The Red Book, 2022-23

The Red Book
Housestaff Manual for Cardiology
Department of Medicine
Massachusetts General Hospital
Harvard Medical School
July 2022 – June 2023
Editors
Krishan Sharma, MD
Christopher Marnell, MD
LETTER FROM THE EDITORS
It is our honor to present the 2022-2023 edition of the Housestaff Manual for Cardiology. Former MGH house
officer, Andrew Sauer, spearheaded the first edition in 2010, with the intention of offering residents a practical
introduction to the major concepts essential to everyday patient care in the Coronary Care Unit (CICU) and the
cardiac Step Down Unit (SDU).
Continuing the efforts of last year’s edition, we hope to present a Red Book that provides an up-to-date,
comprehensive review of core Cardiology topics, yet in a format accessible enough for the busy resident to
pick up and extract critical teaching points to inform their patient care – the core mission the Red Book has
always sought to fulfill.
In 1994, based on the understanding that exceptional patient care is grounded in a rich foundation of evidence,
Albert Shaw and Ravi Thadhani set out to create a reference guide for residents that compiled up-to-date
guidelines for clinical management. This resource, entitled “The MGH Department of Medicine Housestaff
Manual,” has since been updated annually and represents the rigor, autonomy, and pride with which our
residents approach their work. We intend for “The Red Book” to encapsulate these same principles within the
field of cardiology and to pay tribute to the original DOM housestaff manual, now in its 26th year, and known
more affectionately as “The White Book.”
This commitment to well-informed practice is grounded in a genuine desire to understand, connect with, and
improve the lives of our patients, but a more difficult reality emerges when we feel that our efforts have fallen
short. As agents of medical practice, we continuously engage with elusive concepts—illness, intimacy, loss,
grief—and wrestle to ascribe meaning to the intangible. In the year 1980, Dr. Ted Stern, an MGH psychiatrist
and the psychiatric consultant to the medical intensive care unit (MICU), attempted to confront and respond to
these challenges when he purchased a journal, the cover of which was red, and placed it in the MICU. From
then, until 2003, the red book served as a collective forum for resident self-reflection. It supplemented his
weekly “autognosis” (self-knowledge) rounds. After it was filled, seven more volumes followed. Excerpts from
the journals were subsequently complied and incorporated into a book, “On the Edge of Life: Diary of a Medical
Intensive Care Unit” edited by Drs. Mikkael Sekeres (a former MGH house officer) and Ted Stern. While Dr.
Stern’s “Red Book” is no longer in existence, its spirit is still very much alive at MGH, particularly on our
cardiology rotations and exemplified by Dr. Hasan Bazari’s CICU reflection rounds. We hope that this guide will
serve as another reminder to carve out space for introspection and to allow for the projection of kindness and
empathy both inward and outward.
In addition to the individuals mentioned above, we would like to thank the many current and former MGH
housestaff and faculty who have updated and provided original contributions to this guide. We are deeply
appreciative of their dedication, leadership, and commitment, without which “The Red Book” would not be
possible.
The following attending reviewers have provided expert opinion and consultation for past and present editions
of the Red Book:
Kevin Heist Rahul Sakhuja

Sunu Thomas Doreen Defaria-Yeh
Ido Weinberg
We would also like to acknowledge the outstanding leadership of our section editors (bold) and content writers:
Peyton Hanson, Erik Dove ACS and Ischemic Heart Disease

Matthew Nardi, Smirthi Sukumar Heart Failure
Lakotah Hardie, Kyle Saysana Arrythmias and Electrophysiology
Kate Khan, Omar Khan Valvular Heart Disease
Krishan Sharma Vascular Medicine
Chris Marnell, Max Quinn Adult Congenital Heart Disease
Nelson Hsieh, Aditya Achanta Cardio-Obstetrics
Finally, we would like to provide a special thank-you to Dr. Dave Dudzinski, Dr. Jay Vyas, the DOM Chief
Residents, and the DOM Staff for supporting our endeavor.
We hope that this guide will continue to assist with the care of cardiac patients at MGH. As such, it is meant to
serve as a reference to be used in conjunction with other resources and never in place of sound clinical
judgment. Thank you for continuing to provide the highest level of care and compassion to our patients.
Krishan Sharma, MD
Christopher Marnell, MD
The Red Book Editors
2021-2022
Table of Contents
INTRODUCTION TO INPATIENT CARDIOLOGY 6
CCU & SDU Rotation Overview 6
Overview of Cardiac Procedures Relevant to CCU/SDU Patients: 9
ACUTE CORONARY SYNDROMES AND ISCHEMIC HEART DISEASE 11
Classification 11
Diagnosis 12
Management 17
ACS – pharmacologic management 18
Coronary Angiography and Percutaneous Coronary Intervention (PCI) 23
Post-Cath Care 28
Cardiopulmonary Bypass Grafting (CABG) 29
Post-MI Complications 30
Special Populations 34
HEART FAILURE 38
DEFINITIONS 38
HISTORY & INITIAL ASSESSMENT 39
CLASSIFICATION 40
ETIOLOGY 40
HFpEF 45
ACUTE RIGHT VENTRICULAR FAILURE (RV FAILURE) 50
ADVANCED THERAPIES FOR CARDIOGENIC SHOCK: MECHANICAL CIRCULATORY SUPPORT (MCS) 51
INTRA-AORTIC BALLOON PUMP (IABP) 52
ADVANCED THERAPY: LONG-TERM DURABLE MECHANICAL CIRCULATORY SUPPORT (LT-MCS) 54
ORTHOTOPIC HEART TRANSPLANT 56
ARRHYTHMIAS AND ELECTROPHYSIOLOGY 62

Narrow Complex Tachycardias 62
Wide Complex Tachycardias 79
Conduction Diseases and Bradyarrhythmias 86
Device Therapy 91
Electrophysiology Studies and Procedures 104
Quick Reference Guide: Arrhythmias and Electrophysiology 109
Electrophysiology Studies and Procedures 112
Quick Reference Guide: Arrhythmias and Electrophysiology 119
VALVULAR HEART DISEASE 123
Aortic Stenosis (AS) 123
Aortic Regurgitation (AR) 128
Mitral Regurgitation (MR) 133
4
Mitral Stenosis (MS) 140
Tricuspid Regurgitation (TR) 144
VASCULAR MEDICINE 146
Venous Thromboembolism 146
Deep Vein Thrombosis 146
Pulmonary Embolism 148
Catheter-associated thrombosis 150
Peripheral Artery Disease 151
Renal Artery Stenosis 154
Aortic Aneurysm 155
Aortic Dissection 158
Quick Reference Guide: Vascular Medicine 163
Congenital Heart Disease 167
PATENT FORAMEN OVALE (PFO) 168
ATRIAL SEPTAL DEFECT 170
VENTRICULAR SEPTAL DEFECT 171
Basic Physiology of Pregnancy 181
ACLS in Pregnancy 182
Cardiac Medications during pregnancy 184
Peripartum Cardiomyopathy (PPCM) 184
Arrhythmias in Pregnancy 187
Pregnancy and Acute Coronary Syndrome 187
5
Introduction to Inpatient Cardiology
TOC
INTRODUCTION TO INPATIENT CARDIOLOGY

CCU & SDU Rotation Overview
Heart Center Overview: The MGH Corrigan Minehan Heart Center comprises 5 inpatient units. Residents rotate in two
(see below)
- Blake 8 Cardiac surgical ICU
- Ellison 8 Cardiac surgical Step-Down Unit
- Ellison 9 CCU (residents)
- Ellison 10 Cardiac Step-Down (residents)
- Ellison 11 Cardiac "Access" Unit
Introduction to the Ellison 9 CCU:

- 16 bed ICU staffed by distinct Red and Blue teams
- Triage decision re: Red v Blue made by HCICU intensivist (some fluidity based on overall team census and
attending preferences)
Staffing Team Cap Case Mix

CCU Red ● HCICU - ● Post-op cardiac surgery
intensivist ● Advanced HF pts pre/post VAD
● APP ● Advanced HF pts pre/post-transplant
● Heart Failure ● Cardiogenic shock requiring temporary MCS
consult team
● IM resident(s)
on elective
CCU Blue ● CCU 12 (hard cap) ● ACS (no MCS)
Attending* +/- ● Unstable arrhythmia
MICU ● Severe valvulopathy
attending ● Pericardial disease
● MGH/Brigham ● Post-cardiac arrest
cardiology ● Cardiogenic shock (no MCS)
fellow ● MICU 'boarders'
● SAR
● 4 JARs
*Blue attending is often a cardiologist without specific critical care training, may consult the HCICU intensivist for input re:
ventilation, sedation etc.
CCU Blue Team Roles:

● SAR: Primarily responsible for leading rounds, maintaining the handoff, supervising procedures, interfacing with
families, and running codes
● JARs: Rotate through a q4 call schedule as detailed below (Call->Post->Swing->Pre/Plan). Responsibilities include
admitting patients, performing procedures, running plan on rounds, and doing swing.
● Call JAR: Arrives at ~7am and admits until team arrives at 7a the next day, except for new patients that arrive during
rounds if there is a swing JAR present (goal is to keep call JAR on rounds to understand plans and contingencies
going into the night). Depending on attending preference, will usually check in with CCU attending by phone around
~10pm. Sends 5am email and leaves after presenting new admissions on team rounds at 8a.
● Swing JAR: Arrives at ~7am, protects rounds by admitting new patients that arrive during rounds and performing
swing tasks including procedures (depending on experience/comfort). Usually stays through PM rounds
● Pre/Plan JAR: Presents established patients on rounds and signs progress notes. Leaves first, often before PM
rounds. Usually has one afternoon of clinic during the block. Performs afternoon swing tasks if Swing resident is off
Codes in the CCU:

● Day: Run by the native CCU Blue SAR (with support from the CCU fellow, Senior On, and JARs)
● Night: Run by the cardiology night teach/Senior On or overnight fellow (OA will page Senior On/Cardiology Night
Team, fellow/call JAR runs the code until NT arrives)
Codes outside the CCU:

● Day: Call JAR goes to codes on the floors--primary responsibilities are to monitor pulse, place I/O (will be brought by
the MICU intern) and assist as otherwise directed by the senior on/code whisperer.
● Night: Call JAR does not go to codes since they are the only resident on the floor
6
Chris Marnell, Krishan Sharma
TOC
Overnight Support: There are many layers of overnight support in the CCU, each useful in different circumstances
● Cardiology Night Teach: Beginning in AY 2021-2022 there will be a dedicated NT for the CCU and SDU. Can be
contacted for procedural supervision, general cardiology, or critical care questions, or if needing support for
admissions (NT can either help stabilize patients or coordinate with chiefs to hit in an additional admitting resident).
The Cards NT is also responsible for running codes in the CCU overnight and will be paged by the OA
● Overnight Cardiology Fellow: There is now an in-house 1st or 2nd year cardiology fellow who covers the CCU and
SDU in addition to seeing consults on the floors/ED and performing STAT TTEs. The fellow should be first call for
issues with Blue team patients and can help mobilize other cardiology resources as needed (i.e., cath lab, temp wires,
etc.) and guide outreach to other subspecialists overnight.
● Access Fellow: Dedicated in-house fellow who covers the Ellison 11 Access Unit and is first-call for access site
complications on cardiac patients across the hospital (bleeding, suspected ischemia distal to access site, any
questions about TR bands, etc.). They will come hold pressure for access site bleeds (resident not expected to hold
pressure for prolonged periods) and will help direct further management.
● CCU Attending: The native CCU Blue attending can and should be contacted for high-level management questions
on established Blue patients, particularly if there is disagreement with the overnight fellow or if a patient is complex
(the overnight fellow most often will not know the patients). Most attendings will plan a scheduled phone check-in at
~10pm but will remain available thereafter. The Blue attending should also be contacted if needing to involve the
HCICU intensivist or Shock team overnight.
● HCICU intensivist: Available in-house overnight and can be consulted for critical care issues on Blue team patients
(need for intubation, vent/sedation issues, difficult procedures, troubleshooting mechanical support devices). Also
holds the Shock/ECMO consult pager and is responsible for Blue/Red triage decisions.
● Overnight Intensivist: In-house intensivist covering MICU boarders in the CCU (for critical care questions on CCU
Blue team cardiology patients, contact the HCICU intensivist). Available for general management questions, to
supervise procedures, to staff new MICU admissions.
● CCU Red APP: Cardiac surgery PA/NP who sits in the Red Team office near the double doors at the CCU entrance.
Can be a useful resource for questions regarding post-op patients and for help troubleshooting MCS devices.
Tips for CCU Admission/ Presentation:

● Provide the cardiac history in chronological order
● Have details on prior cardiac studies available
● Treadmill stress test: remember to include duration of exercise, METS achieved, HR (and % maximum), BP, peak
double product (“good test” > 20k), EKG/imaging
● Echo: TTE or TEE, EF, valves, wall motion abnormalities, wall, and cavity dimensions (IVS, LVID) and atrial
dimensions
● Catheterizations: Go anatomically! Right heart cath values first in the order obtained (RA, RV, PA, PAOP), then LV
gram results, then coronary angiography (Left main, LAD, LCx, RCA) finally, interventions and complications
● CABG: anatomy is critical; if OSH surgery, you must obtain a copy of the operative report or post-CABG angiogram
● Print relevant EKGs (including a baseline) for review on rounds
Tips for daily CCU rounds:

● Ensure each patient has daily EKG, and ideally print them (SAR can choose whether plan/call/swing JAR does this)
● Find patient’s RN prior to rounding on each patient (often Swing JAR task)
● Engage nursing at bedside, similar to MICU rounds
● Offer a suggested plan but recognize these patients are complicated, and often there are many possible approaches
7
TOC
Introduction to the Ellison 10 SDU: Ellison 10 is a 36-bed cardiology unit which admits patients with primary cardiac
disorders and serves as a step-down unit for the Ellison 9 CCU. Patients in the SDU are cared for by two equivalent
housestaff teams (Red and Blue) and an EP team.
SDU Team Structures: Each team is composed of 1-2 day interns, 2 JARs, 1 SAR, and 1 attending. There is also an
embedded cardiology fellow dedicated to teaching both teams. The Blue and Red teams alternate admitting days. The
JAR admitting cycle is: long rounding – long admit – short rounding – short admit.
Admitting Team roles:

● Day intern: pre-rounds on 2-4 patients with SAR supervision and presents at 8 am rounds. Assigned 1-2 admissions
during the day that are supervised by the SAR and formally staffed in the afternoon.
● Short admit JAR: Arrives at 7 am signs into admitting pager (31010), pre-rounds on list, and card-flips patients
following presentation of overnight admissions. Admits 3 patients until 3:00 pm. The first admission of the day will
typically go to the day intern. Short Call admissions should be staffed with the attending on the day the patients are
admitted, if possible. They sign out to the SAR (if finished before 7:00 pm) or the NF JAR (if finished at 7:00pm).
● Long admit JAR: Arrives at 7 am and card-flips patients after short admit JAR. Begins admitting at 3 pm (or earlier of
short admit is capped) and can admit up to 4 patients before 7 pm. Admissions not staffed the same day will be
passed off to the NF team and formally presented the following morning. Any admissions over-cap will be passed off
and stabilized by the Long SAR and passed off to the NF team.
● Long SAR: supervises admissions, oversees discharges,
Rounding Team roles:

● Day intern: rounds on their list of 2-4 patients and may sign out to Long rounding JAR when swing is complete
● Short rounding JAR: Arrives at 7 am, pre-rounds, and presents any new patients from prior day (when they were
Long admit JAR) at morning rounds, may pass off their list to Long rounding JAR when swing is complete
● Long rounding JAR: Arrives at 7 am, pre-rounds on patients and card-flips after new patient presentations. Takes
pass off from the Day Intern and Short Rounding JAR once they are done with swing and ready to pass off. If the EP
team is available to pass off prior to 7 pm, they will pass off to the Long Rounding JAR to pass off to the NF JAR. The
Long Rounding JAR passes off to the NF team
● Short SAR: supervises day intern rounds, attends case management rounds at 10:30 am oversees discharges
Overnight Support: please refer to the SDU Night Float guide for full details
● Cardiology Night Teach will see and staff all admissions performed by SDU NF interns (JAR does not have to formally
staff)
● For access site issues 🡪 Access fellow
● For acute clinical change requiring a cardiologist within 30 minutes 🡪 in-house cardiology fellows
● For EP patients 🡪 EP Fellow, they may independently request assessment by other in-house cardiology staff
8
TOC
Overview of Cardiac Procedures Relevant to CCU/SDU Patients:
Coronary angiography +/- PCI:

● Indications: Acute coronary syndromes, chronic coronary syndromes refractory to medical therapy or with high-risk
features, workup of heart failure or unexplained ventricular tachycardia, others
● Procedure overview: Arterial access established via radial or femoral arteries, coronary ostia engaged with catheters
and angiogram performed with injection of iodinated contrast under fluoroscopy. Functional assessment of stenotic
lesions sometimes performed with fractional flow reserve (FFR) or instant wave free ratio (iFR) techniques. If
indicated, stents will then be deployed, and the patient loaded with a P2Y12 inhibitor.
● Pre-procedure planning:
● NPO @ MN
● Anti-coagulation management (source: MGH Cardiac Cath Lab Anticoagulation Guidelines, available on Ellucid)
● Questions for pass-off: Procedure (diagnostic findings and interventions), Access (Where and what size access was
used? High stick? Do you want the sheaths pulled? When? By whom? At what PTT? Duration of bedrest? Closure
devices used? TR band in place?), Anticoagulation (What was used in the case? Do you want heparin or bivalirudin
restarted?), Antiplatelets (Was the patient loaded with a P2Y12? What should be ordered going forward?)
Complications?
● Post-procedure evaluation: Check groin yourself for expansile mass, tenderness, bruit (suggestive of
pseudoaneurysm). Document full bilateral neurovascular exam
● Key complications to watch out for: Access site bleeding, retroperitoneal hematoma, arterial pseudoaneurysm, limb
ischemia, coronary perforation resulting in tamponade
● Contingencies: For an acute access site bleed, hold pressure proximal to arteriotomy (several cm proximal to skin
puncture), page fellow who performed procedure (day) or cardiac access fellow (night)
For any procedural/access questions, first port-of-call for help should be cardiology or interventional cardiology
fellow.
Right Heart/Pulmonary Artery Catheterization

● Indications: Suspected cardiogenic shock, pulmonary hypertension, pericardial disease, worsening renal function in
decompensated HF, others
o Must be inserted in cath lab (rather than bedside) if: LBBB, severe PH (PAP>70mmHg), large RV, PPM/ICD,
temp wire, severe TR, prosthetic TV/PV
o Contraindications: RA/RV mass/thrombosis, mechanical TV/PV, endocarditis (TV/PV)
● Procedure Overview: ~8Fr venous sheath ("Cordis") inserted under ultrasound guidance in central vein (RIJ>LIJ>L
subclav>femoral), pulmonary artery catheter inserted into SVC, balloon tip inflated, catheter advanced under
fluoroscopy or while monitoring hemodynamic waveforms until wedge tracing obtained, balloon deflated, line then
removed or secured in place
● Pre-procedure Planning:
o NPO @ MN
o Considered a "low bleeding risk" procedure (relative to procedures requiring arterial access), though
anticoagulants should still be held per the MGH cath lab anticoagulation guidelines listed above
o Need to decide and communicate to cath lab whether you want a one-time diagnostic RHC or "PA line to
stay"--note that PA catheters only allowed in the CCU and Ellison 11.
● Questions for pass-off: Results (i.e. hemodynamics measurements--be sure to note whether reported values were
taken at end-expiration or as the mean value across the respiratory cycle), Access (Where and what size? Sheath
still in place? Should they be pulled? By whom? At what PTT? Activity restrictions?), Anticoagulation (when to
restart), Complications
● Post-procedure evaluation: Examine access site, if line left in place ensure balloon deflated and obtain CXR
(waveform more useful than CXR to assess initial position but helpful to have a baseline in case of issues later)
● Key complications to watch out for: infection, bleeding, PTX, VT, RBBB, CHB, PA rupture (place patient on side with
the catheter “bleeding side down”, order STAT CXR, CBC, coags, CT surgery consult), pulmonary infarct, PE
9
TOC
TAVR (Transcatheter aortic valve replacement):

● Indications: Severe aortic stenosis with symptoms or other high-risk features (see Aortic Stenosis section for full list of
indications)
● Procedure Overview: Femoral artery access obtained using a 14F sheath or greater, transvenous access obtained
and RV pacing wire placed, guide wire placed across aortic valve and dilation performed, prosthesis moved into
position under fluoro + TEE or TTE guidance, rapid ventricular pacing (>180bpm) initiated to decrease stroke volume,
allowing valve to be deployed. Valve either self-expands (Medtronic CoreValve) or is expanded with a balloon
(Edwards Sapien).
● Pre-procedure Planning:
o Standard pre-TAVR workup: TTE, coronary angiography +/- RHC, carotid duplex, CT surg consult,
Panorex + dental evaluation
o Note presence of pre-existing conduction disease, increasing the likelihood of pt requiring PPM post-
TAVR
o NPO @ MN for procedure
o Anesthesia plan (MAC vs general)
● Questions for pass-off: Results (successful? Type and size of valve? Presence of paravalvular leak?), Access
(Where and what size? Sheath still in place? Should they be pulled? By whom? At what PTT? Activity restrictions?),
Anticoagulation (when to restart), Antiplatelets (what is antiplatelet plan? typically DAPT) Complications (Access
site bleeding, paravalvular leak, new/worsening heart block)
● Post-procedure evaluation: Examine access sites, document peripheral pulses, EKG to assess for new/worsening
heart block, screening neuro exam
● Key complications:
o "Big 5" TAVR Complications: Bleeding, stroke, paravalvular leak (PVL), AKI, Complete Heart Block
o "Suicide LV": Acute LVOT obstruction resulting from relief of fixed afterload which unmasks increased
contractility from chronically hypertrophied ventricle, resulting in reduced CO and shock (treat similar to
hypertrophic cardiomyopathy with LVOT obstruction, i.e. fluids, beta blockers, phenylephrine)
o Differential for shock after TAVR: Bleeding, aortic annular rupture, severe PVL, acute MI from inadvertent
occlusion of coronary ostia, suicide LV (examine access sites, EKG, stat TTE)
Pulmonary vein isolation:

● Indications: Symptomatic atrial fibrillation with failure or intolerance of anti-arrhythmic drugs
● Procedure Overview: Bilateral femoral venous access obtained, ablation catheters inserted from the RA->LA via atrial
septal puncture, pulmonary veins isolated via radiofrequency or cryoablation. Additional lesions sometimes created
such as with a posterior wall isolation. Venous access sites often occluded with sutures locked in place via stopcocks.
● Pre-procedure Planning: Patients typically brought in by EP as outpatients then admitted to the SDU for one night
post-procedurally
● Questions for pass-off: Results (PVI alone or additional lesions?) Access and closure technique (typically b/l
femoral veins occluded with stopcocks), Anticoagulation (when to restart patient's DOAC or warfarin),
Complications (any concern for perforation or effusion? TTE performed during procedure?) Meds: (Pred taper?
Sucralfate?)
● Post-procedure evaluation: Examine groin sites, ensure stable blood pressure (high index of suspicion for
perf+tamponade)
● Key complications to watch out for:
o Acute: Access site bleeding, stroke, perforation + tamponade (resulting from excessive overheating of
atrial tissue or catheter puncture)
o Subacute: atrio-esophageal fistula (presents with sepsis, endocarditis, air emboli, or GI bleeding 1-6
weeks after PVI), pulmonary vein stenosis (dyspnea, cough, hemoptysis 2-5 mo after PVI)
o For any significant or sustained hypotension following PVI, page EP for consideration of formal TTE to r/o
tamponade (EP will either do it themselves or ask gen cards fellow to do so)
10
ACS/IHD
TOC
ACUTE CORONARY SYNDROMES AND ISCHEMIC HEART DISEASE

If you suspect ST-elevated myocardial infarction (STEMI) in an admitted patient:
● Call a Rapid Response
● If true STEMI, call 6-8282. This puts you in touch with the interventional attending (if after hours) or the cath lab
charge RN (if during business hours), who can help guide the next steps (i.e. cath lab activation)
● If there is uncertainty about the ECG meeting STEMI criteria, STAT page the general cardiology fellow on call.
On-call cardiology assignments can also be viewed through amion.com, password mghcard
Classification
Angina pectoris: Chest pain caused by myocardial oxygen demand outstripping myocardial oxygen supply.
● Classically: 1) Substernal, 2) Worsened with exertion, 3) Relieved by rest or nitroglycerin
● Stable angina: Occurs predictably at a certain level of exertion and is relieved with rest or nitroglycerin
Acute coronary syndrome (ACS) This is commonly subdivided into non-ST-elevation ACS (NSTE-ACS) – including
unstable angina or NSTEMI – or STEMI. Important features that can distinguish NSTE-ACS from stable CAD.
o Rest angina, which is usually more than 20 minutes in duration
o New onset angina that markedly limits physical activity
o Angina that is more frequent, longer in duration, or occurs with less exertion than previous angina
● STEMI: Designates an MI in patients with chest discomfort or other ischemic symptoms, who develop EKG changes
denoted in "Diagnosis" Section. Often denotes acutely occluded coronary artery from thrombus arising from plaque
disruption or erosion or rarely thromboembolism
● NSTEMI: MI without ST-segment elevation
● Unstable angina: ACS without biomarker elevation
Joint Task Force Classification of Myocardial Infarction JACC 2018;72(18):2231-2264:

● Type 1: Spontaneous MI. Atherosclerotic plaque rupture, ulceration, fissuring, erosion,
or dissection causing intraluminal thrombus in 1+ coronary arteries.
● Type 2: Demand MI. Myocardial injury with necrosis in which a condition other than
CAD contributes to an imbalance between myocardial O2- supply and demand
● Type 3: MI resulting in death but biomarkers unavailable with symptoms suggestive of
MI including new ischemic ECG changes or new LBBB
● Type 4a: MI related to PCI (with cTn > 5x 99th-percentile URL)
● Type 4b: MI related to stent thrombosis.
● Type 4c: MI related to PCI after initial successful PCI due to restenosis or complex PCI
● Type 5: MI related to CABG (with cTn > 10x 99th-percentile URL)
History
When evaluating patients with chest pain for ACS:
● Typical ischemic chest pain: Commonly meets angina characteristics. OPQRST
mnemonic: HYPERLINK
o Onset: Gradual "https://jamanetw
o Provocation/palliation: Provoked by an activity; not changed with respiration or position ork-com.ezp-
o Quality: Substernal pressure (squeezing, burning or tightness)
prod1.hul.harvard
o Radiation: Radiates to the shoulder, neck, jaw, or either arm (may also be inter-scapular
or epigastric) .edu/journals/jam
o Site: Not felt in one specific spot, but diffuse discomfort a/fullarticle/24688
o Time course: Angina (2-5 min), 96"JAMA 2015;314(18):1955-
1965
● Atypical chest pain: Falls short of meeting all three criteria
o Common presentation of ACS, with 10% of individuals reporting dyspnea alone.
o More common in women, elderly, inferior MI, and patients with diabetes
o May rarely present with fatigue, lethargy, syncope, AMS, CVA/TIA, or GI distress
● Non-ischemic chest pain:
o Quality: Pleuritic, sharp, or reproducible with palpation
o Timing: Occurring with cessation of exercise or lasting only seconds or >6 hrs.
o Context: Without evidence of myocardial damage by biomarkers. Chest pain that is not
ischemic may represent other life-threatening etiologies of chest pain, such as aortic
dissection, PE, or pneumothorax. Alternative diagnoses should be ruled out before
disregarding chest pain.
Erik Dove, Peyton Hanson

Heart Failure
TOC
Diagnosis
A. Physical Exam: Exam findings do not predict ACS reliably
● Signs w/ high pre-test probability for CAD: S4, Levine’s sign, signs for disease in other vascular beds
● High-risk features in ACS: syncope, new HF (S3 gallop, rales, or elevated JVP), possible mechanical complication
such as papillary muscle or ventricular septal rupture (sinus tachycardia, hypotension, elevated JVP, or new systolic
murmur)
B. 12-lead ECG: 50% of patients with MI have a normal or non-

diagnostic ECG on presentation, repeat q10-15m if ongoing sx
a. Right sided leads: For RV infarction. Inferior STEMI + V1
STE +/- V2 STD
b. Posterior leads: For posterior MI. STDs in V1-V3, R/S ratio
>1 in V1-V2
NSTEMI ECG Criteria: (Left) Right-sided leads, (Right) Posterior leads

● New horizontal or down-sloping STD of ≥ 0.5mm
● TWI ≥ 0.1mm with a prominent R-wave or R/S ratio > 1 in ≥ 2 contiguous leads
STEMI ECG Criteria: (≥1 of the following)

● New STE: measure ST segment 80ms (2 small boxes) from the J-
point (inflection point between S-wave and ST segment) in 2
contiguous leads
● Pathologic elevations > 1 mm except V2, V3 (M: > 2 mm, F > 1.5)
● *Patients may demonstrate elevations in the anterior precordial
leads (V1–V3) which is NOT pathologic2
● New LBBB
● Posterior MI defined by STD in ≥2 V1–V4. Check posterior leads ECG evolution in STEMI
Sgarbossa Criteria: Used to diagnose AMI in LBBB/Paced Rhythm

● Normal: ST segment should be discordant with the QRS complex.
● Sgarbossa criteria:
o STE > 1mm concordant with QRS in any lead = 5 points
o STD > 1mm concordant with QRS in V1, V2 or V3 = 3 points
o STE > 5mm discordant with QRS in any lead = 2 points
Total Sgarbossa criteria point score ≥ 3 yields 90% specificity and 88% PPV for MI,
but notably only a sensitivity of 20%.3
Localization of Injury (Zimetbaum et al. NEJM 2003;348)

● Contiguous STE may indicate which vessel is involved.
● STE correlate better with a vascular territory than STD or TWIs.
Category Anatomy of Occlusion ECG Findings
Proximal LAD Prox to 1st septal STE V1–6, I, aVL +/– BBB
(antero-lateral MI) perforator
Mid-LAD Distal to 1st septal STE V1–6, I, aVL
(antero-lateral MI) perforator, prox to 1st diag
Distal LAD/Diag Distal to diagonal or
STE V1–6 or I, aVL, V5–6
(apical MI) diagonal itself
High Lateral MI Proximal LCx STE I, aVL +/– V5, V6
“Apical” MI
Distal LCx STE V5, V6
(Low lateral MI)
STE II, III, AVF and:
1. V1, V3R, V4R (RV)
Large Inferior MI Proximal RCA (90%) or LCx (10%) 2. V5-V6 (inferoapical)
3. R>S V1-2, STD V1-V3,
STE V8 (inferoposterior)
Small Inferior MI Distal RCA, LCx branch STE II, III, aVF
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STE >1 mm in aVR AND STE in aVR > V1

Critical Left Main Dz Left main
OR widespread STD
Other Notable ECG patterns:

Pre-existing RBBB: Terminal ST-segments should not be affected by RBBB. Interpret ischemia on ECG as if no BBB. If
deep discordant STD in V1-V3, check posterior leads.
deWinter’s T-waves (2% of STEMIs): Tall symmetric T-waves + >1mm STD at J-point in precordial leads + 0.5-1mm STE
in aVR, may evolve to STEs, consistent w/ acute LAD occlusion.
Wellen’s Pattern: Biphasic T waves (25%; Type A) or symmetric, deeply inverted T waves (75%; Type B) in V2, V3
Wellen’s Syndrome: Wellen’s pattern in patients with resolved CP 🡪 indicates reperfusion of myocardium consistent with
acute LAD occlusion. 75% of pts will have anterior MI in days to weeks if not treated. Do not stress these patients.
● DDx Wellen’s: apical HCM, coronary vasospasm, elevated ICP (long QTc), MI, PE, post-tachycardia/pacing, BBB,
WPW, idiopathic.
DDx ST Elevations DDx ST Depressions
Acute MI Takotsubo/stress cardiomyopathy Ischemia, NSTEMI
Vasospastic Angina Massive PE (V1, V2 occasionally) Posterior wall MI
Benign Early Repolarization Brugada pattern (V1–V3 with RBBB) Digoxin effect
Acute Pericarditis Tumor or Trauma Pericarditis
LVH or LBBB V-paced rhythms LVH or LBBB
LV Aneurysm Hypothermia (Osborn/J wave) LV Aneurysm
Myocarditis Post-DC cardioversion (rarely) Myocarditis
Hyperkalemia (V1, V2) Hypercalcemia (rarely) Hypokalemia
C. Cardiac Biomarkers
Troponin: At MGH, use a high-sensitivity troponin T (hsTnT) assay. An elevated troponin is defined as: hsTnT ≥10 ng/L (in
F) and ≥12 ng/L (in M).
● Peaks within 12-48 hours and returns to normal within 5-14 days. Reaches peak more quickly when revascularized,
more slowly when not.
● Converting numbers between assays (4th generation to hsTnT assay): for > 0.01 multiply by 1000 to get hsTNT
o For values < 0.1, remember: cTnT value of 0.01 ng/ml 🡪 hsTnT of 30 ng/L, 0.03 ng/ml 🡪 hsTnT of 53 ng/L
How to Use hsTnT:
● DO NOT wait for troponin if high suspicion for ACS (classic pain, ECG changes) 🡪 immediately start treatment
● Order troponin at presentation + 3hr repeat. Check after 1hr if worried
● A rising OR falling value (delta) ≥ 5 w/ symptoms or ECG changes 🡪 consider ACS.
● If baseline troponin >99th percentile (more common in CKD or left ventricular hypertrophy patients; mechanism of
action (MOA) not completely understood), a rise and fall of 20% is suggestive of MI. As with the general population
and hsTnT, the “delta” in troponin values is critical to determine the likelihood of an acute coronary syndrome
CK-MB: CK-MB peaks within 24 hrs and normalizes within 48-72 hrs. At MGH, CK and CK-MB are no longer used
routinely except post-PCI (or post-alcohol septal ablation) to evaluate for infarct size or when reinfarction is suspected.
D. Risk Stratification for non-ACS patients with chest pain: for patients with chest pain who do not meet above
criteria for ACS, use HEART score – estimates 6 week risk of MACE 🡪 score >3 consider for non-invasive or stress
imaging
● When compared to TIMI and GRACE, the HEART score was superior at identifying low risk patients, with
negative predictive value > 98% for MACE with 1 single troponin (Int J Cariol 2017;227:656)
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E. Non-invasive Testing
Schematic Approach to Noninvasive Cardiac Testing (adapted from UpToDate)
Stress testing
● Indications:
o Diagnose CAD: sx of stable angina in pts with intermediate-high risk of CAD. Not indicated for low risk or
asymptomatic pts
o Evaluate new or changing sx concerning ischemia in pts with known CAD
o Post-revascularization: evaluate pts with ongoing/recurrent angina or asymptomatic pt if incomplete revasc
o Pre-op risk assessment: not routinely indicated (see Perioperative Medicine)
o Newly diagnosed HF or cardiomyopathy likely due to ischemia, functional capacity (for exercise prescription),
viability testing, valvular disorders
● Contraindications: untreated ACS, MI within 2d, high risk or LM CAD, uncontrolled arrhythmia, acute CHF, recent
DVT/PE, acute myo-/peri-/endocarditis, aortic dissection, uncontrolled HTN
● Preparation: NPO 3h prior, longer if imaging or adenosine. Must reverse DNR/DNI for test. Hold caffeine >12h for
adenosine, > 24h for dobutamine.
o “Does the patient have CAD?” ⭢ hold BB and nitrates
o “How well are meds working in known CAD?” ⭢ continue BB and nitrates
● Caveats:
o Majority of vulnerable plaques are angiographically insignificant (<70% stenosis) ⭢ stress testing unable to
identify the presence of these plaques (CTA more sensitive). CTA may be helpful to rule-out LM disease.
o Angiographically significant (>70% stenosis) 3 vessel disease may produce false-negative vasodilator stress test
⭢ ”balanced ischemia”
● Positive test results: optimize medical tx. Decision re: angiography/revascularization varies by pt.
o ISCHEMIA trial: revascularization did not decrease ischemic CV events for pts with stable CAD (NEJM
2020;382:1395)
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a. Exercise Tolerance Test (ETT) Stress = exercise, Imaging = EKG, SPECT, TTE
i. ETT preferred over pharmacologic testing if pt is able to reach goal exertion (Bruce protocol or modified Bruce)
ii. Assesses exercise duration, METs, BP/HR response, HR recovery, double product (HR x SBP)
iii. Diagnostic: >85% max-predict HR (220-age), peak double product (HRxBP) >20k, HR recovery (HRpeak – HR1min
post-exercise) >12
iv. Increased probability of ischemia: # of leads with STD, degree of max STD, METs when EKG changes
occur, ventricular ectopy during recovery, increased time to recovery of EKG, failure of SBP to rise with exercise
b. Pharmacologic Stress Test Stress = pharmacologic, Imaging = TTE, SPECT, PET, or MRI
i. Choosing an agent:
1. Adenosine/Regadenoson (act via cAMP): stenosed coronary arteries are already maximally dilated, so flow
is “stolen” by healthy vessels (“coronary steal") relative perfusion deficit
a. Side effects: wheezing, bradycardia, HoTN. Caution if ACTIVE bronchospasm, high grade AVB, SSS,
severe AS
b. Regadenoson: decreased respiratory/conduction side effects, more cost-effective in obese pts. Caution if
seizure hx (reversal agent aminophylline seizure risk)
2. Dobutamine: workload induced by positive inotropy and chronotropy via β-1 receptor agonism
a. Extremely high dose of dobutamine is given, dose titrated up to 40 mcg/kg/min
b. Side effects: tachyarrhythmias. Caution if MI<48h, hx of malignant arrhythmia, severe AS, HOCM, severe
HTN, severe PAH, aortic dissection
c. Choosing an imaging modality:
i. Nuclear imaging: utilizes a radioactive tracer to detect areas of perfusion between rest and stress states. More
expensive than TTE and high amount of radiation (SPECT > PET).
ii. PET (92.6% Sn/ 81.3% Sp) is more sensitive and specific than SPECT (88.3% Sn/ 75.8% Sp) with faster image
acquisition. Less widely available and most expensive. Additional uses for imaging in rheumatologic (i.e. cardiac
sarcoid) and oncologic contexts (i.e. cardiac myxoma, metastases)
iii. TTE: Reasonable test characteristics to exclude CAD (76% Sn / 88% Sp). May be helpful for
hemodynamics/valve disorders.
1. Do not use in pts with LBBB, V-pacing or extensive wall motion abnormalities at rest.
Viability Testing
● Up to 20-40% of patients with CAD and LV dysfunction may demonstrate improved function after revascularization.
This is thought to be due to viable myocardium that lacks adequate perfusion (“stunned/hibernating myocardium”). In
contrast, necrotic myocardium is unlikely to benefit from reperfusion. Does not require stressor.
● Indication: determine viability of ischemic myocardial tissue (“hibernating myocardium”).
● Use is controversial since myocardial viability testing did not identify pts w/ a different survival benefit from CABG
compared with medical therapy alone (STITCH trial). Some argue that may have been due to type of viability study
used (i.e. SPECT)
● Imaging modalities: FDG PET, dobutamine TTE, cMRI
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Rest Imaging
● Coronary CTA: used to evaluate for presence and extent of CAD (JACC 2010;55:2663).
● Unlike stress imaging, CCTA is an anatomic assessment, not a functional assessment.
● CT-Fractional flow reserve (FFR). FFR is most validated as an invasive assessment during coronary
angiography. It can be computed on CCTA to determine the hemodynamic relevance of stenosis. FFR derived
from CCTAs closely mimic invasive FFR and may provide some functional data; however, data are limited and
there remain limitations (e.g. ostial lesions)
● Requires cardiac gating (goal HR 60-70, may need to give BB) and respiratory gating (breath hold for 5+ sec) and
vasodilators (nitroglycerin)
● Indications:
o Low to intermediate risk patients in the ED who present with new CP (i.e. to rule out ACS)
▪ Low risk pts: has high NPV (99%) for CAD rule-out (JACC 2008;52:1724)
▪ Moderate risk pts: reasonable for further risk stratification in pts at intermediate risk of CAD or pts with
equivocal stress test results
o Others: Assess patency of CABG, assess for anatomical abnormalities (e.g. course of anomalous
coronaries), CTO planning
● Findings: 2 yr. ACS risk significantly elevated if high-risk plaque (16%) and/or stenotic disease (6%)
(JACC 2015;28:337)
o Higher sensitivity and specificity for coronary stenosis compared to cMRI (Annals 2010;152:167)
● Limitations: calcified coronaries, prior stents (“blooming artifacts”)
● Coronary Artery Calcium (CAC) Scans: CT modality that provides risk assessment score (CAC or “Agatston”
Score) for coronary artery disease. Either performed alone or concurrently with coronary CTA. Non-gated, non-
contrast chest CT scans can be used to provide a qualitative estimation of CAC (Agatston score).
● Indications: To guide in decision making for primary prevention for asymptomatic adults ≥40 years of age at
intermediate risk (7.5 to 19.9 percent 10-year ASCVD risk) if statin therapy decision remains uncertain.
● Do not use: stand-alone test in evaluation of symptoms of myocardial ischemia, other high risk atherosclerosis
patients e.g. familial hypercholesterolemia.
● Findings:
o Agatston scores ≥100 or >75 percentile for age and gender independent of ASCVD risk 🡪 lifestyle changes, risk
factor modification (BP, smoking DM tx), and statin therapy. (JACC 2019;73:285)
o For those with calcium score of 0, reasonable to defer statin therapy for up to 5 years (Circ 2019; 140:496)
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Management
A. Myocardial Injury Without Ischemia
● Evaluate for non-ACS causes of elevated troponin (UpToDate)
B. Stable Ischemic Heart Disease

Anti-Anginal Therapy
● Beta-blockers: 1st line therapy to reduce anginal episodes and improved exercise intolerance.
o Relieve anginal symptoms by decreasing O2-demand (reduce HR and contractility)
o All beta-blockers are effective.
▪ Atenolol may not be cleared in renal dysfunction. May cause less fatigue.
▪ Metoprolol XL should be at least BID
o Improve survival in patients who have had MI or impaired LV (in HF, metoprolol XL, bisoprolol, or carvedilol
are only indicated BB)
● CCB: Add-on therapy to BB if ongoing ischemic symptoms
o Causes coronary artery dilation, reduces contractility
o Diltiazem, verapamil, or amlodipine are preferred
o Short acting dihydropyridines (nifedipine) should be avoided unless using with a long acting BB due to the
increase in mortality seen in patients after MI or increase in MI in those treated for hypertension
● Nitrates: SL nitro should be provided for patient for acute episodes. Long-acting nitrate can be added to daily regimen.
● Ranolazine: Additional anti-anginal add-on therapy
o Inhibits late sodium channel (which frequently fails to inactivate in many myocardial diseases and results in
disturbances of ion homeostasis)
o Initial dose is 500 mg BID but can be increased to 1000 mg BID
o Effective but expensive
Preventative therapy: ASA, statin, ACE/ARB (HTN, DM, HFrEF, CKD), CVD risk factor reduction, flu shot
PCI/CABG:
● Elective for refractory or severe symptoms, change in symptom severity, high-risk coronary anatomy, LV dysfunction
(PCI or CABG as appropriate)
● Mortality: No convincing evidence [ISCHEMIA trial (NEJM 2020;382), COURAGE trial NEJM 2007;356] that
revascularization improves mortality in patients with SIHD as defined by study
o ISCHEMIA excluded: LVEF <35%, LM > 50%, “unacceptable angina,” recent onset CCS III
angina/progressive angina/CCS IV angina, ACS within 2 months, PCI within 12 months, NYHA III-IV, recent
stroke, ESRD, valvular disease, many prior CABG patients.
● Symptoms: For patients w/o adequate control of anginal symptoms with optimal medical therapy PCI and CABG have
been shown to improve symptoms in two trials MASS II (J Am Coll Cardiol 2004;43) and ISCHMIA (NEJM 2020%3B
382). The ORBITA trial (Lancet 2018;391) shows no benefit in anginal symptoms with PCI, but has been highly
criticized.
C. ACS (UA/NSTEMI/STEMI)
Pharmacologic Management: All pts (w/o contraindications) should immediately receive the following:
1) ASA 325 mg, chewed/crushed
2) Atorvastatin 80 mg
3) Heparin (ACS protocol)
4) Nitroglycerin – careful in patients with low-normal SBP + large RCA MI
*Decisions regarding P2Y12 inhibitors and other medications should be had in conjunction with cardiology.
Coronary Angiography: All pts w/ ACS should undergo angiography during hospitalization - Optimize medical therapy
(see ACS – PHARMACOLOGIC MANAGEMENT), PCI (see section), or CABG (see section).
● Directly to Cath Lab:
● STEMI
● UA/NSTEMI accompanied by high-risk feature: Cardiogenic shock, refractory CP, electrical instability (frequent
NSVT, unstable SVT, or sustained VT)
● If the patient has UA/NSTEMI that does not meet criteria for immediate coronary angiography, risk stratify.
● TIMI (JAMA 2000;284:835) and GRACE (BMJ 2006;333:1091) At MGH, the TIMI Risk Score is most often used.
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● TIMI Score of ≥3 or GRACE score of >140 and high clinical suspicion for a Type 1 MI warrants an early invasive
strategy (catheterization ≤ 48hrs), though notably, the TIMCAS NEJM 2009;360 study showed that early
intervention (≤24 hrs) did not differ from delayed intervention (>36 hrs) in preventing death, MI, or stroke in
NSTEMI patients
ACS – pharmacologic management
A. Anti-Platelet
ASA
● Indication: All patients with suspected ACS
● Dose: 325 mg x1, non-enteric coated, chewed/crushed (onset of action 20 min) 🡪 81 mg qD thereafter for lifetime
● MOA: Irreversibly inhibits prostaglandin H synthase (cyclooxygenase-1) in platelets; prevents the formation of
thromboxane A2, a potent vasoconstrictor and platelet aggregator.
● Benefit: Mortality reduction and 50% RR non-fatal reinfarction
● Aspirin allergy: Consider substituting a P2Y12 inhibitor. Less common options: cilostazol, or vorapaxar
o In all cases, ASA desensitization with Allergy/Immunology is recommended when pt stable
P2Y12 Inhibitors
● Indication: STEMI, Type I NSTEMI/UA (regardless of if medical management or an invasive strategy is chosen)
● MOA: Inhibit the G-protein couple receptor P2Y12 that interact with ADP in the process of platelet activation
● Timing: institution-dependent, could delay possible CABG (7 day wash out)
o No significant benefit to pre-loading. Do not start in ACS without cardiology
● Minimum duration (shorter duration associated with worse outcomes - SMART-DATE)
o BMS: DAPT should be continued for at least 1 month (preferably 1 year)
o DES: DAPT should be continued for at least 12 months in patients who underwent PCI for ACS and 6-12
months for patients who underwent PCI for stable ischemic heart disease
o Medical management: at least 1 year
o Post-fibrinolysis: 1 year
o Shorter DAPT durations may be safe in specific circumstances (TWILIGHT, STOPDAPT-2, ONYX ONE)
● Prasugrel (TRITON-TIMI38) or ticagrelor (PLATO) preferred over clopidogrel in ACS. Clopidogrel preferring patients
with high-bleeding risk.
● Continuing DAPT beyond 1 year: Continuation of clopidogrel for longer may be reasonable (Class IIb, LOE A) in pts
who have tolerated minimum course of DAPT w/o a bleeding complication and who are not a high bleeding risk.
o DAPT Trial: continued DAPT reduced rates of stent thrombosis & MACE, but inc rate of mod/severe bleeding.
o PEGASUS-TIMI 54: In patients with MI in the prior 1-3 years, an extended regimen of ticagrelor plus ASA
significantly reduced the risk of CV death, MI
o Can use DAPT score to predict combined ischemic & bleeding risk and guide decision making on continuation
past 6-12 months (http://tools.acc.org/DAPTriskapp/#!/content/calculator/)
o No data to continue DAPT beyond 36 months
● Continuing DAPT less than 1-3 months: pts receiving specific types of DES, high-risk bleeding, check with cardiology
● ACS discharges: always send 1 year of P2Y12 to pharmacy prior to d/c to ensure supply + check coverage
Clopidogrel:
● Dose: 300-600 mg loading dose + 75mg daily
o 600 mg dose vs 300 mg dose: Maximal platelet inhibition is reached within 2 hrs w/ a 600 mg loading dose vs.
15-24h w/ a 300 mg loading dose. This correlates with better outcomes both in those with STEMI (
HORIZONS-AMI, CURRENT-OASIS) and NSTE-ACS (ARMYDA 2) who underwent PCI
● Benefit: Decrease in the primary end point of CV death, non-fatal MI, stroke (PCI-CURE, PCI-CLARITY)
● Important considerations:
o CYP2C19 genotype variants: poor metabolizers of clopidogrel with decreased response based on high
platelet reactivity (unclear relationship to CV events and bleeding). These individuals are at higher risk of
in-stent thrombosis with clopidogrel. Switch to another agent.
▪ Consider genetic testing if patient presents for in-stent thrombosis.
o Generic, much less expensive than other anti-platelet choices; remains the treatment of choice for many
Ticagrelor:
● Dose: 180 mg load + 90 mg BID maintenance
● Pharmacokinetics: Reversible binding (faster acting), shorter duration, BID dosing. Does not require activation by
CYP450 system
● Evidence/Benefit: Compared to clopidogrel: improves primary end point of MI, stroke, vascular death w/o significant
increase in non-CABG related bleeding; reduces in stent thrombosis (PLATO)
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o Consider in ACS/post-PCI
o Consider in those individuals who have had in stent thrombosis on clopidogrel (“non-responders”)
o Side effects: Associated with the development of dyspnea and more rarely, heart block, potentially related to
inhibition of adenosine metabolism. Higher bleeding risk than clopidogrel.
o After 12m, consider ticagrelor 60mg BID for maintenance (or clopidogrel 75mg daily) (PEGASUS-TIMI54)
Prasugrel:
● Dose: 60mg loading dose, followed by 10mg daily
● Pharmacokinetics: Prodrug with more potent inhibitor of platelet aggregation than clopidogrel
● Evidence/Benefit: Reduction in CV death, MI, stroke compared to clopidogrel but high major and life-threatening
bleeding (TRITON-TIMI 38). No significant differences in outcomes compared to ticagrelor (PRAGUE-18
o Contraindicated if prior TIA/CVA, weight < 60 kg, or >75 years old
o No role in pre-cath lab management, or long-term medical management
Cangrelor:
● Dose: 30 mcg/kg bolus followed by 4 mcg/min/kg for PCI
● Pharmacokinetics: Intravenous; short half-life (3-5 min)
● Evidence/Benefit: More effective in patients prior to undergoing urgent or elective PCI than clopidogrel in reducing
death, MI, and ischemia-driven revascularization at 48 hours; also, less in-stent thrombosis compared to clopidogrel;
similar rates of severe bleeding (CHAMPION-PHEONIX)
● Important considerations: May be used in pts awaiting CABG versus high-risk PCI eval. Dosing: 0.75 mcg/kg/min)
(BRIDGE)
Switching between P2Y12 inhibitors: Either for cost or bleeding risk (de-escalation, switching to clopidogrel) or need to
switch to a more potent agent (escalation, switching to ticagrelor), switching between P2Y12 is sometimes necessary. The
most common switches are:
● Switching from ticagrelor to clopidogrel: 24 hours after ticagrelor dose, start clopidogrel load
● Switching from clopidogrel to ticagrelor:
o Acute/early phase (<30 days): 180 mg ticagrelor irrespective of when the last clopidogrel dose was, ticagrelor
maintenance dose given ~24 hours after last clopidogrel dose.
o >30 days: 90 mg ticagrelor 24 hours after maintenance dose
Glycoprotein IIb/IIIa inhibitors

● Indication: Most commonly initiated in the cath lab and may be continued for 12–24 hours after PCI, especially in
those with persistent thrombus. Can be used in NSTEMI with concern for ongoing ischemia awaiting coronary
angiography or as (cheaper) bridge to urgent CABG. Usually not needed in patients who have received DAPT and no
evidence of ongoing ischemia.
● Drugs: Eptifibatide, abciximab (no longer avail in US), and tirofiban. Eptifibatide (Integrilin) most often used at MGH.
● MOA: Block the glycoprotein IIb/IIIa receptor, the binding site for fibrinogen, von Willebrand factor and other ligands
critical to platelet aggregation. Inhibition of this final common receptor reversibly blocks platelet aggregation and
prevents thrombosis.
● Evidence/Benefit: Mortality benefit in patients presenting with STEMI not treated with P2Y12 inhibitors. A meta-
analysis of 11 trials showed that apiciximab lowered rate of death at 30 days (JAMA 2005;293(14)). Lack of benefit
when used with P2Y12 inhibitors w/ increased risk of bleeding (NEJM 2009;360(21))
B. Lipid Lowering Therapy

Statins
● Indication: All patients who present with ACS
● Dose: High intensity statin – Atorvastatin 80 mg or Rosuvastatin 40 mg PO 🡪 Target LDL < 70 mg/dL
● MOA: 1) LDL-C lowering through hepatic upregulation of LDL receptors secondary to inhibition of cholesterol
biosynthesis, 2) plaque stabilization and prevention of plaque rupture, 3) anti-inflammatory, anti-thrombotic and
endothelial stabilization effects
● Evidence/Benefit: Benefit of high intensity statin (vs prava) seen as early as 15 days post MI (PROVE-IT TIMI 22).
Associated with reductions in death, adverse cardiac events, readmission for recurrent angina, atherosclerosis, and
reduction in infarct size (MIRACL, REVERSAL)
Ezetimibe
● Indication: patients with MI who have an LDL >70 despite high dose statin
● Dose: 10 mg daily
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● MOA: LDL-C lowering through inhibition of an intestinal enterocyte cholesterol transporter thus reducing dietary
cholesterol uptake and ultimately promoting hepatic LDL uptake
● Evidence/Benefit: In patients with recent ACS (prior 10d), addition of ezetimibe to a moderate intensity statin is
associated with a reduction in CV mortality, major CV event or non-fatal stroke when compared to statin therapy
alone. No reduction in all-cause mortality or stroke. Of note, patients already on a high-potency statin were
excluded (IMPROVE-IT).
PCSK-9 inhibitors (evolocumab, alirocumab)

● Indication: consider if LDL remains > 70 mg/dL on statin + ezetimibe
● Dose: evolocumab 140 mg subq every 2 weeks or 420 mg subq monthly; alirocumab 75 mg subq every 2 weeks
● MOA: PCSK9 binds LDL-R on surface of hepatocytes leading to degradation of LDL-R and higher levels of plasma
LDL. PCSK9 antibodies interfere with binding of PCSK9 to LDL-R leading to higher hepatic LDL-R expression and
lower plasma LDL levels. Net effect is reduction in LDL-C by as much as 60% in patients on statins.
● Evidence/benefit: FOURIER trial showed reduced risk of cardiovascular death, MI, CBA, stroke, revasc, and unstable
angina in patients already on statin therapy with a LDL > 70 (though no decrease in CV mortality or all-cause
mortality). ODYSSEY OUTCOMES trial showed reduction composite of death from CAD, nonfatal MI, CVA, unstable
angina in patients that had a prior history of MI in 1-12 months prior to enrollment and LDL of at least 70 mg/dL. Also
effective as monotherapy (e.g. statin intolerant, GASUS-2, ODYSSEY ALTERNATIVE).
Icosapent Ethyl
● Indication: Consider for use in addition to maximally tolerated statin therapy in patients with triglyceride levels ≥150
mg/dL and either established CVD or T2DM plus ≥ 2 risk factors for cardiovascular disease
● Dose: 2g BID
● MOA: reduction in hepatic production of triglyceride-rich vLDL
● Evidence/benefit: REDUCE-IT (NEJM 2019;380)
C. Beta Blockers
● Indication: Initiated within 24 hours of STEMI/NSTEMI in patients without contraindication 🡪 reduce the magnitude of
infarction, rate of reinfarction, and frequency of life-threatening ventricular tachyarrhythmias
● Dose/Route: Start with metoprolol tartrate 6.25mg PO q6h and titrate up for goal HR 55–60.
o IV beta blockers should not be routinely given to patients with NSTEMI due to inc risk of cardiogenic shock,
though can consider for HTN mgmt if no contraindication (COMMIT)
● MOA: Reduce the magnitude of infarction, rate of reinfarction, and frequency of life-threatening ventricular
tachyarrhythmias by decreasing myocardial oxygen demand and sympathetic tone. This occurs by decreasing heart
rate, systemic arterial pressure, and myocardial contractility. In addition, prolongation of diastole secondary to the
reduction in heart rate may augment perfusion to ischemic myocardium, particularly to the sub endocardium.
● Evidence/Benefit: No RCTs in STEMI pts post-PCI. Studied in STEMI pts and under certain revascularization
approaches:
o No reperfusion: 25% reduction in mortality at 1 year (however, pts did not receive statin or P2Y12 therapy)
o Fibrinolysis: No high-quality evidence
o PCI: Conflicting data. One observational study showed significant mortality benefit (JACC 2014;7(6)), others
have not (Am J Cardiol 2015;115(11))
● Contraindications (CI): Signs of HF. Relative CI: asthma/reactive airways, PR > 240ms, 2 nd or 3rd degree heart block
D. Nitroglycerin
● Indication: Ongoing ischemic discomfort.
o IV nitroglycerin is indicated within the first 48 hours after NSTEMI for relief of ongoing ischemic discomfort,
control of hypertension, or management of pulmonary congestion.
o IV nitroglycerin should not preclude other mortality-reducing interventions, such as beta-blockers and/or
ACEI. Symptom reduction, not mortality benefit.
● Dose: Sublingual 0.4 mg q5m x3 dose; assess for need of IV if ongoing CP
● MOA: Induces smooth relaxation and vasodilation in peripheral veins and arteries 🡪 reduces cardiac oxygen demand
by decreasing preload, with modest effects on afterload and dilation of coronary arteries
● Contraindications: SBP < 90 or ≥ 30 mm Hg below baseline, suspected RV infarction (V4R elevation), or patients who
have received a PDE-5 inhibitor (e.g. sildenafil, tadalafil) within 24h
● Side effect: headache, may limit IV titration
E. ACE-I and ARBs

● Indication: within first 24h of (N)STEMI to patients with any of the following: Anterior MI, DM, LVEF < 40%
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● Dose/Agent: Can start with short-acting captopril for titration and convert long-acting agent prior to discharge. ARBs
with fewer side-effects
● MOA: Attenuate the remodeling of the myocardium, preservation of ischemic preconditioning, reduction of recurrent
MI and ischemia (through reducing afterload and mitigating vasoconstriction induced by angiotensin II) and reduction
in sudden cardiac death through decreased sympathetic activity and reduced ventricular remodeling
● Evidence/Benefit: ISIS-4, CONSENSUS-II, AIRE, SAVE
● Contraindications: Hypotension (SBP < 100 mm Hg or > 30 mm Hg below baseline)
F. Anticoagulation
● Indication: IV anticoagulation for all patients with NSTEMI/STEMI without contraindication.
● Agent/Dose:
o Heparin: Unfractionated heparin (at a dose of 60 U/kg bolus followed by 12 U/kg/hr drip, titrating to goal PTT
50–70) is the anticoagulant of choice, especially if the patient will proceed to catheterization as the activated
clotting time (ACT) can be followed during the procedure, leading to lower bleeding rates
o Bivalirudin, Argatroban: Reserved for patients with HIT
o Enoxaparin: Dose is 1 mg/kg BID. For patients in whom a conservative strategy is selected, Class IIa
recommendation to select enoxaparin or fondaparinux over UFH. This is based on evidence of decrease in
primary composite end-points as compared to heparin (ESSENCE, TIMI11B, and Phase A to Z trials). Of
note, enoxaparin resulted in higher rates of bleeding in patients age > 75 years, though the rate of bleeding
was greatest when patients were transitioned from LMWH to UFH or vice versa (SYNERGY). Prefer last
dose 8h prior to coronary angiography and possible PCI.
● If on existing oral AC: if warfarin, do not start until INR < 2; if DOAC, consult with pharmacy.
● MOA: Treat/stabilize intra-coronary thrombus and thrombogenesis that leads to acute reduction in blood flow
● Length of therapy:
o After PCI: Stop unless pt has another indication for anticoagulation (see triple therapy below)
o Medical management: If PCI is not performed (but CAD seen on angiography), can consider continuing:
▪ Intravenous UFH for at least 48 hours or until discharge; or
▪ Enoxaparin or fondaparinux for duration of the hospitalization, up to 8 days; or
▪ Bivalirudin 0.25 mg/kg per hour for up to 72 hours
o Heparin rebound syndrome: D/C’ing UFH results in a brief period of hypercoagulability during which
patients may experience worsening angina (NEJM 1992;327(3))
▪ Managed through the use of ASA or progressive weaning of UFH drip
▪ In patients who cannot receive ASA, another antiplatelet should be utilized consider UFH wean
● Triple Therapy: Ongoing concurrent DAPT and oral anticoagulant therapy increase the risk of bleeding with no
significant difference in MI, cardiac death, thrombotic events (WOEST, ISAR-TRIPLE)
● MGH common practice: treat with triple therapy (ASA/clopidogrel/AC) for 1-4w and subsequently discontinue
ASA, continuing AC and clopidogrel (preferred over ticagrelor/prasugrel due to increased bleeding risk)
● DOAC is preferred over warfarin in most patients (reduced bleeding risk, no lab monitoring). The following
DOACs have been studied with antiplatelet therapy in atrial fibrillation:
o Dabigatran 150 mg BID (RE-DUAL)
o Apixaban 5 mg BID or 2.5 mg BID in pts w/ at least two of the following: age ≥80 years, body weight ≤60
kg, or serum creatinine ≥1.5 mg/dL (AUGUSTUS)
o Low dose rivaroxaban (15 mg qPM) was studied in PIONEER-AF-PCI RCT trial but was underpowered to
exclude increased risk of stroke therefore some still use the suggested 20 mg qPM for stroke prevention
o Edoxaban 60 mg daily (ENTRUST-AF PCI); however when compared to warfarin + clopidogrel,
edoxaban does not reduce bleeding risk.
● If pt needs triple therapy, give PPI or H2 blocker for GI ppx (PPI may interact with clopidogrel. No clinical impact
suggested, but study terminated early. Expert consensus recommendation).
● Mechanical heart values: DOACs deemed contraindicated due to an association of worse outcomes in this cohort
(RE-ALIGN), <10% of pts included in WOEST and ISAR-TRIPLE studies had mechanical heart valves.
G. Oxygen
● Indication: O2 should be used to maintain SaO2 > 90%. Avoid routine use of supplemental O2 in cardiac patients
without hypoxemia as it is not beneficial and may be harmful (Circulation 2015;131(24))
● Evidence/Benefit: No difference in rate of all-cause mortality or rehospitalization in 1 year when comparing patients
with SaO2 > 90% randomized to supplemental O2 vs ambient air (DETO2X-AMI)
H. Morphine
● Indication: almost never 🡪CP unresponsive to NG gtt is an indication for urgent intervention. Morphine can be used
in refractory pain en route to cath.
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● MOA: Reduction in pain decreases sympathetic activity

● Of note: Delays antiplatelet effect of clopidogrel and attenuates ticagrelor exposure and action (J Am Coll Cardiol
2014;63(7), IMPRESSION). Associated with increased mortality in NSTEMI patients (CRUSADE)
I. Fibrinolysis
● Indication: STEMI pts who cannot receive primary PCI w/in 120 mins of first medical contact (Catheter Cardiovasc
Interv 2013;82(1)). In UA/NSTEMI there is no benefit of fibrinolysis (possible harm).
● Timing: Time from hospital arrival to initiation of fibrinolysis should be < 30 min. Fibrinolysis has not improved
outcomes in patients who present > 12 hrs after symptom onset and thus is not recommended for patients who are
stable or asymptomatic.
● P2Y12 inhibitors: Patients receiving fibrinolysis benefit from pretreatment with clopidogrel but not GpIIb/IIIa inhibitors.
Ticagrelor may be safe with regards to bleeding (TREAT)
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Coronary Angiography and Percutaneous Coronary Intervention (PCI)

Coronary Angiography: A minimally invasive procedure performed in the cardiac catheterization (“cath”) lab under
fluoroscopic guidance in which iodine contrast is injected into the coronary arteries for structural evaluation
Percutaneous Coronary Intervention (PCI): This is when an intervention is performed on the coronary arteries during
coronary angiography. This includes percutaneous transluminal coronary angioplasty (PTCA), in which a balloon-
tipped catheter is inflated to open narrow arteries, with or without stent placement.
A. Access
Most commonly transradial (TRA) or transfemoral (TFA) approach
● The RIVAL trial demonstrated that TRA was non-inferior to TFA in terms of death, MI, stroke, and non-CABG related
bleeding; in STEMI subset, TRA was associated with a 30-d all-cause mortality benefit1
● Strong evidence to suggest ↓ rates of bleeding and ↓ vascular complications with TRA vs TFA
● AHA endorses a “radial-first” strategy for PCI in ACS2
Radial Access: After catheterization, a clear plastic band (TR Band) with an inflatable pressure pad is secured around the
access site. The sheath (catheter through which procedure was performed) is withdrawn and the inflatable pressure band
is adjusted to prevent access site bleeding, while allowing sufficient blood flow to transport hemostatic factors to the hand
(“patent hemostasis”). There is a specific nursing protocol to deflate and remove the band when hemostasis achieved (at
MGH 2h for diagnostic procedure or 4h post-PCI).
● TR Bands at MGH are managed by the cardiac access fellow, page if any concern for bleeding/expanding hematoma
Femoral Access: After catheterization, the FA sheath can be removed when the activated clotting time is <150-160sec.
Manual pressure is applied and the sheath is removed with ongoing pressure for hemostasis (timing determined by size of
sheath). Vascular closure devices (e.g. Perclose™ > AngioSeal™) may be used in the Cath Lab in fully anticoagulated
patients, patients who have difficulty lying flat and other select scenarios to achieve faster hemostasis. The size of the
sheath should be noted post-catheterization as it correlates with bleeding risk.
B. Angiographic Nomenclature and Anatomy

In the cath lab, the x-ray source is underneath
the table the patient is laying on. The x-ray
image is captured by an image intensifier (II)
directly above the patient. The body surface of
the patient that is closest to the image
intensifier determines the specific view.
- Right Anterior Oblique (RAO): II is anterior
and on the patient’s right-side
- Left Anterior Oblique (LAO): II is anterior
to and on the patient’s left-side
- Cranial View: II is closest to the pt’s head
- Caudal View: II is closest to the pt’s feet
Standard Views

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Imaging the LCA:

Left Main (LM): Best viewed with
the LAO Caudal (“Spider view”)
and LAO Cranial
LAD: Best viewed in cranial
projections
LCx: Best viewed in caudal
projections
RAO Caudal (LCA): RAO Cranial (LCA):

Spine & catheter are Spine and catheter are
on screen left. LCx is on left. Diaphragm is
clearly delineated. Its seen. LAD runs anterior
branches are named to the apex of heart and
obtuse marginals in ends in a shape that
numerical order from resembles “Salvador
proximal to distal Dali’s mustache.” Septal
(OM1, OM2 etc.) perforators come off the
LAD on L, diagonals on
R.
LAO Cranial (LCA): LAO Caudal (LCA,

Spine and catheter Spider View): Spine and
are on screen right. catheter are on screen
Diaphragm is seen. left. LM, proximal LAD
LAD and its branches and proximal circumflex
are seen (septal are in view.
branches and
diagonal branches)
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LAO Cranial (RCA): Spine and catheter

are screen right. Small branches supplies
conduction system. Acute marginal
branches (e.g. RV marginal) originate from
mid-vessel. Distal RCA branches into the
PDA and PLV. The PDA (lowest artery on
film), runs in the inferior portion of the
interventricular and supplies the posterior
portion of the RV, LV and septum. PDA
has septal perforators.
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C. Identifying Significant Lesions

Fractional Flow Reserve (FFR): ratio of pressures proximal to (aortic pressure) / distal to stenosis (measured by
intracoronary wire) at maximal myocardial blood flow (“hyperemia”). Used to evaluate if a stenosis is functionally
significant.
● Stable Ischemic Heart Disease: reasonable to use FFR to evaluate functional significance of intermediate-severe
coronary stenosis (50-90%). (DEFER, FAME, FAME II)
● ACS: FFR is not used in evaluating culprit lesion, however there is evidence that demonstrates utility in using FFR to
revascularize non-culprit lesions in ACS.
o Stenting of non-infarct related lesions significant by FFR to achieve complete revascularization reduces
subsequent revascularization (DANAMI-3-PRIMULTI, Compare-Acute)
● See Fig. 1 for algorithm: https://www.acc.org/latest-in-cardiology/articles/2017/05/25/08/34/ffr-in-2017-current-status-
in-pci-management
Instant Wave Free Ratio (iFR): adenosine independent resting-pressure derived index. Non-inferior to FFR (iFR-
SWEDEHEART trial)
● Cutoff < 0.89 suggestive of physiologically significant disease and reasonable to consider intervention
● See Fig. 2 for algorithm: https://www.acc.org/latest-in-cardiology/articles/2017/05/25/08/34/ffr-in-2017-current-status-
in-pci-management
Intravascular Ultrasound (IVUS): can assist evaluation of left main disease and/or PCI planning (by measuring vessel
diameter, lesion length and calcification, as well as confirm stent expansion).
● Use of IVUS supported by meta-analyses suggesting reduced MACE, mortality, and complications with IVUS vs.
angiography alone.
● Optical Coherence Tomography (OCT) has higher spatial resolution than IVUS but less depth penetration. Data
suggest equivalence to IVUS; trials ongoing.
PCI of Non-culprit Lesions

● NSTEMI/UA: Controversial. No RCTs, only observational studies. Most studies support complete revascularization.
● STEMI: There are 4 options in the management of non-culprit lesions in STEMI: 1) no revascularization, 2) PCI at
time of primary PCI, 3) Staged PCI either during index hospitalization or post-discharge, 4) CABG in those that have
clear indications
o Evidence that PCI of non-culprit lesions leads to better outcomes (especially need for repeat
revascularization): PRAMI, CvLPRIT, DANAMI-3-PRIMULTI. Timing of intervention remains uncertain.
▪ 2015 ACC/AHA guideline: IIb recommendation for PCI to non-culprit lesions.
o May be harmful in STEMI with cardiogenic shock: CULPRIT-SHOCK
● Which non-culprit lesions? Any lesion that looks unstable, stenosis ≥ 70%, use FFR in lesions ≥ 50%. If there is a
question regarding viability of the tissue to the area, viability imaging may be reasonable prior to PCI.
● CTO (chronic total occlusion): Optimal management of non-culprit CTO in STEMI is not known. CTO-PCI is primarily
indicated for morbidity benefit in patients with refractory angina +/- LVEF recovery. Would defer to outpatient
evaluation once optimally medically managed for angina/HF.
D. Aspiration Thrombectomy
2015 ACC/AHA guidelines recommend against aspiration routine thrombectomy in patients undergoing PCI for STEMI.
This is based on three large trials (TOTAL, TASTE, TAPAS) and the subsequent meta-analysis, that did not find improved
outcomes with this strategy.
E. Stent Placement – Bare Metal Stent (BMS) vs Drug Eluting Stent (DES)
BMS: Consider in pts w/ high bleeding risk, need for invasive procedures, or difficulty with adherence to 1yr DAPT
● More likely to develop early in-stent restenosis due to re-epithelization within the first 30 days
● Requires DAPT for at least 1 month (preferred 1 year)
● With reduction in stent thrombosis in newest generation of DES and short-DAPT regimens in high-bleeding risk
individuals, BMS are rarely used.
DES: Contain anti-proliferative drug and polymer that serves as vehicle for the drug and controls the rate of release. The
drug inhibits the growth of the neointima, which is the major cause of restenosis. Associated with increased rate of late
(>30 day) stent thrombosis due to prolonged foreign body exposure
● Requires DAPT for at least 6 months in SIHD (preferred 1 year) so theoretically increases bleeding risk
● The NORSTENT trial comparing 2nd generation DES vs. BMS found no significant difference in mortality, but noted ↓
repeat revascularization in DES group
● Emerging evidence suggests newer generation DES w/ shorter DAPT may be considered (LEADERS FREE II, ZEUS,
ONYX-ONE)
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Assessment of Blood Flow Before & After Intervention:

- TIMI 0 Flow (no perfusion): Absence of any antegrade flow beyond a coronary occlusion
- TIMI 1 Flow (penetration w/o perfusion): Faint antegrade flow beyond the occlusion, w/ incomplete filling distal to the
coronary bed
- TIMI 2 Flow (partial reperfusion): Delayed or sluggish antegrade flow with complete filling of the distal territory
- TIMI 3 Flow: Normal flow fills the distal coronary bed completely
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Post-Cath Care
Pass-off Essentials in SDU/CCU:
● Type of access used for procedure (Arterial v Venous, Femoral v Radial v Jugular)
● Sheaths: What sheaths are in place, by whom they should be removed, removed in post-cath holding area vs. if
closure device used (relevant for bedrest), for how long should bedrest be?
● Medications in cath lab (ex. Anti-platelet loads)
● Drips (heparin, eptifibatide, cangrelor, etc) and parameters to stop
● Planned course for anti-platelet agents & a/c, especially P2Y12 (P2Y12 ordered prior to transfer by cardiology fellow).
● Findings of procedure and devices/stent details (DES v BMS, size, location)
● Complications of procedure
Post-Cath Orders/Vascular Access Questions:

● Interventional fellow will place some post-cath orders (IVF, AC); always clarify AC with fellow
● Day questions/issues about procedures directed to procedural fellow during day
● Night questions/issues
o Re: vascular access: Direct to moonlighting fellow on Cardiac Access Unit for interventional procedures
(Ellison 11, call floor, ask for fellow) and to EP fellow for EP procedures
o Other issues are not responsibility of access fellow (ex if patient unstable and needs to return to cath lab,
notify daytime cards attending or on-call PDW cards fellow). For STEMI, call 6-8282 to speak with Cath Lab
during the day or Interventional Cardiology Attending at night.
Sheaths and Removal:

● When FA sheaths (catheter through which procedure is performed) in place, patients must strictly lie flat (head of bed
< 30-degrees), after removal need to remain flat for 4-6hrs (reverse Trendelenburg used if patient needs to sit forward
to eat, take meds, or reduce aspiration)
● Arterial sheaths removed by interventional fellow (or Access Fellow on E11 at night) and require at least 20-30min
manual pressure
● Vascular closure devices occasionally used to remove sheath despite an elevated PTT (otherwise heparin gtt needs
to be off and PTT checked)
● PTT goals vary but achieving near normal PTT ↓ bleeding complications
● SBP goal <140 if possible, to reduce pressure on platelet plug
● If radial access, TR band used for hemostasis there are few activity restrictions (removal is nursing protocol driven)
● Common restrictions: No lifting > 10 lbs x 7 days (with affected hand if radial access); no driving at least 48h post-proc
Vascular Closure Devices (VCD):

● Gold standard is manual compression for hemostasis
● VCDs placed in cath lab to continue AC, shorten bedrest, and reduce manual pressure time
● Most common femoral devices in MGH lab: Angio-seal (endovascular pad with extravascular collagen plug), PerClose
(uses sutures), StarClose (extravascular clip)
● TR band used for radial access, removal on floor/unit per nursing protocol
Access Site Complications

● Hematoma: more common w/ femoral access.
o Apply pressure (arteriotomy site is 2 fingerbreadths proximal to skin puncture). Fem-O-Stop device can
be used to apply constant pressure if uncontrolled bleeding or unable to interrupt anti-platelets (carefully
monitor distal perfusion with help of fellow); only when advised by procedural fellow/attending.
o IVFs, control blood pressure, and consider reversing AC (after discussing with attending
● Retroperitoneal Bleed: may present with HD instability, ipsilateral flank pain and ecchymosis; up to 20% mortality •
Risk ↑ in females with very low or high BMIs.
o Assume that any hypotension post-procedure is RP bleed (especially with femoral arterial access is)
o Management includes immediately notifying attending, large bore IV access, IVFs, blood products, and
consider stopping/reversal of antiplatelet/anticoagulant agents
o Only proceed to non-contrast CT if patient is stable. Otherwise, defer and treat as if were RP bleed
● Limb ischemia: due to thrombus, dissection or complication of closure device
o Be sure to exam access sites (pulse, bruit) and distal pulses (Doppler PRN) PRIOR to procedure for
comparison post-procedure
o Evaluate distal pulses with Doppler and consider PVRs to further assess location of compromise
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Cardiopulmonary Bypass Grafting (CABG)

A. Indications for CABG
Class I: Significant (>50%) L Main Disease or equivalent (>70% prox LAD + prox LCX), 3VD, Significant (proximal, long)
LAD Disease with 1-2VD and EF<50%, 1-2VD without LAD involvement but large area of at-risk myocardium
Class IIa: Significant proximal LAD Disease with 1-2VD without high-risk features. PCI may be reasonable.
Class IIb: 1-2VD without LAD and without high-risk features. PCI often preferable.
B. Bypass Grafts
Arterial: Arterial grafts >> long-term survival compared to vein grafts: >90% patency rate at 10 years, ↑ survival, ↓ MI, ↓
less recurrent angina, ↓ reoperations; arterial ↑ grafts difficulty to harvest compared to SVG so may not be used in
emergent situations
● Internal Thoracic Arteries (ITA) [LIMA/RIMA]: Native take off from the subclavian with end-to-side anastomosis to
coronary, limited by vessel length to proximal touchdown on coronaries (for bypassing proximal stenosis)
o ITA grafts confer 20 yr. survival benefit compared to SVGs alone
o LIMA anatomically favorable for LAD, so most common graft
o RIMA technically challenging, increases pump time; can be used in-situ to bypass RCA or OM w/ critical stenosis
(>90%) or in Y-graft with LIMA to other target vessels.
o Prefer to avoid bilateral ITA in poorly controlled diabetics due to concern for sternal wound healing
● Radial Arteries: 80-85% patency at 5yrs; ↑ patency and ↓ adverse cardiac events compared to SVGs31
o Can bypass severe (>70%) L sided stenosis or critical (>90%) R sided stenosis
o Safe harvest, sometimes numbness/tingling in hand ipsilateral to harvest but generally no motor compromise
● Gastroepiploic Arteries: 15 yr. patency rate >92%, rarely used
Venous: SVG 5-7 yr. patency ~50%
● Requires ASA within 48hrs s/p CABG, continued indefinitely
● Smoking, HTN, HLD, DM ↑ risk for graft failure
Key Points:
● Arterial grafts ↑ patency compared to SVGs; may not be limited to RIMA/LIMA with increased radial artery grafting
● Arterial grafts ↑ difficulty to harvest compared to SVGs, so less conducive in emergencies
C. Concomitant Medical Therapy

● ASA 81-325 mg/day (clopidogrel 75mg/day if intolerant/allergic to ASA): Associated w/ decrease in-hospital mortality,
MI, stroke, and renal failure in patients who received w/in first 48 hours. Should be continued post-operatively.32
● P2Y12 therapy: Controversial and practice-dependent. Some surgeons use if prior stents (esp. if not bypassed) or
limited operative outflow from grafts. Subset of the CURE trial suggested a non-significant decrease in CV death, MI,
stroke.33
● Statin: High intensity statin for all <75 unless drug-drug interaction or intolerance
● Beta-blocker starting peri-operatively to reduce post-operative AF.
o No difference between BB and amiodarone re: AF at follow-up (Gillinov et al. NEJM 2016;374)
o 2014 review, there was no mortality benefit in beta blocker seen in patients undergoing CABG without ACS in
the past 21 days.34
● Anticoag: COMPASS-CABG Study demonstrated that rivaroxaban 2.5mg BID + ASA 100 daily or rivaroxaban 5mg
BID vs ASA 100 alone did not reduce graft failure, but rivaroxaban 2.5mg BID + ASA 100 associated with ↓MACE. 35
D. CABG vs PCI
Syntax Score: Developed for SYNTAX Trial, which randomized patients with 3VD or LMCA to CABG vs PCI
● Syntax Score is a semi-quantitative tool based on coronary angiography that grades anatomic complexity
● ↑ Syntax Score = better outcomes with CABG, while ↓ Syntax Score = non-inferior outcomes compared to PCI
● Multidisciplinary Heart Team meetings at MGH between cardiothoracic surgery, interventional cardiology, and primary
team to decide intervention in complex situations
Specific Considerations:
LMCA Disease: Historically CABG was standard for LMCA disease, some recent randomized trials showing PCI with
DES may be reasonable for certain patients but the data are mixed (SYNTAX, PRECOMBAT, NOBLE, EXCEL, MAIN-
COMPARE)
DM w/ limited overall CAD: No difference in 5yr survival, but rate of MACE was lower in CABG (BARI-2D)
DM w/ advanced CAD: CABG is superior to PCI in the management of patients with DM2 and multivessel disease with
respect to prevention of MI and death, although at a cost of a higher risk of stroke (FREEDOM)
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CABG + OMT vs. OMT alone in Ischemic Cardiomyopathy: All-cause mortality, cardiovascular mortality and
hospitalization for cardiovascular causes were significantly lower in patients who underwent CABG + medical therapy
than those who received medical therapy only. Benefit seen over time; at least 5 year-survival (STICHES)
Post-MI Complications
Mechanical Complications (JACC 2013;61:e78, JACC 2019;12(18):1825-1836.)
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Electrical Complications:
● Bradyarrhythmia/conduction block: may be due to coronary artery occlusion (see below) or Bezold-Jarisch reflex
(Anes 2003;98:1250)
● Tachyarrhythmia: related to creation of re-entrant circuit from scar formation and/or ⭡ automaticity from adrenergic
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Special Populations
Myocardial Infarction with Non-obstructive Coronary Arteries (MINOCA):

Definition: Rise & fall of troponins with symptoms suggestive of ischemia, but angiogram with non-obstructive disease (≤
50% stenosis)
Epidemiology: 1-14% in patients presenting with MI
Risk Factors: ~ CAD (DM, HTN), more likely to be younger (mean age=55) and female
Ddx: Coronary spasm, microvascular disease, missed lesion on cath (indeterminate/eccentric plaque, fibrinolysis prior to
angiography), SCAD, takotsubo cardiomyopathy, coronary artery embolism, viral myocarditis
Treatment: Depends on etiology. For patients that have some evidence of CAD and no evidence of alternative etiology,
reasonable to assume ACS and medically manage with ASA, P2Y12, beta-blocker, and statin
Prognosis: Meta-analysis of 8 studies showed in-hospital mortality of 0.9% with 12-month mortality of 4.7%. Generally, the
mortality is lower than in patients with MI with obstructive CAD
Spontaneous Coronary Artery Dissection (SCAD):

Definition: non-traumatic dissection of the coronary arterial wall
Epidemiology: Accounts for 1-4% of all MIs, may account for up to 35% of MIs in women ≤ 50, most common cause of
ACS in pregnancy 43%; 1.81 events per 100,000 pregnancies. Average age of women 45-53
Risk Factors: Female gender, pregnancy (usually third trimester, early post-partum), FMD and other arthropathies.
Classically associated with physical or emotional stress
Pathophysiology: Creation of a false lumen with intramural hemorrhage either by intimal tear or bleeding of the vasa
vasorum. The enlarging hematoma then encroaches on the true lumen causing myocardial ischemia. The LAD is the most
commonly effected artery (32-46%). The mid-distal sections are most commonly affected.
Clinical Manifestations: Vast majority present with ACS with STE, 2-5% present in cardiogenic shock
Diagnosis:
● Coronary Angiography (gold standard): angiographic classification due to the different appearances of SCAD on
angiography. Coronary angiography carries more risk of iatrogenic coronary artery dissection than in other cases
(3.4% vs 0.2%)
● CTA Coronary: Sometimes able to identify SCAD but lower sensitivity than coronary angiography. Often used for
follow-up
Treatment:
● Conservative management (no revascularization) generally recommended in patients that are hemodynamically
stable without high risk anatomy. Angiographic healing has been shown to occur in patients that had repeat
angiography in the weeks to months after (70-97%). Early complications may occur in these patients – 5-10% develop
recurrent MI within the first 7 days. These patients commonly need urgent angiography with PCI. Monitor inpatient for
3-5 days for signs and symptoms of ongoing ischemia.
● PCI: Only considered if ongoing ischemia or HDUS. Increased complications in patients with SCAD that underwent
PCI due to the risks of complications that occur with stent placement (extension of dissection, etc).
● CABG: Consider if LM, proximal 2-vessel dissection, or if complication of PCI.
● Medical therapy: Lack of consensus w/ wide practice variation; discuss with cards. 2017 AHA Expert Opinion SCAD:
o Anticoagulation: Once SCAD is diagnosed, reasonable to stop heparin given concern for propagation of
intramural hematoma (although could reduce thrombus formation).
o Anti-platelet: Wide variation in use and recommendations of DAPT. Generally, aspirin is prescribed.
o Beta-blockers: Should be considered in all patients with low EF or arrhythmias. Low HR decreases shear
stress on arteries.
o Statins: Not recommended routinely after SCAD but is indicated if have concomitant hyperlipidemia.
● Activities after SCAD: patients should be referred to cardiac rehab (SCAD-specific if available). Target HR during
exercise should generally not exceed 50-70% of HR reserve and systolic blood pressure should generally be < 130.
Avoid lifting heavy weights (W < 20-30 lbs, M < 50 lbs). A dedicated SCAD rehab program was shown to be beneficial
in patients (reduced chest pain, improving exercise capacity, and reducing CV events)
Prognosis:
● Pregnancy-related SCAD has worse prognosis than non-pregnancy related SCAD
● In-hospital mortality: 4.2%
● Recurrent in-hospital MI: 4.6%, unplanned revascularization: 4.3%
● At intermediate follow up (2-3 years), recurrent MI reported in 10-30%
● At long term follow up (10 years): MACE in ~50%, most commonly recurrent SCAD
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Microvascular Angina
Definition: Symptoms of angina + signs of ischemia on non-invasive testing, but on evaluation of epicardial coronary
arteries, no obstructive coronary disease
Epidemiology: More likely to be younger and female, more likely to have CV risk factors than the general population
Clinical Presentation: Some patients present with ACS and then are diagnosed with MINOCA. Others have stable
coronary disease that get the diagnosis after persistent and severe symptoms lead to coronary angiography without
evidence of obstructive CAD
Pathophysiology: Various mechanisms proposed, but it has been shown that these patients have higher sensitivity to
vasoconstrictor stimuli and less ability to vasodilate. Other mechanisms include endothelial dysfunction, luminal
obstruction (microthrombi), vascular remodeling, extramural compression, pain sensitivity. Can coincide with other CV
conditions, such as HCM, LVH, aortic stenosis due to one of the many mechanisms proposed
Diagnosis: Stress testing, PET-stress in particular can assess coronary flow reserve/microvascular disease. Coronary
angiography +/- provocative testing.
During angiography:
● Coronary Flow Reserve (CFR): More commonly measured by PET-stress. Can administer intra-coronary
vasodilator and measure the flow reserve during coronary angiography. If the CFR is low (<2-2.5) and there is no
epicardial disease, microvascular dysfunction can be diagnosed
● Provocative testing with Ach: diagnostic if have symptoms + EKG changes without evidence of epicardial disease
Non-invasive
● Fractional flow reserve using CT, PET, or CMR
Treatment:
● Risk factor modification
● Aspirin and statin if have any evidence of atherosclerotic disease
● Anti-anginal: as listed in SIHD
● ACE-I: There is some evidence of benefit. For example, in the WISE trial, women who had received quinapril had
improved CFR after 16 weeks. They also had improved symptoms of angina
● Imipramine: Small study showed 50% reduction in chest pain
Cocaine-induced myocardial infarction

Treatment:
● ASA 325 mg unless suspicion of acute aortic dissection
● Sublingual nitroglycerin 0.3-0.4 mg q5min until chest pain is relieved up to 3 doses
● Calcium channel blockers are adjunctive treatments for ongoing/recurrent symptoms of ischemia despite optimal
therapy with nitroglycerin. Usually IV diltiazem 5-20 mg or verapamil 2.5-5 mg is used
● For agitation 2/2 cocaine, benzodiazepines (diazepam 5-10 mg IV q3-5 min) EW also used (Grade 2C
recommendation)
● Beta blockers are NOT recommended for cocaine-associated MI or ischemia prior to elimination of cocaine on
theoretical considerations of coronary artery vasoconstriction and systemic hypertension from unopposed alpha
adrenergic stimulation. However, this is not universally accepted and some still give beta blockers. If beta blockers are
to be used, mixed alpha/beta blockers such as labetalol and carvedilol are favored over nonselective beta blockers
● Reperfusion is an important early part of management
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Discharge planning and outpatient management:

Standardizing the discharge process for post-AMI patients as much as possible is crucial to improve their comfort level
upon discharge and to reduce readmission rates. The section’s purpose is to review necessary diagnostic tests and
adjunct medicines that should be considered for any patient being discharged from MGH with AMI during their
hospitalization. The most salient references for this information are: ACC/AHA guidelines for management of STEMI, as
well as the ACC/AHA/SCAI Focused update on primary PCI for patients with STEMI.
A. Pre-discharge consults
Once an ACS patient is admitted to the SDU or CCU, they should be admitted using the E10/E11 admission template,
which will standardize their admission orders. Included in that template are consults for:
● PT, Nutrition, smoking cessation (~50% reduction in subsequent cardiac mortality; Arch Intern Med 2000; 160: 939-
44)
● Cardiac rehab (it is cost effective and associated with improvement in clinical outcomes; 20-26% lower mortality rates
in modern era of secondary prevention; Am J Med. 2004; 116:682–92)
● Vaccines: Influenza & Pneumococcal vaccination
o All patients with CVD, regardless of age, should receive PSV23. (For pts previously vaccinated, a
minimum 5-year interval is recommended)
● ***Please make sure that these are ordered prior to the day of discharge.***
B. Assessment of LV function
● Class I recommendation: All patients should have a TTE performed pre-discharge in order to evaluate LV function if
they did not have a ventriculogram performed during catheterization.
● In patients with significant LV systolic dysfunction, a post-discharge plan for re-evaluation ≥ 40 days later should be
made, especially to address potential need for ICD therapy after allowing for recovery from myocardial stunning.
C. Lipid Lowering For Secondary Prevention

● In patients that have had ACS, lipids should be aggressively managed. Start all patients on high intensity statin that
were not on one already. Recheck LDL in 6-8 weeks and if not ≤ 70, then start ezetimibe. If persistently elevated after
ezetimibe, consider PCSK-9. In a patient who was reliably taking a high intensity statin prior to ACS event or cannot
tolerate statin therapy, consider adding ezetimibe or PCSK-9. Consider icosapent ethyl for triglycerides > 150mg/dL.
D. Management of Diabetes
● Goal: HbA1c is < 7%. Less stringent goals may be appropriate for some patients.
● SGLT-2 inhibitors: SGLT2-inhibitors empagliflozin, canagliflozin, dapagliflozin decrease cardiovascular mortality and
morbidity in T2DM patients who have CAD/high CVD risk factors (CANVAS, EMPA-REG OUTCOME, subanalysis of
DECLARE-TIMI 58)
o Adverse events: CANVAS showed increased risk of amputations, which occurred more often in those with
prior history of PAD or prior amputation. Similar data has not been seen in EMPA-REG OUTCOME
● GLP-1: liraglutide lowered cardiovascular mortality and all-cause mortality (LEADER)
E. Adjunctive Medications on discharge

All AMI patients should be discharged on the following medications, unless there are contraindications:
● Aspirin: 81 mg daily for lifetime
● Second anti-platelet agent (clopidogrel, ticagrelor, prasugrel): Submit the prescription to the patient’s pharmacy as
soon as this decision is made as many patients require prior authorization for these medications (ticagrelor and
prasugrel) and this can hold up their discharge. Follow up to make sure affordable. Contact Interventional Cardiologist
prior to changing medication
● High intensity statin
● Beta-blocker if tolerable, can titrate as outpatient
● PPI/H2 blocker: if sending home on triple therapy, hx of GIB, or high risk as shown to decrease rate of GIB in pts on
DAPT w/o increasing the rate of ischemic events (NB: observational studies that have raised concern of interaction
between clopidogrel and PPI). (COGENT)
● ACE-I/ARB if anterior MI, DM, or LVEF < 40%
● PRN sublingual nitro: Most likely to be forgotten on discharge.
o Below is an example of the instructions to give to patients regarding how to take nitroglycerin:
o Sit or lie down if you can.
o Place one tablet under your tongue and wait 5 minutes.
o If you still feel chest pain, take a second tablet, and wait 5 more minutes.
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o If you still feel chest pain, take a third tablet and wait 5 more minutes.
o If you rarely require nitroglycerin or if you feel chest pain 5 minutes after taking the third pill, call 911.
o Always tell your doctor if you had to take this medicine
o Keep medicine in the original bottle in a dark, dry place and check the expiration date often.
o If you need to open the bottle, write the date you opened it in permanent marker.
o The bottle is good for only 6 months after it is opened.
● NSAIDs: Patients who routinely took nonsteroidal anti-inflammatory drugs (except for aspirin) before NSTEMI should
discontinue these agents because of increased risks of mortality, reinfarction, hypertension, heart failure, and
myocardial rupture (Class III Recommendation: Harm)
F. Follow up
● Appointments: The patient should be scheduled to see a cardiologist or their PCP within one month of discharge. For
patients who do not have a primary cardiologist, they should be referred to the MGH MI clinic or will be set up with the
PDW fellow on service. They should also be given a phone number to call for their cardiologist (even if an
appointment is not scheduled at the time of discharge) so that they can call if they have symptoms.
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HEART FAILURE
DEFINITIONS
Cardiomyopathy (CM): disease of myocardium. This can lead to heart failure, but is not synonymous with heart failure
● Dilated CM: dilation or impaired contraction of one/both ventricles
o Left ventricular internal diameter end diastole (LVIDd) >59mm males, >53mm females
● Restrictive CM: nondilated or small ventricle(s) with diastolic dysfunction
● Hypertrophic CM: increased LV mass, with nondilated, hypertrophied LV (IVS >15mm)
● Also: arrhythmogenic right ventricular cardiomyopathy/dysplasia (ARVC/D); unclassified CMs
Heart failure (HF): clinical syndrome characterized by typical symptoms and signs that are caused by cardiac
dysfunction. Hemodynamically, it is a failure to provide commensurate cardiac output to the body, or in which output is at
cost of elevated cardiac filling pressures
● Heart failure with preserved ejection fraction (HFpEF) (EF ≥ 50%) accounts for 40-50% of patients with HF
● Heart failure with reduced EF (HFrEF) (EF≤ 40%) accounts for 40-50% of patients with HF
● Heart failure with midrange EF (HFmrEF) (EF 41-49%) accounts for approximately 10-20% of patients with HF
KEY PHYSIOLOGY CONCEPTS

Preload: describes the myocardial wall stretch at the end of diastole
● Most accurate measure: LV end diastolic volume (LVEDV); rarely directly measured, can be approximated by some
imaging methods or bedside hemodynamic assessments
o Closest proxy LV end-diastolic pressure (LVEDP) – can only be measured during LHC
● Closest estimate of LVEDP = left atrial pressure (LAP), when there is equal pressure gradient from ventricle to atrium
o LAP best estimate: pulmonary capillary wedge pressure (PCWP), measured by RHC
● AKA, in a normal heart: LVEDV → LVEDP ≈ LAP ≈ PCWP
● In hearts with diastolic disease, ventricular volume and pressure may become uncoupled.
o Increased LV stiffness (pericardial restriction or myo/endocardial), higher LVEDPs required to create same
EDV
Afterload: describes the force opposing LV ejection

● Most accurately described as aortic impendence or elastance
● Afterload ≈ myocardial wall stress, which is defined according to Laplace’s Law
(𝑝𝑟𝑒𝑠𝑠𝑢𝑟𝑒× 𝑟𝑎𝑑𝑖𝑢𝑠)
o 𝑤𝑎𝑙𝑙 𝑠𝑡𝑟𝑒𝑠𝑠 = (2× 𝑤𝑎𝑙𝑙 𝑡ℎ𝑖𝑐𝑘𝑛𝑒𝑠𝑠)
.
● Increased afterload 🡪 ↑ intraventricular pressure needed open the aortic valve 🡪 ↑ increased wall stress.
o If exposed to chronically ↑ afterload 🡪 myocardial hypertrophy (increased thickness) to restore normal wall
stress
Contractility/Inotropy: inherent capacity of the myocardium to contract independent of changes in preload or afterload.
● ↑ contractile function a/w enhanced ventricular relaxation (lusitropy),
● Frank-Starling curve relates ventricular EDV (preload) to contractility
o ↑ in force of contraction as EDV ↑ with increasing sarcomere length and optimization of the overlap between
actin + myosin filaments
o There is a limit to this optimization after which LVEDV / EDP will increase without additional increase in SV
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HISTORY & INITIAL ASSESSMENT

● HPI:
o See table below for key symptoms
o Identify precipitant (medication issues, dietary indiscretion [salt, fluid, alcohol], arrhythmia, ischemia, infection)
o Ask for dry weight, recent weights, and functional status (number of blocks/flights of stairs they can walk)
● Medical history:
o HF etiology, most recent EF, frequency of exacerbations
o Other cardiac history (ischemic, valvular, arrhythmia, etc)
o Prior testing: Prior echo, stress test, coronary CT, or CT chest that shows atherosclerosis
o Associated conditions: HTN, DM, OSA/OHS, obesity, anemia, nutritional deficiencies
● Medications:
o GDMT dosing
o Diuretic dosing, any recent changes or pauses
● Social history:
o EtOH, cocaine, methamphetamine, tobacco use
● Vitals/Exam:
o O2 requirement compared to baseline and pulse pressure
o See below table for common exam findings
● Studies/Imaging:
o Labs:
▪ BNP (compare to baseline), Troponin (eval for ischemia)
▪ Cr (cardiorenal or low output), lactate (low output), LFTs (congestive hepatopathy)
▪ Consider infectious workup if concern for causing exacerbation
▪ New HF etiology labs as below
o ECG: baseline and current EKG for signs of ischemia, arrythmia, or device malfunction that explain HF etiology
and/or exacerbation
o CXR:
▪ 1) Left sided HF: pulmonary edema, pleural effusions, +- worsened cardiomegaly if large pericardial
effusion
▪ 2) Right sided HF: opacified upper portion of abdomen may suggest ascites
▪ 3) R/o other causes of dyspnea (pneumothorax, pneumonia, ILD, etc)
o TTE:
▪ Required for every potential new diagnosis of HF
Symptoms Signs
Shortness of breath Sensitivity: 84-100% S3 gallop Sensitivity: 13%
Specificity: 17-34% Specificity: 99%
Orthopnea Sensitivity: 22-50% Tachycardia Sensitivity: 7%

Specificity: 74-77% Specificity: 99%
Paroxysmal nocturnal Sensitivity: 39-41% Pedal edema Sensitivity: 10%

dyspnea Specificity: 80-84% Specificity: 93%
Edema, abdominal Sensitivity: 23% Elevated JVP > 6cm Sensitivity: 39%
distention, RUQ pain Specificity: 80% Specificity: 93%
(right sided HF)
Crackles Sensitivity: 60%
Specificity: 78%
Hepatojugular reflex Sensitivity: 24%
Specificity: 96%
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Ascites Sensitivity: 1%
Specificity: 97%
▪ Not required for every patient with known HF. Useful in evaluating progressive valvular ,
ischemic, or pericardial disease
▪ Most accurate assessment (especially of RV/LV function and valvular pathologies) is at euvolemia, in
sinus rhythm and at normal rates
CLASSIFICATION
General classification: ACC/AHA, Stages A-D. Grades based on structural changes and symptoms
Functional classification: NYHA, Functional Classes 1-4. Grades severity of symptoms and exercise tolerance
● Since this captures symptomatic only, lowest NYHA grade starts at equivalent point to ACC/AHA B (see graphic)
Severe/decompensating: INTERMACS, Profiles 1-7. Gradations scale from NYHA III (7) to critical cardiogenic shock (1).
● Most commonly applied to advanced HF patients admitted to CCU/CS-ICU, not used in terminology as much day-to-
day as other classifications above
ETIOLOGY
In general, when describing patients with the clinical syndrome of heart failure, try to delineate the type of heart failure
from the underlying condition that led or put them at risk of that syndrome, if identifiable. Example: 62 year old male with
HFrEF (EF 32%) and ischemic cardiomyopathy
You can have heart failure syndrome without a cardiomyopathy, as cardiomyopathy refers only to the disease of
the heart muscle.
Initial workup for new diagnosis of heart failure:

● Ischemic: EKG, troponins, HbA1c, lipids, stress test (exercise vs pharmacologic), imaging (coronary CTA), coronary
angiography
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● Non ischemic – see table below. Most important studies bolded
Type Etiologies Workup

Dilated Infectious ● Viral: RVP, serologies
Bolded: etiologies ● Viral: flu, HIV, adeno, coxsackie, ● Bacterial: BCx, GAS screen
that may or hepatitis B/C, parvovirus, CMV, EBV (more likely historical),
commonly present ● Bacterial: Strep (Rheumatic fever), ● Parasitic: Toxo, T. cruzii
acutely typhoid, diptheria, brucellosis, serologies
mycobacteria, psittacosis ● Fungal: serum
● Parasitic: toxo, T. cruzii (Chagas’), galactomannan, 1,3B-d-
schistomiasis, trichinosis glucan
● Fungal: histoplasma, crypto ● Syphilis Ab screen, Leptospira
● Other: rickettsia, syphilis, leptospira, Ab, Lyme screen with reflex
?Lyme ● Biopsy for path + culture may
be necessary
Medications: ● Springboard report in Epic

● Chemo (doxorubicin; cyclophosphamide; gives lifetime dose
Herceptin) doxorubicin
● ART (zidovudine, didanosine, ● Serial TTEs used to monitor
zalcitabine) Herceptin
● HCQ/chloroquine ● Others gathered from patient
● Psychiatric/CNS meds (phenothiazines, HPI
clozapine) ● ICI myocarditis +- presents
● Immune checkpoint inhibitors with dilated LV
Rheumatologic Auto-Antibodies:
● SLE ● SLE: ANA, anti-dsDNA, -Ro, -
● Dermatomyositis, scleroderma*, RA La
● Sarcoid ● Dermato: anti-Jo1, -Mi2, -
● GCA, Kawasaki’s disease MDA5
● Giant cell myocarditis ● Scl: anti-centromere, -Scl70,
● Eosinophilic myocarditis RNApol III
● Hypersensitivity myocarditis ● RA: anti-RF, -CCP
● GCA/Kawasaki: ANCA
Labs:
● Sarcoid: ACEI level
Path:
● GC myocarditis, eos:
endomyocardial biopsy
o Often associated with
significant arrhythmias
Imaging:
● CXR, TTE
● Vasculitides: CT cardiac vs
CTA chest, +/- head+neck
Genetic ● Genetic profiling: can be
● Familial or sporadic targeted to first degree
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● Duchenne’s MD*, Erb dystrophy, relatives, or broader screen in

myotonic dystrophy, FXA, ARVC new diagnosis
Endocrine ● HgbA1c
● DM ● Serum, urine metanephrines
● Pheochromocytoma* ● Cushing’s: AM cortisol to
● Cushing’s screen; ACTH level; dex
● TSH (hyper or hypo*) suppression to confirm
● GH (high* or low) ● TSH with reflex
● GH: IGF-1
Toxins ● UTox, serum tox
● EtOH, cocaine, amphetamines ● Heavy metals screen
● Heavy metals – lead, cobalt, mercury ● Li level
● Lithium ● Methemoglobin
● CO
Miscellaneous ● Tachycardia is diagnosis of
● Tachycardia-mediated exclusion
● Peripartum CM ● PPCM: final mo. of pregnancy
● Heat/hypothermia 🡪 5mo. post partum
● OSA ● Radiation: less common now
● Radiation induced* with highly specific mapping
Deposition diseases ● HC: screen - ferritin; confirm -
● Hemochromatosis*, amyloid* HFE gene
● Amyloid: TTR scan,
SPEP/SFLC, UPEP
Restrictive All “starred” above can present with restrictive
picture
Storage & deposition diseases ● Gaucher: low β-glucosidade
● Gaucher’s disease ● HC: ferritin + HFE
● Hemochromatosis ● Amyloid: TTR scan,
● Amyloid SPEP/SFLC, UPEP
Endomyocardial diseases ● TTE + biopsy to confirm
● Loeffler’s endocarditis ● Loeffler’s: diffuse eosinophilic
● Endomyocardial fibrosis infiltration
● EMF: endemic areas –
Venezuela, Brazil, W. Africa,
Uganda, S. India
Genetic/Familial ● Family history often enough to
● Hypertrophic phenotypes can have suggest
restrictive features ● Targeted genetic profiles in
first degree relatives
Miscellaneous
● Radiation
● Primary neoplasma/metastatic dz
● ^GH /Pheo
● Scleroderma
Hypertrophic Hypertension
Genetic/familial ● Targeted genetic profile in first

degree relatives
Endocrine ● Serum, urine metanephrines
● Hypothyroidism ● TSH with reflex
● Pheochromocytoma ● GH: IGF-1
● Acromegaly
Hereditary disorders ● Biopsy and path
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● Storage diseases: glycogen storage ● Fabry’s: alpha-GAL level

diseases; Fabry’s (low); females also genetic
● Friedrich’s ataxia test
● Neurofibromatosis ● NF: clinical phenotype;
genetics
HFrEF (EF <40%)
Guideline Directed Medical Therapy (GDMT)

● Good data that GDMT (especially multi-drug regimens) reduces mortality/hospitalizations and improves quality of life
● Goal of initial phase/initiation: start as many different classes of therapy as blood pressure and renal function allow
● Goal is not to reach target dose early. ADHF hearts are extremely sensitive – too rapid titration may lead to shock
● See table below for target doses associated with best outcomes
● Transcatheter mitral valve repair should be considered for symptomatic patients with chronic moderate-severe to
severe MR despite optimal doses of GDMT (COAPT Trial).
● Loop diuretics are not associated with improvements in mortality, but they do improve QoL
Therapy Target Dose Key Trials and notes

BETA-BLOCKERS ● CIBIS-II, COPERNICUS, COMET, MERIT-HF
Bisoprolol 10 mg Daily ● Carvedilol (non-selective BB with α-blocking capacity) has
Carvedilol 25 mg BID greater effect on BP than metoprolol
(<85kg) or 50 mg ● Contraindicated in severe conduction disease
BID (>85kg) ● Use with caution in patients with tenuous cardiac index
Metoprolol 200 mg Daily (e.g. immediately post-MI and ADHF), asthma or
bronchospastic COPD
ARNI ● PARADIGM-HF, PIONEER-HF
Sacubitril/valsartan 97/103mg BID ● Do not administer with ACEi/ARBs due risk of angioedema
● Transitioning from ACE to ARNI requires a 36 hour
washout period to reduce risk of angioedema (not required
for ARB)
● Contraindicated in severe hepatic impairment, caution in
RAS, BP < 100 and volume depletion
● ARNI is preferred over ACE-I or ARB if no
contraindications
ACE-I ● SAVE, CONSENSUS, SOLVD, V-HeFT II, ATLAS, AIRE
Captopril 50mg TID ● Don’t use if history of angioedema, bilateral RAS,
Enalapril 10-20mg BID symptomatic hypotension or SBP < 90
Lisinopril 20-40mg Daily ● Can cause dry cough, angioedema, azotemia,
Ramipril 10mg Daily hyperkalemia, and transient renal insufficiency upon
initiation of therapy
● Reduction in eGFR of up to 30 percent in first 6-8 weeks
post initiation of therapy is tolerated
ARBS ● CHARM-ALTERNATIVE, VAL-HeFT, HEAAL
Candesartan 32mg Daily ● Consider for patients intolerant of ACE-I due to side effects
Losartan 150mg Daily (cough or angioedema); avoid ACE-I/ARB combination
Valsartan 160mg BID due to risk of hyperkalemia, hypotension and renal
dysfunction
ALDOSTERONE ANTAGONIST ● RALES, EPHESUS, EMPHASIS-HF
Eplerenone 50mg Daily ● Avoid in patients with K > 5; be careful with use in AKI or
Spironolactone 25-50mg Daily Cr > 2.0
● Spironolactone can cause gynecomastia and breast pain
in men; eplerenone has fewer endocrine side effects
SGLT2-INHIBITORS ● DECLARE-TIMI 58, DAPA-HF, EMPA-REG, EMPEROR-
Dapagliflozin 10mg Daily Reduced
Empagliflozin 10mg Daily ● For HF, dapagliflozin can be used eGFR ≥30 and
empagliflozin for eGFR ≥20
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● Side effects: yeast infections, hypotension, volume

depletion, euglycemic DKA (if DM), UTI (including
complicated UTI)
ADJUNCT THERAPIES
VASODILATORS ● V-HeFT, A-HeFT
Hydralazine 75mg TID ● Isosorbide mononitrate (Imdur) has not been studied and
Isosorbide dinitrate 40mg TID is not recommended according to ACC/AHA guidelines.
If-CHANNEL BLOCKERS ● SHIFT, BEAUTIFUL, SHIFT-HF
Ivabradine 75 mg TID ● Titrate to HR 50-60 BPM; indicated for patients in sinus
rhythm with HR >70bpm at rest once BB therapy is
maximized
LOOP DIURETICS ● IV > PO for ADHF, can function as a vasodilator and
Furosemide 40-240 mg QD decreases RA and PCWP; starting dose is typically given
Torsemide 10-200 mg QD as 2-2.5 times home PO dose; start with intermittent bolus
Bumetanide 1-5 mg QD and consider continuous infusion if congestions is
refractory to boluses
● Conversions: 40 mg PO Lasix = 20 mg IV Lasix = 20 mg
PO torsemide = 1 mg IV/PO Bumex
THIAZIDE DIURETICS ● Useful in refractory diuresis. Administer 30 minutes before
Hydrochlorothiazide 12.5-100 mg QD loop diuretic for maximum effect.
Metolazone 2.5-10 mg QD
ICD ● SCD-HeFT, MADIT-II, DEFINITE
● Primary prevention of sudden cardiac death in patients with non-ischemic
dilated cardiomyopathy or ischemic heart disease at least 40 days post MI with
EF of 35% or less and NYHA class II-III symptoms on GDMT with expectation
of at least one year survival
● MADIT-CRT, CARE-HF, MIRACLE, RAFT
● CRT is indicated for patients with LVEF 35% or less, sinus rhythm, LBBB with
CRT QRS duration of 150ms or greater and NYHA Class II-IV symptoms on GDMT;
can be useful for patients with reduced EF and LBBB pattern with QRS 120-
149ms or non-LBBB pattern with QRS duration of 150ms or greater
● CRT should also be considered in patients on GDMT with LVEF 35% or less
who are undergoing device implantation with expectation of ventricular pacing
>40% of time
Iron ● FAIR-HF, CONFIRM-HF, IRONOUT-HR, RED-HF, AFFIRM-AHF
● IV iron repletion (ferritin 15-100 or 100-299 with transferrin saturation < 20%)
improves NYHA functional status, 6-min walk test and several quality-of-life
assessments. These improvements not seen with PO iron
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HFpEF
Diagnosis may be challenging given normal EF and non-specific signs and symptoms.
● The H2FPEF score was developed to help distinguish HFpEF from other causes of dyspnea.
● European Society of Cardiology (ESC) has developed the HFA-PEFF diagnostic algorithm to diagnose HFpEF.
● For inpatients, RHC (+/- provocative maneuvers such as exercise) should be considered
Reddy, Y et. al. Circulation

2018
Pieske, B. et. al. EHJ

2019
HFpEF Treatment
● HFpEF patients often elderly and/or highly symptomatic, ∴ aim of therapy 🡪 alleviate symptoms and improve QoL
o SGLT2i (EMPEROR-PRESERVED trial). Improved outcomes for patients w/ and w/o diabetes
o +/- spironolactone (controversial TOPCAT trial)
Diuretics, blood pressure control, address underlying valvulopathy/arrhythmia/ischemia
Therapy Key Trials and Notes

SGLT2i EMPEROR-PRESERVED: NEJM 2021; 385:1451-1461. Decreased cardiovascular-
related death and hospitalizations regardless of concomitant diabetes
ACE-I PEP-CHF: Eur Heart J 2006; 27: 2338-45. Non-significant trend toward reduced mortality.
ARB CHARM-Preserved: Lancet 2003; 362: 777-8. Trend toward reduced hospitalizations
I-PRESERVE: NEJM 2008; 359: 2456-67. No improvement of outcomes
ARNI PARAMOUNT: Lancet 2012; 380: 1387-95 (vs. Valsartan). Reduced NT-proBNP
PARAGON-HF: NEJM 2019; 381:1609-1620. Narrowly missed primary end point
(composite of HF hospitalizations or CV death) but did reduce risk in HFpEF patients at
lower end of range (45-57%).
PARALLAX: clinicaltrials.gov (on-going trial)
Aldosterone TOPCAT: NEJM 2014; 37:1383-92. Spironolactone decreased hospitalizations due to HF
antagonists but no effect on mortality. ALDO-DHF: JAMA 2013; 309: 781-791. No effect on exercise
capacity or QoL
Sildenafil RELAX: JAMA 2013; 309: 1268-77. No benefit.
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Imdur NEAT-HFpEF: NEJM 2015;373:2314-24. Worse outcomes (reduced daily activity).

Digoxin DIG: NEJM 1997;336:525-33. No effect.
Diltiazem MDPIT subgroup analysis: Circ 1991; 83: 52-60
ACUTE DECOMPENSATED HEART FAILURE (ADHF)
Characterized by signs and symptoms of venous

congestion (‘volume overload’). This may cause
hypoperfusion, i.e. shock.
● Classify by perfusion and congestion (see
table)
o ‘Wet’ – proxy for elevated intracardiac
pressures
o ‘Warm/Cold’ – proxy for systemic
vascular resistance
Specific etiologies of new, severe LV or

biventricular dysfunction that are commonly seen
in the CCU include:
● ACS
● Acute valvular disease
● Stress cardiomyopathy: new transient
decrement in LV function (<21 days) related to
emotional or physical stress
o Takotsubo’s CM: subtype
characterized by i) midsegment
RWMAs and basal hyperkinesis, ii)
absence of CAD/ruptured plaque, iii) ischemic ECG changes and iv) exclusion of myocarditis
● Myocarditis:
o infectious (viral, bacterial – specific etiologies above)
o toxin/medication (immune checkpoint inhibitors most often seen)
o inflammatory/rheumatologic (giant cell myocarditis, eosinophilic myocarditis)
Cardiogenic shock (CS) is shock [tissue hypoperfusion] secondary to reduced cardiac output of a primary cardiac
etiology. The SCAI stages of CS (A-E) can aid in the timely diagnosis and management.
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● Tailored therapy: refers to use a pulmonary artery catheter (PAC) to obtain intracardiac pressures and
hemodynamic measurements to guide therapy.
o PAC (or Swan-Ganz): quad lumen catheter; RIJ, occasionally L 🡪 RA 🡪 RV 🡪 R or L main PA
o Uses: Determine etiology of shock, tailored treatment
o Complications:
▪ Infection/PTX/bleeding, arrhythmia, PA rupture, IJ injury/erosion (long term); pulm. infarct; PE
o Relative CI/indications for cath lab placement:
▪ LBBB: at risk for developing RBBB and then complete heart block
▪ ICD or PPM placed within the last 6 months; temp. wire
▪ Valves: prosthetic/stenotic, or severe tricuspid regurgitation (challenging); TV or pulmonic valve IE
▪ Severe pHTN: systolic PA pressures > 70 mmHg: ↑ risk PA rupture
▪ R. heart mass (thrombus, tumor)
o Placement: assess with waveform & CXR – tip at edge of middle 1/3 of thorax, ideally inferior to level of LA on
CXR (West Zone 3 in V/Q map of lung
Hemodynamic Normal How to Calculate or Assess Using PAC

Parameter Value
Cardiac output CO: 4-7 Thermodilution method using PAC (not accurate in shunt or TR)
𝑉𝑂2 𝑉𝑂2
Cardiac index L/min Fick method: (𝐶𝑎𝑂2−𝐶𝑣𝑂2) ≈ (13.4×𝐻𝑔×[𝑆𝑎𝑂2−𝑆𝑣𝑂2])
(CO/BSA) CI: 2.6-4.2
L/min/m2 VO2 is measured with metabolic cart or estimated using body weight
PCWP (≈ 6-12 mmHg PAC balloon is inflated; PCWP is measured prior to c wave, or if
LAP) difficult to identify can average peak/trough of a wave. If AF (thus no a
wave), PCWP is measured 130-160ms after QRS complex before v-
wave; should be measured at end-expiration when intrathoracic
pressure ≈ 0. See below for description of PCWP waveform.
SVR 770-1200 (𝑀𝐴𝑃 − 𝐶𝑉𝑃
) × 80
dynes 𝐶𝑂
PVR < 2 Woods (𝑚𝑃𝐴𝑃 − 𝑃𝐶𝑊𝑃
) × 80
units / 20- 𝐶𝑂
130 dynes
(WU x 80)
CVP (≈RAP) 0-6 mmHg CVP waveform is similar to PCWP and should be assessed similarly
MVO2 (or 65-70% Oxygen saturation of mixed venous blood obtained from the
SvO2) pulmonary artery
CVO2 (or >65% Oxygen saturation of central venous blood obtained from the superior
ScvO2) vena cava (does not reflect venous return from lower body or
myocardium)
PAPi >2 (𝑃𝐴𝑆𝑃 − 𝑃𝐴𝐷𝑃)
𝑅𝐴𝑃
Pulmonary artery pulsatility index (PAPi) is an indicator of right heart
function
CPO >0.6 W (𝑀𝐴𝑃 × 𝐶𝑂)
451
Low cardiac power output (CPO) is a strong predictor of mortality for
patients with CS
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CVP/PCWP waveform
a-wave: atrial contraction, lost in AF/flutter, increased in tricuspid/mitral
stenosis, cannon a-waves in junctional, VT and CHB due to contraction
against closed TV/MV
c-wave: closure of TV/MV
v-wave: rapid filling of atria, TR/MR causes fusion of c and v waves into
one wave (called cv-wave) and blunted x descent
x-descent: atrial relaxation
y-descent: early ventricular filling
ACUTE DECOMPENSATED HEART FAILURE MANAGEMENT

Therapy Target Management
Oxygen Spo2 Administer O2 if SpO2 < 92% and sit upright.
>92%; NIPPV if pulmonary edema 🡪 PEEP helps improve oxygenation in congested alveoli.
88-92% Caution with RV failure, severe COPD, or altered mental status (inability to protect
in airway).
COPD If severe hypoxemia, hypercarbia, shock or AMS 🡪 intubation
Diuretics PCWP < ⭣CVP and PCWP to optimize Starling curve mechanics & relieve
18 symptoms.
CVP 8 – Initial dose: IV bolus loop diuretics 2-2.5 times the home PO dose.
12 If UOP does not augment within two hours, consider escalation in diuretic dose, Lasix
🡪 Bumex, bolus 🡪 gtt, or addition of a thiazide
Infusion with gtt may be preferable to IV pushes in patients when hypotension is a
concern for ease of titration
Vasodilators SVR Relieve symptoms by ⭣ preload and PCWP, ⭣ afterload and ⭡ stroke
<800 volume
SBP > NB NB if severe HTN, acute MR, acute AR
Nitroglycerin 90 Vasodilator effect on veins > arteries. Reduces cardiac O2 demand by ⭣
MAP >
preload; may ⭣ afterload mildly as well.
65
Gtt: initial dose 5 to 10 mcg/min up to 200
SE: headache and hypotension. Tachyphylaxis common in time.
Isosorbide PO version nitroglycerin. Often used in combo w/hydralazine
dinitrate Initial dose: 20 to 30 mg PO TID or QID
SE: hypotension
Nitroprusside ⭡ CO by ⭣ afterload
Continuous IV infusion: Initial dose 5 to 10 mcg/min
SE: coronary steal (do not use in patients with un-revascularized CAD), cyanide
toxicity, hypotension, increased ICP
Inotropes CI >2.2 Consider in cold/wet patients with minimal UOP despite escalating diuretics
Dobutamine MvO2 β1>β2 agonist (inodilator)
>65 Continuous IV infusion: Initial dose 0.5 to 5mcg/kg/min
SE: arrhythmias, hypotension, tachycardia and ventricular ectopy
Milrinone PDE-3 inhibitor (inodilator)
Continuous IV infusion: Initial dose 0.125mcg/kg/min
Longer half-life, greater pulmonary vasodilatation, slightly less chronotropy, fewer
arrhythmic events than dobutamine; caution with AKI
SE: arrhythmias and hypotension
Dopamine Adrenergic and dopaminergic receptors (inopressor)
o Low dose: dopaminergic
o High dose: dopaminergic and β1
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o Large dose: alpha adrenergic

Consider use if severe hypotension, unable to tolerate inodilators
Continuous IV infusion: Initial dose 2 to 20mcg/kg/min
SE: Arrhythmias, tachycardia, end-organ hypoperfusion
Vasopressors CI >2.2 Use if severe hypotension and unable to tolerate inodilators
MvO2 SE: tachycardia, arrhythmias, end-organ hypoperfusion
Norepinephrine >65 α > β1 🡪 ⭡ vasoconstriction primarily + contractility, HR
Continuous IV infusion: Initial dose 0.05-1mcg/kg/min
Can be useful in mixed shock
Epinephrine α, β1, β2 leading to ⭡ cardiac stimulation, ⭡inotropy and
⭡chronotropy
⭡ Myocardial O2 consumption
Continuous IV infusion: Initial dose 0.01- 0.5mcg/kg/min
Vasopressin Risk of cardiac, digital, splanchnic ischemia; used in mixed cardiogenic & distributive
Phenylephrine Pure α-agonist 🡪 vasoconstriction 🡪 ⭡ afterload
Use in cardiogenic shock with HCM physiology (increased afterload reduces LVOT
gradients, reflex bradycardia beneficial) and aortic stenosis (fixed CO, want to
prioritize perfusion pressure; reflex bradycardia promotes diastolic filling and
maximizes output)
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ACUTE RIGHT VENTRICULAR FAILURE (RV FAILURE)
Acute right ventricular failure: characterized by elevated right heart filling pressures in the setting of acute pulmonary
hypertension (acutely elevated RV afterload).
● The RV is an embryologically, histologically and functionally different structure to the LV. It is more fibrous, with
significantly less muscle mass and capability to functionally compensate for changes in pressures or volumes.
o In the setting of acutely elevated afterload (PA pressure), the RV compensates initially by dilating –
additional pressure is dissipated by creating greater volume
▪ Unlike the LV, additional pressure does not increase RV stroke volume as effectively
▪ As pressure/volume increases, this leads to increased RV wall tension and flattening of the
interventricular septum (IVS)
o The coronary arteries fill during times of low wall tension; as RV WT , myocardial perfusion decreases 🡪
 contractility 🡪  RV output
o The same pressure changes that lead to RV WT  lead to progressive flattening 🡪 bowing of IVS towards
and into LV
▪ This reduces LV EDV 🡪 reduced preload 🡪 reduced overall cardiac output
▪ Reduced RV output also not providing as adequate preload
o State of low cardiac output 🡪 systemic HoTN 🡪 acidosis, inflammation 🡪  pHTN,  coronary O2 delivery
o This type of cardiogenic shock and spiraling deterioration is known as the RV death spiral
Konstantinides, S. et. al. EHJ 2014
Haddad, F. et. al. Circulation 2008
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ADVANCED THERAPIES FOR CARDIOGENIC SHOCK: MECHANICAL CIRCULATORY SUPPORT (MCS)
Indications Contraindications
Refractory cardiogenic shock (CPO < Anoxic Brain Injury
0.6W, CI < 2.2L/min/m2 or elevated lactate Irreversible End Organ Failure
despite pharmacologic therapy) Prohibitive Vascular Access
High risk interventional procedures DNR
● Type of MCS device is determined by indication, INTERMACS profile, predominant ventricle involved (left, right or
both) and presence of hypoxemia
● If concern for worsening cardiogenic shock on pharmacotherapy, the CARDIOGENIC SHOCK team (staffed by
HCICU Attending) should be paged at 29151 for early consideration of MCS.
● As IABP is the main therapy residents are exposed to, this will be discussed in detail next. Please see chart below for
brief description and comparison of other available MCS options.
Tehrani, B. et. al. JACC HF. 2020

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INTRA-AORTIC BALLOON PUMP (IABP)

A. Access
● 30-50 cc balloon; inserted into the descending aorta via percutaneous femoral artery access, less commonly via
surgical cut-down of the axillary artery.
● Correct positioning: tip of the IABP should be 1cm distal to L subclavian so as not to occlude proximal (L subclavian, L
common carotid) or distal (splenic or renal) arteries
o Daily CXR to assess placement: tip radio-opaque, should be at L 2nd intercostal space, at level of L main
bronchus
B. Indications
Cardiogenic shock and hemodynamic instability after a
STEMI refractory to pharmacological management (Class IIa
based on findings from IABP-SHOCK II)
Mechanical complications of MI (VSD, severe MR)
Refractory ischemia (intractable angina with impaired LV
function or large territory infarct, refractory polymorphic VT)
Prophylactic placement prior to high risk procedures (PCI,
CABG)
Inability to wean from cardiopulmonary bypass after
C. Contraindications
Severe aortic regurgitation
Severe bilateral peripheral arterial disease
Aortic dissection, aneurysm, or intramural hematoma
Severe coagulopathy or sepsis
D. Mechanism Mandawat, A. Rao, S. Circulation.

2017
● Counter pulsation: Inflates with helium in diastole, actively deflates during systole.
● Key principles:
● Amount of blood displaced is proportional to the volume of the balloon
● LV and aortic diastolic filling times are inversely proportional to heart rates; shorter diastolic filling times (higher
heart rates) produce less balloon augmentation per unit time
● as aortic compliance ↑ (or SVR decreases), the magnitude of diastolic augmentation decreases
IABP Waveform
Normal: IABP inflates after AoV closes
(dicrotic notch), leading to diastolic
augmentation > than SBP. Balloon
inflation leads to a sharp and deep V at
the dicrotic notch. Deflation starts
immediately before the opening of the
aortic valve, leading to reduced end-
diastolic pressure.
Early Inflation: Loss of deep V 🡪

premature AoV closure 🡪 incomplete LV
emptying, AI, ↑LV EDV / LV EDP, ↑
afterload and ↑ myocardial oxygen
demand.
Late Inflation: Deep V becomes a W 🡪
decreased augmented coronary
perfusion, ↓ O2 to coronaries and
reduced overall benefit of the IABP.
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Early Deflation: Premature deflation 🡪

increase aortic pressure prior to
isovolumetric contraction 🡪 ↑ afterload
and ↑ myocardial demand. Diastolic
augmentation is also suboptimal.
Late Deflation: IABP remains inflated

during isovolumetric contraction, thus the
LV is contracting against an inflated
balloon leading to ↑↑ increase in
afterload. This requires immediate
attention.
E. Complications:
● Anemia and thrombocytopenia
● Insertion site complications (bleed, infection, aneurysm, fistula)
● Limb ischemia (daily pulse checks and vascular exam; requires device removal)
● Vascular injury including dissection or pseudoaneurysm (12-40%) or stroke
● Balloon rupture (suspect if blood seen in helium line; device detect, will attempt to aspirate helium from aorta to
prevent gas embolism).
Any suspected complication should prompt an immediate call to the fellow/attending or HCICU Intensivist.
F. Weaning/Removal:
● Depending on hemodynamic status and indication for device, the IABP is programmed to assist every beat (1:1) or
less often (1:2, 1:4, 1:8). Improvements 🡪 decrease cycling frequency
● Thrombosis risk increases at frequencies <1:1 (stasis) – AC required for these
● Wean stepwise, with assessment of hemodynamics, rhythm, symptoms during each phase. Before removal, return to
1:1 x hours due to risk of thrombus dislodgement
● Remove after holding heparin x hours, generally when PTT <40
● Per policy at MGH, IABPs are removed only by fellows or more senior
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ADVANCED THERAPY: LONG-TERM DURABLE MECHANICAL CIRCULATORY SUPPORT (LT-MCS)
Indications Absolute Contraindications

NYHA functional class IIIB-IV, EF < 25% and Irreversible hepatic, renal or neurological disease
at least one of the following criteria: Medical non-adherence
● INTERMACS profile 2-4 Active mental illness or psychosocial instability
● Inotrope or acute MCS dependence
● Progressive end-organ dysfunction Relative Contraindications
● Peak VO2 < 14 ml/kg/min (or 12 Age > 80
ml/kg/min on beta blockers) Morbid obesity (BMI >35) or cachexia
● Acute MCS dependence
● To reverse elevated PVR or renal Active systemic infection or prolonged intubation
failure in potential heart transplant Untreated malignancy
candidates
Severe peripheral artery disease or cerebrovascular
● To allow time for transplant
disease
contraindications to be reversed
such as recent cancer, obesity and Significant aortic insufficiency unable to be corrected
recovery drug/alcohol dependence Drug, tobacco or alcohol use within 6 months
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According to indication, LT-MCS use may be categorized as a:

● Bridge to candidacy: use of LT-MCS to improve end-organ function (or buy time) for an ineligible patient to
become eligible for heart transplantation
● Bridge to transplantation: use of LT-MCS to keep patient alive who is otherwise at high risk of death before
transplantation until a donor organ becomes available
● Bridge to recovery: use of LT-MCS to keep a patient alive until cardiac function recovers sufficiently to remove
MCS
● Destination therapy: use of LT-MCS as an alternative to transplantation in patients with end-stage HF ineligible
for transplantation or long-term waiting for heart transplantation
Devices: LT-MCS most commonly refer to ventricular assist devices (VAD) which are FDA approved to provide support to
the left ventricle (LVAD).
● NB: VADs are also used off-label for RV support (RVAD) or to support both ventricles (BiVAD). RV support
cannot be done outside of an ICU.
● Total artificial heart (TAH) is FDA approved for biventricular support but is not available at MGH.
Principles of VAD
● Blood to LV pump via inflow cannula (surgically
implanted in apex) 🡪 blood to ascending aorta via
outflow graft
● Driveline: Surgically tunneled cable that connects the
pump to an external control unit which operates and
monitors pump function (LVAD speed, flow, power,
pulsatility index). Driveline exits the body through
abdominal wall. The external controller is connected to
a power source.
● The rotor or impeller within the pump propels blood by
spinning at a high speed. Blood flow is proportional to
pump speed though the relationship is not linear. The
speed is set by the provider to ensure adequate LV
unloading. Inadequate loading may result in pulmonary
edema while excessive unloading could lead to suction
events, resulting in hypotension or arrythmias.
● Continuous flow devices do not generate a pulse. However, the interaction with native ventricular function
leads to phasic changes in blood flow through the LVAD called the pulsatility index for the HeartMate II and is
displayed as the waveform for HVAD.
● Given risk of thrombus with continuous flow devices, VADs mandate anticoagulation (heparin 🡪 warfarin)
Complications intrinsic to the pump

Driveline Accidental mechanical impact/pulling cable, weight gain. Treatment of lead fractures is a
repair but some may require pump exchange.
Pump Malfunction Mainly a consequence of pump thrombosis; technical failure can occur less commonly
Outflow graft Due to thrombus, stenosis, compression, malposition. Pump flow decreases, and power
occlusion increases to maintain speed. Work-up includes a CT scan of chest.
Complications related to pump-patient interface
Infection Driveline infections and blood stream infections may mandate chronic antibiotic therapy,
device exchange or emergent transplantation depending on the clinical severity
Pump thrombosis Hemodynamic changes seen = power spikes (abrupt increases in power consumption),
slow increase in power requirements, clinical evidence of hemolysis (abrupt rise in LDH).
Early pump thrombosis 🡪 pump exchange or heart transplant; late pump thrombosis
sometimes treated with IV heparin
GI bleeding Common cause of hospital readmissions both early and later. Often no intervenable
source. AC interrupted until bleeding resolves; recurrent bleeding 🡪 lower target INR.
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CVA Leading cause of long-term mortality; VAD patients are at risk of both ischemic and
hemorrhagic stroke. Ischemic stroke = emboli from pump thrombosis. Hemorrhagic stroke
= due to the need for chronic AC or risk of hemorrhagic conv. of isch. NCHCT for any
acute mental status or neurologic change.
Arrythmia Burden of arrythmias is high in LT-MCS; reasonably well tolerated with low risk of
immediate hemodynamic collapse since output independent of native myocardium
Aortic insufficiency In ~10 to 53%; fusion of commissures and degenerative changes of cusps from persistent
aortic valve closure. Assessed by TTE.
RHF Risk of developing right heart failure is an important consideration in assessing
candidacy for LVAD; exacerbation of pre-existing RHF, or by changes to RV structure
(septal bowing) due to off-loading of the left ventricle. Assessment of PVR critical.
Alarm type Advisory (non-critical) Critical Evaluation and

Management
Low flow or suction ● Speed too high/ low Same differential as Obtain MAP, ECG, TTE
● Hypovolemia advisory alarm, but Trial of volume (albumin) if
● RV dysfunction associated with suction
● Tamponade extremely low flow Manage HTN/treat VT
● HTN/Arrhythmia Page HF or VAD pager
● Inflow/outflow (11045)
obstruction
Low power ● Power disconnected Driveline disconnect Examine driveline
● Low battery power Depleted batteries Replace batteries
Power modules Page HF or VAD pager
disconnect (11045)
High power ● Pump thrombosis Same as advisory LDH, LFT, INR, U/A, CBC
● Poorly controlled HTN column. Treat HTN. Page HF
● Electric fault service or VAD pager
ORTHOTOPIC HEART TRANSPLANT
Indications Absolute Contraindications Relative Contraindications

End-stage HF with ● Systemic illness with life ● Age > 72
severe symptoms, expectancy < 2 years ● Active infection (except VAD related)
poor prognosis and ● Fixed pulmonary ● Severe comorbidities including DM, PAD,
no remaining hypertension – i.e. CVA, PUD, morbid obesity, cachexia)
alternative treatment pulmonary pressures do ● Renal/liver failure – can be dual listed
options not improved with ● Active mental illness or psychosocial
improved LV function instability
Peak VO2 ≤14 (theoretically could ● Medication non-adherence
ml/kg/min favor listing receive heart-lung) ● Recent HIT
● EtOH/tobacco/drug use
.
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Truby L. and Rogers J. JACC 2020
Immunosuppression: Post-transplant immunosuppression typically consists of a triple regimen that includes calcineurin
inhibitors (such as cyclosporine and tacrolimus), purine synthesis inhibitors (such as MMF and azathioprine) and
corticosteroids.
● MMF is superior to azathioprine in preventing rejection and mortality.
● Steroids prescribed in high doses initially with gradual taper starting at 6 months post-transplantation.
● Patients undergo routine cardiac biopsies to grade level of rejection post-transplant (per below table)
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Early Complications Following Cardiac Transplantation

Primary graft Most common cause of mortality in 1st month post transplant.
dysfunction Risk factors: older donor or recipient age, female donor, non-head trauma cause
of death, CAD in donor, prolonged ischemic time.
Assess: TTE. Management: inotropes; potential MCS
Acute right Preoperative PH is associated with high incidence of RHF and perioperative
ventricular failure mortality.
Conduction Denervation of donor heart 🡪 loss of PNS efferents from vagus to SA node and
abnormalities loss of SNS efferents to the atria/ventricles. RBBB/LBBB may result from trauma
to conduction system.
Epicardial pacing used intraoperatively to maintain CO with HRs 100-120.
Late Complications Following Cardiac Transplantation
Chronic Allograft Accelerated atherosclerosis of blood vessels after cardiac transplantation.
Vasculopathy Risk factors include older donor/recipient age, DM, HTN, mismatch of body size
and HLA mismatch.
Due to denervation of donor heart, patients do not have typical anginal pain but
presents with HF, arrythmia or SCD.
IVUS and coronary angiogram 4-6 weeks after transplant at min. Non-invasive
testing with stress TTE, MRI or PET can also be done at regular intervals.
Treatment: stenting with PCI if disease is localized; if diffuse, modify IS, statins
Infection Common in acute and chronic setting post-transplant.
Posttransplant, prophylaxis for PJP, HSV, toxoplasmosis and oral candidiasis is
started.
CMV -Recipients of CMV+ hearts: antiviral prophylaxis.
Chronic Kidney Up to 50% of patients 5 years after transplant.
Disease Risk factors: older age, female, lower eGFR pretransplant, pretransplant
inotrope/MCS use, CNI use.
Steroid related All patient should receive calcium/vitamin D and possibly bisphosphonates.
complications Consider early withdrawal of steroids is possible.
Cardiac Rejection
Hyperacute Occurs immediately after aortic cross-clamp is removed and the donor heart is
rejection exposed to recipients blood cells. This is now uncommon due to cross-matching
of blood type and panel reactive antibodies.
Acute cellular Mediated by the recipient’s T cells recognizing donor HLA molecules;
rejection characterized by an inflammatory infiltrate on EMB.
Classified based on the severity of lymphocytic infiltrate and myocyte:
● Grade 0 (no rejection),
● Grade 1R (mild),
● Grade 2R (moderate)
● Grade 3R (severe)
MGH also uses the 1990 ISHLT histologic criteria,
● Grade 0 (no evidence of ACR)
● Grade 1A (focal infiltrate without myocyte damage)
● Grade 1B (diffuse infiltrate without myocyte damage)
● Grade 2 (one focus of infiltrate with associated myocyte damage)
● Grade 3A (multifocal infiltrate with myocyte damage)
● Grade 3B (diffuse infiltrate with myocyte damage)
● Grade 4 (diffuse injury with extensive myocyte damage)
Treatment includes high dose corticosteroids or antithymocyte antibodies if no
response to steroids. Repeat EMB is performed 1-2 weeks after treatment for
follow-up.
Antibody mediated ● Donor antigens and recipient antibodies forms an antigen-antibody complex
rejection or membrane attack complex that results in endothelial and vascular injury.
● Diagnosis is confirmed by presence of donor specific antibodies and via EMB
with evidence of complement activation
● Management includes IVIG, plasmapheresis, antilymphocyte antibodies and
high dose steroids.
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41. DOSE: Felker GM, et al. "Diuretic strategies in patients with acute decompensated heart failure". The New
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45. MADIT-CRT: Moss AJ, et al. "Cardiac-resynchronization therapy for the prevention of heart-failure events". The
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49. PEP-CHF: “The perindopril in elderly people with chronic heart failure (PEP-CHF) study”. Eur Heart J 2006; 27:
2338-45. PMID: 16963472
50. CHARMED-PRESEVERED: Yusuf S, et al. "Effects of candesartan in patients with chronic heart failure and
preserved left-ventricular ejection fraction: The CHARM-Preserved Trial". The Lancet. 2003. 362(9386):777-781.
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51. I-PRESERVE: “Irbesartan in patients with heart failure and preserved ejection fraction.” The New England Journal
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53. PARAGON-HF: Solomon SD, et al. "Angiotensin–neprilysin inhibition in heart failure with preserved ejection
fraction". The New England Journal of Medicine. 2019. 381(17):1609-1620. PMID: 32187481
54. PARALLAX: “Angiotensin receptor neprilysin inhibition versus individualized RAAS blockade: design and rationale
of the PARALLAX trial” ESC Heart Failure 2020 Jun;7(3):856-864. PMID: 32297449
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Heart Failure with Preserved Ejection Fraction". JAMA. 2013. 309(12):1268-1277. PMID: 23478662
57. NEAT-HFpEF: Redfield MM, et al. "Isosorbide mononitrate in heart failure with preserved ejection fraction". New
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59. MDPIT: “Diltiazem increases late-onset congestive heart failure in postinfarction patients with early reduction in
ejection fraction. The Adverse Experience Committee; and the Multicenter Diltiazem Postinfarction Research
Group” Circulation. 1991 Jan;83(1):52-60. PMID: 1984898
60. A standardized and comprehensive approach to the management of cardiogenic shock. PMID: 33121700
61. Intra-aortic balloon support for myocardial infarction with cardiogenic shock. PMID: 22920912
62. Percutaneous Mechanical Circulatory Support Devices in Cardiogenic Shock. PMID: 28500136
63. A prospective, randomized clinical trial of hemodynamic support with Impella 2.5 versus intra-aortic balloon pump
in patients undergoing high risk percutaneous coronary intervention. PMID: 22935569
64. Percutaneous Mechanical Circulatory Support versus Intra-aortic balloon pump in cardiogenic shock after acute
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65. Recover I: a multicenter prospective study of Impella 5.0/LD for post-cardiotomy circulatory support. PMID:
22405676
66. Impella ventricular support in clinical practice: Collaborative Viewpoint from a European expert user group PMID:
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67. Left ventricular assist devices 101: shared care for general cardiologist and primary care. PMID: 31635239
68. Temporary circulatory support for cardiogenic shock. PMID: 32682486
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71. Refractory cardiac arrest treated with mechanical CPR, hypothermia, ECMO and early reperfusion. PMID:
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75. Anderson MB et al. Benefits of a Novel Percutaneous Ventricular Assist Device for Right Heart Failure: The
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76. Slaughter MS et al. Advanced heart failure treated with continuous-flow left ventricular assist device. N Engl J
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77. Mehra MM et al. A fully magnetically levitated circulatory pump for advanced heart failure. N Engl J Med. 2017;
376:440-450. PMID: 27959709
78. Sheu JJ et al. Early extracorporeal membrane oxygenator-assisted primary percutaneous coronary
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80. Cardiac Transplantation: Update on a road less traveled. PMID: 3190306
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ARRHYTHMIAS AND ELECTROPHYSIOLOGY
Narrow Complex Tachycardias
A narrow complex tachycardia (NCT) refers to a tachycardia with QRS duration <120ms and typically implies normal
electromechanical conduction from a supraventricular origin. Generally, it is helpful to organize NCTs by mechanism
(automaticity, re-entry, or triggered activity) and anatomic origin (sinus node, atria, AV node).
PATHOPHYSIOLOGY
Tachyarrhythmias are caused by one of three mechanisms: re-entry, automaticity, or triggered activity
1. Re-entry: most common mechanism of NCT and is thought to be the result of cyclic conduction around an electrical
circuit. Reentry can occur when the following three criteria are met:
1. There are two distinct but parallel conducting pathways connected proximally and distally
2. One pathway must have a substantially longer refractory period than the other pathway
3. The pathway with a shorter refractory period must conduct electrical impulses slower than the other pathway
Initiation: re-entry can be initiated when an appropriately timed premature impulse is introduced to the circuit. If a pre-
mature impulse is blocked by the longer refractory period of one limb of the circuit and preferentially conducts down the
slowly conducting limb of the circuit, enough time can elapse such that the current can travel in retrograde fashion up the
newly repolarized limb and reenter the circuit from the beginning, forming a continuous circuit. Re-entry can also be “set
up” by scar and/or ischemia that produce areas of tissue heterogeneity (though this is more common in ventricular
arrythmias).
2. Automaticity: “automatic” depolarization of electrical foci in different areas of the heart (atria, AV junction, ventricles)
which may be physiologic (e.g. automatic pacemaker function of the SA resulting in normal sinus rhythm or sinus
tachycardia). Abnormal automaticity at specific location(s) of the heart can trigger tachyarrhythmias (both atrial and
ventricular), typically in response to metabolic insults (ischemia, hypoxemia, sympathetic tone, and electrolyte and acid-
base derangements).
3. Triggered activity: shares features of both automaticity and re-entry and occurs when there is interruption of normal
cardiac repolarization by “afterdepolarizations,” early or delayed depolarizations that either proceed (early
afterdepolarizations) or follow (delayed afterdepolarizations) the cardiac action potential. These spontaneous or triggered
beats cause extrasystoles and lead to tachyarrhythmias. In early afterdepolarization, abnormal oscillations in the
membrane potential are seen during phase 2 (plateau) and early repolarization in phase 3 (e.g. long QT syndrome,
Torsades). In delayed afterdepolarization, the oscillations occur after full repolarization (e.g. digitalis toxicity due to
enhanced calcium influx). Either early or delayed after depolarizations can lead to self-sustaining arrhythmic events.
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Tachycardia by Site of Origin: SINUS NODE

NCTs involving the sinus node include sinus tachycardia and sinus node re-entry tachycardia.
Sinus tachycardia
● Presentation: HR 100–150 in older pts. Can be as high as 200 in young patients (max HR ~ 220-age)
o Initiation is gradual (heart rate trend on telemetry increases over seconds)
o P wave axis and morphology unchanged compared to baseline ECG
● Pathophysiology: most frequently secondary to other cause (physiologic) Due to an underlying process (pain, fever,
hypovolemia/shock, CHF, PE, anemia, hyperthyroidism, AV fistula) or drugs (intoxication of caffeine, anticholinergics,
catecholamines, nicotine, or withdrawal from EtOH, benzos, opiates). May be seen in roughly one-third of patients
with acute MI (Circulation 1972;45:681)
o Idiopathic (primary):
▪ Inappropriate Sinus Tachycardia (IST) is idiopathic resting sinus tachycardia, typically with very high sinus
rates on exertion
▪ Paroxysmal Orthostatic Tachycardia Syndrome (POTS) is a separate diagnosis characterized by marked
sinus tachycardia upon standing
▪ Both IST and POTS are diagnoses of exclusion after physiologic ST is ruled out
● Treatment: physiologic treat the underlying cause
o IST or POTS: treatment is primarily for symptoms (tachyarrhythmia-mediated cardiomyopathy is exceedingly
rare). BB is the most common treatment vs less often non-dihydropyridine CCB, catheter ablation of SA node,
ivabradine (off label but can be effective)
Sinus Tachycardia: https://litfl.com/sinus-tachycardia-ecg-library/
Sinus node re-entry tachycardia (SANRT)

● Presentation
o Can often occur in the presence of structural heart disease
o Initiation and termination are abrupt (paroxysmal) and can be brought on by pacing
o P wave axis and morphology are unchanged compared to baseline (sinus) ECG
o There is often little that will differentiate this from sinus tachycardia on ECG and telemetry and will often require a
high index of clinical suspicion and invasive EP studies for diagnosis
● Pathophysiology
o Re-entry within or adjacent to the SA node
● Treatment
o Acute: Vagal maneuvers, modified Valsalva (passive leg raise after Valsalva terminated SVT 43% of time vs 17%
of time with Valsalva alone, Lancet 2015; 386: 1747), adenosine, rapid atrial pacing
o Chronic: BB, non-dihydropyridine CCB and digoxin can be used to prevent recurrence (although evidence for
benefit still lacking); catheter ablation
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Tachycardia by Site of Origin: ATRIOVENTRICULAR NODE

These include non-reentrant junctional tachycardias, AV nodal re-entrant tachycardia (AVNRT), and AV reciprocating
tachycardia (AVRT).
Junctional Tachycardia
● Presentation
o These generally include junctional ectopic tachycardia (JET) and accelerated junctional rhythm (which is known
as non-paroxysmal junctional tachycardia of NPJT). Junctional tachycardias can be difficult to distinguish from
other arrhythmias, particularly AVNRT. Retrograde P waves can be observed, and incomplete A-V dissociation is
frequent with intermittent capture of sinus beats by the AV node leading to irregular ventricular rates that can also
mimic atrial fibrillation
o Junctional ectopic tachycardia (JET):
● Rare and relatively benign in adults; more commonly associated with, and often incessant in infants after
cardiac surgery for CHD
● Rapid, occasionally irregular NCT, with rates typically 120 to 220
o Non-paroxysmal junctional tachycardia(NPJT):
● More common in adults than junctional ectopic tachycardia
● Also referred to as accelerated junctional rhythm, rates typically 70 to 130
● Pathophysiology
o Junctional ectopic tachycardia: Arises from an accelerated, ectopic focus in the AV junction (including the His
bundle)
o Non-paroxysmal junctional tachycardia: Most often due to digitalis toxicity (digitalis can enhance phase 4
depolarization of the His-Purkinje fibers) but also seen in acute MI
● Treatment
o Junctional ectopic tachycardia: Acute :IV nodal blockade in the acute setting, Chronic: PO for ongoing
management; ablation can be considered if symptomatic and resistant to medical therapy, but is very risky (can
result in AV block)
o Non-paroxysmal junctional tachycardia: Treatment of underlying condition (digitalis toxicity, MI)
Junctional Tachycardia: https://litfl.com/accelerated-junctional-rhythm-ajr/
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AV nodal re-entrant tachycardia (AVNRT)

● Presentation
o Initiated by a PAC or PVC and onset and initiation are abrupt
o There is always a 1:1 AV relationship, generating a regular rhythm with ventricular rates typically between 150–
220
o Ps usually buried within QRS, or found immediately before or after QRS.
● Pathophysiology: re-entry circuit within the AV node with dual pathway physiology
Typical (“slow-fast”): Represents >90% of AVNRT in which the impulse travels antegrade down the slow
pathway and retrograde up the fast pathway. This classically generates a short RP tachycardia
o Atypical (“fast-slow”, “slow-slow”): In these cases, the impulse travels initially via the fast pathway, then returns via
the slow. This usually generates a long RP tachycardia
● Treatment
o Acute: Initial management usually involves vagal maneuver and/or adenosine to terminate, but if the patient is
unstable, DCCV should be attempted upfront. To increase the chance of success with vagal maneuvers, have the
patient strain (e.g. blow into a syringe) in a semi-recumbent position (60 seconds) and then perform a passive leg
raise (45 degrees, 60 seconds) which increases the chance of success from 17% to 43% compared to standard
Valsalva (REVERT RCT in Lancet, 2015)
o Additional effective therapies involve medications that block the AV node, such as BBs and CCBs
o Definitive Tx involves radiofrequency catheter ablation, which has a cure rate > 95%
Typical slow-fast AVNRT: https://litfl.com/supraventricular-tachycardia-svt-ecg-library/
Ladder diagrams of typical (slow-fast) AVNRT (left) and atypical (fast-slow) AVNRT (right). In typical AVNRT, a PAC
triggers re-entry that beings anterograde along the slow pathway (while the fast pathway is refractory). Retrograde
conduction occurs along the fast pathway, generating a “short RP.” In atypical AVNRT, a PVC triggers re-entry with
anterograde conduction via the fast pathway and retrograde atrial depolarization via the slow pathway, generating a “long
RP.”. A = atrial depolarization, V = ventricular depolarization, F = fast pathway, S = slow pathway, ATR = atrium, AVN =
AV node, VENT = ventricle. For more information regarding laddergrams, consider the following link and source
https://ecg-interpretation.blogspot.com/2013/06/ecg-interpretation-review-69-pvc-pjc.html
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AVNRT with retrograde P forming a pseudo r’ in V1 and pseudo-S in II, III, aVF (A). These are absent in NSR (B).
AV nodal reciprocating tachycardia (AVRT)

● Presentation: Similar to AVNRT in that there is a 1:1 AV relationship generating a regular rhythm but ventricular rates
are often faster and P waves tend to be further separated from the QRS complex (following the QRS either on the ST
segment or in the T wave)
o In contrast to AVNRT, AVRT requires the presence of at least one accessory pathway, which may be “concealed”
(i.e. normal baseline ECG) or “manifest” (i.e. evidence of accessory pathway on baseline ECG such as a delta
wave in WPW)
● Pathophysiology
o Anterograde conduction can occur via the AV node (with retrograde conduction up the accessory
pathway, i.e. orthodromic AVRT) or via the accessory pathway (with retrograde conduction either through
the AV node, or less commonly, via another accessory pathway, i.e. antidromic AVRT).
▪ Orthodromic AVRT: More common (95%). Anterograde conduction though the AV node produces a narrow
QRS complex unless there is aberrant conduction
▪ Antidromic AVRT: Less common. Anterograde conduction down the accessory pathway produces a wide,
maximally pre-excited QRS complex which may be mistaken for VT
● Notable case reports and discussions of variants of AVRT:
o Permanent junctional reentrant tachycardia (PJRT): https://doi.org/10.1016/S0735-1097(20)33848-1 39
o Mahaim tachycardias: https://doi.org/10.1016/j.hrcr.2021.07.012 40
o Lown-Ganong-Levine Syndrome: https://doi.org/10.12659/ajcr.906767 41
● Treatment
o Orthodromic AVRT (narrow QRS): AV nodal blockade: vagals > IV adenosine > IV verapamil, IV beta blockers
including metoprolol > IV procainamide.
o Antidromic AVRT (wide QRS): IV procainamide is the preferred option anywhere outside the EP lab. While
antidromic AVRT can be treated with rate control if the diagnosis is absolutely certain, co-occurring atrial
fibrillation and VT must to be excluded as nodal blockade can cause the rhythm to degenerate and acutely
worsen.
o Atrial fibrillation with preexcitation: IV procainamide > IV ibutilide. It is critical to avoid nodal blockade with
adenosine, CCB’s, BB’s, amiodarone, and digoxin in patients with atrial fibrillation with pre-excitation because
they will slow conduction through the AV node and facilitate anterograde conduction through the accessory
pathway, which can lead to VF. However, a regular rhythm effectively rules out atrial fibrillation.
o Acute or refractory , DCCV
o Definitive treatment requires ablation of the accessory pathway, which carries a success rate between 85–
98% depending on the pathway’s location
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Tachycardia by Site of Origin: ATRIA
Orthodromic AVRT: https://litfl.com/atrioventricular-re-entry-tachycardia-avrt/
Antidromic AVRT: https://litfl.com/atrioventricular-re-entry-tachycardia-avrt/
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Atrial tachycardia (AT)

● Presentation: atrial rate 100–250. Ventricular rate typically 90–150 (due to variable block).
o P wave morphology is different from baseline sinus P wave,
▪ When AV block present, baseline between P wave is isoelectric in all leads.
● Pathophysiology: Often idiopathic in young patients. Commonly seen in structural heart disease or dig toxicity (which
can be exacerbated by hypokalemia)
● Treatment: Extremely difficult to control with nodal blockade alone. Radiofrequency ablation is often required if AT is
incessant, symptomatic/hemodynamically significant, and medically refractory.
AT with variable block. When P’s are consecutive, RP > PR.
Multifocal Atrial tachycardia (MAT)

● Presentation
o Atrial rate 100–250. Ventricular rate typically 90–150 (due to variable block).
o 3 different P morphologies, often with varying R-P and P-R intervals
o When AV block present, baseline between P waves is isoelectric in all leads.
● Pathophysiology: Seen in older patients with chronic lung disease or atrial enlargement. Often preceded or followed
by atrial fibrillation/flutter, paroxysmal AT, or frequent PACs (Am Heart J 1988;115:680)
● Treatment: Can typically be monitored in the absence of decompensation. Replete both magnesium and potassium
prior to medical therapy. Rate control is reported to work better than rhythm control for MAT. In the presence of
cardiopulmonary disease, choose non-DHP CCB’s such as verapamil > BBs. If unstable, consider DCCV or ablation.
MAT with variable Ps and PR, RP intervals.
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Atrial flutter
● Presentation
o Atrial rate 250–350, often 300. Ventricular rate can be around 150 bpm if there is 2:1 A-V conduction.
o Typical (“CTI’”): 90% of patients have typical flutter with counterclockwise reentry around the tricuspid valve.
Sawtooth “F” waves are negative in the inferior leads based on counterclockwise conduction down the right
atrial anterolateral free wall, across the cavotricuspid isthmus, and more slowly up the interatrial septum
o Atypical forms of atrial flutter also exist, with a wide variety of atrial rates and p wave morphologies. These are
more common after catheter/surgical ablation of atrial fibrillation
● Pathophysiology: Macro-reentrant circuit
● Treatment:
o If 2:1 block, can first trial vagal maneuvers. Adenosine may also be trialed and generally will transiently slow
A:V conduction and the ventricular rate but will not terminate atrial flutter (6mg rapid IV push, followed by
12mg push if no response; if administered through a central line, the doses are 3mg-->6 mg).
o Medical management: Anticoagulation and rate/rhythm control, similar to AFib
o Always rate control first with BB, CCB, and/or digoxin before attempting rhythm control with class IA or IC agents
(because these anti-arrhythmics can facilitate embolization of an atrial thrombus as well as faciliatate 1:1 ventricular
conduction with rates in the 300’s. Amiodarone 200mg QD can be used to prevent recurrence. DCCV can be
considered if atrial flutter is associated with hypotension or decompensated heart failure. Typical flutter is most
amenable to catheter ablation
Atrial fibrillation
● Nomenclature:
o Paroxysmal: Recurrent AF (≥ 2 episodes) that terminates spontaneously within 7 days. Episodes of AF of ≤ 48
hours duration that are terminated with electrical or pharmacologic cardioversion should also be classified as
paroxysmal AF episodes.
o Persistent: Continuous AF that is sustained beyond 7 days. Episodes in which a decision to cardiovert the patient
after ≥ 48 hours of AF, but prior to 7 days, should also be classified as persistent AF episodes.
o Long-standing persistent: Duration > 12 months; efforts to terminate, either chemically or electrically, are typically
unsuccessful although catheter ablation may restore sinus rhythm in some patients.
o Permanent: Persistent AF where further attempts at rhythm control are indefinitely deferred
● Pathophysiology: AF results from an abnormal atrial response to reentry and/or rapid focal ectopic firing. In
the case of reentry, fibrillatory activity may be generated from a single localized reentry circuit or result
from multiple functional reentry circuits that vary in time and space. Alternatively, there may be an ectopic
focus that generates regularly firing, rapid discharges.
o Natural history of AF may involve progression from paroxysmal to persistent to long-standing persistent
forms. At the tissue level, this can result from atrial remodeling caused by the arrhythmia itself,
progressive fibrosis, and worsening of underlying heart disease. AF-related electric remodeling results
from altered expression and function of cardiac ion channels, which favor the development of
functional reentry substrates. With AF termination, some of these changes can be reversible, a process
known as reverse remodeling. If left untreated, however, the remodeling and fibrosis can progress
which contribute to persistent AF.
● Management
o Stable AF: rate versus rhythm control. If AF is self-limited, or has a potentially reversible cause,
restoration of normal sinus rhythm should be pursued. Pharmacological or direct current cardioversion
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(DCCV) has a higher success rate when AF has been present for less than 24 hours. Remember the
adage, “AF begets AF” (through irreversible electrical remodeling).
▪ Studies that have examined rate control vs medical rhythm control have not detected differences in
mortality or stroke rates.
▪ Caveats: these studies enrolled predominantly older patients (average age 70), most of whom had
persistent AF in the setting of structural heart disease and were able to tolerate AF from a
symptomatic standpoint; younger patients and those with severe symptoms from AF were
underrepresented. In addition, follow-up was limited to just a few years. Thus, the results of these
trials do not necessarily apply to younger patients without heart disease or those whose
dependency on SR is likely to change appreciably over time.
o Unstable AF 🡪 DCCV: patients with hypotension, hypoxemia, decompensated heart failure, pre-
excitation, worsening ischemia, angina or decreased responsiveness often necessitate emergent
DCCV, ideally preceded by sedation (usually fentanyl/midazolam or propofol depending on patient
stability and coordinated by cardiac anesthesia, CCU or ER team). Alternatively, amiodarone may be
used in conjunction with neo (given reflex bradycardia) in patients who are hypotensive. In addition,
amiodarone may help to maintain SR after DCCV.
o Acute rate control usually achieved through AV nodal blockers (see Table 2).
▪ While in the CCU/SDU, be aware of the negative inotropic effects of BB & CCB
▪ In the case of atrial fibrillation in sepsis, a recent large retrospective analysis showed that IV BBs
were associated with reduced hospital mortality when compared with CCBs, digoxin, and
amiodarone.8
Atrial Fibrillation with RVR: https://litfl.com/atrial-fibrillation-ecg-library/
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Table 1: Summary of Trials Examining Rate vs Rhythm Control in AF
Trial Characteristics Results

Pharmacological -Randomized trial (N=252) -No difference in primary endpoint
Intervention in Atrial -Primary endpoint: Symptom improvement -Rhythm control strategy
Fibrillation2 -Rate control with diltiazem (N=125) vs demonstrated improved exercise
(PIAF) rhythm control with DCCV+amiodarone tolerance, but hospital admissions
Lancet, 2000 (N=127) were more frequent in this group
-F/u interval: 1 year
Atrial Fibrillation Follow- -Randomized multicenter trial (N=4060) -No difference in primary endpoint
up Investigation of -Primary endpoint: Overall mortality overall
Rhythm Management3 -Rate control with digoxin/BB/or -Rate control strategy demonstrated
(AFFIRM) CCB+warfarin vs rhythm control (many mortality reduction for patients over
NEJM, 2002 different agents used) the age of 65 (HR 0.76) and those
-F/u interval: 3.5 years who did not have a history of heart
failure (HR 0.69)
-Rhythm control group with more
hospitalizations and adverse drug
effects
Rate Control versus -Randomized trial (N=522) -Rate control non-inferior to rhythm
Electrical Cardioversion -Primary endpoint: Composite of CV death, control in terms of primary endpoint
for Persistent Atrial admission for CHF, severe bleeding, need
Fibrillation Study Group4 for PPM, or severe drug side effect
(RACE) -Rate control with digoxin/BB/or CCB
NEJM, 2002 (N=256) vs rhythm control with DCCV+anti-
arrhythmic (many agents used) (N=266)
-F/u interval: 2.3 years
Randomized trial of rate- -Randomized multicenter trial (N=200) -No difference in terms of mortality,
control versus rhythm- -Primary endpoint: Composite of death, morbidity, and quality of life
control in persistent need for CPR, CVA, and systemic -However during follow up period,
atrial fibrillation5 embolism only 23% of rhythm control group
(STAF) -Rate control (N=100) vs rhythm control remained in NSR, after up to 4
JACC, 2003 (N=100) DCCVs
-F/u interval: 1.6 years
Rate control vs rhythm -Randomized multicenter trial (N=205) -No difference in primary endpoint
control in patients with -Primary endpoint: Composite of all-cause -Rhythm control strategy
nonvalvular persistent mortality, number of thromboembolic demonstrated improved exercise
atrial fibrillation: the events, and major bleeding tolerance, but hospital admissions
results of the Polish How -Rate control (N=101) vs rhythm control were more frequent in this group
to Treat Chronic Atrial with stepwise regimen of: disopyramide, (74% vs 12%)
Fibrillation6 propafenone, sotalol, and amiodarone
(HOT CAFE) (N=104)
Chest, 2004 -F/u interval: 1.7 years
Rhythm control versus -Randomized multicenter trial (N=1376) in -Rhythm control strategy does not
rate control for atrial patients with both AF and CHF reduce the rate of CV death when
fibrillation and heart -Primary endpoint: Time to death from all compared to rate control
failure7 cardiovascular causes -Also no difference in all-cause
(AF-CHF) -Rate control (N=694) vs rhythm control mortality, stroke, and worsening HF
(N=682)
NEJM, 2008 -F/u interval: 3.1 years
Early Rhythm-Control -Randomized multicenter trial (N=2789) - Rhythm control strategy reduced
Therapy in Patients with -Primary endpoint: composite CV death, composite of CV death, CVA, or
Atrial Fibrillation36 CVA, or hospitalization hospitalization (HR, 0.79; P=0.005)
- Rhythm control vs usual care - No statistical difference in safety
NEJM, 2020 -F/u interval: 5.1 years (stopped early) outcomes between groups
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Rhythm Control Strategies: Before initiating antiarrhythmic drug (AAD) therapy, treatment of precipitating or reversible
causes of AF should be pursued. The goal of AAD therapy include a reduction in the frequency and duration of episodes
of AF as well as an emerging goal of reducing mortality and hospitalizations associated with this condition. See Figure 1
and Table 3.
Electrical Cardioversion (See EP Procedures section for more information)

● DCCV is the most effective method of restoration of SR, and is successful at least 80% of the time.
● If the first attempt fails, a repeated shock can be delivered following the administration of an AAD (amiodarone,
flecainide, ibutilide/dofetilide, propafenone or sotalol). However, if DCCV continues to fail, particularly if only able to
induce short periods of SR between relapses, repeated attempts are not recommended. DCCV is relatively
contraindicated in those with digitalis toxicity or hypokalemia.
● Pre-procedure anticoagulation: patients with AF of 48 hour duration or longer should be anticoagulated for at least 3
weeks prior
o An alternative strategy is to perform TEE in search of LA thrombus. If no thrombus can be found, DCCV can be
performed immediately after anticoagulation with UFH or another agent has been started. Patients are then
transitioned to oral anticoagulation. In the ACUTE trial, outcomes with TEE guidance have been found to be
similar to the traditional prolonged anticoagulation strategy.9
● Post-procedure anticoagulation: all patients should receive AC for at least 4 weeks following DCCV as risk of
thromboembolism is high in the post-cardioversion period due to changes in cardiac conduction and myocardial
stunning.
Chemical Cardioversion and Maintenance of SR therapy

● In general, chemical cardioversion is less effective than DCCV. The success is significantly higher for acute (< 7
days) compared with longer-duration AF. Moreover, drug-induced torsades de pointes and other serious
arrhythmias may result when using AADs for cardioversion. If desired, flecainide, propafenone or ibutilide are the
recommended agents, see table 3 for further details.
Catheter Ablation - Trials
AATAC (2016): In patients with symptomatic (NYHA II-III) heart failure with reduced ejection fraction (HFrEF, LVEF
●
≤40%) and persistent atrial fibrillation (AF) chosen for a rhythm control strategy, AF ablation was associated with a
36% absolute increase in AF-free survival at 24 months. There was also a 26% absolute reduction in unplanned
hospitalizations and a 10% absolute reduction in overall mortality with AF ablation.10
●
FIRE AND ICE (2016): In patients with symptomatic paroxysmal atrial fibrillation (pAF) resistant to antiarrhythmic
drugs referred for pulmonary vein isolation (PVI), balloon cryoablation is noninferior to radiofrequency ablation in
regards to a primary outcome of composite clinical failure (recurrent AF, prescription of antiarrhythmic drugs, or repeat
ablation) more than 90 days after the index procedure.11
CASTLE-AF (2018): In patients with AF and symptomatic (NYHA II-IV) systolic heart failure (LVEF ≤ 35%), catheter
●
ablation is associated with a 16.1% absolute reduction in death or hospitalization for heart failure when compared to
medical therapy (rate or rhythm control). This difference was driven both by a 11.6% absolute reduction in death and
a 15.2% absolute reduction in hospitalization for heart failure. Catheter ablation was also associated with greater
improvement in LVEF and long-term maintenance of sinus rhythm. 12
●
CABANA (2019): In patients with atrial fibrillation (AF) requiring treatment, catheter ablation was not associated with a
significant reduction in death, disabling stroke, serious bleeding, or cardiac arrest when compared to medical therapy
at 12 months. The results of this trial were incorporated in the AHA/ACC 2019 AF guidelines and as a result AF
ablation in patients without systolic heart failure is likely to remain an elective procedure performed with the primary
purpose of symptom relief in patients who have failed, are intolerant of, or decline anti-arrhythmic therapy. 13
●
EAST-AFNET4 (2020): In patients recently diagnosed with AF (~1month) rhythm control was superior to usual care
and the trial was stopped early, because the primary-outcome composite (CV death, CVA, or hospitalization) was
significantly lower in the rhythm control group. While rhythm control was mostly with AAD, about 8% of participants
underwent catheter ablation by 1 year and 20% by 2 years. This trial has not dramatically altered guidelines as of yet,
but its findings alongside those from CABANA and CASTLE-AF suggest that normal sinus rhythm matters. 36
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Table 2: IV and Oral Agents for HR control in AF
Maintenance
Drug LOE Loading Dose Onset Major Side Effects
Dose
500 mcg/kg IV 60–200
Esmolol* I-C 5 min ↓ BP/HR; HB; asthma, HF
over 1 min mcg/kg/min IV
2.5–5 mg IV
Metoprolol* I-C over 2 min; up 5 min NA ↓ BP/HR; HB; asthma, HF
to 3 doses
Propranolol* I-C 0.15 mg/kg IV 5 min NA ↓ BP/HR; HB; asthma, HF
0.25 mg/kg IV 2-
Diltiazem* I-B 5–15 mg/h IV ↓ BP; HB, HF
over 2 min 7min
0.075–0.15
3-
Verapamil* I-B mg/kg IV over NA ↓ BP; HB, HF
5min
2 min
↓BP; HB, pulmonary toxicity, skin discoloration,
150mg IV over hypo-/hyperthyroidism, corneal deposition, optic

Amiodarone^ IIa/C Days 0.5–1 mg/min IV
10 min neuropathy, warfarin interaction, sinus
bradycardia
1.5 mg load:
0.25 mg IV q2
60+ 0.125–0.375 mg
Digoxin*^ I-B x6 Digitalis toxicity, HB, ↓ HR
min daily IV/PO
OR 0.75 mg IV
+ 0.375 Q6H
LOE: Level of evidence. *Avoid in patients with known or suspected accessory pathway. ^Useful in patients with
concomitant HF.
Figure 1: Choice of Antiarrhythmic Drug (AAD) Based on Cardiovascular Comorbidities
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Table 3: Agents maintenance of SR

Agents for Conversion to SR (please refer to pharmacy for institutional dosing protocols)
An intravenous IKr blocker that also enhances the late inward sodium current is
~50% effective at restoring SR. It is slightly more effective for AFL than for AF.
When used, patients need to be monitored closely for QT prolongation and TdP
Ibutilide
for at least 2 hours after infusionIncreases success rate of cardioversion and
prevents relapses by suppressing atrial ectopy, however high incidence of
potentially severe extracardiac side effects limits its use and makes it second-line
or last-resort agent in non-critically ill patients.
A high dose of flecainide (200–300mg) can be used as an outpatient strategy
once treatment has proven safe in-hospital for selected patients without sinus or
Flecainide AV node dysfunction, BBB, QT-interval prolongation, Brugada syndrome or
structural heart disease. The overall rate of conversion tends to be >85%. Before
these agents are initiated, a BB or CCB should be given to prevent atrial flutter
with 1:1 ventricular conduction.
Most useful in paroxysmal afib and can be used in a style similar to flecanide as a
Propafenone pill in the pocket outpatient strategy. Avoid in those with ischemic heart disease
or LV dysfunction as can be pro-arrhythmic. Before this agent is initiated, a BB or
CCB should be given to prevent atrial flutter with 1:1 ventricular conduction.
Maintenance Daily Dose (OR vs. control of maintaining SR after AF conversion, # of trials)
More effective than class I drugs, sotalol or placebo in the long-term maintenance
of SR in paroxysmal or persistent AF refractory to other drugs. Drug of choice in
Amiodarone patients with LVH, HF, CAD or prior MI since associated with low risk of pro-
100–400 mg arrhythmia. Also effective for HR control (BB properties). Increases success rate
(6.8, 2 trials) of cardioversion and prevents relapses by suppressing atrial ectopy, however
high incidence of potentially severe extracardiac side effects limits its use and
makes it second-line or last-resort agent in non-critically ill patients.
Flecainide Effective in postponing the first recurrence of AF and overall time spent in AF.
100–300 mg Limited to patients with no structural (LV dysfunction) or ischemic heart disease.
(4.3, 3 trials) Adverse effects include VT, HF and conversion to AFL with RVR.
Propafenone Useful to prevent first recurrence of AF and post-DCCV. Avoid in those with
450–900 mg ischemic heart disease or LV dysfunction as can be pro-arrhythmic.
(3.0, 4 trials)
Prevents recurrent AF after DCCV. Considered first-line therapy in vagally
Disopyramide
induced AF; has negative inotropic and dromotropic effects that may cause HF or
400–750 mg
AV block; this negative inotropic effect may be desirable in HCM associated with
(2.9, 2 trials)
dynamic outflow tract obstruction. Associated with TdP.
Sotalol Not effective for chemical cardioversion but useful to prevent AF. Min effective
160–320 mg dose is 160mg daily. Avoid in patients with asthma, HF, renal failure or prolonged
(2.5, 4 trials) QT. Requires inpatient initiation of therapy.
Useful for chemical cardioversion and maintenance of SR. Can be used in
Dofetilide
structural heart disease/CHF. Due to risk of pro-arrhythmia (QT prolongation), it
500–1000 mcg
must be started as inpatient, titrate to renal function.
Prolongs time to recurrence of AF. Decreases hospitalization rates. Not useful for
chemical cardioversion or improving success of DCCV. Less efficacious than
Dronedarone amiodarone but better tolerated. Associated with a significant reduction in the risk
800 mg of stroke. Avoid in class IV or recently decompensated HF, particularly if
depressed LV function (< 35%). Associated with increased mortality in patients
with CHF or permanent AF.
Anticoagulation: General Considerations

All patients with AF should be on anticoagulation except those at the lowest risk of thromboembolic stroke. Risk is greatly
increased by personal history. The CHA2DS2VASc risk score is a useful tool for assessing ischemic stroke risk in patients
with AF. Note that the AHA/ACC 2019 guidelines for atrial fibrillation recommend that NOACs – including dabigatran,
rivaroxaban, apixaban and edoxaban – are now the preferred recommended drug class over warfarin to reduce stroke risk
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in appropriate AFib patients in men with a CHA2DS2VASc of 2 or more and 3 or more in women. In men with a
CHA2DS2VASc of 1 and women with a score of 2, the decision to initiate oral anticoagulation depends on if the extra
point is conferred by age 65-74 as this is the strongest risk factor. Female gender alone does not confer significantly extra
risk for embolic stroke in the absence of other risk factors and does not necessitate anticoagulation by itself. Patients who
have moderate-to-severe mitral stenosis or a mechanical heart valve should continue to be anticoagulated with warfarin. 1
Anticoagulation: Specific Agents
Agent Commentary
Warfarin therapy should be targeted to an INR 2–3, as measured weekly during initiation of therapy and
Warfarin monthly thereafter. On average, warfarin provides an annual reduction of 68% in relative risk for stroke.
Approved as an alternative to warfarin for non-valvular AF, with superiority in the prevention of stroke
Dabigatran compared to warfarin in the RE-LY trial.15 Pro-drug, rapidly converted to active direct thrombin inhibitor.
It is administered in fixed doses without laboratory monitoring of anticoagulation intensity. At a dose of
150 mg bid, it reduced the rate of stroke by 34% with no increase in major bleeding when compared to
warfarin. For those with CrCl 15–30, a dose of 75 mg bid was also approved (dabigatran is not indicated
for patients with CrCl < 15).
A direct-thrombin inhibitor. In ROCKET-AF trial, it proved to be non-inferior to warfarin for the prevention
Rivaroxaban of stroke and systemic embolism, with no difference in risk of major bleeding although ICH and fatal
bleeding occurred less frequently with rivaroxaban. 16 It is administered at a dose of 20 mg daily, with
dose reduction to 15 mg if renal impairment.
Apixaban A direct-thrombin inhibitor, found to be superior to warfarin in preventing stroke or systemic embolism in
the ARISTOTLE trial. It also caused less bleeding and lower mortality.17 It is administered at a dose of 5
mg BID, or 2.5 mg BID if any two of the following: Age ≥ 80 years old, body weight ≤ 60 kg, serum Cr ≥
1.5. In the AVERROES trial in patients with AF thought to be unsuitable candidates for anticoagulation
with VKA, Apixaban reduced the risk of stroke without increasing the risk of major bleeding compared to
aspirin.18
Edoxaban A direct-thrombin inhibitor, found to be equal in efficacy to warfarin in preventing stroke or systemic
embolism in ENGAGE AF-TIMI 48. It caused less bleeding.19 It was also noted to be non-inferior to
warfarin in atrial fibrillation following TAVR, but with more bleeding in the ENVISAGE-TAVI AF trial in
2021.42 It is administered at a dose of 60 mg daily (or 30 mg daily for CrCl 15-50mL/min). Edoxaban is
currently less commonly used given more frequent clinical experience with rivaroxaban and apixaban as
well as equivalence rather than superiority to warfarin.
Aspirin A poor substitute for anticoagulation, though perhaps a plausible alternative in a very low-risk patient
(i.e., CHA2DS2-Vasc = 1) or one at very high risk of bleeding. The relative risk reduction for stroke is
variable, but perhaps around 20%.
Anticoagulation: Special Considerations for Patients Post-PCI

Up to 1 in 10 patients undergoing PCI have AF, and in general, the literature is in the early stages of understanding
optimal anticoagulation in these cases. The WOEST trial found that in patients on oral anticoagulation undergoing PCI,
use of clopidogrel + warfarin (double therapy) was associated with reduction in bleeding complications as well as lower
combined secondary endpoints (death, MI, revascularization, stroke, stent thrombosis) when compared to the use of
clopidogrel + warfarin + ASA (triple therapy).20 Since the publication of WOEST, the ACC/AHA guidelines suggest that
patients with nonvalvular AF undergoing PCI be maintained on oral anticoagulation and clopidogrel without aspirin. 14
There is increasing evidence supporting the use of DOACs in patients with AF (RE-LY, ARISTOTLE, ROCKET AF). 15-17 A
more recent study, PIONEER AF-PCI, assessed the use of DOACs in patients with nonvalvular AF undergoing PCI with
stent placement and found that low-dose rivaroxaban plus either single or dual antiplatelet therapy reduces the risk of
bleeding when compared to warfarin + DAPT at 1 year post-procedure without having a significant effect on the rate of
major adverse cardiovascular events.21 Note that the doses of rivaroxaban (15 mg daily or 2.5 mg BID) used in this trial
are not FDA approved for AF or ACS and the results of this trial are preliminary with further trials now ongoing.
Patient with Contraindications to AC: Percutaneous and Surgical Left Atrial Appendage (LAA) Closure
● LAA closure has emerged as a mechanical alternative to pharmacologic stroke prevention in patients with a
contraindication to anticoagulation. There are multiple LAA occlusion devices, including the WATCHMAN, Amulet,
WaveCrest, and LARIAT system devices (Amulet and WaveCrest are currently investigational in the U.S.).
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● PROTECT-AF trial: showed that percutaneous LAA closure with the WATCHMAN device was non-inferior to
warfarin for the prevention of the composite endpoint of ischemic stroke, hemorrhagic stroke, cardiovascular death,
and systemic embolism.22 The PREVAIL Trial subsequently found that LAA occlusion was non-inferior to warfarin
for ischemic stroke prevention, although non-inferiority was not achieved for the overall efficacy endpoint (stroke,
systemic embolism, and cardiovascular/unexplained death).23
● Based on PROTECT & PREVAIL, the WATCHMAN device was approved by the in March 2015 for patients with
nonvalvular AF for whom long-term anticoagulation is indicated but who have a contraindication.
o After placement of an LAA occlusion device, patients are treated with oral anticoagulation + ASA for 6
weeks, followed (if successful LAA closure is documented by TEE at 6 weeks post-implant) by clopidogrel
+ ASA for 6 months, followed by ASA for life. Patients with absolute contraindication to oral anticoagulants
are given DAPT for 6 months.
● In the LAAOS III trial, investigators were able to conclude that surgical occlusion of the LAA in patients with atrial
fibrillation undergoing cardiac surgery and who went on to be anticoagulated had a lower risk of stroke than those
who did not.43
Other Special Considerations in AF

● Post-MI AF: incidence of AF after AMI varies between 10–20% at 30 days. It is more common in older patients with
higher Killip class (more severe AMI) and more severe LV dysfunction. Post-MI AF is associated with higher 30 day
mortality compared to NSR (29.3% vs. 19%). Stroke rates are also higher in this population. Management includes
urgent DCCV if RVR produces intractable ischemia or instability. IV beta-blockers are also indicated if stable.
● AF and Pre-Excitation (WPW):
o As a general rule, IV beta-blockers, CCB, digitalis, and adenosine are contraindicated, as they can facilitate
anterograde conduction through the accessory pathway and result in acceleration of the ventricular rate,
hypotension or VF.
o For hemodynamically stable: a class IA antiarrhythmic IV (typically procainamide) or amiodarone
● “Reversible” AF: Guidelines have proposed that AF can occur as an isolated event due to a reversible stressor (e.g.,
thyrotoxicosis, infection, MI, cardiac surgery).
o In the Framingham cohort, 62% of patients with an isolated episode of AF due to a “reversible” cause had
recurrent AF at 15 years. 24 Overall stroke risk and mortality were similar in groups with and without a reversible
stressor
o Given higher risk for recurrent AF and elevated stroke risk, AC should be considered. However, more research is
still needed here.
●
AF after Cardiac Surgery: This is a relatively common post-surgical complication, with an incidence of 20-50%. A
recent study found that there was no difference between rate and rhythm control in regards to total number of hospital
days, rates of death, and serious adverse events such as thromboembolism or bleeding. At 60 days after AF onset,
both patients receiving rate and those receiving rhythm control had similarly low rates of persistent AF. 25
●
AF and Heart Failure: The 2016 Ablation versus Amiodarone for Treatment of persistent Atrial fibrillation in patients
with congestive heart failure and an implanted device (AATAC) trial evaluated the efficacy of AF ablation versus
amiodarone in patients with symptomatic HFrEF and persistent AF. At 2 years, ablation was associated with a 36%
absolute increase in AF-free survival compared to amiodarone. Patients receiving AF ablation also experienced a
26% absolute reduction in unplanned hospitalizations and 10% absolute reduction in overall mortality.
o AATAC trial suggests that among patients with HFrEF and AF, AF ablation is potentially superior to amiodarone
as a method for achieving and maintaining sinus rhythm in terms of AF-free survival as well as in regards to
cardiovascular outcomes and mortality.26
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28. Giugliano, Robert P., et al. "Edoxaban versus warfarin in patients with atrial fibrillation." New England Journal of
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30. Gibson, C. Michael, et al. "Prevention of bleeding in patients with atrial fibrillation undergoing PCI." New England
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device in patients with atrial fibrillation versus long-term warfarin therapy: the PREVAIL trial." Journal of the
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Wide Complex Tachycardias
A wide complex tachycardia (WCT) refers to a tachycardia with QRS duration QRS ≥ 120ms. Generally, the approach to
WCT is to assume it is a ventricular tachycardia (VT) until proven otherwise. VT is the most common and most malignant
of the WCTs, however a broader differential should be considered.
Differential Diagnosis of WCT:
● Ventricular Tachycardia(70% of the time): ectopic or reentrant ventricular impulse spreads electrical activity slowly
through the ventricular myocytes and produces a wide QRS. It originates below or very rarely at the bundle of His.
o Monomorphic VT: has a variety of etiologies (infarct/scar being a common one)
o Polymorphic in the setting of a normal QTc (<500 ms) is often due to ischemia
● Supraventricular Tachycardia (SVT) with Aberrancy( 30% of the time): SVT (e.g. AT, AF) conducts an electrical
impulse into the ventricles along the standard His-Purkinje system, but is slowed along that path as a result of:
o Pre-existing or rate-related aberrant intraventricular conduction (e.g. bundle-branch block)
o Drugs (e.g. class 1C anti-arrhythmics, digoxin), electrolyte abnormalities (e.g. hyperkalemia), or ischemia
o Slowing of electrical conduction through the ventricles results in wide complex QRS
● Supraventricular Tachycardia with Pre-excitation: SVT conducts an electrical impulse into the ventricles through an
aberrant conduction pathway in which depolarization advances slowly through the ventricular myocytes rather than
quickly along the His-Purkinje system (for example, an underlying RBBB)
● Pacemaker-Related Tachycardia
o Pacemaker-mediated tachycardia: “Endless loop” tachycardia in which the aberrant circuit is generated by the
pacemaker
▪ Electricity arising from the ventricular pacing lead conducts retrograde (typically, through the AV node) to the
atria, producing atrial depolarization (seen as a retrograde P wave)
▪ The atrial depolarization is sequentially recognized by the pacemaker, leading to atrial-sensed ventricular
pacing
▪ Another ventricular depolarization can conduct in retrograde fashion again through the AV node and produce
a circuit
o Pacemaker-tracked tachycardia: SVT is tracked by the pacemaker
▪ SVT is sensed by the pacemaker, producing a wide complex beat.
(This rhythm is less common now that devices have become sophisticated at mode switching to non-tracking
modes such as VVI or DDI when the algorithm recognizes SVT or AF
o *Note: Both pacemaker-tracked and pacemaker-mediated tachycardia can be terminated by the application of a
magnet to the pacemaker, which changes the pacing mode to an asynchronous mode (VOO or DOO). This is not
true for most ICDs, in which the magnet will temporarily disable ICD therapy, but will not alter the pacing mode.
ECG diagnosis of WCT
Quick reference:
1. Consider the substrate:

a. History of CAD or cardiomyopathy favors VT
b. Young age, known history of atrial tachyarrhythmias, or baseline bundle branch block favors SVT with
aberrancy
c. Medications in overdose: Class 1A/3 antiarrhythmics, antipsychotics, antidepressants, antiemetics all
favor WCT
2. Consider classical ECG features of VT:
a. AV dissociation (including fusion/capture beats)
b. Positive concordance (RS waves in V1-V6, suggesting basal VT focus)
c. Negative concordance (QS waves in V1-V6, suggesting apical VT focus)
3. Consider the axis and the QRS width:
a. Extreme axis deviation: northwest axis (positive in aVR, suggesting a ventricular focus or negative in I
and AVF) or with a superior axis (II, III, aVF are negative)
b. Wide QRS (RBBB > 140 ms, LBBB > 160 ms)
4. Consider using the Brugada Algorithm:
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Clarifying the Brugada Algorithm:
1. Absence of an RS complex in all precordial leads? If yes, then VT.

a. This basically means that the QRS morphology in every precordial lead is either a Q wave or an R wave -
i.e. positive or negative concordance.
2. R to S interval >100 ms in one precordial lead? If yes, then VT.
a. This criteria means that you find an RS complex in one of the precordial leads, and measure the distance
from the beginning of the R wave to the nadir of the S wave. If this distance is > 100 ms, this is likely VT.
b. Why? Well, in a typical RBBB or LBBB, remember that the other bundle is working normally. So the initial
part of the RBBB or LBBB complex should be a quick (sharp deflection) because ventricular activation is
occurring through the His-Purkinje system. The second part of the complex is wide/slurred, because
electricity is moving through the myocardium (rather than through the conduction system, and thus is
inherently slow) in order to depolarize the other ventricle.
c. This means that if the initial part of QRS complex is wide (rS >100 ms), rather than a nice sharp
deflection, that is more typical of direct myocardial activation (that is, VT), since typically conduction
through the His-Purkinje tends to be much faster.
3. AV dissociation? If yes, then VT.
a. AV dissociation, including fusion or capture beats (examples below), are consistent with VT.
4. Morphology criteria for VT present both in precordial leads V1-2 and V6.
a. This criteria is more complicated, and comes down to an understanding of what a normal RBBB and
LBBB should look like:
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a. A typical RBBB looks like an RSR' complex in V1, with R smaller than R', and an RS complex in V6, with
R/S >1. So any complex that looks significantly different than this (for example, a monophasic R, qR
complex, or RSR' complex with R > R') favors a diagnosis of VT.
b. A typical LBBB looks like an rS complex in V1, and an R in V6. So any complex that looks significantly
different than this (for example, a wide R wave or wide notched S wave in V1, or a Q wave in V6) favors a
diagnosis of VT.
Additional Tips for Identifying Types of WCTs

Examine the telemetry strip: Look for R-on-T at the start of the WCT, also look for AV dissociation (P waves
marching through discordant to QRS, capture beats, fusion beats)
● Capture beat (labeled “C” in strip below): Atrial depolarization that is able to normally conduct a narrow QRS
and transiently interrupts the spread of electricity from the VT focus
● Fusion beat (labeled “F” in strip below): Simultaneous conduction and blending on ECG of supraventricular beat
and wide complex ventricular beat
● Beat-to-beat variability in QRS morphology: Characteristic in polymorphic VT or SVT/AF with varying degrees of
pre-excitation/fusion or rate-related aberrancy.
● Pacer spikes: may indicate pacemaker etiology (paced QRS followed by retrograde P)
QRS morphology:
● A QRS > 160 msec has a 20:1 likelihood ratio of being VT. VT can be narrow (<140 msec) if it arises near the His-
Purkinje system
● If LBBB or RBBB pattern, look for morphologies suggestive of VT:
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● Note: If there is VT with a RBBB pattern + inferiorly directed axis in a patient with a structurally normal heart, consider
LVOT VT. Interestingly, this rhythm can respond to drugs that reduce cAMP, such as adenosine, verapamil or beta-
blockers
● Note: If there is VT with a LBBB pattern + inferiorly directed axis in a patient with a structurally normal heart, consider
RVOT VT. This rhythm also responds to drugs that reduce cAMP
There are many formal criteria for distinguishing VT from other causes of WCT with two others listed below in addition to
the Brugada criteria discussed in depth above. They are more time consuming and unwieldy in comparison to the quick
approach above. If in doubt, assume VT.
1. Vereckei criteria
2. R wave peak time (RWPT)
Clinical Management of WCT
Consider all WCT as VT until proven otherwise. At least 80% of WCT in patients with ischemic or structural heart disease
is VT.
Initial Management According to Stability
● Pulseless: Immediately start the pulseless VT ACLS algorithm and prepare for unsynchronized DCCV
● Hemodynamically unstable or highly symptomatic: Prepare for synchronized DCCV (+ fentanyl/versed for sedation)
and start amiodarone (150 mg x 1 Q 3–5 min, then drip @ 1 mg/min), and/or lidocaine (100 mg x 1, then drip @ 1–4
mg/min) unless concern for TdP (prolongs QTc)
o Put pads on the patient
o CALL FOR HELP:
▪ Fellow resident(s) and your attending
▪ Ward Cardiology fellow and/or EP Fellow on Call
▪ RICU if anticipate potential need for intubation
▪ Cardiac anesthesia for conscious sedation (though often no time)
o Worry about etiology after stabilization
▪ If regular, monomorphic, and there is some suspicion for SVT, consider adenosine as both a diagnostic (can
slow down rhythm to make easier to dx) and therapeutic intervention
▪ If pacemaker-mediated or tracked WCT→ apply magnet
● Hemodynamically stable:
o Put pads on patient, call for help; you have some time to determine etiology of WCT, but most patients do not
tolerate persistent VT (particularly if critically ill) and will likely develop hemodynamic instability
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o If you suspect VT→ start amiodarone and/or lidocaine

o Be ready to cardiovert, consider cardioverting stable VT that persists for many minutes (requires the same
algorithm as above)
Further Management According to Etiology
Monomorphic VT:
● Anti-arrhythmic drugs (AAD): Temporizing measure while reversing underlying cause. Do not reduce mortality or
prevent SCD, may increase mortality when used as monotherapy for VT/VF prevention.
o Recurrent, stable VT: Amiodarone and procainamide
o WPW possible: Lidocaine or procainamide preferred (both reduce accessory pathway conduction)
o Amiodarone: 150 mg IV bolus over 3–5 min (re-bolus as needed), followed by gtt load at 1mg/min for 6hrs
and then 0.5 mg/min for 18 hours.
▪ Effective for both ventricular and supraventricular arrhythmias (Na+ and K+ channel blocker; slows AV nodal
conduction as well) and has superior efficacy over lidocaine
▪ AV nodal blockade effects predominate until 6–7 grams administered. A full “amio load” for VT is 10 grams
(given over a period of days)
▪ AVOID IN TdP: nodal-blocking activity slows HR and K+ channel blocking effect prolongs the QTc, which can
promote TdP
o Lidocaine: 1–1.5 mg/kg IV bolus over 2–3 minutes (often 100mg), followed by 1–4 mg/min infusion (often
start at 1)
o Procainamide: Infuse at 20–50 mg/min until arrhythmia is controlled (stop if hypotension or if QRS complex
widens by 50% of original width, or total of 17 mg/kg is given). Maintenance infusion usually 1–6 mg/min
● Electrolytes: replete Magnesium and potassium
● Electricity: Asynchronous DCCV (for pulseless VT) vs synchronized DCCV (for VT w/ pulse). Other options if
patient has a Pacemaker include:
o Over-drive pacing (anti-tachycardia pacing) at a faster rate than the VT may be useful in some cases (call Ward
fellow and/or EP for help w/ ATP).
Refractory monomorphic VT:

● Definitions: refractory to above pharmacologic measures
o Incessant VT = Hemodynamically stable VT >1hr
o VT Storm = Multiple bouts of unstable VT within 24hr
● Management:
o Sedation with intubation: reduces autonomic tone
o Treatment of underlying ischemia: revascularization, IABP support
o Catheter-based ablation therapy: Radiofrequency (RF) ablation is often performed for refractory VT or VT storm.
Acute procedural success (no inducible VT) rates are approximately 70%
Polymorphic VT:
● Torsades/PMVT w/ prolonged QT (on ECG from earlier in day)
o Electrolytes: Repletion of Mg2+ with 1–2 g IV bolus, with a total dose of 2–4 g over 10–15 min, can successfully
terminate TdP within 5 minutes in up to 75% of patients, and 15 minutes in most patients. Replete K+ as well.
o AAD: Lidocaine avoid nodal agents and amiodarone
o Chronotropes: Goal HR 80-100bpm will shorten the QTc and can abort the PMVT. Start IV infusion of
isoproterenol (2–6 mcg bolus followed by 2–20 mg/min OR dopamine at a starting rate of at least 300 mcg/min
o Electricity: Asynchronous DCCV (for sustained PMVT) or over-drive pacing at rates in the range of 80–100
bpm (to suppress pause-dependent initiation of PMVT).
● PMVT with normal QT (on ECG from earlier in day) is ischemia until proven otherwise 🡪 ACS pathway with
emergent cardiology evaluation for cath/revasc, can use AAD as above
SVT with Aberrancy:

● AAD: Treat as you would any other SVT; consider adenosine, BB, CCB, amiodarone, correct toxicities/drug
effect/electrolyte abnormalities
● Electricity: Synchronized DCCV if unstable or refractory symptoms
SVT with Pre-Excitation:

● AADs
o 1st line: Procainamide (1 gm over 50 min IV)
o 2nd line: Ibutilide (0.01 mg/kg over 10 minutes, max dose 1 mg, can repeat once after 20 mins)
o 3rd line: Amiodarone (150 mg IV x 1, can repeat many times🡪then 1mg/min gtt)
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o Caution: Adenosine should not be used in pre-excited AF (presents as irregular, WCT); refer to AVRT section for
management of SVT associated with WPW
● Electricity: DCCV for extremely symptomatic or unstable patients
Pacemaker-Mediated WCT:
● Magnet is 1st line therapy. Magnet will also stop the arrhythmia by mode switching to VOO or DOO to stop
sensing the atria. The magnet does not change the pacing mode for an ICD (it will disable the defibrillator
therapies) and thus will not terminate a PPM-mediated tachycardia in a patient with an ICD.
o EP will need to reprogram pacemaker reprogramming to prevent further episodes of PMT
● AAD: 2nd line: Adenosine, verapamil or beta-blockers can abort retrograde conduction and stop the circuit
Pacemaker-Tracked WCT: Treat SVT as you would any other SVT. Mode switch PPM to a non-tracking mode either by
EP interrogation or with magnet.
Maintenance Therapy
● Devices: ICDs are recommended for secondary prevention of VT/VF unless a reversible trigger is identified/treated
o The AVID trial demonstrated a 10% absolute mortality benefit with this strategy when compared to AAD alone
(see ICD Section for more information)
o Specific guidelines are available for IHD, NICM, and other specific cardiomyopathies (e.g. HCM)
● Medical management:
o Beta-blockers: reduce sympathetic tone, have some direct antiarrhythmic effect, and may reduce mortality in
patients with previous VT/VF
o AADs are often continued unless a reversible VT/VF trigger (e.g. ischemia) is identified and treated, although
there is no established mortality benefit with this strategy
o Patients with HFrEF should be treated with a BB, mineralocorticoid antagonist, ACEi/ARB/neprolysin inhibitor to
reduce SCD and all-cause mortality
● Procedures:
o Patients with VT/VF and ischemic heart disease should be revascularized as appropriate
o VT ablation:
▪ VT ablation is recommended in: patients with sustained VT that recurs despite AAD, when AAD are not
tolerated, incessant VT without a reversible cause
▪ Evidence:
o Among the earliest trials in VT ablation was SMASH-VT (NEJM, 2007) in which VT ablation was
associated with reduced incidence of ICD therapies.
o The VANISH trial (NEJM, 2016) randomized patients to escalation of AAD versus VT in patients
with ischemic cardiomyopathy with recurrent VT. VT ablation was associated with a 10% absolute
reduction in the primary endpoint (composite of death, VT storm, ICD shocks); there was no
difference in mortality
▪ See Chapter 5 – Electrophysiology Studies and Procedures for further details
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References:
1. Antunes, Eduardo, et al. "The differential diagnosis of a regular tachycardia with a wide QRS complex on the 12-
lead ECG: ventricular tachycardia, supraventricular tachycardia with aberrant intraventricular conduction, and
supraventricular tachycardia with anterograde conduction over an accessory pathway." Pacing and clinical
electrophysiology: PACE 17.9 (1994): 1515
2. Trial, Cardiac Arrhythmia Suppre4ssion. "Preliminary report: effect of encainide and flecainide on mortality in a
randomized trial of arrhythmia suppression after acute myocardial infarction." N. Engl. J. Med. 321 (1989): 406-
412
3. Jain, Rahul, et al. "Electrocardiographic features of arrhythmogenic right ventricular dysplasia." Circulation 120.6
(2009): 477
4. Bakker, Annelies LM, et al. "The Lewis lead: making recognition of P waves easy during wide QRS complex
tachycardia." Circulation 119.24 (2009): e592-e593
5. Brugada, Pedro, et al. "A new approach to the differential diagnosis of a regular tachycardia with a wide QRS
complex." Circulation 83.5 (1991): 1649-1659
6. Vereckei, András, et al. "New algorithm using only lead aVR for differential diagnosis of wide QRS complex
tachycardia." Heart rhythm 5.1 (2008): 89-98
7. Exner, Derek V., et al. "Beta-blocker use and survival in patients with ventricular fibrillation or symptomatic
ventricular tachycardia: the Antiarrhythmics Versus Implantable Defibrillators (AVID) trial." Journal of the
American College of Cardiology 34.2 (1999): 325-333
8. Defibrillators, Antiarrhythmics Versus Implantable. "Investigators. A comparison of antiarrhythmic-drug therapy
with implantable defibrillators in patients resuscitated from near-fatal ventricular arrhythmias." N Engl J
Med 337.22 (1997): 1576-1583
9. Sapp, John L., et al. "Ventricular tachycardia ablation versus escalation of antiarrhythmic drugs." New England
10. Tung, Roderick, et al. "Freedom from recurrent ventricular tachycardia after catheter ablation is associated with
improved survival in patients with structural heart disease: an International VT Ablation Center Collaborative
Group study." Heart rhythm 12.9 (2015): 1997-2007
11. Al-Khatib, Sana M., et al. "2017 AHA/ACC/HRS guideline for management of patients with ventricular arrhythmias
and the prevention of sudden cardiac death: a report of the American College of Cardiology/American Heart
Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society." Journal of the American
College of Cardiology 72.14 (2018): e91-e220
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Conduction Diseases and Bradyarrhythmias
A narrow complex tachycardia (NCT) refers to a tachycardia with QRS duration <120ms and typically implies normal
electromechanical conduction from a supraventricular origin. Generally, it is helpful to organize NCTs by mechanism
(automaticity, re-entry, or triggered activity) and anatomic origin (sinus node, atria, AV node).
Management of Unstable Bradycardia: CALL CODE, follow ACLS bradycardia protocol
Protocol: atropine 0.5mg IV q3-5min (max 3mg) 🡪 transcutaneous pacing +/- epinephrine gtt +/- dopamine gtt
Medications:
● atropine 0.5mg IV q3-5min (max 3mg) [avoid in Mobitz II/CHB]
● dopamine 5-15μg/kg/min (β1 predominant; usually 200-800 μg/min)
● epinephrine 2-10μg/min
● isoproterenol 2-10μg/min
● glucagon 3-10mg bolus followed by 3-5mg/h gtt for βB or CCB overdose
Transcutaneous pacing
1. Place Zoll pads, sedate (ideally fentanyl/midazolam with Anesthesia present, but can use morphine/lorazepam if
emergent)
2. set mode to pace, increase rate to 100bpm, and set pacing output (stimulus needed to capture) to 140mA (if code
setting, otherwise start lower), and ensure capture w/ pulse.
3. Intubation is not necessary for pacing, but can be considered for airway protection as part of ACLS protocol
4. Will require placement of transvenous pacing wire See Chapter 4 – Device Therapy
Pathophysiology of Bradyarrhythmias
Broadly, bradyarrhythmias can be characterized by one of two mechanisms:

1. Failure of impulse generation: decreased or failed SA node automaticity can result in too few electrical impulses
originating from the SA node. The most common bradyarrhythmia originating from the sinus node is sinus
bradycardia. When symptoms develop from such slowed rates that symptoms develop, a patient is said to have sick
sinus syndrome.
2. Failure of impulse propagation: when normal electrical impulses generated by the SA node (or another ectopic atrial
pacemaker) are not conducted properly from the atria down to the ventricles (by way of the AV node and His-Purkinjie
system) is termed heart block. This arises from abnormal conduction velocity and/or refractory periods throughout the
conducting system, almost exclusively owing to disease of the AV node or His-Purkinjie conduction pathways.
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Bradyarrhythmia by Site of Origin: SINUS NODE

Conduction disease involving the sinus node include sinus bradycardia and sinus node dysfunction
Sinus bradycardia
● ECG: HR less than 50-60 bpm, normal p wave axis
● Pathophysiology:
o Most often physiologic and asymptomatic, seen in healthy individuals, endurance athletes, and during sleep
where it is not uncommon to see rates briefly in the 30s or pauses of up to 2 seconds
o Pathophysiologic causes include SA node dysfunction, medications, 15-25% of MI (RCA supplies SA node in
60% of individuals), sleep apnea, and exaggerated vagal tone (e.g. vasovagal syncope) (Circulation, 2020;
142:15)
● Treatment:
o Acute, unstable: Call code + initiate ACLS Bradycardia algorithm with immediate placement of temporary
pacing pads on the patient (see management of unstable bradycardia section)
o Chronic treatment: See Chapter 4 – Device Therapy for indications for pacemaker therapy
Sinus node dysfunction (SND) (formerly sick sinus syndrome)

● Presentation: symptomatic bradycardia (dizziness, palpitations, pre-syncope, syncope)
o Numerous ECG abnormalities may contribute including Sinus bradycardia, Sinus pauses (greater or equal to 2 s),
Sinus arrest, SA nodal exit block (delay in impulse leaving SA node), Chronotropic incompetence
o If accompanied by SVT (atrial fibrillation, flutter, or tachycardia) can be termed tachycardia-bradycardia syndrome
● Pathophysiology: failure of SA node to generate HR that meets individual’s physiologic needs
o Most mechanism is SA node fibrosis, other causes include infiltrative disease (amyloid, sarcoid,
hemochromatosis), inflammatory diseases (rheumatic fever, pericarditis, diphtheria, Chagas disease), SA nodal
artery disease (most commonly RCA disease)
● Treatment
o Acute, unstable: ACLS
Chronic: medical therapy alone typically fails (due to unacceptable bradycardia with adequate control of
tachycardia) 🡪 often, a combination of meds (e.g., βB, CCB, digoxin) for tachycardia and permanent pacemaker
for bradycardia
Bradyarrhythmia by Site of Origin: AV NODE and BELOW

Overview: Conduction diseases at the level of the AV node and Bundle of His typically refer to various failures of impulse
propagation, or “AV blocks”.
● When the block is within the AV node (first-degree or Mobitz I), subsidiary pacemakers at the AV junction usually take
over the pacemaker function of the heart, resulting in a relatively stable, non-life-threatening heart rhythm.
● Infra-nodal blocks (within the His bundle) typically result in unstable escape rhythms that may require temporary or
permanent pacing
First degree AV block

● ECG: Prolonged PR (>200ms), all atrial impulses conducted (1:1)
● Pathophysiology: prolonged or slower conduction through the AV node
o Monitoring prolongation of a PR interval may have clinical implications in patients in whom there is concern for
aortic pathology, such as an aortic root abscess
● Treatment: Typically benign and asymptomatic with a narrow escape rhythm and with no indication for treatment.
Second-Degree AV Block Mobitz Type I (Wenckebach)
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● ECG: Progressive PR prolongation until an atrial impulse is not conducted

o Look at the first PR interval after a pause; the PR after the pauses should be the shortest PR in Mobitz I
o The relative increase in the PR interval decreases with each sequential beat; in other words, the PR intervals may
look something like this: 220ms-->260ms-->280ms. This is why it is easiest to see a prolonging PR interval
between the first and second beat of a cycle.
o RR interval progressively shortens with each beat in the cycle prior to the dropped beat (due to the above
phenomenon)
● Pathophysiology: reversible conduction delay within the AV node
o Physiologic: high vagal tone such as athletes, young people
o Iatrogenic: AV nodal blocking agents, post-cardiac surgery, post-ablation, post-TAVR
o Pathologic: myocardial ischemia involving the conduction system (RCA usually supplies the AV node as well as
SA node), cardiomyopathy, myocarditis (Lyme)
● Treatment: typically benign and asymptomatic, if symptomatic may warrant EP study to identify location of block
(supra-His block i.e. AV node 🡪 no treatment, infranodal 🡪 may warrant PPM)
Second-Degree AV Block Mobitz Type II

● ECG: intermittent non-conducted P-waves without progressive prolongation of the PR interval
o Note: difficult to distinguish Mobitz type I vs II AV block on ECG if 2:1 block present (as there is no chance to
observe PR prolongation)
● Pathophysiology:
o Whereas a Mobitz I block suggests AV nodal disease, a Mobitz II block always indicates a more distal block
below the AV node.
o Etiologies overlap with Mobitz Type I (iatrogenic, pathologic), though rarely seen in patients without underlying
heart disease, often seen following anterior MI with infranodal conduction injury.
● Treatment:
o Mobitz Type II is an unstable rhythm, if identified, pacing pads should be placed and cardiology should be
urgently involved for consideration of temp wire
o Treat reversible causes if present (myocardial ischemia, electrolyte abnormalities, AV nodal agents,
hypothyroidism)
▪ If no reversible cause is identified, high likelihood of progression to complete heart block, therefore require
PPM implantation during that admission See Chapter 4 – Device Therapy)
Third-Degree AV Block (Complete Heart Block)

● ECG: complete dissociation of atrial and ventricular conduction
o Nearly all patients with complete heart block present with some degree of symptoms (fatigue, dyspnea, chest
pain, pre-syncope, syncope, arrest) secondary to the typically slow (~ 40 bpm) escape rhythms
● Pathophysiology: Etiologies are similar to first- and second-degree AV block
o Hemodynamics become entirely dependent upon subsidiary escape pacemaker which are typically fascicular or
ventricular and therefore considered unstable
Treatment: Prepare for transcutaneous pacing while awaiting urgent temp wire placement and likely PPD implantation if
no reversible cause can be identified and treated (See Chapter 4)
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Bradyarrhythmia by Site of Origin: DISTAL (bundle and fascicular) BLOCKS
Right bundle branch block (RBBB)

● ECG criteria:
o QRS > 120 ms (“incomplete” if less than 120 ms)
o Rsr’, rsR’, rSR’ in leads V1 or V2
o S wave of greater duration than R wave or >40 ms in I and V6 in adults
o Normal R peak time in leads V5 and V6 but > 50 ms in V1
o Rightward axis; if left axis, then diagnostic of a bifascicular block (RBBB + LAFB)
● Pathophysiology: impaired conduction down the right bundle branch (see diagram above)
● Etiology: Most often idiopathic or associated with structural heart disease
▪ Chronically increased RV pressures
▪ Sudden increase in RV pressure 🡪 stretch (e.g. PE)
▪ Myocardial ischemia, infarct, or inflammation (e.g. myocarditis)
▪ Cardiomyopathies, including congenital heart disease
▪ Transient RBBB may be induced during right heart catheterization
● Treatment: none
● Prognosis: RBBB in setting of acute MI or CHF is associated with higher mortality REFERENCE
Left bundle branch block (LBBB)

● ECG
o QRS > 120 ms (“incomplete” if less than 120 ms)
o Broad notched R waves in I, aVL, V5, V6 with absent q waves in I, V5, V6
o R peak time >60 ms in V5 and V6 but normal in V1, V2, V3
o ST and T waves are in opposite direction of QRS (“negative concordance”)
▪ See ACS section: STEMI Sgarbossa criteria for discussion of ECG ischemia interpretation in setting of LBBB
● Pathophysiology: usually result of progressive degenerative disease of conduction system that can be hastened by
common CV risk factors like HTN, CAD, DM
o Other notable etiologies: ischemia (acute anterior MI), iatrogenic (septal myomectomy, TAVR)
● Treatment: see Chapter 4 – Device Therapy for indications (HFrEF, syncope)
● Prognosis: is an independent predictor of worse outcomes in CAD, MI, and CHF
o MI: complicates diagnosis of MI (Sgarbossa interpretation), and may correlate with infarct size
o CHF: LBBB produces disordered LV contraction which can further worsen systolic function
Chronic bifascicular blocks

● ECG: RBBB + left anterior fascicular block OR left posterior fascicular block
o Left anterior fascicular block (LAFB): Left axis, QRS <120, qR in I, aVL, rS in II, III, aVF
o Left posterior fascicular block (LPFB): Right axis, QRS <120, rS in I, aVL, qR in II, III, aVF
● Treatment: benign finding, though may warrant additional monitoring if history of syncope as intermittent LBBB +
bifascicular block results in intermittent complete heart block that may require PPM
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References:
Fogoros, Richard N. Electrophysiologic Testing. Chichester: Wiley-Blackwell, 2012.
Patterson E, Scherlag BJ et al. Decremental conduction in the posterior and anterior AV nodal inputs. Journal of
Interventional Cardiac Electrophysiology (2002) 7 (2): 137–48.
Tisdale et al. Drug- Induced Arrythmias: A Scientific Statement From the American Heart Association. Circulation 142
(2020
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Device Therapy
The purpose of this section is to review the specific indications for temporary pacing; permanent pacemakers (PPMs),
cardiac resynchronization therapy (CRT), and implantable cardioverter-defibrillator (ICD) therapy.
Temporary Pacing
Transcutaneous Pacing
Indications: Formal indications for transcutaneous pacing are provided in Table 1 below. Indications for pad placement (to
allow for transcutaneous pacing instantly if needed) are also included and designated by an asterisk. These patients will
generally proceed to urgent insertion of transvenous pacing wire.
Table 1: Indications for Transcutaneous Pacing and Placement of Pacing Pads

Class I
Sinus bradycardia (HR <50) with symptomatic hypotension (SBP < 80), refractory to drug therapy†
3ºAVB†
Mobitz Type II 2ºAVB†
Bilateral BBB (alternating BBB or RBBB + alternating LAFB/LPFB)*
Newly acquired or age LBBB, LBBB and LAFB, RBBB and LPFB*
RBBB or LBBB and 1ºAVB*
Class IIa
Stable bradycardia (SBP >90, no hemodynamic compromise or responsive to pharmacologic
therapy)*
Newly acquired or age-indeterminate 1ºAVB*
Class IIb
Uncomplicated acute MI without evidence of conduction system disease*
† Indication for demand pacing, * Indication for pad placement only
1. Place pads: Note that all MGH defibrillators can provide transcutaneous pacing. Proper pad placement is shown in the
figure below. Ensure that the pads are connected to the defibrillator and that the ECG leads are connected to the patient
(white is right, smoke over fire = white lead on R shoulder, black lead on left shoulder, red lead on left leg) and the
defibrillator.
Anterior pad
Posterior pad (usually
placed over L apex)
2. Administer sedation: Involve anesthesia for all non-ACLS protocol transcutaneous pacing to assist with administration
of medications that may cause respiratory compromise (such as IV midazolam/fentanyl). If pacing must be initiated
immediately, IV Dilaudid +/- IV Ativan may be used.
3. Initiate Pacing: Turn the defibrillator dial to “pacer” and set the pacing rate and output, which is the electrical stimulus
needed to produce capture; a higher output represents more energy and will generally be more painful. A reasonable
initial rate and output are 100 bpm and 100 mA, but note that the upper limit is around 140 mA. In non-emergent
situations where you do not need to ensure immediate capture, it is reasonable to start with a lower output around 40 mA
and increase by 5-10 mA until capture is achieved.
4. Verify Capture: Because the pacing rate should be well above the patients native rate, all beats should be paced.
Appropriate capture is confirmed if pacing spikes precede all QRS complexes (and fire at the set rate, e.g. 100 bpm). If
this is not the case, increase the output by 5-10 mA up to 140 mA. Confirm that paced/captured beats are perfusing with
either palpation or Doppler of femoral pulse.
5. Set Final Output: If capture is achieved immediately (e.g. with an initial output set to 100 mA), find the capture
threshold by decreasing the output slowly until capture is lost. The minimum output needed to maintain output will then be
10% higher than the capture threshold. In healthy patients, theoretical thresholds should range from 40-80 mA
(corresponding to an output range of 44-88 mA or, more practically, 45-90). In clinical practice, thresholds tend to be more
variable, with a range between 20-140 mA.
Transvenous Pacing
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Indications: Transvenous pacing is a more durable option than transcutaneous pacing and is employed as a temporary
bridge to recovery or to PPM placement.
Table 2: Indications for Transvenous Pacing

Class I
● Asystole
● Symptomatic bradycardia
● Bilateral BBB (alternating BBB or RBBB w/ alternating LAFB/LPFB)
● New or age-indeterminant bifascicular block (RBBB w/ LAFB/LPFB + first degree AVB)
● Mobitz Type II second degree AVB
Class IIa
● RBBB with 1ºAVB
● New or age-indeterminate LBBB
● Incessant VT for overdrive pacing
● Recurrent sinus pauses (> 3 sec) not responsive to atropine
Class IIb
● Age-indeterminate bifascicular block
● New or age-indeterminate RBBB
Non-guideline based but commonly encountered indications
● AVB after MI or cardiac surgery
● AVB due to Lyme disease or infective endocarditis (e.g. aortic paravalvular abscess)
● Intra/post-procedural support for AVNRT ablation, alcohol septal ablation, heart transplant, or
TAVR
● Overdrive pacing for polymorphic VT
Special considerations: In contrast to transcutaneous pacing (which can be performed urgently without input from
cardiology), placement of a temp wire for transvenous pacing must be performed in the cath lab. The pacing lead is
inserted into the right ventricle via the right internal jugular, left subclavian, or femoral veins (less reliable and increased
risk for dislodgement). Temp wires may remain in place for up to 7-10 days but carry a risk of infection. For this reason,
prophylactic antibiotics are indicated during and after implantation.
Additional complications include: lead dislodgement, bleeding, RV perforation, tamponade, thrombophlebitis, PE or air
embolism, pneumothorax, subdiaphragmatic stimulation, arrhythmias (ectopy/asystole), and/or permanent RBBB.
Temporary Pacing Settings:
The control box has four set parameters (Figure 1):

● Heart Rate: This sets the backup/pacing rate (if rate set to 80, pacing will only occur if intrinsic rate is < 80)
● Output: Electrical stimulus (mA) needed to produce capture (often set 5-10x higher) to ensure reliable capture.
Must be assessed daily, as increased threshold may be an early sign of lead malfunction (e.g. migration,
fracture). Note that the control box has separate dials for the atrial lead (if present) and ventricular lead (always
present). Most medical patients will have only a single RV lead. In contrast, post-cardiac surgery patients with
epicardial wires will often have both atrial and right ventricular leads.
● Pacing Mode: Most often set to VVI (ventricular pacing and sensing, allowing for inhibition of pacing if native rate
is sensed at or above the backup rate)
● Sensitivity: Sets the device detection limit and represents the minimum energy generated by the heart that the
device can detect. If the sensitivity is too low, the device will fail to detect intrinsic cardiac activity and may fire
inappropriately. Alternatively, if the sensitivity is too high, the device may fail to fire
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To test the output threshold:
1. Increase heart rate on device such that all beats are paced
2. Decrease output until pacing ceases and native rhythm is seen, this defines the output threshold of the temporary
pacer
3. Increase output back up to its initial value (or 5-10x the threshold) and turn the rate back to its initial value
4. Do not touch sensitivity, unless troubleshooting
5. Document the threshold, output (in mA), and patient’s native (underlying) rhythm
Note that for RV pacing, the ECG should show LBBB, with left superior axis-usually upright in I and aVL. Any change in
pacing morphology is lead displacement until proven otherwise. If there is concern for change in lead position, perform
threshold testing again and get a STAT CXR.
Troubleshooting common issues:
Failure to pace: Absence of pacing spikes and no paced QRS:
1. Oversensing: pacer senses noise artifact (background activity) as a QRS complex and does not pace. Decrease
sensitivity or turn off sensing (asynchronous pacing, VOO).
2. Battery or connection problem: Replace battery and check connections.
Failure to capture: pacing spikes present but no paced QRS complex.
1. Increased capture threshold due to fibrosis. Increase output to capture.
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2. Lead migration (epicardial lead migration can result in ventricular perforation). Troubleshoot with unipolar ECG:
connect V1 electrode to distal-most pacing electrode. Normal endocardial contact should result in negative QRS
deflection with ST elevation. A positive or biphasic QRS is suggestive of lead migration.
3. Physiologic effect: Such as ischemia, hypoxia, acidosis, alkalosis, hyperglycemia, hypercapnia, medication
related. Attempt to reverse the underlying condition
4. Battery or connection problem. Replace battery and check connections.
Failure to sense: The device does not detect intrinsic cardiac activity and fires inappropriately. Pacing spikes can be
seen on top of or after native QRS (increases risk of R on T).
1. Lead migration. Troubleshoot as above.

2. Sensitivity too low. Troubleshoot by increasing the sensitivity on the control box.
3. Ectopic beats. Consider/address reversible causes such as electrolytes
4. Pulse generator failure. Troubleshoot by replacing generator
Permanent Pacing
Permanent pacing is indicated for symptomatic or dangerous forms of bradycardia that are not due to transient or
reversible causes.
Table 3: Class I Indications for Implantable Pacemaker

Sinus Node Dysfunction
Symptomatic bradycardia or frequent, symptomatic sinus pauses
Symptomatic chronotropic incompetence
Symptomatic bradycardia resulting from drug therapy or medical conditions
AVB
o 2°AVB causing symptomatic bradycardia
o 2° or 3°AVB during exercise without evidence of myocardial ischemia
o 3°AVB with HR≥40 if cardiomegaly or LV dysfunction present or if block below AV node
o 3° or adv. 2°AVB causing symptomatic bradycardia or VT/VF
o 3° or adv. 2°AVB and awake/asymptomatic in NSR w/ pause ≥3s, infranodal escape or
escape HR<40
o 3° or adv. 2°AVB and awake/asymptomatic in AF w/ bradycardia and pause ≥5s
o Persistent 3° or advanced 2°AVB occurring after AV node ablation or cardiac surgery
Chronic Bifascicular Block
Advanced 2° or 3°AVB
Type 2° with alternating bundle branch block
AV Block after Acute MI
Persistent and symptomatic 2° or 3°AVB
Persistent 2° infranodal AVB with alternating BBB or 3° infranodal AVB
Hypersensitive Carotid Sinus Syndrome/Neurocardiogenic Syncope
Recurrent syncope due to spontaneous carotid sinus stimulation with asystole ≥3 seconds
Pacemaker modes:
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There are many different pacing modes which are

designated by a 1-5 letter code, although typically only
the first three positions are used in practice.
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Figure 4: Algorithm for Choice of Optimal Pacing Mode
Note: AVM: AV delay management, SND: Sinus node dysfunction, AF: Atrial fibrillation, CRT: Cardiac
resynchronization therapy.
AAI: Single right atrial lead paces unless native atrial activity is sensed. Useful for patients with isolated sinus node
dysfunction, manifesting as sinus bradycardia or sinus pauses. Rate-responsiveness can be added for patients who
cannot accelerate their heart rates (AAI-R). Patients must have intact AV conduction. A major disadvantage is that there is
no protection from ventricular bradyarrhythmias in the setting of AV block which develops in 0.6–5% of patients with sick-
sinus syndrome per year. Pacemaker upgrade is often a higher-risk procedure than de novo implantation of a dual-
chamber system. In patients with sinus node dysfunction, the presence of bundle-branch block at implantation is a
relatively accurate predictor of subsequent AV block, and dual chamber pacemaker should be considered instead.
VVI: Single right ventricular lead with paces unless ventricular activity is sensed. Very common mode for prevention of
ventricular bradyarrhythmias or asystole. Virtually all devices currently in use are capable of VVI(R) pacing. Unlike AAI
pacing, VVI pacing is effective even in patients with impaired AV conduction or in patients at risk for future development
of AV block. VVI(R) pacing in particular is indicated in patients with chronic atrial fibrillation with a slow ventricular
response. The drawback to VVI pacing is that this mode cannot maintain AV synchrony and lack of AV synchrony can
result in pacemaker syndrome as well as increased risk of atrial fibrillation.
DDD: Right atrial and right ventricular leads which are both capable of pacing in the absence of native activity sensed in
either respective chamber, but inhibited if it is. Provides closest mimic of physiologic pacing conditions and maintains AV
synchrony which reduces the risk of AF in sick sinus syndrome, resulting in a lower incidence of thromboembolic events,
improves hemodynamics by preserving the atrial kick, and helps to avoid pacemaker syndrome. Results in one (or more
at any given time) of four different rhythms: normal sinus rhythm, atrial pacing with intact AV conduction, AV sequential
pacing, and atrial sensing and ventricular pacing (P-synchronous ventricular pacing).
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Figure 5: The “Four Faces” of DDD pacing
1.
2. 3.
4.
1: a-paced, v-sensed. 2: a-sensed, v-sensed (normal conduction). 3: a-paced, v-paced. 4: a-sensed, v-paced.
Subsection References:
1. Tracy, Cynthia M., et al. "2012 ACCF/AHA/HRS focused update incorporated into the ACCF/AHA/HRS 2008
guidelines for device-based therapy of cardiac rhythm abnormalities: a report of the American College of
Cardiology Foundation/American Heart Association Task Force on Practice Guidelines and the Heart Rhythm
Society." Journal of the American College of Cardiology 61.3 (2013): e6-e75
2. Kusumoto, Fred M., et al. "2018 ACC/AHA/HRS guideline on the evaluation and management of patients with
bradycardia and cardiac conduction delay: a report of the American College of Cardiology/American Heart
Association Task Force on clinical practice guidelines and the Heart Rhythm Society." Journal of the American
3. Trohman, Richard G., Michael H. Kim, and Sergio L. Pinski. "Cardiac pacing: the state of the art." The
Lancet 364.9446 (2004): 1701-1719
4. Fitzpatrick, Adam, and Richard Sutton. "A guide to temporary pacing." BMJ: British Medical Journal 304.6823
(1992): 365
5. Gammage, Michael D. "Temporary cardiac pacing." Heart 83.6 (2000): 715-720
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Implantable Cardioverter-Defibrillator (ICD) Therapy
Overview: These devices have been shown to be 97% effective in terminating arrhythmias with defibrillation,
cardioversion or antitachycardia pacing (ATP). Additionally, all ICDs can function as a pacemaker (though note that the
reverse is not true). ICDs can be single-chamber (RV-lead) or dual chamber (RA/RV-lead) devices. They can be
distinguished from dual chamber PPMs on CXR by presence of coils.
Indications: Per AHA/ACC guidelines, 1-3 implantation of ICD should be considered in patients on optimal medical therapy
who have an estimated survival of at least 1 year (with good functional status). There are Class I indications for both
primary and secondary prevention, as well as Class II indications for conditions that increase the risk of SCD.
Class I
Secondary Prevention: Survivors of cardiac arrest due to VF or sustained VT without reversible causes
Primary Prevention:
- Ischemic cardiomyopathy and LVEF ≤ 30-40% at least 40 days post-MI (DINAMIT) or at least 3 months post-
CABG (CABG-PATCH)
- LVEF ≤ 30% and NYHA Class I, II, or III (MADIT-II)
- LVEF ≤ 35% and NYHA Class II or III (SCD-HeFT)
- LVEF ≤ 40% and inducible VF or sustained VT at EP study (MUSTT)
- Non-ischemic cardiomyopathy with at least 3 months of documented
- CHF, LVEF ≤ 35%, and NYHA Class II or III (SCD-HeFT)*
- Syncope of unknown origin and VT/VF induced at EP study
- Spontaneous sustained VT (+/- hemodynamic instability) with structural heart disease (*DANISH Study: RCT of
non-ischemic heart failure with EF ≤ 35%, showed no overall mortality benefit from ICD versus optimal medical
therapy, however risk of SCD was reduced and a mortality benefit was observed in the subgroup that was <68
years old)
Class II
For numerous conditions that increase risk of SCD, with limited RCT data
- Hypertrophic cardiomyopathy: LV thickness >/= 30mm, family history of SCD, abnormal exercise BP
- Arrhythmogenic right ventricular cardiomyopathy (ARVC): extensive RV, LV involvement
- Long-QT syndrome: syncope and/or VT while on beta-blockers
- Brugada syndrome: syncope and/or VT
- Catecholaminergic polymorphic VT: syncope and/or sustained VT on beta-blockers
- Cardiac sarcoid, giant cell myocarditis, Chagas disease
- Unexplained syncope, significant LV dysfunction, and non-ischemic dilated cardiomyopathy
- Sustained VT with normal ventricular function
- Non-hospitalized patient awaiting heart transplant
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Cardiac Resynchronization Therapy (CRT)
CRT is an important therapy among patients with HFrEF which portends a robust mortality and reverse remodeling
benefit. Initially shown to improve exercise capacity, clinical symptoms, and LVEF in the MIRACLE Study. Further
investigation demonstrated a mortality benefit in patients with HFrEF and widened QRS.
CRT implantation involves RA, RV, and coronary sinus (for epicardial pacing of LV) leads. This allows for optimization of
A-V synchrony as well as V-V synchrony, which has been shown to improve stroke volume. For this reason, CRTs
represents an important component of guideline directed medical and device therapy. CRT devices may only provide BiV
pacing (CRT-P) or may allow for BiV pacing plus defibrillation with ICD function (CRT-D).
Indications for CRT are divided into two groups, those in sinus rhythm (table 4) and those who are in persistent or
permanent atrial fibrillation who either cannot undergo ablation or who have received ablation and failed (table 5). For
those who fall into those mentioned groups with atrial fibrillation, further consideration can be for AV junction ablation and
simultaneous CRT which can both improve symptoms and reduce mortality (see figure 5 for further decision making and
patient selection for ablation and/or CRT) in patients who either cannot tolerate or who do not respond to other methods of
rate and rhythm control with the understanding that AVJ ablation will effectively render them pacemaker dependent. Most
of the evidence for either group of patients are based on RCT’s who enrolled patients who are NYHA II-IV with LVEF 35%
or less with some exceptions in the atrial fibrillation groups detailed below who have received optimal medical therapy or
OMT for at least 3 months after being diagnosed with HFrEF or at least 40 days following diagnosis of a myocardial
infarction in addition to treatment of any reversible cardiomyopathy such as ischemic or tachycardia-induced
cardiomyopathy. Additional recommendations for those with pre-existing ICD’s can be found in the 2021 ESC guidelines
on cardiac pacing and cardiac resynchronization therapy from which the below tables are pulled. 15
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Table 4: 2021 ESC/EHRA Guidelines for CRT for patients in SR
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Table 5: 2021 ESC/EHRA Guidelines for CRT for patients in Afib
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Figure 6. Management of AVJ Ablation in Patients with Afib
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References:
1. Tracy, Cynthia M., et al. "2012 ACCF/AHA/HRS focused update incorporated into the ACCF/AHA/HRS 2008
guidelines for device-based therapy of cardiac rhythm abnormalities: a report of the American College of
Cardiology Foundation/American Heart Association Task Force on Practice Guidelines and the Heart Rhythm
Society." Journal of the American College of Cardiology 61.3 (2013): e6-e75
2. Kusumoto, Fred M., et al. "2018 ACC/AHA/HRS guideline on the evaluation and management of patients with
bradycardia and cardiac conduction delay: a report of the American College of Cardiology/American Heart
Association Task Force on clinical practice guidelines and the Heart Rhythm Society." Journal of the American
3. Higgins, Steven L. "Impact of the Multicenter Automatic Defibrillator Implantation Trial on implantable cardioverter
defibrillator indication trends." The American journal of cardiology 83.5 (1999): 79-82
4. Klein, Helmut U., and Sven Reek. "The MUSTT study: evaluating testing and treatment." Journal of Interventional
Cardiac Electrophysiology 4.1 (2000): 45-50
5. Moss, Arthur J., et al. "Prophylactic implantation of a defibrillator in patients with myocardial infarction and
reduced ejection fraction." New England Journal of Medicine 346.12 (2002): 877-883
6. Bardy, Gust H., et al. "Amiodarone or an implantable cardioverter–defibrillator for congestive heart failure." New
7. Hohnloser, Stefan H., et al. "Prophylactic use of an implantable cardioverter–defibrillator after acute myocardial
infarction." New England Journal of Medicine 351.24 (2004): 2481-2488
8. Myerburg, Robert J. "Implantable cardioverter–defibrillators after myocardial infarction." New England Journal of
Medicine359.21 (2008): 2245-2253
9. Tang, Anthony SL, et al. "Cardiac-resynchronization therapy for mild-to-moderate heart failure." New England
10. Bristow, Michael R., et al. "Cardiac-resynchronization therapy with or without an implantable defibrillator in
advanced chronic heart failure." New England Journal of Medicine 350.21 (2004): 2140-2150
11. Cleland, John GF, et al. "The effect of cardiac resynchronization on morbidity and mortality in heart failure." New
12. Curtis, Anne B., et al. "Biventricular pacing for atrioventricular block and systolic dysfunction." New England
13. Ruschitzka, Frank, et al. "Cardiac-resynchronization therapy in heart failure with a narrow QRS complex." New
14. Olgin, Jeffrey E., et al. "Wearable cardioverter–defibrillator after myocardial infarction." New England Journal of
Medicine379.13 (2018): 1205-1215.
15. Michael Glikson et al, ESC Scientific Document Group, 2021 ESC Guidelines on cardiac pacing and cardiac
resynchronization therapy: Developed by the Task Force on cardiac pacing and cardiac resynchronization therapy
of the European Society of Cardiology (ESC) With the special contribution of the European Heart Rhythm
Association (EHRA), European Heart Journal, Volume 42, Issue 35, 14 September 2021, Pages 3427–3520.
.
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Electrophysiology Studies and Procedures
The purpose of this section is to provide background/basic information on three commonly employed EP procedures:
synchronized cardioversion and defibrillation, diagnostic EP studies, and catheter ablations.
Synchronized Cardioversion and Defibrillation
Cardioversion (DCCV) and defibrillation are non-invasive interventions that can terminate tachyarrhythmias by delivering
an electrical shock to the heart. Cardioversion is performed by synchronizing the shock to a QRS complex while
defibrillation is unsynchronized and delivers a random shock during the cardiac cycle.
Indications and Contraindications
Emergent DCCV and defibrillation are indicated in cases of clinical instability. Elective DCCV may also be performed as
an effective treatment for SVTs.
Table 1: Cardioversion & defibrillation indications and energy dosing
CARDIOVERSION Monophasic (J) Biphasic (J)*

AVRT/AVNRT1 50-100 <50-100
Atrial flutter2 100 50-100
Atrial fibrillation2 200 120-200
VT (with pulse) 200 100
DEFIBRILLATION
VT (pulseless) 360 150-200
VF 360 150-200
¹includes reentry arrhythmias AVRT and AVNRT (attempt adenosine first)
²includes:
AF/AFL of ≥48h (or unknown) duration and anticoagulated for 3–4 weeks (INR 2–3)
AF/AFL of <48h duration, for which anticoagulation is optional depending on risk
AF/AFL of unknown duration with CHF and absence of thrombus in LA on TEE acute onset AF/AFL with
hemodynamic compromise: MI, pulmonary edema, hypotension
*
All MGH defibrillators are biphasic which are typically effective at lower energy levels. Large patients may be
difficult to cardiovert/defibrillate even at 360 J biphasic.
In general, DCCV/defibrillation is contraindicated in the following cases:
1. Known atrial or ventricular thrombus without emergent indication

2. Unknown duration AF/AFL without anticoagulation (unless with TEE or emergent)
3. Rhythms associated with increased automaticity or triggered activity (MAT, junctional tachycardia, AIVR) which typically
recur within seconds after shock, and the release of endogenous catecholamines from the shock may further exacerbate
the arrhythmia.
4. Digitalis toxicity
5. Severe electrolyte imbalance
Additionally, the following considerations exist for these special populations:
1. Patients who are pregnant: Can be performed without affecting the rhythm of the fetus. Fetal heart rate monitoring
during the procedure is recommended.
2. Patients who have pacemakers/ICDs: Can be performed but the electrode should be > 12 cm from the pulse
generator and an anteroposterior electrode orientation is recommended. The pacemaker/ICD should be interrogated
afterward to ensure proper functioning.
Mechanism and Procedure

The delivered shock depolarizes all or most excitable cardiac tissue and induces a refractory period that terminates
reentrant activity. Cardioversion restores sinus rhythm in 70–95% of patients. Efficacy decreases with increased
resistance (tissue density, physical distance due to habitus), prolonged arrhythmia duration, presence of structural
heart disease, and involvement of multiple reentry circuits.
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Step-by-step instructions for emergent cardioversion and defibrillation:

Cardioversion:
16. Turn the mode selector to DEFIB (red area). Select the desired energy using the up and down arrow keys in the
front panel. See above for desired energy, or in general:
a. Narrow, regular: 50 – 100 J (atrial flutter often converts with 50 J)
b. Narrow, irregular: 120 – 200 J (atrial fibrillation typically requires 150 J)
c. Wide, regular: 100 J
d. Wide, irregular: 150 – 200 J (defibrillation dose)
17. Press the Sync On/Off button
a. Confirm that a Sync marker appears on the monitor above each detected R wave to indicate where
discharge will occur
b. If necessary, use the LEAD and SIZE buttons to establish settings that yield the best display
18. Press the CHARGE button on the front panel
19. Ensure all are clear from the bed then press and hold the illuminated SHOCK button on the front panel. The
defibrillator will discharge with the next detected R wave
20. If additional shocks are necessary, increase the energy level as needed
Defibrillation:
1. Turn the mode selector to DEFIB (red area)
a. The unit displays DEFIB 120J SEL on the monitor
b. The default energy selections for adult patients are Shock 1: 120J, Shock 2: 150J, Shock 3: 200J. You
can use energy select (UP and DOWN arrow keys) to change settings
2. If the monitor shows a shockable rhythm, press the CHARGE button on the front panel. If patient is pulseless,
continue CPR while charging
3. Ensure all are clear from the bed then press and hold the illuminated SHOCK button
4. If patient is pulseless, resume CPR for 2 minutes before the next pulse and rhythm check
For non-emergent and routine procedures: NPO for at least 6-8h. Some patients may require periprocedural
anticoagulation to prevent thromboembolism. TEE is frequently used to look for the presence of a LA thrombus.
Complications: After shocking, ST & T wave changes may occur and typically resolve within 5 minutes. However, the
following complications may also occur:
● Arrhythmias/Conduction abnormalities:
o Self-limited and include sinus tachycardia, PAC, PVC, NSVT, VT, VF, and LBBB.
o May cause hemodynamic instability requiring further intervention
● Thromboembolism: Approximately 1% with anticoagulation, 5% without anticoagulation
● Myocardial necrosis: Severity depends on strength and number of shocks delivered
● Myocardial dysfunction/stunning:
o Global LV dysfunction can be present until 48 hours after shock
o Interpret cardiac studies within this 48h window with caution
● Pulmonary edema: Rare complication seen in patients with AF and/or LV dysfunction
● Hypotension: Transient, may last several hours, typically fluid-responsive
● Cutaneous burns:
o Seen in 20-25% of patients
o May use prophylactic steroid cream or topical NSAIDs at the site of electrodes
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Electrophysiology Study (EPS)
EPS is an elective, invasive, intracardiac catheter-based intervention that measures specific intervals within the
cardiac cycle to better understand the etiology, clinical significance, and management of brady- and tachy-
arrhythmias.
Indications:
1. Bradyarrhythmias: acquire corroborative data in symptomatic patients with episodic bradyarrhythmia or define level
of AV conduction abnormality
2. Tachyarrhythmias: define mechanism of NCT or WCT or reproduce a clinically defined tachycardia for mapping
and ablation
3. ICD implantation and programming: search for EPS-induced VT or VF in patients with structural heart disease,
NSVT, or reduced LVEF to justify ICD implantation and define optimal ICD parameters
4. Syncope of unknown etiology: to assess SN function, AV conduction, and search for VT/VF in patients with
syncope and organic heart disease
5. After cardiac surgery: to assess the effect of cardiac surgery on arrhythmia risk
Contraindications: active ACS, bacteremia, ADHF (not caused by the arrhythmia), critical AS, severe HOCM, severe left
main or 3-vessel CAD, presence of a major bleeding diathesis, presence of an acute lower extremity DVT (if femoral vein
cannulation is required).
Performed in the EP lab and patients are given at least conscious sedation. Standard ECG leads and defibrillation pads
are applied. Multiple sites of venous (and at times, arterial) access are acquired for intracardiac catheter placement.
Femoral access is most common. Catheters with electrode tips are placed in specific locations to both pace and record.
● High right atrium: Reflects SA node function, AV

conduction, and direction of atrial activation
● Coronary sinus: Reflects LA activation. Obtained in
patients with SVT or pre-excitation
● Tricuspid annulus (His): Tracings from low septal RA,
His bundle, and high septal RV depolarization reflect His
bundle activity
● RV apex: Reflects RV activity
● Left heart (via transseptal or retrograde aortic
approach for mapping/ablation)
Mapping
At the conclusion of the diagnostic EPS, a subset of patients may

undergo additional mapping and ablation for treatment of an arrhythmia. The created “map” is used to guide and localize
potential ablation sites. Mapping prior to ablation is not necessary for certain types of arrhythmias that have a defined
anatomical course (i.e. typical atrial flutter).
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Catheter Ablation Therapy
Indications
1. WPW, accessory pathway-mediated, and other variant pre-excitation states

2. Refractory atrial fibrillation/flutter and/or with severe symptoms
3. Refractory sinus, atrial or junctional tachycardia and/or with severe symptoms
4. Idiopathic ventricular premature depolarization from the right ventricular outflow tract associated with severe
symptoms
5. Monomorphic VT (can consider cases of polymorphic VT)
6. VF (uncommon indication)
7. PVC-induced cardiomyopathy
Contraindications are generally the same as for EPS (see prior section).
Pulmonary Vein Isolation (PVI) for the treatment of AF:
Indications, Technique, & Outcomes:
Indicated for patients with symptomatic AF who have either failed pharmacologic therapies for rhythm control or cannot
tolerate medication side effects. Among patients with HFrEF and NYHA II-III symptoms with persistent AF who are chosen
for a rhythm control strategy, PVI leads 36% absolute increase in AF-free survival at 24 months, 26% absolute reduction
in unplanned hospitalizations, and a 10% absolute reduction in overall mortality with AF ablation as compared to
amiodarone.
Can be accomplished with radiofrequency (RFA) or cryoablation. In patients with drug refractory, symptomatic paroxysmal
AF, cryoablation is non-inferior, reduces procedural time, but increases fluoroscopy time as compared to RFA. The
procedure aims to electrically isolate the antral portion of the pulmonary veins, a region identified as containing >90% of
the ectopic beats involved in the generation and maintenance of AF. As a result, cavotricuspid isthmus line ablation can
be performed during the same procedure if atrial flutter is co-occurring.
Efficacy at 1 year has been reported to be as high as 80-85% for paroxysmal AF but decreases to 50-60% for persistent
AF.
Anticoagulation:
As with any cardioversion, there is a risk of thromboembolism with PVI. All patients should be on anticoagulation peri-
procedurally. Patients with AF >48 hours should be on therapeutic anticoagulation for at least 3 weeks or have a TEE
prior to PVI. Anticoagulation should continue for at least two months after the procedure, although based on patient
wishes, risk factors/stratification, and aggressive post-ablation monitoring some EP physicians will choose to discontinue
anticoagulation.
Complications:
1. Complete heart block 5. Pericarditis
2. Thromboembolism 6. Pulmonary vein stenosis
3. Cardiac tamponade 7. Phrenic nerve paralysis
4. Acute MI 8. Atrioesophageal fistula
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References:
1. American Heart Association, American Heart Association, and American Heart Association. "guidelines for
cardiopulmonary resuscitation (CPR) and emergency cardiovascular care (ECC) of pediatric and neonatal
patients: neonatal resuscitation guidelines." Pediatrics 117.5 (2006): e1029-e1038
2. Jacobs, Ian, et al. "Part 6: defibrillation: 2010 international consensus on cardiopulmonary resuscitation and
emergency cardiovascular care science with treatment recommendations." Circulation 122.16_suppl_2 (2010):
S325-S337
3. Lown, Bernard, Raghavan Amarasingham, and Jose Neuman. "New method for terminating cardiac arrhythmias:
use of synchronized capacitor discharge." JAMA 256.5 (1986): 621-627
4. Knight, B. “Basic principles and techniques of cardioversion and defibrillation.” UpToDate 2018
5. Knight, B. “Cardioversion for specific arrhythmias.” UpToDate 2019
6. Kadish, Alan H., et al. "ACC/AHA clinical competence statement on electrocardiography and ambulatory
electrocardiography: A report of the ACC/AHA/ACP–ASIM Task Force on Clinical Competence (ACC/AHA
Committee to Develop a Clinical Competence Statement on Electrocardiography and Ambulatory
Electrocardiography) Endorsed by the International Society for Holter and Noninvasive Electrocardiology." Journal
of the American College of Cardiology 38.7 (2001): 2091-2100
7. Zipes, Douglas P., et al. "Guidelines for clinical intracardiac electrophysiological and catheter ablation procedures:
a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines
(Committee on Clinical Intracardiac Electrophysiologic and Catheter Ablation Procedures), developed in
collaboration with the North American Society of Pacing and Electrophysiology." Journal of the American College
of Cardiology 26.2 (1995): 555-573
8. Homoud, M. “Invasive cardiac electrophysiology studies.” UpToDate 2019
9. Dagres, Nikolaos, et al. "Complications of atrial fibrillation ablation in a high‐volume center in 1,000 procedures:
Still cause for concern?." Journal of cardiovascular electrophysiology 20.9 (2009): 1014-1019
10. Haissaguerre, Michel, et al. "Spontaneous initiation of atrial fibrillation by ectopic beats originating in the
pulmonary veins." New England Journal of Medicine 339.10 (1998): 659-666
11. Oral, Hakan, et al. "Circumferential pulmonary-vein ablation for chronic atrial fibrillation." New England Journal of
Medicine354.9 (2006): 934-941
12. Pappone, Carlo, and Vincenzo Santinelli. "Atrial fibrillation ablation: state of the art." The American journal of
cardiology96.12 (2005): 59-64
13. Ganz, L. “Overview of catheter ablation of cardiac arrhythmias.” UpToDate 2019
14. Passman, R. “Catheter ablation to prevent recurrent atrial fibrillation.” UpToDate 2018
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Quick Reference Guide: Arrhythmias and Electrophysiology
Narrow Complex Tachycardia (NCT)

● If unstable with NCT ⇒ DCCV with following energy
o Regular → 50-100J
o Irregular → 120-200J biphasic or 200J monophasic
● The following table characterizes the NCTs by mechanism and location
MECHANISM
↑ AUTOMATICITY RE-ENTRY
S
Sinus Tachycardia Sino-Atrial Nodal Reentrant Tachycardia
I
● Secondary cause (HoTN, pain, fever, ● Reentry within or around SA node
N
PE, CHF, acute MI, fistula, etc.) vs drug ● Paroxysmal, abrupt on/off
U
effect/toxicity/withdrawal ● P wave morphology similar to baseline
S
● HR 100-150 in older pts; up to 200 in ● Treat w/ vagal maneuvers, Valsalva;
N
younger pts nodal blockade; ablation
O
● Gradual onset
D
● Treat underlying cause
E
Atrial Tachycardia Atrial Flutter

● Focal vs multifocal ● Macro-reentrant circuit
● Atrial rate 100-250, vent rate 90-120 ● Atrial rate 250-300, vent rate 150 (if 2:1
A (variable block) conduction)
T
● Focal AT: Structural heart dz vs Dig ● Slow and diagnose with vagal
R
toxicity; d/c Dig, rate control (BB vs maneuvers ± adenosine
I
CCB), ablation. ● Similar mgmt. to atrial fib: rate/rhythm
LO U
● MAT: ≥3 P-wave morphologies, a/w control, anticoagulation
CA M
chronic pulmonary disease; prefer CCB ● Prefer BB, CCB, Dig to class 1A/1C
TI > BB if severe lung disease meds → can enable 1:1 conduction
ON
● Typical flutter is amenable to ablation
Non-Reentrant AVNRT
Junctional Tachycardia ● Reentry thru dual pathways in AV node
● JET (junctional ectopic tach): infants > ● Abrupt on/off, rates 150-220
adults, particularly post-cardiac surgery ● Retrograde P, can be buried in QRS
A for CHD; due to ectopic focus; high ● Acute: vagal, adenosine
V morbidity ● Mgmt: BB, CCB; ablation is definitive
N ● NPJT (non-paroxysmal JT): adults >
O children; “accelerated junctional AVRT
D rhythm”; a/w digoxin toxicity and acute ● Reentry thru acc. pathway + AV node
E MI; difficult to distinguish from AVNRT ● Narrow = orthodromic (antegrade thru
w/o EP study; treat underlying cause AV node, retrograde thru acc. path);
use nodal blockade
● Wide/pre-excitation = antidromic; avoid
nodal blockade (see WCT chapter)
● Definitive tx: ablation
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Wide Complex Tachycardia (WCT)

● Refers to rate > 100bpm and QRS ≥ 120ms
● The DDx for WCTs include
o VT
o SVT with aberrancy
o SVT w/ pre-excitation, and
o Pacemaker-related tachycardias
● The clinical presentation of WCT can be variable, from asymptomatic runs of NSVT to a patient who has coded.
Because most patients do not tolerate VT for long periods of time, when you see WCT, assume it is VT🡪 feel for
a pulse and obtain BP ASAP!
● Approach the initial management of WCT according to patient stability (as below). See chapter for more details on
mgmt according to etiology
o Pulseless: Immediately start the pulseless VT ACLS algorithm and prepare for unsynchronized DCCV
o Hemodynamically unstable or highly symptomatic: Worry about etiology AFTER YOU’VE STABILIZED
PATIENT
▪ Prepare for synchronized DCCV (fentanyl/versed for sedation), put pads on the patient, and call
for help (e.g. cardiology, EP, RICU, etc.)
▪ Start amiodarone (150 mg x 1 Q 3–5 min, then drip @ 1 mg/min), and/or lidocaine (100 mg x 1,
then drip @ 1–4 mg/min). Amiodarone typically is an appropriate anti-arrhythmic to start unless
there is QT prolongation and concern or TdP
▪ If regular, monomorphic, and there is some suspicion for SVT, you can consider using adenosine
as both a diagnostic and therapeutic intervention
Atrial Fibrillation (AF)

● Atrial fibrillation is the most common sustained cardiac rhythm disturbance, increasing in prevalence with age
(0.4% to almost 20%)
● In general, AF results from an abnormal atrial response to reentry and/or rapid focal ectopic firing
● Patients can be asymptomatic, but many describe palpitations, fatigue, dyspnea, lightheadedness and
diaphoresis
o Thromboembolic CVA is the initial manifestation in 10–40% of patients
● TTE should be performed in all patients who present with new-onset AF in order to evaluate for a structural
etiology. In addition, thyroid function testing should routinely be performed, as hyperthyroidism predisposes to AF.
Also consider renal and liver function tests, as well as cardiac biomarkers (including troponin and NT-proBNP)
based on clinical presentation
● Rate versus rhythm control: no mortality difference
● Anticoagulation: All patients with AF should be on anticoagulation except those at the lowest risk of
thromboembolic stroke
o The AHA/ACC 2019 guidelines recommend DOACs (including dabigatran, rivaroxaban, apixaban and
edoxaban) over warfarin to reduce stroke risk in appropriate AFib patients, unless moderate-to-severe
mitral stenosis or a mechanical heart valve
Temporary Pacing and Pacemaker Therapy

● Temporary pacing includes transcutaneous and transvenous pacing, both of which are indicated as urgent or
emergent therapy in patients with hemodynamically significant bradyarrhythmia
● Transcutaneous pacing can be performed urgently without input from cardiology, but should involve the Senior
ON and nursing supervisors
o Short-acting sedation (e.g. with Dilaudid/Ativan) is indicated in non-ACLS setting (consider early
involvement of Anesthesia)
o Pace by turning defibrillator to “Pacer” mode; a good rule of thumb is to set the HR and output at a
starting rate 100 bpm and 100 mA, respectively
● Transvenous pacing is a more durable option than transcutaneous pacing, and is often employed as a temporary
bridge to recovery or to PPM placement
o In contrast to placement of a temp wire for transvenous pacing must be performed in the cath lab
o The pacing lead is inserted into the right ventricle via the right internal jugular, left subclavian, or femoral
veins (less reliable and increased risk for dislodgement)
o Temp wires may remain in place for up to 7-10 days but carry a risk of infection
o Daily maintenance includes CXR, threshold testing, and ECG (all to assess for lead migration)
● Permanent pacing is indicated for irreversible symptomatic bradycardia, chronotropic incompetence, or unstable
conduction disorders
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● There are many different pacing modes, which are designated by a 1-5 letter code. In the chart below, “position”
refers to letter position
o As an example, in the 4-letter code DDDR, the D in position I implies that both chambers (the atria and
the ventricles) can be paced, the D in position II indicates that both chambers (the atria and the
ventricles) can be sensed, the D in position III indicates that the device can respond to sensing by
either triggering activity or inhibiting itself, and the R in position IV indicates that the device allows for
rate modulation
Implantable Cardioverter-Defibrillator Therapy

● Per AHA/ACC guidelines, ICDs are indicated for both primary and second prevention in patients on optimal
medical therapy who have an estimated survival of at least 1 year (with good functional status)
● Class I indications for secondary prevention include:
o Survivors of cardiac arrest due to VF or sustained VT without reversible causes (AVID)
● Class I indications for primary prevention (with trial references) include:
o Ischemic cardiomyopathy and LVEF ≤ 30-40% at least 40 days post-MI (DINAMIT) or at least 3 months
post-CABG (CABG-PATCH)
o LVEF ≤ 30% and NYHA Class I, II, or III (MADIT-II)
o LVEF ≤ 35% and NYHA Class II or III (SCD-HeFT)
o LVEF ≤ 40% and inducible VF or sustained VT at EP study (MUSTT)
o Non-ischemic cardiomyopathy with at least 3 months of documented: CHF, LVEF ≤ 35%, and NYHA
Class II or III (SCD-HeFT)
o Syncope of unknown origin and VT/VF induced at EP study
o Spontaneous sustained VT (+/- hemodynamic instability) with structural heart disease
● Wearable cardiac defibrillators (WCDs) are externally worn defibrillators, generally considered as interval therapy
in patients awaiting ICD
o The VEST Trail showed that among post-MI patients with EF ≤35%, WCDs did not reduce SCD and
ventricular tachyarrhythmias but did reduce the secondary endpoint of all-cause mortality up to 90 days

● Cardiac resynchronization therapy (CRT) devices have an RA, RV, and coronary sinus (epicardial pacing of LV)
leads, allowing for optimization of A-V and V-V synchrony, which has been shown to improve stroke volume
o Class I indications: CRT implantation is recommended for patients with chronic heart failure (NYHA
function class II, and ambulatory IV) with LVEF ≤ 35% and LBBB w/ QRS duration > 150 ms and should
be considered in these patients if QRS duration is 120-150 ms
o CRT devices may only provide BiV pacing (CRT-P) or may allow for BiV pacing plus defibrillation with ICD
function (CRT-D)
Procedures in EP and EP Studies

● Cardioversion (DCCV) and defibrillation are non-invasive interventions that can terminate tachyarrhythmias by
delivering an electrical shock to the heart
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● Emergent DCCV and defibrillation are generally indicated in cases of clinical instability. Planned DCCV may also
be performed as an effective treatment for SVTs
● The delivered shock depolarizes all or most excitable cardiac tissue and induces a refractory period that
terminates reentrant activity
● Cardioversion is performed by synchronizing the shock to a QRS complex (thus requires a rhythm in which the
QRS complex is present) and restores sinus rhythm in 70–95% of patients. The procedure is as follows:
front panel. In general:
● Defibrillation is unsynchronized and delivers a random shock during the cardiac cycle.
6. If the monitor shows a shockable rhythm, press the CHARGE button on the front panel. If patient is
pulseless, continue CPR while charging
7. Ensure all are clear from the bed then press and hold the illuminated SHOCK button on the front panel
● An electrophysiology study (EPS) is an elective, invasive, intracardiac catheter-based intervention that
measures specific intervals within the cardiac cycle. The purpose is to better understand the etiology,
clinical significance, and management of brady-and tachy-arrhythmias
● A common procedure in EP is Pulmonary Vein Isolation (PVI), performed with either radiofrequency (RFA)
or cryoablation, which involves electrical isolation of the antral portion of the pulmonary veins, which
contains >90% of the ectopic beats involved in AFib.
PVI is indicated in patients with symptomatic atrial fibrillation who have either failed pharmacologic therapies for
rhythm control or cannot tolerate medication side effects. Importantly, ablation does not negate the need for
therapeutic anticoagulation
Electrophysiology Studies and Procedures
The purpose of this section is to provide background/basic information on three commonly employed EP procedures:
synchronized cardioversion and defibrillation, diagnostic EP studies, and catheter ablations.
Subsection 1 – Synchronized Cardioversion and Defibrillation
Subsection 2 – Electrophysiology Study (EPS)
Subsection 3 – Catheter Ablation Therapy
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Synchronized Cardioversion and Defibrillation
Cardioversion (DCCV) and defibrillation are non-invasive interventions that can terminate tachyarrhythmias by delivering
an electrical shock to the heart. Cardioversion is performed by synchronizing the shock to a QRS complex while
defibrillation is unsynchronized and delivers a random shock during the cardiac cycle.
Indications and Contraindications
Emergent DCCV and defibrillation are indicated in cases of clinical instability. Elective DCCV may also be performed as
an effective treatment for SVTs.
Table 1: Cardioversion & defibrillation indications and energy dosing
CARDIOVERSION Monophasic (J) Biphasic (J)*

AVRT/AVNRT1 50-100 <50-100
Atrial flutter2 100 50-100
Atrial fibrillation2 200 120-200
VT (with pulse) 200 100
DEFIBRILLATION
VT (pulseless) 360 150-200
VF 360 150-200
¹includes reentry arrhythmias AVRT and AVNRT (attempt adenosine first)
²includes:
AF/AFL of ≥48h (or unknown) duration and anticoagulated for 3–4 weeks (INR 2–3)
AF/AFL of <48h duration, for which anticoagulation is optional depending on risk
AF/AFL of unknown duration with CHF and absence of thrombus in LA on TEE acute onset AF/AFL with
hemodynamic compromise: MI, pulmonary edema, hypotension
*
All MGH defibrillators are biphasic which are typically effective at lower energy levels. Large patients may be
difficult to cardiovert/defibrillate even at 360 J biphasic.
In general, DCCV/defibrillation is contraindicated in the following cases:
1. Known atrial or ventricular thrombus without emergent indication

2. Unknown duration AF/AFL without anticoagulation (unless with TEE or emergent)
3. Rhythms associated with increased automaticity or triggered activity (MAT, junctional tachycardia, AIVR) which typically
recur within seconds after shock, and the release of endogenous catecholamines from the shock may further exacerbate
the arrhythmia.
4. Digitalis toxicity
5. Severe electrolyte imbalance
Additionally, the following considerations exist for these special populations:
1. Patients who are pregnant: Can be performed without affecting the rhythm of the fetus. Fetal heart rate monitoring
during the procedure is recommended.
2. Patients who have pacemakers/ICDs: Can be performed but the electrode should be > 12 cm from the pulse
generator and an anteroposterior electrode orientation is recommended. The pacemaker/ICD should be interrogated
afterward to ensure proper functioning.
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The delivered shock depolarizes all or most excitable cardiac tissue and induces a refractory period that terminates
reentrant activity. Cardioversion restores sinus rhythm in 70–95% of patients. Efficacy decreases with increased
resistance (tissue density, physical distance due to habitus), prolonged arrhythmia duration, presence of structural
heart disease, and involvement of multiple reentry circuits.
Step-by-step instructions for emergent cardioversion and defibrillation:

Cardioversion:
front panel. See above for desired energy, or in general:
Defibrillation:
10. If the monitor shows a shockable rhythm, press the CHARGE button on the front panel. If patient is pulseless,
continue CPR while charging
11. Ensure all are clear from the bed then press and hold the illuminated SHOCK button
For non-emergent and routine procedures: NPO for at least 6-8h. Some patients may require periprocedural
anticoagulation to prevent thromboembolism. TEE is frequently used to look for the presence of a LA thrombus.
Complications: After shocking, ST & T wave changes may occur and typically resolve within 5 minutes. However, the
following complications may also occur:
● Arrhythmias/Conduction abnormalities:
o Self-limited and include sinus tachycardia, PAC, PVC, NSVT, VT, VF, and LBBB.
o May cause hemodynamic instability requiring further intervention
● Thromboembolism: Approximately 1% with anticoagulation, 5% without anticoagulation
● Myocardial necrosis: Severity depends on strength and number of shocks delivered
● Myocardial dysfunction/stunning:
o Global LV dysfunction can be present until 48 hours after shock
o Interpret cardiac studies within this 48h window with caution
● Pulmonary edema: Rare complication seen in patients with AF and/or LV dysfunction
● Hypotension: Transient, may last several hours, typically fluid-responsive
● Cutaneous burns:
o Seen in 20-25% of patients
o May use prophylactic steroid cream or topical NSAIDs at the site of electrodes
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Electrophysiology Study (EPS)
EPS is an elective, invasive, intracardiac catheter-based intervention that measures specific intervals within the
cardiac cycle to better understand the etiology, clinical significance, and management of brady- and tachy-
arrhythmias.
Indications:
6. Bradyarrhythmias: acquire corroborative data in symptomatic patients with episodic bradyarrhythmia or define level
of AV conduction abnormality
7. Tachyarrhythmias: define mechanism of NCT or WCT or reproduce a clinically defined tachycardia for mapping
and ablation
8. ICD implantation and programming: search for EPS-induced VT or VF in patients with structural heart disease,
NSVT, or reduced LVEF to justify ICD implantation and define optimal ICD parameters
9. Syncope of unknown etiology: to assess SN function, AV conduction, and search for VT/VF in patients with
syncope and organic heart disease
10. After cardiac surgery: to assess the effect of cardiac surgery on arrhythmia risk
Contraindications: active ACS, bacteremia, ADHF (not caused by the arrhythmia), critical AS, severe HOCM, severe left
main or 3-vessel CAD, presence of a major bleeding diathesis, presence of an acute lower extremity DVT (if femoral vein
cannulation is required).
Performed in the EP lab and patients are given at least conscious sedation. Standard ECG leads and defibrillation pads
are applied. Multiple sites of venous (and at times, arterial) access are acquired for intracardiac catheter placement.
Femoral access is most common. Catheters with electrode tips are placed in specific locations to both pace and record.
● High right atrium: Reflects SA node function, AV

conduction, and direction of atrial activation
● Coronary sinus: Reflects LA activation. Obtained in
patients with SVT or pre-excitation
● Tricuspid annulus (His): Tracings from low septal RA,
His bundle, and high septal RV depolarization reflect His
bundle activity
● RV apex: Reflects RV activity
● Left heart (via transseptal or retrograde aortic
approach for mapping/ablation)
Mapping
At the conclusion of the diagnostic EPS, a subset of patients may

undergo additional mapping and ablation for treatment of an arrhythmia. The created “map” is used to guide and localize
potential ablation sites. Mapping prior to ablation is not necessary for certain types of arrhythmias that have a defined
anatomical course (i.e. typical atrial flutter).
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Catheter Ablation Therapy
Indications
1. WPW, accessory pathway-mediated, and other variant pre-excitation states

2. Refractory atrial fibrillation/flutter and/or with severe symptoms
3. Refractory sinus, atrial or junctional tachycardia and/or with severe symptoms
4. Idiopathic ventricular premature depolarization from the right ventricular outflow tract associated with severe
symptoms
5. Monomorphic VT (can consider cases of polymorphic VT)
6. VF (uncommon indication)
7. PVC-induced cardiomyopathy
Contraindications are generally the same as for EPS (see prior section).
Pulmonary Vein Isolation (PVI) for the treatment of AF:
Indications, Technique, & Outcomes:
Indicated for patients with symptomatic AF who have either failed pharmacologic therapies for rhythm control or cannot
tolerate medication side effects. Among patients with HFrEF and NYHA II-III symptoms with persistent AF who are chosen
for a rhythm control strategy, PVI leads 36% absolute increase in AF-free survival at 24 months, 26% absolute reduction
in unplanned hospitalizations, and a 10% absolute reduction in overall mortality with AF ablation as compared to
amiodarone.
Can be accomplished with radiofrequency (RFA) or cryoablation. In patients with drug refractory, symptomatic paroxysmal
AF, cryoablation is non-inferior, reduces procedural time, but increases fluoroscopy time as compared to RFA. The
procedure aims to electrically isolate the antral portion of the pulmonary veins, a region identified as containing >90% of
the ectopic beats involved in the generation and maintenance of AF. As a result, cavotricuspid isthmus line ablation can
be performed during the same procedure if atrial flutter is co-occurring.
Efficacy at 1 year has been reported to be as high as 80-85% for paroxysmal AF but decreases to 50-60% for persistent
AF.
Anticoagulation:
As with any cardioversion, there is a risk of thromboembolism with PVI. All patients should be on anticoagulation peri-
procedurally. Patients with AF >48 hours should be on therapeutic anticoagulation for at least 3 weeks or have a TEE
prior to PVI. Anticoagulation should continue for at least two months after the procedure, although based on patient
wishes, risk factors/stratification, and aggressive post-ablation monitoring some EP physicians will choose to discontinue
anticoagulation.
Complications:
1. Complete heart block 5. Pericarditis
2. Thromboembolism 6. Pulmonary vein stenosis
3. Cardiac tamponade 7. Phrenic nerve paralysis
4. Acute MI 8. Atrioesophageal fistula
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References:
17. American Heart Association, American Heart Association, and American Heart Association. "guidelines for
cardiopulmonary resuscitation (CPR) and emergency cardiovascular care (ECC) of pediatric and neonatal
patients: neonatal resuscitation guidelines." Pediatrics 117.5 (2006): e1029-e1038
18. Jacobs, Ian, et al. "Part 6: defibrillation: 2010 international consensus on cardiopulmonary resuscitation and
emergency cardiovascular care science with treatment recommendations." Circulation 122.16_suppl_2 (2010):
S325-S337
19. Lown, Bernard, Raghavan Amarasingham, and Jose Neuman. "New method for terminating cardiac arrhythmias:
use of synchronized capacitor discharge." JAMA 256.5 (1986): 621-627
20. Knight, B. “Basic principles and techniques of cardioversion and defibrillation.” UpToDate 2018
21. Knight, B. “Cardioversion for specific arrhythmias.” UpToDate 2019
22. Kadish, Alan H., et al. "ACC/AHA clinical competence statement on electrocardiography and ambulatory
electrocardiography: A report of the ACC/AHA/ACP–ASIM Task Force on Clinical Competence (ACC/AHA
Committee to Develop a Clinical Competence Statement on Electrocardiography and Ambulatory
Electrocardiography) Endorsed by the International Society for Holter and Noninvasive Electrocardiology." Journal
of the American College of Cardiology 38.7 (2001): 2091-2100
23. Zipes, Douglas P., et al. "Guidelines for clinical intracardiac electrophysiological and catheter ablation procedures:
a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines
(Committee on Clinical Intracardiac Electrophysiologic and Catheter Ablation Procedures), developed in
collaboration with the North American Society of Pacing and Electrophysiology." Journal of the American College
of Cardiology 26.2 (1995): 555-573
24. Homoud, M. “Invasive cardiac electrophysiology studies.” UpToDate 2019
25. Dagres, Nikolaos, et al. "Complications of atrial fibrillation ablation in a high‐volume center in 1,000 procedures:
Still cause for concern?." Journal of cardiovascular electrophysiology 20.9 (2009): 1014-1019
26. Haissaguerre, Michel, et al. "Spontaneous initiation of atrial fibrillation by ectopic beats originating in the
pulmonary veins." New England Journal of Medicine 339.10 (1998): 659-666
27. Oral, Hakan, et al. "Circumferential pulmonary-vein ablation for chronic atrial fibrillation." New England Journal of
Medicine354.9 (2006): 934-941
28. Pappone, Carlo, and Vincenzo Santinelli. "Atrial fibrillation ablation: state of the art." The American journal of
cardiology96.12 (2005): 59-64
29. Ganz, L. “Overview of catheter ablation of cardiac arrhythmias.” UpToDate 2019
30. Passman, R. “Catheter ablation to prevent recurrent atrial fibrillation.” UpToDate 2018
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Quick Reference Guide: Arrhythmias and Electrophysiology
Narrow Complex Tachycardia (NCT)

● If unstable with NCT ⇒ DCCV with following energy
o Regular → 50-100J
o Irregular → 120-200J biphasic or 200J monophasic
● The following table characterizes the NCTs by mechanism and location
MECHANISM
↑ AUTOMATICITY RE-ENTRY
S
Sinus Tachycardia Sino-Atrial Nodal Reentrant Tachycardia
I
● Secondary cause (HoTN, pain, fever, ● Reentry within or around SA node
N
PE, CHF, acute MI, fistula, etc.) vs drug ● Paroxysmal, abrupt on/off
U
effect/toxicity/withdrawal ● P wave morphology similar to baseline
S
● HR 100-150 in older pts; up to 200 in ● Treat w/ vagal maneuvers, Valsalva;
N
younger pts nodal blockade; ablation
O
● Gradual onset
D
● Treat underlying cause
E
Atrial Tachycardia Atrial Flutter

● Focal vs multifocal ● Macro-reentrant circuit
● Atrial rate 100-250, vent rate 90-120 ● Atrial rate 250-300, vent rate 150 (if 2:1
A (variable block) conduction)
T
● Focal AT: Structural heart dz vs Dig ● Slow and diagnose with vagal
R
toxicity; d/c Dig, rate control (BB vs maneuvers ± adenosine
I
CCB), ablation. ● Similar mgmt. to atrial fib: rate/rhythm
LO U
● MAT: ≥3 P-wave morphologies, a/w control, anticoagulation
CA M
chronic pulmonary disease; prefer CCB ● Prefer BB, CCB, Dig to class 1A/1C
TI > BB if severe lung disease meds → can enable 1:1 conduction
ON
● Typical flutter is amenable to ablation
Non-Reentrant AVNRT
Junctional Tachycardia ● Reentry thru dual pathways in AV node
● JET (junctional ectopic tach): infants > ● Abrupt on/off, rates 150-220
adults, particularly post-cardiac surgery ● Retrograde P, can be buried in QRS
A for CHD; due to ectopic focus; high ● Acute: vagal, adenosine
V morbidity ● Mgmt: BB, CCB; ablation is definitive
N ● NPJT (non-paroxysmal JT): adults >
O children; “accelerated junctional AVRT
D rhythm”; a/w digoxin toxicity and acute ● Reentry thru acc. pathway + AV node
E MI; difficult to distinguish from AVNRT ● Narrow = orthodromic (antegrade thru
w/o EP study; treat underlying cause AV node, retrograde thru acc. path);
use nodal blockade
● Wide/pre-excitation = antidromic; avoid
nodal blockade (see WCT chapter)
● Definitive tx: ablation
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Wide Complex Tachycardia (WCT)

● Refers to rate > 100bpm and QRS ≥ 120ms
● The DDx for WCTs include
o VT
o SVT with aberrancy
o SVT w/ pre-excitation, and
o Pacemaker-related tachycardias
● The clinical presentation of WCT can be variable, from asymptomatic runs of NSVT to a patient who has coded.
Because most patients do not tolerate VT for long periods of time, when you see WCT, assume it is VT🡪 feel for
a pulse and obtain BP ASAP!
● Approach the initial management of WCT according to patient stability (as below). See chapter for more details on
mgmt according to etiology
o Pulseless: Immediately start the pulseless VT ACLS algorithm and prepare for unsynchronized DCCV
o Hemodynamically unstable or highly symptomatic: Worry about etiology AFTER YOU’VE STABILIZED
PATIENT
▪ Prepare for synchronized DCCV (fentanyl/versed for sedation), put pads on the patient, and call
for help (e.g. cardiology, EP, RICU, etc.)
▪ Start amiodarone (150 mg x 1 Q 3–5 min, then drip @ 1 mg/min), and/or lidocaine (100 mg x 1,
then drip @ 1–4 mg/min). Amiodarone typically is an appropriate anti-arrhythmic to start unless
there is QT prolongation and concern or TdP
▪ If regular, monomorphic, and there is some suspicion for SVT, you can consider using adenosine
as both a diagnostic and therapeutic intervention
Atrial Fibrillation (AF)

● Atrial fibrillation is the most common sustained cardiac rhythm disturbance, increasing in prevalence with age
(0.4% to almost 20%)
● In general, AF results from an abnormal atrial response to reentry and/or rapid focal ectopic firing
● Patients can be asymptomatic, but many describe palpitations, fatigue, dyspnea, lightheadedness and
diaphoresis
o Thromboembolic CVA is the initial manifestation in 10–40% of patients
● TTE should be performed in all patients who present with new-onset AF in order to evaluate for a structural
etiology. In addition, thyroid function testing should routinely be performed, as hyperthyroidism predisposes to AF.
Also consider renal and liver function tests, as well as cardiac biomarkers (including troponin and NT-proBNP)
based on clinical presentation
● Rate versus rhythm control: no mortality difference
● Anticoagulation: All patients with AF should be on anticoagulation except those at the lowest risk of
thromboembolic stroke
o The AHA/ACC 2019 guidelines recommend DOACs (including dabigatran, rivaroxaban, apixaban and
edoxaban) over warfarin to reduce stroke risk in appropriate AFib patients, unless moderate-to-severe
mitral stenosis or a mechanical heart valve
Temporary Pacing and Pacemaker Therapy

● Temporary pacing includes transcutaneous and transvenous pacing, both of which are indicated as urgent or
emergent therapy in patients with hemodynamically significant bradyarrhythmia
● Transcutaneous pacing can be performed urgently without input from cardiology, but should involve the Senior
ON and nursing supervisors
o Short-acting sedation (e.g. with Dilaudid/Ativan) is indicated in non-ACLS setting (consider early
involvement of Anesthesia)
o Pace by turning defibrillator to “Pacer” mode; a good rule of thumb is to set the HR and output at a
starting rate 100 bpm and 100 mA, respectively
● Transvenous pacing is a more durable option than transcutaneous pacing, and is often employed as a temporary
bridge to recovery or to PPM placement
o In contrast to placement of a temp wire for transvenous pacing must be performed in the cath lab
o The pacing lead is inserted into the right ventricle via the right internal jugular, left subclavian, or femoral
veins (less reliable and increased risk for dislodgement)
o Temp wires may remain in place for up to 7-10 days but carry a risk of infection
o Daily maintenance includes CXR, threshold testing, and ECG (all to assess for lead migration)
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● Permanent pacing is indicated for irreversible symptomatic bradycardia, chronotropic incompetence, or unstable
conduction disorders
● There are many different pacing modes, which are designated by a 1-5 letter code. In the chart below, “position”
refers to letter position
o As an example, in the 4-letter code DDDR, the D in position I implies that both chambers (the atria and
the ventricles) can be paced, the D in position II indicates that both chambers (the atria and the
ventricles) can be sensed, the D in position III indicates that the device can respond to sensing by
either triggering activity or inhibiting itself, and the R in position IV indicates that the device allows for
rate modulation
Implantable Cardioverter-Defibrillator Therapy

● Per AHA/ACC guidelines, ICDs are indicated for both primary and second prevention in patients on optimal
medical therapy who have an estimated survival of at least 1 year (with good functional status)
● Class I indications for secondary prevention include:
o Survivors of cardiac arrest due to VF or sustained VT without reversible causes (AVID)
● Class I indications for primary prevention (with trial references) include:
o Ischemic cardiomyopathy and LVEF ≤ 30-40% at least 40 days post-MI (DINAMIT) or at least 3 months
post-CABG (CABG-PATCH)
o LVEF ≤ 30% and NYHA Class I, II, or III (MADIT-II)
o LVEF ≤ 35% and NYHA Class II or III (SCD-HeFT)
o LVEF ≤ 40% and inducible VF or sustained VT at EP study (MUSTT)
o Non-ischemic cardiomyopathy with at least 3 months of documented: CHF, LVEF ≤ 35%, and NYHA
Class II or III (SCD-HeFT)
o Syncope of unknown origin and VT/VF induced at EP study
o Spontaneous sustained VT (+/- hemodynamic instability) with structural heart disease
● Wearable cardiac defibrillators (WCDs) are externally worn defibrillators, generally considered as interval therapy
in patients awaiting ICD
o The VEST Trail showed that among post-MI patients with EF ≤35%, WCDs did not reduce SCD and
ventricular tachyarrhythmias but did reduce the secondary endpoint of all-cause mortality up to 90 days

● Cardiac resynchronization therapy (CRT) devices have an RA, RV, and coronary sinus (epicardial pacing of LV)
leads, allowing for optimization of A-V and V-V synchrony, which has been shown to improve stroke volume
o Class I indications: CRT implantation is recommended for patients with chronic heart failure (NYHA
function class II, and ambulatory IV) with LVEF ≤ 35% and LBBB w/ QRS duration > 150 ms and should
be considered in these patients if QRS duration is 120-150 ms
o CRT devices may only provide BiV pacing (CRT-P) or may allow for BiV pacing plus defibrillation with ICD
function (CRT-D)
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Procedures in EP and EP Studies

● Cardioversion (DCCV) and defibrillation are non-invasive interventions that can terminate tachyarrhythmias by
delivering an electrical shock to the heart
● Emergent DCCV and defibrillation are generally indicated in cases of clinical instability. Planned DCCV may also
be performed as an effective treatment for SVTs
● The delivered shock depolarizes all or most excitable cardiac tissue and induces a refractory period that
terminates reentrant activity
● Cardioversion is performed by synchronizing the shock to a QRS complex (thus requires a rhythm in which the
QRS complex is present) and restores sinus rhythm in 70–95% of patients. The procedure is as follows:
6. Turn the mode selector to DEFIB (red area). Select the desired energy using the up and down arrow keys in
the front panel. In general:
● Defibrillation is unsynchronized and delivers a random shock during the cardiac cycle.
14. If the monitor shows a shockable rhythm, press the CHARGE button on the front panel. If patient is
pulseless, continue CPR while charging
15. Ensure all are clear from the bed then press and hold the illuminated SHOCK button on the front panel
● An electrophysiology study (EPS) is an elective, invasive, intracardiac catheter-based intervention that
measures specific intervals within the cardiac cycle. The purpose is to better understand the etiology,
clinical significance, and management of brady-and tachy-arrhythmias
● A common procedure in EP is Pulmonary Vein Isolation (PVI), performed with either radiofrequency (RFA)
or cryoablation, which involves electrical isolation of the antral portion of the pulmonary veins, which
contains >90% of the ectopic beats involved in AFib.
PVI is indicated in patients with symptomatic atrial fibrillation who have either failed pharmacologic therapies for
rhythm control or cannot tolerate medication side effects. Importantly, ablation does not negate the need for
therapeutic anticoagulation
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Valvular Heart Disease
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VALVULAR HEART DISEASE

Aortic Stenosis (AS)
Epidemiology / Natural History
• Incidence: 0.2% in patients aged 50-59 years, but increases to 9.8% at age 80-89
• Bicuspid aortic valve incidence worldwide is 0.5–2%, but accounts for 50% of severe AS requiring AVR
• Following diagnosis, the aortic valve area decreases by ~ 0.1 cm2 per year, although can be highly variable
• Once symptoms develop, the average survival in patients with severe AS is 1-3 years. If the aortic valve is replaced,
however, average survival returns to that of the general population.
Etiology: clinical risk factors for calcific AS mirror risk factors for CAD.
• AS is more common in men, advanced age, CKD (in part related to metastatic calcification), and vascular disease
• Rheumatic heart disease is responsible for the majority of cases in the developing world.
• Radiation-induced valve disease is increasingly recognized after mediastinal radiation therapy
• Aortic sclerosis, or calcification of the valve with no hemodynamic effects, is increasingly common with age, though
over 5 years, only 10-15% of these patients will develop AS.
Pathophysiology: Left sided pressure changes
Figure 1. Aortic Stenosis. CVPhysiology.com. Note increased LVEDP, LA pressures and decreased systemic pressures.
Presentation:
• Symptoms generally occur only in severe AS; LV remodeling often precedes symptom onsetAngina: results from
several mechanisms including increased total LV oxygen demand in setting of LV hypertrophy, decreased coronary
perfusion gradient due to elevated LVEDP, reduced diastolic perfusion time during tachycardia (later AS); ~ 50% of
angina in AS have CAD
• Syncope: exercise-induced decrease in total peripheral resistance is uncompensated because CO is restricted by
stenotic valve. 15% present with syncope.
• Heart failure: LV hypertrophy from chronic afterload results in diastolic dysfunction and/or systolic dysfunction
Figure 2. The natural history and rate of progression in aortic stenosis.1
Initial Clinical Evaluation

• Physical exam findings:
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o Systolic ejection murmur at the R upper sternal border that radiates to the neck; occasionally a different quality of
murmur which radiates to the apex (Gallavardin phenomenon).
o Decreases with maneuvers that decrease preload, such as standing and Valsalva. The severity of valvular
disease may not correlate with the intensity of the murmur.
o Indicators of severe AS include a late-peaking murmur, delayed carotid upstroke (pulsus parvus et tardus),
radiation to the left clavicle, and obliteration of the A2 component of S2.
• Diagnostics
o EKG may show LVH, LAE, LAFB or LBBB
o Transthoracic echocardiography (TTE) is used to evaluate valve anatomy and structure, valve gradients, and
LV structure and function. Multiple views can show reduced leaflet excursion with a small aortic orifice. Short axis
views “en-face” to the valve can demonstrate a bicuspid valve. Doppler echocardiography permits measurement
of jet velocity and calculation of the LV-Aortic gradient, which are the standard parameters used for evaluation of
severity (See Table 1).
o Cardiac catheterization may be indicated for hemodynamic assessment if clinical and echo data are
inconclusive or to evaluate for CAD prior to aortic valve replacement.
o Particularly for patients with suspected LFLG severe AS, need to optimized blood pressure control prior to
diagnostic studies to accurately assess AS severity
Grading AS Severity
Echocardiographic criteria (Table 1).
Table 1: 2020 ACC/AHA guidelines for grading of severity in aortic stenosis
Valve area (cm2) Mean gradient (mmHg) Jet velocity (m/s)

Mild > 1.5 < 20 2.0-2.9
Moderate 1.0–1.5 20-39 3.0–3.9
Severe < 1.0 > 40 > 4.0
Severe LFLG <4 at rest

(reduced LVEF) < 1.0 <40 ≥4 w/ dobut. stress echo
Clinical progression is separated into stages A-D. Patients with bicuspid aortic valve or valvular sclerosis are termed
Stage A, or “at risk.” Mild-to-moderate AS defines Stage B, or “progressive AS.” Patients with Severe AS may be
categorized as Stage C (asymptomatic) or Stage D (symptomatic).
Aortic Valve Replacement (AVR)

Determining indications for valve replacement is based on (1) presence of symptoms (2) severity of TTE criteria and (3)
LV function. AVR is indicated in the following cases:
• Symptomatic severe AS (Stage D):
o These patients require prompt AVR due to risk of sudden death. Exercise testing is contraindicated.
• Asymptomatic, severe AS (Stage C2):
o Asymptomatic, severe AS with LVEF <50% have class I indication for AVR
o Normal LVEF: exercise stress testing can be useful in asymptomatic patients to confirm lack of symptoms and
evaluate physiologic change. If symptoms are provoked with exercise, patient is considered symptomatic and
AVR is indicated. If poor exercise tolerance or fall in systolic pressure by ≥10 mmHg, AVR can be considered.
• Low Flow Low Gradient AS:

In patients with reduced LV function (either from long-standing AS or concomitant systolic dysfunction), the gradient
across the valve may be lower than expected (<40 mmHg) despite AVA <1 cm2
o Evaluation of LFLG AS is via dobutamine stress echo
▪ In LFLG AS, the mean AV gradient should increase to >40mmHg or increase Vmax > 4m/s when the heart
function is augmented with dobutamine. AVR is indicated in these patients.
▪ Some patients fail to show an increase in stroke volume by ≥20% with dobutamine, referred to as “lack of
contractile reserve”
▪ Conversely, a normal valve may appear to have a low area if the ejection fraction and the flow across it are low
(so termed “pseudo-severe” AS).
▪ In “pseudo-severe” AS, the increased cardiac output may “stent” open the valve, and increase calculated
aortic valve area (to an AVA >1cm2), while the mean AV gradient does not change or may even be reduced.
AVR is NOT indicated in these patients
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Medical Management
Only AVR has been shown to improve symptoms and mortality in AS patients. Guidelines for medical management
involve treatment of HTN in patients at risk of developing AS (stage A) or with asymptomatic AS (stages B and C).
• Hypertension: Reduces the “double load” of afterload related to both the stenotic valve and systemic vasculature. No
optimal regimen. ACEi may reduce fibrosis; caution as diuretics can reduce preload and CO, vasodilators can reduce
coronary perfusion, and BB can reduce myocardial contractility. Up-titrate cautiously.
• Volume status: Volume status can be difficult to optimize in hospitalized patients with severe aortic stenosis.
Adequate preload is necessary to ensure sufficient cardiac output. Nitrates and diuretics should be used with caution
to avoid rapidly decreasing preload. High afterload can further potentiate high wall tension and diastolic dysfunction,
resulting in flash pulmonary edema. Initial management of hypovolemia in patients with severe AS may require small
fluid boluses (250cc) with careful monitoring of respiratory status. Patients with severe stenosis may easily “tip over”
with volume overload and can rapidly experience pulmonary edema.
• Statin therapy: has not been shown to reduce progression of AS and therefore is not indicated for prevention of
hemodynamic progression of AS.
Interventional Management:
▪ Bioprosthethic vs mechanical valve: depends on age (if <50, mechanical preferred for durability), contraindications
to anticoagulation (required lifelong for mechanical valve), and surgical risk (mechanical valve only done surgically)
▪
▪ TAVR versus SAVR: Recommendation of transcatheter AVR versus surgical AVR is made in multi-disciplinary
consultation between surgery and structural cardiology.
▪ Use of the Society of Thoracic Surgeons (STS score) risk calculator is helpful in determining surgical risk. An
STS score <4% qualifies as low risk, 4-8 % as intermediate risk, >8% as high risk
▪ Main risk factors that are not included in STS risk score are frailty, pulmonary hypertension, liver
disease, and porcelain aorta. Consider these in addition to STS.
TAVR was initially shown to be effective in patients with prohibitively high surgical risk (PARTNER trial), but has
since been shown to be non-inferior to surgical AVR in patients with:
▪ High surgical risk (PARTNER 1A, CoreValve trials), intermediate and low surgical risk (PARTNER-2,
PARTNER-3, SURTAVI, NOTION, STACCATO, Siontis GCM trials)
▪ TAVR has a slightly lower mortality risk and is associated with a shorter hospital length of stay, more rapid return
to normal activities, lower risk of transient or permanent AF, less bleeding, and less pain than SAVR. However, it
does have a higher risk of paravalvular leak, valve reintervention, and need for permanent pacemaker (PARTNER
3, NOTION)
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Preparing a patient for TAVR and Periprocedural Considerations

• To begin the process, consult structural cardiology, cardiac surgery. Patients should have a recent TTE, a TAVR-
protocol cardiac CT, and have undergone dental clearance (Panorex).
• Steps of Procedure for Percutaneous Route (most commonly transfemoral)
o Femoral artery access obtained using a 14F sheath or greater
o Transvenous access obtained and RV pacing wire placed
o Cross the aortic valve with a guide wire and balloon dilation performed
o With prosthetic valve in place (with fluoro +TEE or TTE guidance), rapid ventricular pacing (>180bpm) is used to
decrease stroke volume and allow valve to be deployed.
o Should immediately see reduction in transvalvular gradient
• Periprocedural considerations
o Access:
▪ Bleeding: Large bore sheaths and access sites and distal pulses (often with PVRs) require frequent
monitoring, and patients are heparinized during the procedure followed by DAPT so at high risk for bleeding.
• Complications include: retroperitoneal hemorrhage, femoral or iliac artery dissection, and development of
femoral pseudoaneurysm. The major bleeding rates have decreased over the years with newer
generation valves and catheters ( ~4% in the TVT registry)
o Hemodynamics:
▪ Hypertension: Due to sudden reduction in obstruction after TAVR; can often be controlled with IV pushes of
vasodilators (i.e. hydralazine) PRN, though occasionally will require drips
▪ Hypotension: Due to decreased preload. Left ventricular hypertrophy and diastolic heart disease means
patients are usually volume responsive, so gentle fluid resuscitation should be attempted. Target a mean
arterial pressure of 60-80.
o Rhythm:
▪ High degree AV block: Occurs more often in patients who have baseline conduction abnormalities
(particularly RBBB) and those who are receiving self-expanding valves (ie Corevalve). In those cases,
temporary pacing wires are left in place. Risk of PPM ~8% in the Siontis GCM metanalysis.
Antithrombotic Management Post-Valve Replacement

The incidence of transcatheter heart valve (THV) thrombosis following TAVR is 7% (majority subclinical), with larger valve
size predisposing to higher rates of thrombosis. 7 The risk of stroke or TIA is greatest in the first 24 hours postoperatively
and neurologic events peak in the first week. 8 Emerging data also suggests that there may be a role for intraoperative
neuroprotective strategies given reports of changes in cognition in the post-TAVR period. Guidelines for anticoagulation
after AVR (institutional preferences may vary, check with structural team, surgeon and/or fellow/attending):
• SAVR
o Bioprosthetic AVR:
▪ ASA 81 mg, 3-6 month of Coumadin for INR 2–3 after surgery. (Consider lifetime if AF, EF<30–35%, prior
clot, hypercoagulable)
▪ Stop Coumadin 48–72 hours before procedure, restart 24h afterwards
o Mechanical AVR:
▪ ASA 81 mg, INR 2–3 for life; if other risks factors (EF < 30%, AFib, prior clot, procoagulable disorder, Starr-
Edwards Valve), INR goal 2.5–3.5.
▪ IV heparin when INR < 2
o If reversal of anticoagulation is urgent, FFP can be used (Class II), and is preferred over Vitamin K since it is
thought to reduce the incidence of thrombotic complications (data is limited)
• TAVR
o ASA 81 mg monotherapy is recommended, unless there is a concurrent indication for DAPT(i.e. recent PCI)
▪ Aspirin monotherapy is non-inferior to DAPT for composite thrombotic events and associated with less
bleeding (NEJM 2020; 383:1447-1457)
o If patient has separate indication for anticoagulation (i.e. AFib) and no concurrent indication for antiplatelet
therapy, they should be continued on the anticoagulant post-TAVR without addition of aspirin
▪ GALILEO trial was stopped early due to higher rate of adverse events in Rivaroxiban + aspirin group
References:
1. Lester SJ et al. The natural history and progression of aortic stenosis. Chest. 1998;113(4):1109-14
2. Makkar RR et al. Transcatheter aortic-valve replacement for inoperable severe aortic stenosis. N Engl J Med.
2012;366(18):1696-704
3. Kodali SK et al. Two-year outcomes after transcatheter or surgical aortic-value replacement. N Engl J Med.
2012;366(18):1686-95
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4. Adams DH et al. Transcatheter aortic-valve replacement with a self-expanding prosthesis. N Engl J Med.
2014;370(19):1790-8
5. Popma JJ et al. Transcatheter aortic valve replacement using a self-expanding bioprosthesis in patients with
severe aortic stenosis at extreme risk of surgery. J Am Coll Cardiol. 2014;63(19):1972-81
6. Leon MB et al. Transcatheter or surgical aortic-valve replacement in intermediate-risk patients. N Engl J Med.
2016;374(17):1609-20
7. Hansson NC et al. Transcatheter aortic valve thrombosis: Incidence, predisposing factors, and clinical
implications. J Am Coll Cardiol. 2016;68(19):2059-2069
8. Tay EL et al. A high -risk period for cerebrovascular events exists after transcatheter aortic valve implantation.
JACC Cardiovasc Interv. 2011;4(12):1290-7
9. Makkar RR et al. Possible subclinical leaflet thrombosis in Bioprosthetic aortic Valves. N Engl J Med.
2015;373(21):2015-24.
10. Auffret V et al. Serial changes in cognitive function following transcatheter aortic valve replacement. J Am Coll
Cardiol. 2016;68(20):2129-2141
11. Spaziano M et al. Imaging and functional testing to assess clinical and subclinical neurological events after
transcatheter or surgical aortic valve replacement: a comprehensive review. J Am Coll Cardiol. 2014;64(18):1950-
63
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Aortic Regurgitation (AR)
Acute and chronic AR have different etiologies, pathophysiological consequences, natural histories, and management
strategies. In general, AR occurs when the aortic valve does not close (or coapt) completely and blood flows back into
the LV from the aorta during diastole. As shown in Figure 1, this results in a rapid descent of aortic diastolic pressure
(AP tracing). Backflow from Aorta to LV → Increase in LVEDV → increased LV preload → increased SV and SBP.
Increased SBP and decreased DBP as described above result in characteristic wide pulse pressure.
Figure 1. Aortic Regurgitation. CVPhysiology.com.
Acute AR:
Etiology and Epidemiology
Results from abnormalities of the valve, such as infective endocarditis, or cusp prolapse, or acute abnormalities of the
aorta, primarily aortic dissection. Acute AR may also occur among patients with mechanical or bioprosthesis if there is
prosthetic leaflet dysfunction.
Pathophysiology:
In the uncompensated heart with acute AR, an increase in LVEDV (without acute LV enlargement) results in a large
increase in left-sided pressures, which leads to congestive heart failure and pulmonary edema. Marked and rapid volume
overload pushes the LV to the edge of its Frank-Starling curve. The LV cannot acutely increase total stroke volume,
resulting in a decline in forward stroke volume and cardiac output.
Acute AR may be an emergency; if a patient is symptomatic from acute AR, surgical consultation should be
pursued.
Chronic AR:
Etiology/Epidemiology:
The most common causes of chronic AR in the United States and other developed countries are bicuspid aortic valve,
thoracic aneurysms and calcific valve disease. Rheumatic heart disease is the leading cause in many developing
countries. AR also arises from primary diseases causing dilation of the ascending aorta or sinuses of Valsalva (e.g.
genetic syndromes such as Marfan’s Syndrome, systemic rheumatic disorders such as ankylosing spondylitis, and
infectious aortitis).
The 2018 AHA/ACC Adult Congenital Cardiology guidelines provide a Class IIa recommendation to screen first-degree
relatives of individuals with bicuspid aortic valve for valvular disease (present in 10% of relatives) and aortopathy (present
in 32% of relatives).1
Pathophysiology and Clinical Course

Chronic AR typically leads to progressive LV and LA dilation. The added volume produces an increased wall tension and,
over time, spherical remodeling and eccentric ventricular hypertrophy. Ventricular compliance increases to accommodate
high volumes. The combination of ventricular hypertrophy and increased preload raises the stroke volume, and cardiac
output is initially maintained. In this way, patients with moderate-severe AR may remain asymptomatic for years.
Over time, however, the LV continues to dilate and the hypertrophy is unable to keep pace, which eventually leads to a
decline in both LV contractility and ejection fraction (EF). Interstitial fibrosis increases, compliance declines, and LVEDP
rises, and symptoms of congestion ensue. Bradycardia is poorly tolerated because slow HRs increase diastolic filling (and
regurgitant volume) time, which reduces effective forward stroke volume.
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Initial Clinical Evaluation

Physical exam:
▪ Early decrescendo diastolic murmur at the LUSB or RUSB. This murmur typically increases with sitting
forward, expiration, or handgrip (increase in afterload). The murmur is louder with more severe AR, except if
AR is acute or in its late-stage when LV filling pressure rises and aortic pressure drops.
▪ The Austin Flint murmur, a diastolic rumble at the apex, may also be audible if the AR jet is directed
posteriorly and interferes with mitral inflow.
▪ An S3 is common and can be heard in patients with AR and a preserved EF (due to LV dilation that is part of
the normal pathophysiologic response to AR).
▪ Pulses may be bounding, and the pulse pressure is widened. These and dozens of other eponymous signs
become increasingly prominent as the AR becomes more severe.
Radiographic evaluation:
▪ TTE is indicated in patients with signs or symptoms of AR for accurate diagnosis of the cause of regurgitation;
assessment of regurgitant severity, LV size and LV systolic function; and for determining timing of valve
intervention. See Figure 2 and Table 1 below for echocardiographic/clinical grading criteria.
▪ If TTE images are sub-optimal in moderate/severe AR, or clinical and echocardiographic findings are discrepant,
can consider TEE or cardiac MRI (less useful in acute setting), to distinguish between moderate and severe MR
Note: In cases of acute AR when aortic dissection is suspected, the sensitivity and specificity of TTE for
dissection is only around 60 to 80%. In these instances, TEE or CTA should be employed, as the
sensitivities and specificities for diagnosing aortic dissection exceed 95% for these modalities.
▪ AR is quantified by measuring the jet width in the LVOT and vena contracta (the narrowest width of the
regurgitant jet before the LVOT) on Doppler as well as the regurgitant orifice size and regurgitant volume. With
severe AR, Doppler shows steep deceleration in the jet velocity due to elevated LV end-diastolic pressure and
prolonged diastolic flow reversal in the descending aorta.
▪ LV systolic and diastolic diameters, EF, and aortic width on TTE are key parameters that influence decision for
surgical intervention. Depressed ejection fraction and increased LVESV are associated with development of
HF symptoms or death in asymptomatic patients.
Figure 2. Echocardiographic assessment of aortic regurgitation severity. Asecho.org.

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Table 1: 2020 ACC/AHA Guidelines for Staging Chronic AR3

Progressive (stage Asymptomatic Symptomatic Severe
B) Severe (Stage C) (Stage D)
Hemodynamics
Jet width (% of Mild: <25% Severe: ≥65% Severe: ≥65%

LVOT)
Moderate: 25-64%
Vena contracta Mild: <0.3 cm Severe: >0.6 cm Severe: >0.6 cm

(cm) Moderate: 0.3-0.6 cm
Regurgitant Mild: <30 ml Severe: ≥60 ml Severe: ≥60 ml

volume (ml/beat) Moderate: 30-59 ml
Regurgitant Mild: <30% Severe: ≥50% Severe: ≥50%

fraction (%) Moderate: 30-49%
Effective Mild: <0.10 cm 2 Severe: ≥0.3 cm 2 Severe: ≥0.3 cm 2

regurgitant orifice Moderate: 0.10-0.29 cm 2
(cm2)
Diastolic aortic Sub-holosystolic Holosystolic Holosystolic
flow reversal
LV size/function Normal LV volume or C1: LVEF ≥55%, mild- Moderate-to-severe LV

mild dilation. moderate LV dilation. dilation is present.
Normal LV systolic C2: LVEF <55% or Can occur with normal
function severe LV dilation LVEF (≥55%), mild-
(LVESD>50mm) moderate dysfunction
(40-55%) or severe LV
dysfunction (<40)
*Note: Stage A refers to “at-risk” patients, such as patients with bicuspid aortic valve, diseases of the aortic sinus or
ascending aorta, history of rheumatic fever, or infective endocarditis.

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Surveillance:
Repeat TTE should be performed to re-evaluate asymptomatic patients with AR, with recommended frequency
determined by the severity of regurgitation (Severe: every 6-12 months, Moderate: every 1-2 years, Mild: every 3-
5 years).
Management
Medical Management
Acute or decompensated AR: The management of acute severe AR (most often resulting from infectious endocarditis or
aortic dissection) consists of hemodynamic temporization and urgent surgical evaluation. Propensity-matched cohort
studies among patients with infective endocarditis have demonstrated a 6% absolute risk reduction with early versus
delayed surgery.2
Medical therapy:
• IV afterload reduction with agents like nitroprusside. Avoid vasoconstrictors which may increase diastolic
regurgitant flow
• Inotropic support with dobutamine/milrinone as needed
• Chronotropic support with overdrive pacing or isoproterenol to reduce diastolic regurgitation time as needed.
• Beta blockers are generally avoided in severe AR (blocks compensatory tachycardia, increasing diastolic
regurgitation time), except in the case of acute aortic dissection where it is first line for impulse control therapy
• Diuretics as needed to reduce LV filling pressures
• Consider PA line placement for guidance of above therapies
Mechanical Circulatory Support

• Intra-aortic balloon pumps are contraindicated in severe AR: inflate during diastole → increase diastolic
regurgitant flow dramatically
• VA ECMO is contraindicated in patients with severe aortic regurgitation
• LVAD implantation can worsen AR. Significant AR can lead to ineffective LVAD output and end-organ
malperfusion.
Chronic compensated AR:

▪ In asymptomatic patients with chronic AR (stages B and C), treatment of hypertension to maintain SBP <140 mm
Hg is recommended
▪ Guidelines recommend the use of ACE inhibitors/ARBs in patients with severe AR who have symptoms and/or LV
dysfunction and are not candidates for surgical intervention. RCTs have not shown conclusively that these drugs
alter the natural history of asymptomatic patients with chronic asymptomatic AR and normal LV systolic function,
but cohort studies support their use in patients with systolic impairment.
Valvular intervention
- Proceed to AVR if patient is symptomatic, LVEF <50%, LV end-systolic dimension >50 mm, and/or if concomitant
CT surgical procedure is being planned (i.e. CABG or other valve). See Figure 3.
- Outcomes are optimal when surgery is performed before LVEF decreases below 55%.
- In asymptomatic patients with LV systolic dysfunction, postoperative outcomes are better if AVR is
performed before onset of symptoms.

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Figure 3. Timing of Valvular Intervention. 2014 ACC/AHA Guidelines 2014.
Additional Notes:
o Once AR has been diagnosed, follow up evaluations should focus on the identification of symptoms.
Symptomatic AR is an indication for surgical intervention, and intervening as early as possible—before LV
systolic failure ensues or worsens—is paramount. Without AVR, these patients have a very high mortality rate
(25% for NYHA class III/IV, 6% for NYHA Class II), and post-operative survival is significantly higher in patients
who are still NYHA I/II at time of surgery compared with NYHA class III/IV (10 year survival of 80% vs 45%).4
o Even in symptomatic patients with severely depressed systolic function, surgery is recommended over medical
therapy. The sooner AVR is performed after depressed EF is noted, the more systolic recovery occurs.
References:
1. Stout KK et al. 2018 AHA/ACC Guideline for the management of adults with congenital heart disease. J am Coll
Cardiol. 2019;73(12):1494-1563
2. Lalani T et al. Analysis of the impact of early surgery on in-hospital mortality of native valve endocarditis: use of
propensity score and instrumental variable methods to adjust for treatment-selection bias. Circulation.
2010;121(8):1005-13.
3. 2014 AHA/ACC guideline for the management of patients with valvular heart disease. J Am Coll Cardiol. 2014 Jun
10;63(22):2438-88
4. Klodas E et al. Optimizing timing of surgical correction in patients with severe aortic regurgitation: role of
symptoms. J Am Coll Cardiol. 1997;30(3):746-52

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Mitral Regurgitation (MR)
Acute.
Etiologies: Acute ischemia (most often inferior STEMI) with papillary muscle rupture/dysfunction, infective endocarditis,
spontaneous chordal rupture in myxomatous mitral valve disease
Chronic.
(1) Primary (degenerative). Valvular incompetence via pathology of a component of the valve itself (leaflets/chordae
tendinae/papillary muscles/annulus).
o Most common cause in United States is MVP and ischemic heart disease. Additional etiologies:
infective endocarditis, rheumatic heart disease, collagen vascular disease, annular calcification
o Young patients: myxomatous degeneration
o Elderly patients: fibroelastic degeneration of valve
(2) Secondary (functional). Valve is normal but becomes displaced via papillary muscle displacement (usually from dilated
ventricle and severe LV dysfunction). Annulus dilates, leaflet becomes tethered, and valve leaflets cannot coapt.
Figure 1. Mitral regurgitation. CVphysiology.com.
Acute Mitral Regurgitation.

• Acute MR and sudden volume overload cannot be compensated by LV → risk of pulmonary edema, reduced SV
and CO, cardiogenic shock
Chronic Primary Mitral Regurgitation.

• ↑ LA volume and pressure → ↑ pulmonary circulation pressures and ↑ LVEDV → enlarged LV.
o Increased LV size leads to risk of atrial fibrillation and worsens MR by dilating mitral annulus/regurgitant
orifice.
o LV undergoes eccentric hypertrophy with compensatory dilation (volume overload pattern). Initially
maintains CO, but decompensates and leads to left, then right sided heart failure and ↑risk sudden death.
In those who are symptomatic, exertional dyspnea, fatigue, and atrial fibrillation are the most common manifestations.
Severe MR results in poor clinical outcomes (survival rates 33% at 8 years without MVR, mortality 5% per year). Most
deaths are due to heart failure. There is a substantial rate of sudden death, highlighting the importance of ventricular
arrhythmias.
Evaluation: 1. Distinguish between acute and chronic. 2. Identify etiology. 3. TTE to confirm and grade severity.
Acute.
History: New onset dyspnea, PND, orthopnea, edema. Exam: New apical holosystolic murmur radiating to left axilla.
Rales, edema, JVD, cardiogenic shock.

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Chronic.
History: Progressive exertional dyspnea, exercise intolerance.
Exam: Apical holosystolic murmur radiating to left axilla (half patients with chronic secondary MR lack audible
murmur, especially if low systolic LA-LV pressure gradient i.e. ↑LA pressure, ↓systemic arterial pressure) decreased with
maneuvers which decrease venous return (Valsalva). Specific findings per etiology: mid-systolic click (MVP), S3 gallop,
lateral PMI (LV dilatation), rales (pulmonary edema). AF highly associated with chronic MR with LA dilatation.
• Other possible findings: Early diastolic rumble, left sided S4, soft S1 and widely split S2. Sharp and high volume
carotid upstroke when severe. Cardiac impulse brisk, hyperdynamic, laterally displaced.
Radiographic findings other than TTE:

• EKG: Acute MR usually no specific findings. Chronic MR: Large LA, large LV. P-mitrale often associated mostly
with chronic MR
• CXR: Large LA, large LV, pulmonary edema occasionally unilateral (RUL common from posteriorly directed
regurgitant jet)
• RHC: large V waves suggestive (Figure 1)
TTE is most common modality for diagnosis of MR. Echo criteria are used to grade MR (Tables below). ACC/AHA
guidelines support the use of TTE for initial evaluation (EF, LV and LA sizes, and PA pressure). Consider TEE as well
before surgical intervention if TTE not sufficient for mechanism of MR and feasibility of repair (although sedation during
TEE can reduce degree of MR via vasodilation and afterload reduction).
Figure 2. Algorithm for determining etiology of MR.
The criteria for grading MR are shown in Table 1-2. The clinical progression of the disease is separated into stages A-D.
Stage A is mild MR. Stage B is moderate MR. Stage C-D are severe MR. For severe, chronic MR, only one
echocardiographic criteria must be met.

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Table 1: 2020 ACC/AHA guidelines for Stages of Chronic Primary MR

Stage A B C D
Definition At risk of MR `Progressive MR Asymptomatic Symptomatic
severe MR Severe MR
Valve Anatomy - Mild MVP - Mod-severe MVP - Severe MVP
- Normal coaptation - Normal coaptation - Loss of coaptation or flail leaflet
- Mild valve
thickening and - Rheumatic valve changes - Rheumatic valve changes with leaflet
leaflet restriction with leaflet restriction and restriction and loss of central coaptation
loss of central coaptation
- Prior IE - Prior IE
- Thickening of leaflets with radiation heart

disease
Valve
Hemodynamics
Doppler MR jet - No or small - Central jet MR 20-40% LA - Central jet MR >40% LA or holosystolic
area central jet area or late systolic eccentric jet eccentric jet MR
<20% LA MR
Doppler vena <0.3cm <0.7cm ≥0.7cm

contracta
Regurgitant <60mL ≥60mL

volume (mL/beat)
Regurgitant <50% ≥50%

fraction <50%
ERO <0.40cm2 ≥0.40cm2
Angiographic 1+ to 2+ 3+ to 4+
grade
Hemodynamic None Mild LA enlargement Mod-severe LA Mod-severe LA

Consequences enlargement enlargement
No LV enlargement
LV enlargement LV enlargement
Normal pulmonary pressure
Pulmonary HTN at rest Pulmonary HTN at
or with exercise rest
C1: LVEF>60% and

LVESD<40mm
C2: LVEF≤60% and/or
LVESD ≥40mm
Symptoms None None None Decreased exercise
tolerance
Exertional dyspnea
Not all criteria for each valve hemodynamic criteria need to be present in each patient. Parameters should be integrated with other
clinical evidence. ERO, effective regurgitant orifice; IE, infective endocarditis; LA, left atrium; LV, left ventricular; LVESD, left
ventricular end-systolic dimension; MVP, mitral valve prolapse.

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Table 2: 2020 ACC/AHA guidelines for Stages of Chronic Secondary MR
Stage A B C D
Definition At risk of MR Progressive MR Asymptomatic Symptomatic
severe MR Severe MR
Valve Anatomy Normal valve leaflets, - Regional wall - Regional wall motion abnormalities and/or LV
chords, and annulus in a motion abnormalities dilation with severe tethering of mitral leaflet
patient with CAD or with mild tethering of Annular dilation with severe loss of central
cardiomyopathy mitral leaflet coaptation of the mitral leaflets
Annular dilation with
mild loss of central
coaptation of the
mitral leaflets
Valve
Hemodynamics
Doppler MR jet - No or small central jet
area area <20% LA
Doppler vena <0.3cm

contracta
Regurgitant <60mL ≥60mL

volume
(mL/beat)
Regurgitant <50% ≥50%

fraction <50%
ERO <0.40cm2 ≥0.40cm2
Associated Normal or mildly dilated LV Regional wall motion Regional wall motion abnormalities with
Cardiac Findings size with fixed (infarction) or abnormalities with reduced LV systolic function
inducible (ischemia) reduced LV systolic LV dilation and systolic dysfunction
regional wall motion function attributable to primary myocardial disease
abnormalities LV dilation and
Primary myocardial disease systolic dysfunction
with LV dilation and systolic attributable to
dysfunction primary myocardial
disease
Symptoms Symptoms attributable to coronary ischemia or HF may be HF symptoms attributable to MR
present that respond to revascularization and appropriate persist even after revascularization
medical therapy and optimization of medical
therapy
Decreased exercise tolerance
Exertional dyspnea
Not all criteria for each valve hemodynamic criteria need to be present in each patient. Parameters should be integrated with other
clinical evidence. ERO, effective regurgitant orifice; IE, infective endocarditis; LA, left atrium; LV, left ventricular; LVESD, left
ventricular end-systolic dimension; MVP, mitral valve prolapse.

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Management
Acute MR:
Surgical repair > transcatheter repair. Consider early revascularization if ischemia.
Additional notes: This usually requires urgent and early surgical repair. Worse prognosis than chronic MR. Early
revascularization (if ischemic) may arrest local maladaptive LV modeling, restore valve competence, and obviate
the need for surgical repair. Surgical repair generally preferred over transcatheter repair.
Medical management to stabilize for surgery. Reduce afterload, maintain CO and diminish pulmonary congestion with IV
nitroprusside, dobutamine, or intra-aortic balloon pump.
Chronic primary MR: Mainstay is surgery.
The decision to proceed depends on symptoms, LVEF, LVESD. Recommendations:

• Mitral valve intervention recommended irrespective of LV systolic function: symptomatic patients with severe primary
MR
• Mitral valve surgery recommended: asymptomatic patients with severe primary MR and LVEF <60%, LVESD >40mm
• Mitral valve repair is reasonable: Asymptomatic patients with severe primary MR and LVEF >60 and LVESD <40mm,
when performed at a primary or comprehensive valve center and has a high likelihood of a successful and durable
repair (chance of no residual MR >95%, mortality <1%)
• Mitral valve surgery can be considered : asymptomatic patients with severe primary MR and LVED>60 and LVESD
<40mm but with progressive increase in LV size of decrease in EF on >3 serial imaging studies (do not need to
consider likelihood of a successful and durable repair)
• Mitral valve repair can be considered: symptomatic patients with severe primary MR attributable to rheumatic valve
disease, at a comprehensive Valve Center if durable and successful repair is likely.
• Transcatheter edge-to-edge repair is reasonable: severely symptomatic patients (NYHA class III or IV) with primary
severe MR and high/prohibitive surgical risk, if anatomy favorable and life expectancy at least 1 year.
Additional notes: If surgery will proceed, the next determination is mitral valve repair vs replacement followed by the
decision of mechanical vs bioprosthetic valve. Among patients with severe symptomatic MR, mortality is as high as 8%
per year, and the mainstay of therapy is surgery.
Mitral valve repair is preferred over replacement if valve morphology is amenable, as valve repair is associated with
superior post-operative survival and ventricular function. Involvement of the anterior leaflet (or both leaflets) may preclude
repair and require replacement. Repair further eliminates the risks and pitfalls associated with prosthetic valves, including
prosthesis degeneration. Around half of patients with bioprosthetic MVR will need another replacement within 15 years.
For those who are symptomatic despite GDMT and have prohibitive surgical risk, transcatheter mitral valve
repair with MitraClip can be considered
Medical management:
• Treat patients with symptomatic chronic primary MR stage D and LVEF<60% with GDMT as bridge to surgery or
if prohibitive surgical risk.
• Treat concomitant hypertension per standard therapy.
• Patients with asymptomatic chronic primary MR stages B and C with normal LV systolic function do not receive
medical treatment.
Chronic secondary MR: In contrast to primary MR, the utility of surgical intervention in chronic secondary MR is generally
low due to the pathophysiology of this disease. If concomitant HFrEF, treat with GDMT.
There are no Class I indications for MV surgery for chronic secondary MR. Class II recommendations:
▪ MV surgery is reasonable: undergoing CABG concurrently for myocardial ischemia
▪ MV surgery can be considered: preserved LV systolic function (LVEF >50) with severe persistent symptoms
(NYHA class III, IV) despite therapy for HF and comorbidities.
▪ MV surgery can be considered: reduced LV systolic function (LVEF <50) with severe persistent symptoms (NYHA
class III, IV) on optimal GDMT
▪ Cardiac resynchronization therapy (CRT) can also be helpful in reducing the severity of functional MR if otherwise
clinically indicated. 1
▪ If surgery will proceed, mitral valve replacement is preferred over repair.

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There are no Class I indications for TEER for chronic secondary MR. Class II recommendations:
• In patients with chronic severe secondary MR related to LV dysfunction LVEF<50% with NYHA class II, III, or IV
symptoms while on optimal GDMT, TEER is reasonable with appropriate anatomy on TEE and LVEF 20-50%,
LVESD <70, PASP <70mmHg.
Monitoring:
Repeat TTE if there are changes in symptoms.
In the absence of clinical change, repeat TTE every 6–12 months for patients with severe MR for evaluation of
EF (more frequently if evidence of LV dilatation), every 1-2 years for moderate MR, every 3-5 years for mild MR.
Guidelines for anticoagulation after MVR (institutional preferences may vary, check with fellow/attending). Note that if
reversal of anticoagulation is urgently needed, FFP can be used (Class II) and is preferred over Vitamin K since it is
thought to reduce the incidence of thrombotic complications (though no good data).
o Bioprosthetic MVR: 81 mg ASA, 3 month of Coumadin for INR 2–3 after surgery (lifetime if rheumatic MR or if
EF<30–35, hypercoag, hx clot, AFib)
o Mechanical MVR: 81 mg ASA, INR 2.5–3.5 for life with IV heparin when INR <2.5
Figure 3. Indications for Intervention for Primary MR. ACC/AHA 20202

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Figure 4. Indications for Intervention for secondary MR. ACC/AHA 20202
References:
1. van Bommel RJ et al. Cardiac resynchronization therapy as a therapeutic option in patients with moderate-severe
functional mitral regurgitation and high operative risk. Circulation. 2011;124(8):912-9.
2. 2020 AHA/ACC guideline for the management of patients with valvular heart disease. J Am Coll Cardiol. 2014 Jun
10;63(22):2438

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Mitral Stenosis (MS)
Etiologies: rheumatic fever, then senile calcific MS. Other rare cause is congenital (parachute, supramitral ring, part of
Shone’s complex)
• Rheumatic → progressive, thickening of leaflet edges, fusion of commissures, chordal shortening and fusion.
Latent phase between initial illness and valve stenosis.
• Senile calcific → benign calcification of annulus extends into leaflets → narrowing of annulus and rigidity of
leaflets without commissural fusion. Can also be caused by radiation induced valve disease, often in survivors of
Hodgkin’s lymphoma.
Figure 1. Mitral Stenosis. CVPhysiology.com.
• ↓LA flow to LV → ↑LA pressure, ↑pressure in pulmonary vasculature, ↑right sided pressures.
• Nonspecific presentation: exertional dyspnea, poorly tolerated AF from loss of atrial kick or rapid heart rate,
unexplained cardio embolism, hemoptysis from increased pulmonary congestion, hoarseness from LA
compression of recurrent laryngeal nerve (Ortner’s Syndrome). Clinical history of childhood rheumatic fever or
characteristic cardiac exam.
• Generally diagnosed echocardiographically
• If untreated: progressive pulmonary edema → pulmonary hypertension and right heart failure (60% of cases)
→death. Mortality can also result from systemic thromboembolic events in the context of atrial fibrillation.
Evaluation
TTE is indicated to 1. Diagnose MS. 2. Determine etiology. 3. Grade severity. 4. Typify valve morphology to determine
suitability for percutaneous mitral balloon commissurotomy (PMBC)
• TTE can show:

o Characteristic diastolic doming of mitral valve (seen on parasternal long-axis)
o Commissural fusion and planimetry of mitral orifice (seen on short-axis, better done with 3D TTE)
o Doppler hemodynamics (Seen on apical 4-chamber view)
o Mitral valve morphology and PMBC suitability scored via Wilkins/MGH score on a 16-point scale (>8 less
favorable)
• TEE is alternative with technically limited transthoracic windows, is necessary to exclude LAA thrombus prior to
PMBC and to evaluate presence of concomitant MR
Exam:
Loud S1 leading to softer S1 as leaflets become more calcified, opening snap heard best at base, low pitched diastolic
rumble (most prominent at apex in left lateral decubitus during held expiration using stethoscope bell),
The criteria for grading MS are shown in Table 1. The clinical progression of the disease is separated into stages A-D.
Table 1. 2020 ACC/AHA Guidelines for Staging MS
Chris Valle 140

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Stage A B C D
Definition At risk of MS `Progressive MS Asymptomatic Symptomatic
severe MS Severe MS
Valve Anatomy Rheumatic valve Rheumatic valve changes with
changes with commissural fusion and diastolic doming
Visual appearance Mild valve commissural fusion of mitral valve leaflets
doming and diastolic
during doming of mitral
diastole valve leaflets
Mitral Valve Area
(planimetered) >1.5cm2 ≤1.5cm2
Valve Hemodynamics
Normal Increased
transmitral transmitral flow
flow velocity velocities
Mitral Valve Area (by
continuity equation) >1.5cm2 ≤1.5cm2
Diastolic pressure half <150ms ≥150ms

time
Hemodynamic
Consequences
LA enlargement None Mild to moderate Severe
Pulmonary artery
systolic pressure Normal >50 mmHg
Symptoms None Decreased exercise tolerance
Exertional dyspnea
The transmitral mean pressure gradient should be obtained to further determine hemodynamic effect of MS and is
usually >5-10mm Hg in severe MS; However, due to the variability of the gradient with HR and output, it is not
included in criteria for severity. LA left atrial; MS, mitral stenosis; PASP, pulmonary artery systolic pressure
Follow up and Surveillance
Repeat TTE should be performed to re-evaluate asymptomatic patients with MS. For Very Severe: every year, Severe:
every 1-2 years, Progressive MS: every 3-5 years. The mean rate of progressive valve narrowing is ~0.1cm2 per year
with appreciable variability.

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Management
Anticoagulate in rheumatic MS with AF and prior embolic events. It has been shown to reduce incidence of arterial
embolization. There is evidence for VKA, but not for NOACs (patients with MS were excluded from AF trials).
If rheumatic MS and AF with RVR, or with symptomatic resting/exertional sinus tachycardia, use a beta blocker.
Additional notes: Negative dromotropes (e.g. beta blockers) can be beneficial in patients with rheumatic MS and
either AF with RVR or with symptomatic resting or exertional sinus tachycardia. Studies of beta blockers and
ivabradine demonstrated only benefit in younger patients without chronotropic incompetence; thus although there
is theoretical benefit in reducing HR and prolonging diastolic filling (thereby preventing a rise in mean mitral
gradient and increased LA pressures), this is balanced by limitation of stroke volume and chronotropic
incompetence. Rheumatic disease itself can lead to fibrosis of conduction tracts and predispose to hard to control
AF. Beta blockade is used in pregnant pts with MS to blunt the physiologic tachycardia of pregnancy and prolong
diastole, prevent pulmonary edema.
Diuretics are a mainstay of medical management to keep LA pressures down and manage pulmonary edema prior to
intervention.
PMBC or open/closed commissurotomy are mainstay of therapy over medical management. Mitral valve replacement is
an option only if no other options with severe limiting symptoms.
Additional notes: PMBC involves puncturing the septum during cardiac catheterization to access the stenotic
mitral valve via RA to LA. A balloon is then inflated to force open the valve a separate the fused commissures;
this is also what occurs during surgical commissurotomy. Other approaches with expanding roles in MS include
transcatheter mitral valve replacement (TMVR) and mitral valve bypass. IN TMVR, for patients who cannot
receive PMBC or surgery, an expandable transcatheter valve is inserted into the MV leaving the native MV tissue
in place. In MV bypass a conduit is sewed from the LA to the LV apex and a prosthetic valve is incorporated into
the conduit, avoiding direct manipulation of the mitral annulus.
Recommendations:
• PMBC is recommended: patients with NYHA class II, III, IV, and severe rheumatic MS and favorable valve
morphology with less than 2+ MR in the absence of LA thrombus, if at a Comprehensive Valve Center.
• Mitral valve surgery is indicated: patients with NYHA III or IV with severe rheumatic MS who are not candidates
for PMBC, have failed a previous PMBC, require other cardiac procedures, or do not have access to PMBC.
• PMBC is reasonable: asymptomatic patients with severe rheumatic MS and favorable valve morphology with less
than 2+MR in the absence of LA thrombus with elevated PASP>50mmHg, if at a comprehensive Valve Center
• PMBC may be considered: asymptomatic patients with severe rheumatic MS and favorable valve morphology
with less than 2+MR in the absence of LA thrombus who have new onset of AF, if at a Comprehensive Valve
Center.
• PMBC may be considered: NYHA II, III, IV with rheumatic MS, mitral valve area >1.5, if evidence of
hemodynamically significant rheumatic MS with PAWP >25 or mean mitral valve gradient >15 during exercise, if
at a Comprehensive Valve Center
• PMBC may be considered: NYHA III, IV with severe rheumatic MS with suboptimal anatomy and are not
candidates for surgery, if at a Comprehensive Valve Center.
Calcific MS (or mitral annular calcification) is increasingly frequent in USA, but is usually high risk for any intervention
given extensive calcification, advanced age, and comorbidities. Intervention only in highly symptomatic (NYHA III or IV)
with severe MS (mitral valve area <1.5) attributable to extensive mitral annular calcification, with discussion of procedural
risk and patient preferences and values. PMBC is not often performed here; feasibility studies show that TMVR may have
a role. Nonrheumatic MS can also occur after radiation therapy or after a mitral valve repair with a small annuloplasty ring.

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Figure 2. Indications for Intervention for MS. ACC/AHA 2020

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Tricuspid Regurgitation (TR)

Some degree of TR is present in 70% of normal adults. TTE is indicated to determine etiology of TR (primary or
secondary) and consequence on RV. Catheterization is of clinical value if TTE and clinical presentation are insufficient.
• (1) Primary.
o Rheumatic disease, infective endocarditis, marantic endocarditis (SLE, RA), congenital (Ebstein’s),
myxomatous changes, blunt chest/deceleration trauma, carcinoid, drugs
(fenfluramine/phentermine/pergolide), radiation, iatrogenic (leads, biopsies), ischemic heart disease
causing papillary dysfunction or rupture, CTD (e.g. Marfan’s)
o In younger patients is mostly congenital, Ebstein’s most common. Less common is trauma, IE, IVDU, and
small ASD injuring valve through a jet.
• (2) Secondary. Most common form. TR with apparently anatomically normal leaflets/chords
o Tricuspid annular dilation and leaflet tethering after RV remodeling from pressure or volume overload in
pulmonary HTN or dilated cardiomyopathies. Also annular dilation associated with AF, and RV volume
overload from shunts or high output states.
o Disorders which induce RV dilatation and pulmHTN: left-sided HF, mitral stenosis/regurgitation, any
primary pulmonary disease (e.g. PE), left-to-right shunt (ASD, VSD), Eisenmenger’s syndrome, pulmonic
valve stenosis, hyperthyroidism

- Similar to MR
Evaluation
TTE is indicated to 1. establish diagnosis. 2. characterize severity. 3. measure velocity of TR for estimation of systolic RV
to RA gradient 4. identify mechanism responsible for TR.
• TTE can show:
o RV or RA dilation and RV function, tricuspid annulus dilation, paradoxical interventricular septal
movement
o Degree of pulmonary hypertension via estimation of RV to RA systolic gradient from TR jet peak velocity
using modified Bernoulli equation
o Doppler color flow using vena contracta method
Exam:
Clinical findings can be absent in TR and when present are often related to the underlying cause of TR, or its sequela,
right-sided heart failure. In severe TR there may be a sensation of pulsation in the neck.
• Right-sided HF: painful hepatosplenomegaly, ascites, peripheral edema. When severe, cachexia, cyanosis,
sometimes jaundice.
• Jugular veins: distended and prominent veins, distinct “c-v” wave from systolic regurgitation, pulsatile jugular vein
(which can be confused with carotid arterial pulse), Kussmaul’s sign (JVD more prominent with inspiration),
systolic thrill felt over jugular vein when severe.
• Other findings: dynamic RV heave, dullness and prominent pulsation over left second intercostal space,
peripheral edema, pleural effusions (if secondary to left-sided problem), hepatomegaly with possible thrill
(transmission of systolic murmur)
• Auscultation: Holosystolic murmur best heard at left mid sternal border or subxiphoid area. No radiation and
generally no palpable thrill. Murmur is soft/absent when TR is severe. Increases with inspiration/leg
raise/exercise/hepatic compression. Standing decreases intensity of murmur. S3 often heard if RV very dilated;
S4 possible if significant RV hypertrophy.

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Table 1. 2020 ACC/AHA Guidelines for Staging Tricuspid Regurgitation
Stage B C D
Definition Progressive TR Asymptomatic Symptomatic
severe TR Severe TR
Valve Hemodynamics
Color Doppler jet Central jet <50% Central jet ≥50% RA

RA
Doppler vena contracta width (cm) ≥0.7cm
<0.7cm
Regurgitant volume (mL/beat)
≥45mL
<45mL
<0.40cm2 ≥0.40cm2
ERO
Dense continuous wave signal with triangular
shape
Hepatic vein systolic flow reversal
Hemodynamic Consequences
RV/RA dilation None Yes
Elevated RA with “c-V” wave

Yes
Clinical Symptoms and Presentation None Elevated venous Elevated venous

pressure pressure
No symptoms Dyspnea on exertion,
fatigue, ascites, edema
Management
Treatment of primary TR with medical management alone are poor. Management of secondary TR is of underlying
pulmonary hypertension or myocardial disease. Surgery can be considered in a subset of patients with isolated primary or
secondary TR (without pulmonary hypertension or dilated cardiomyopathy).
Treat heart failure, right or left-sided: diuretics, aldosterone antagonists.
Treat causes of pulmonary HTN (e.g. mitral stenosis or CTEPH).
TVR if: severe symptomatic primary TR OR asymptomatic w/ RV dilation/dysfunction

- For secondary severe TR, consider TVR if undergoing left-sided valve surgery OR if tricuspid annular dilation >4 cm
and/or sx of right heart failure (Circ 2021;143:e)
- Isolated TV surgery a/w high mortality, although may be recommended for severe TR refractory to medical therapy
- Numerous transcatheter therapies are potential options but still lack long-term clinical outcome/performance data (JACC
2018;71:2935)

Vascular Medicine
TOC
VASCULAR MEDICINE
Venous Thromboembolism
Deep Vein Thrombosis
A. Definition/ Classification
Clot formation within the deep venous system. Typically classified as:
● Proximal/ “above the knee” (external iliac, popliteal, femoral veins including superficial femoral)
● Distal/ “below the knee” (ant. tibial, post. tibial, peroneal, gastrocnemius and soleus vein)
● Upper extremity (includes the internal jugular vein)
B. Clinical Presentation
Patients may be asymptomatic or complain of unilateral leg pain, swelling, erythema, or warmth.
1. Always consider DVT in signs, symptoms and diagnosis of PE.
Risk Factors
Anatomic risk factors
Iliac vein compression (aka “May-Thurner
syndrome”): compression of the left iliac vein
between the right iliac artery and lumbar spine within
the deep pelvis. Compression on the right is also
possible.
Effort induced thrombosis (aka “Paget-Schroetter

syndrome”): Upper extremity venous thrombosis
usually due to underlying compressive anomaly at
the thoracic outlet.
IVC abnormalities: Congenital venous malformations

of the IVC that may lead to DVT. Primarily occurs in
Image adapted from McMaster young patients
Pathophysiology review. Jan 2021
C. Diagnostics
● Diagnosis of an acute DVT in the lower extremity begins with an assessment of the pre-test probability for that patient
and incorporates US and D-dimer based upon this pre-test probability assessment 1.
o Consider Well’s Criteria for DVT to risk stratify likelihood of DVT.
● Venous doppler US is the most practical test to make the diagnosis of DVT.
D. Management
● Therapeutic anticoagulation is mainstay of treatment in absence of contraindications (i.e. increased bleeding risk)
● Always indicated in patients with lower extremity proximal DVT, Upper extremity DVT, and in some cases of distal
DVT
o Proximal lower extremity DVTs are associated with a high risk of PE and mortality
1. Medical therapy:
● Direct oral anticoagulants (DOACs) (apixaban, rivaroxaban, edoxaban and dabigatran) are considered first-line
agents for VTE in the majority of patients.
● Warfarin favored in patients with APLAS (TRAPS)2.
● LMWH was considered the only preferred method of AC in active malignancy until recently where DOACs have
shown to have similar safety and effectiveness in patients with active malignancy who do not have gastric cancer or
gastroesophageal lesions (ASH 2021 Guideline)3
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Krishan Sharma
Vascular Medicine
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Agent Mechanism Indications Dose
Unfractionated Inactivates ● Treatment of DVT/PE Treatment: 80U/kg bolus +

Heparin thrombin & factor initiate gtt at 18U/kg/hr and titrate
Xa through AT- per protocol for goal PTT 70-100
dependent
mechanism
Warfarin Vitamin K ● Treatment of DVT/PE Treatment: Dose depends on

(Coumadin) antagonist INR measurements and varies
for typical INR goal 2-3
Requires bridging with parenteral
agent if INR <2
Apixaban Factor Xa inhibitor ● Treatment of DVT/PE Treatment: 10 mg BID x 7 days,

(Eliquis) ● DVT prophylaxis after then 5 mg BID during the first 6
hip/knee replacement months, and 2.5 mg BID
surgery thereafter for most patients
● Reduction in risk of Prophylaxis: 2.5 mg BID
recurrent DVT/PE after 6
Rivaroxaban Factor Xa inhibitor months of therapeutic Treatment: 15 mg BID x 21
(Xarelto) anticoagulation days, then 20 mg QD for the first
6 months, and 10 mg QD
thereafter for most patients
Prophylaxis: 10 mg QD
Should not be used in patients
with CrCl <30 mL/min
Edoxaban Factor Xa inhibitor ● Treatment of DVT/PE Treatment: 60 mg QD (30 mg

(Savaysa) after 5-10 days of therapy QD if CrCl 15-50 mL/min)
with UFH/LMWH Prophylaxis: Not approved
Dabigatran Direct thrombin ● Treatment of DVT/PE Treatment: 150 mg BID (CrCl

(Pradaxa) inhibitor after 5-10 days of therapy >30 mL/min)
with UFH/LMWH Prophylaxis: 110 mg once, then
● DVT/PE prophylaxis after 220 mg QD
hip replacement surgery Should not be used in patients
● Reduction in risk of with CrCl <30 mL/min
recurrent DVT/PE
following initial therapy
Enoxaparin Activates ATIII to ● Prophylaxis and Treatment: 1 mg/kg BID or 1.5

(Lovenox) inactivate Xa > IIa treatment of DVT/PE mg/Kg QD
Prophylaxis: 40 mg QD (30 mg
BID if high-risk)
Should be used with caution in
patients with reduced CrCl.
Titration by anti-Xa may be
useful
Fondaparinux Activates ATIII to ● Prophylaxis and Treatment: 5 mg QD (if <50 kg),

(Arixtra) inactivate Xa only treatment of DVT/PE 7.5 mg QD (if 50-100 kg), 10 mg
QD (if >100 kg)
Prophylaxis: 2.5 mg QD
Should not be used in patients
with CrCl <30 mL/min
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Krishan Sharma
Vascular Medicine
TOC
Bivalirudin Direct Thrombin ● Treatment of DVT/PE Treatment: 0.15-0.2 mg/kg/hr

(Angiomax) inhibitor particularly in patients (Dose reduction if CrCl<60
with HIT mL/min
Argatroban Direct IIa inhibitor ● Treatment of DVT/PE Treatment: 0.2-1 mcg/kg/min

particularly in patients
with HIT
● Duration:
o First episode of provoked VTE: Minimum of three months of therapeutic anticoagulation4.
o If persistent risk factors (e.g. immobility, obesity, HRT) and low risk of bleeding: Minimum 6-12 months.
o If unprovoked VTE, recurrent provoked VTE, active malignancy: Indefinite AC may be considered.
o Careful consideration of bleeding risk should always be considered when planning duration of therapy.
2. Catheter-directed thrombolysis (CDT):

CDT is usually reserved for patients with phlegmasia cerulea dolens or highly symptomatic proximal clot (typically ilio-
femoral).
● Suitable candidates should have fresh clot (<21 days old as organized clot is less likely to respond to lysis) and low
bleeding risk.
● CDT may decrease post-thrombotic syndrome (PTS) incidence and severity, esp. w/acute ileo-femoral DVT. 5,6 7
3. Inferior vena cava (IVC) filters:

IVC filters are not routinely inserted as a stand-alone or adjunctive therapy for patients with acute DVTs.
● IVC filters are considered in patients with acute DVTs and PE with absolute contraindications to AC (e.g., recent
surgery, hemorrhagic stroke, active bleeding).
● IVC filters may be permanent or retrievable, although the latter have become increasingly popular due to the long-
term complications associated with indwelling IVC filters (including filter migration, IVC wall penetration, and
thrombosis).
● IVC filter retrieval should be considered once the contraindication to anticoagulation has resolved
● In general, if an inpatient has IVC filter placed during admission, they should leave with an appointment
scheduled for its removal.8
.
Pulmonary Embolism
A. Definitions
● Acute: acute obstruction within the pulmonary arteries by material (e.g. thrombus, tumor, air, fat) from elsewhere in
the body
● Chronic thromboembolic pulmonary hypertension (CTEPH): symptomatic post-embolic pulmonary obstruction
leading to pulmonary hypertension.
B. Clinical Presentation
● Presenting symptoms: dyspnea, tachypnea, chest pain, pleuritic pain, palpitations, pre-syncope, cough, hemoptysis,
low grade fever, syncope, and cardiac arrest.
● Signs: tachycardia (sinus most common, also new RV strain patter, RAD), hypoxemia, hypotension; e/o LE DVT
Image from StatPearls Jan 2021
C. Diagnostics
● CT chest angiogram is the gold standard test to diagnose PE.
● V/Q scan is an alternative for those with contraindications.
● Consider Transthoracic echo (TTE) and lower extremity ultrasound (LENIs) for risk stratification.
Pre-test probability:
There are several externally validated scoring systems to assess for the pretest probability of pulmonary embolism. 9 They
include the original Wells score, the Geneva score and the pulmonary embolism rule-out criteria (PERC) score10.
1. Wells Criteria for PE (10,11,12) (100% Sn, 85% Sp) Highly sensitive when used to exclude the diagnosis of PE in patients
with low clinical probability of PE (score ≤2). Critiques of the Wells score point to its subjective criteria that cannot
otherwise be standardized across users.
2. Geneva score(10,13) Developed as an objective measurement of pre-test probability but has not been demonstrated to be
superior to the Wells score.
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3. PERC score(10,14) (97% SN, 22% Sp) To be used only in instances of low pre-test probability by either the Wells score
or Geneva score.
Labs:
● D-dimer 15: D-dimer has a high sensitivity (80%-100%) and low specificity (23%-63%). Obtain when the pre-test
probability for PE is low (i.e., a rule out test).
● Can be elevated in many different diseases associated with fibrinolysis (cancer, inflammation/infection, DIC,
arterial thrombus, aortic dissection, CHF, ESLD, and ESRD). Use Age-adjusted D-dimer16 for patients >50 years
of age (age x 10ng/mL = cut off value in ng/mL). Normal levels cut off to rule out PE is <500 ng/mL.
Imaging:
● CTPE17 (98% sp, 86% sn) Most definitive diagnostic test. Contraindicated (relative) in pregnancy, renal insufficiency or
contrast allergy.
● V/Q scan17 (93% sp, 83% sn) Alternative image modality in those with contraindications to CTPE
● LENI17 (86% sp, 44% sn): Obtained in conjunction with CTPE or V/Q scan or in some instances to aid in treatment
decisions when chest imaging cannot be obtained promptly (e.g. pregnancy).
● TTE: Obtained with CTPE or V/Q scan. Utilized in risk stratification.
Risk Stratification
Risk stratification of PE depends on the presence or absence of hemodynamic instability, increased respiratory effort
and right heart strain. Overall patient risk taken into context as well as alluded to in the PESI score
● RV strain can be assessed via multiple modalities
o Cardiac biomarkers (NT-proBNP, hsTnT),
o EKG (RBBB, R axis deviation, anterior T wave inversions, S1Q3T3),
o CT-PE (RV/LV ratio >0.9), or
o TTE (RV dilation, hypokinesis, or McConnell’s sign [diffuse RV wall hypokinesis with apical sparing]).
Low Risk Intermediate Risk High Risk
Mortality risk (3-15%) Mortality risk (>15%)

● No evidence of Right heart Intermediate-low: ● Hemodynamic instability
strain and no hemodynamic ● +biomarkers, RV (SBP <90mmHg for
instability dysfunction, or low PESI >15mins)
● (Low risk PESI) score (III-V) ● Cardiac arrest
Intermediate-high:
● +Troponin and RV
dysfunction on Echo or CT
imaging
● NB: the presence/ absence of hemodynamic instability does not always correlate with the anatomic location or the
degree of clot burden.
● The Pulmonary Embolism Severity Index (PESI)14 helps to risk stratify patients who can safely be treated outpatient
once a diagnosis is made.
Management
Low risk: Initiate therapeutic oral AC provided there is no contraindications and risk of bleeding is low.
● If no other reason for hospitalization and adequate home support can discharge home, direct from ED
Intermediate risk: Initiate AC; monitor closely for clinical signs of deterioration. PERT c/s recommended.
● Generally recommended that most patients without hypotension are not treated with thrombolytic therapy. 4
● Thrombolysis or catheter-based therapies can be considered weighing the risks and benefits of the procedure.
● If persistent dyspnea, consult PERT
High-risk:
Consult PERT ASAP.
● Consider systemic thrombolysis 🡪 decreased all-cause mortality but increased risk of major bleeding and intracranial
hemorrhage4
● Catheter-directed thrombolysis
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● For those with high bleeding risk, invasive stabilizing measures (e.g., ECMO) and surgical thrombectomy.
PERT: The Pulmonary Embolism Response Team (x47378) at MGH is a rapid response, multidisciplinary team that can
be activated for prompt assessment and management of patients with intermediate to high-risk PEs.
Catheter-associated thrombosis
Clinical considerations
● Incidence as high as 14-18%.
● Duplex ultrasound is the diagnostic imaging modality of choice.
● Current guidelines recommended that systemic anticoagulation be administered for at least three months after the
catheter has been removed.
● If central access is required, the CVC can remain in place as long as it is appropriately positioned and functioning
correctly without evidence of infection.
● If the catheter remains for > 3 months on therapeutic AC, LMWH prophylaxis is recommended until the line is
removed.4
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Peripheral Artery Disease

A. Definition
Peripheral artery disease (PAD) is an atherosclerotic disease leading to peripheral artery stenosis or obstruction. PAD is
prevalent worldwide and is estimated to affect 202 million people. 22
●
Acute critical limb ischemia is a sudden decrease in limb perfusion presenting within 2 weeks of an inciting event.
Etiologies of arterial occlusion include thrombosis at site of atherosclerotic plaque in native artery (most common
cause), thromboembolism, thrombosis of stent/graft, thrombosis of aneurysm, arterial dissection, and iatrogenic from
arterial access sites.
●
Chronic limb ischemia is ischemia of >2 weeks duration sufficient to threaten the limb. This typically corresponds to
an arterial-brachial index (ABI) <0.4 usually due to multilevel > single vessel occlusions (i.e., aortoiliac and
femoropopliteal vs isolated tibial vessel disease in diabetics)23
B. Risk Factors
Age ≥70 yo, Male, black, Smoking, DM, H/o Atherosclerosis, HTN, HLD, Elevated homocysteine
C. Clinical presentation
Classic claudication: exertional buttock, hip, thigh, calf, or foot pain that is relieved with rest.
Presentation Percent of PAD pts ≥ 50 y.o.

Asymptomatic (screening) 20-50%
Atypical leg pain 40-50%
Classic claudication 10-35%
Threatened limb (ulceration, gangrene) 1-2%
● Acute Critical Limb Ischemia

● 6 P’s (Pain, Paresthesia, Paralysis, Poikilothermic (coolness), Pallor, reduced Pulses
● ABI <0.4 in conjunction with the above symptoms indicates severe ischemia
D. Diagnosis
Screening
The USPSTF has stated there is insufficient evidence to recommend routine screening for PAD with an ABI. 24 However,
the detection of PAD may identify patients at risk for atherosclerosis at other sites and can result in early interventions to
lower overall CVD risk.
Diagnostics
The diagnosis of PAD can be suspected clinically based on history of symptoms, risk factors for PAD, and physical exam
findings. Ankle-brachial index (ABI) should be used to confirm the diagnosis.
1. ABI (90% sn, 98% sp for detecting ≥ 50% stenosis.24

a. < 1 indicates PAD. May be falsely elevated from calcifications and (e.g. in patients with DM)
2. Segmental pressure and pulse volume recordings
a. Formal recordings using blood pressure cuffs and Doppler waveforms in the vascular lab
b. Helpful for identifying site and severity of disease
3. Exercise testing
a. Exercise adds sensitivity to inconclusive tests and should always be ordered as a component of ABI or
segmental pressures (unless patients cannot negotiate the necessary walking component)
4. Vascular imaging when anatomical information is required (often before / after a procedure)
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Diagnostic performance of computed tomography angiography in peripheral arterial disease: a systematic

review and meta-analysis. Met et al JAMA 2009
a. Catheter-based arteriography - preferred imaging modality as it can be diagnostic and therapeutic.

- CTA is highly specific/ sensitive. MRA accuracy is center dependent and may delay urgent
intervention if concerned for critical ischemia.
b. Duplex US is a safe, cheap, alternative that is unfortunately under-utilized.
E. Management
Management of PAD: Management depends on presentation (asymptomatic, intermittent claudication or critical limb
ischemia). Revascularization is an option for patients with significant or disabling symptoms unresponsive to other
treatment options.
Non-invasive therapy focused on symptom relief:

● Supervised Exercise Therapy: First-line treatment that improves walking time and distance. Supervised exercise is
more effective and has a lower dropout rate.25 It is comparable to stent revascularization in improving functional status
and QOL and both better than medical therapy alone. 26
● Cilostazol: Use for lifestyle-limiting claudication. Start 100 mg BID & titrate as tolerated. SE: HA, diarrhea, rhinitis.
Contraindicated in the presence of systolic heart failure.
Medical therapy focused on lowering risk of PAD progression:

● Risk factor modification: Aggressive DM & HTN management. Smoking cessation. Weight loss.
● Antiplatelet agents:
o Aspirin 81 or clopidogrel 75 mg are first line agents. The benefits of these agents in PAD are unclear as
recommendations for PAD have been extrapolated from studies in CVD.
o DAPT is not recommended unless there is another indication due to increased bleeding risk without benefit. 27
● Statin: Moderate and high-intensity statins provide reduction in cardiovascular events and may also improve
symptoms.
● Rivaroxaban: The COMPASS trial showed that rivaroxaban (2.5mg BID) plus aspirin (100mg QD) led to lower risk of
major adverse cardiovascular events but increased risk of major bleeding.28 Rivaroxaban is typically offered to
patients with evidence of atherosclerosis in multiple arterial beds.
Revascularization is recommended for patients with limb-threatening ischemia such as ischemic rest pain or ulceration
and patients with significant or disabling symptoms unresponsive to above.29 Options include percutaneous intervention or
open surgical intervention depending on the location and extent of disease. Most patients are offered endovascular
intervention.
Management of acute critical limb ischemia:

1. Immediate anticoagulation with heparin gtt
2. Place patient in “reverse Trendelenburg” if possible (to increase gravity dependent perfusion)
3. Revascularization
a. Factors that favor surgical revascularization: immediately threatened limb, large proximal lesion, long
segment lesion, diffuse multilevel disease
b. Factors that favor endovascular revascularization: comorbidities that increase surgical risk, multi-level
disease undergoing staged approach (endovascular-first), no suitable vessel for bypass graft
4. If irreversible ischemia (non-salvageable), amputation may be unavoidable
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Clinical categories of acute critical limb ischemia23
Category Clinical features Doppler pulses Management and Prognosis

Viable No sensory loss or Audible No immediate threat of tissue
muscle weakness loss
Obtain vascular imaging
Marginally Minimal pain with no Arterial pulses inaudible Need to be treated promptly, but
threatened sensory loss and Venous pulses audible salvageable
weakness Obtain vascular imaging
Immediately Sensory loss, rest Arterial pulses inaudible Need immediate
threatened pain, mild-to-moderate Venous pulses audible revascularization (no time for
weakness imaging), but salvageable
Irreversibly Tissue loss or nerve Inaudible Require amputation,
ischemic damage 🡪 Profound revascularization may allow for
sensory loss and healing or lower amputation
weakness
Paralysis or rigor
possible
Management of chronic limb ischemia:

A subset of patients can be treated with conservative management consisting of aggressive wound care, pain control, and
medical management. However for most patients, intervention is recommended.
Options for revascularization include endovascular therapy or bypass surgery. There has been persistent, widespread
clinical uncertainty about the best means by which to revascularize patients with chronic limb threatening ischemia. In
modern practice most patients receive endovascular therapy first. The BEST-CLI trial is currently enrolling patients and is
designed to compare best endovascular therapy with best open surgical treatment in patients eligible for both treatments.
Amputation may be considered in patients with sepsis, limb paralysis, uncorrectable flexion contracture, or significant
necrosis of weight-bearing parts of the foot.
Wound care consult and referral to wound clinic is highly recommended
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Renal Artery Stenosis

A. Definition: Renal artery stenosis (RAS) is characterized by narrowing of one or both renal arteries leading to impaired
blood flow to the kidney resulting in a spectrum of clinical syndromes that range from asymptomatic obstruction
(incidental RAS), renal vascular hypertension (RVH) and ischemic nephropathy.30
B. Risk Factors and Etiology: RAS likely accounts for 1-5% of patients with hypertension. Prevalence is higher in patients
with acute, severe, or refractory HTN.31 Risk factors include age, HLD, HTN, and elderly patients with comorbidities
such as diabetes, PAD, or CAD.32
1. Atherosclerotic RAS (ARAS) accounts for 90% of all RAS.33 Patients with ARAS are likely to have atherosclerotic
disease in other areas of the body including CAD and PAD.
2. Fibromuscular Dysplasia (FMD) is a non-inflammatory, non-atherosclerotic vascular condition that commonly
affects the renal arteries. 34 According to the FMD registry, the majority of patients affected with FMD are female
(90%) and the mean age at diagnosis was 52 years.35 In this registry FMD was identified in the renal artery in
66% of patients. Similar data exist in the international / European registry.
3. Other non-atherosclerotic forms of RAS include aneurysms, congenital/ traumatic AV fistulas, vasculitis,
neurofibromatosis, trauma, embolization, post-radiation therapy, dissection, and extrinsic compression of the
renal arteries due to tumors. 36
C. Clinical Presentation: Patients present with severe or resistant hypertension. Physical exam findings of include a
unilateral systolic-diastolic abdominal/ flank bruit (Sn 40% Sp 99). Labs may show HypoK and metabolic acidosis.
Suspect in non-obese patients <30 y.o. with no family history of HTN. RAS is associated with an unexplained rise in
serum Cr > 50% within 1 week of ACE/ ARB initiation, however unilateral RAS is not a contraindication to these
medications.
D. Diagnostics Testing for renovascular disease is indicated for patients who present with clinical findings consistent with
secondary hypertension with moderate-high pre-test probability.
Study Sens (%) Spec (%) Comments
Pros: No IV contrast; Inexpensive

Duplex Doppler *For detecting stenosis >60%
84-98* 62-99*
US Cons: Technically challenging and requires local expertise.
Accessory renal arteries may be missed
Pros: Visualizes adjacent structures including accessory renal
arteries; less time-consuming/operator-dependent
CTA 86-93 90-100
Cons: Radiation; iodine contrast; difficult to eval severity in presence
of significant calcification
Pros: A non-contrast MRA is an alternative to CTA in pts with renal
85 vs 93 insufficiency or allergy. Can assess renal perfusion using gad
94 vs 97
(non vs clearance
MRA (non vs gad-
gad- Cons: $$$; quality is center-dependent, incompatible with some
enhanced)
enhanced) implanted medical devices; cannot evaluate in-stent restenosis, many
patients cannot tolerate the small space in the machine
Pros: GOLD STANDARD if performed in conjunction with pressure
Arteriography measurements
Cons: invasive, iodine contrast, risk of complications
Adapted from 2011 ACC/AHA Practice Guidelines for the Management of Patients with PA
E. Management
● Medical therapy remains the mainstay of treatment for RAS. Treatment focuses on lowering cardiovascular risk
through smoking cessation, glucose control, cholesterol reduction, ASA, and blood pressure control. Choice of anti-
HTN medication should follow published guidelines as if for non-RAS patients.
o Importantly, ACE and ARB are not contraindicated in RAS. ~50% of patients with RAS will usually have a
mild increase in creatinine after the administration of an ACE/ARB. ACE/ARB may be of benefit given
elevated RAAS activity in RAS.
● Revascularization: Options for revascularization include percutaneous angioplasty +/- stenting and surgical
revascularization. Several RCT’s, including, the CORAL trial demonstrated that renal artery stenting plus medical
therapy did not confer a significant benefit with respect to the prevention of clinical events. 37 However, some patients
do benefit from revascularization and it is recommended for those who have a high likelihood of benefit. 38 That
includes patients with hemodynamically significant atherosclerotic RAS AND at least one of the following 1) recurrent
“flash” decompensated HF; 2) refractory ACS; 3) typically new-onset resistant HTN; or 4) acutely progressive CKD
stage IV. Revascularization strategy may vary depending on etiology of RAS (i.e., atherosclerotic RAS vs FMD).
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Aortic Aneurysm
A. Definition
Thoracic Aortic Aneurysm (TAA): is a full-thickness dilation of a segment of the
thoracic aorta that is at least 50% larger than the expected diameter of that
segment. The normal aortic diameter varies according to age, sex, and body size. 39
Abdominal Aortic Aneurysm (AAA): A full-thickness dilation of a segment of the
abdominal aorta typically ≥3 cm. Classified by location (suprarenal, pararenal, or
infrarenal) and morphology (fusiform vs saccular). 40,41
B. Risk Factors
Thoracic Aortic Aneurysm (TAA):
Sporadic (Degenerative) Genetically mediated
Hypertension (Most common. Marfan syndrome
occurring in 60% of pts w/ Ehlers-Danlos syndrome CT image of ascending thoracic aortic
TAA2) Loeys-Dietz syndrome aneurysm. Adapted from JACC
2010;55:e27.
Male Turner syndrome
Age Familial TAA & dissection
Smoking history Bicuspid aortic valve disease
Hypercholesterolemia
Prior aortic dissection
Aortitis (vasculitis/ infection)
Abdominal Aortic Aneurysm (AAA) 40:

Risk Factors Protective Factors
Older age African American heritage
Smoking history (>90% of pts with AAA42) Asian heritage
First-degree relative with AAA Hispanic ethnicity
History of other large vessel aneurysms Diabetes
Atherosclerosis Female sex
Hypercholesterolemia
Obesity
Hypertension
Risk of rupture:
TAA: The risk of rupture or dissection increases abruptly as thoracic aneurysms approach 6 cm because at this size,
distensibility of the aorta rapidly falls. The annual risk of rupture is 2% for TAAs <5 cm and 7% for TAAs >6 cm. 43
AAA: Risk of rupture increases with aneurysm size with <1% annual rupture risk for AAA <4 cm in diameter and >10%
annual rupture risk for AAA >6 cm in diameter. 42 Rupture is often lethal with mortality cited as 85-90%44. Female sex
appears to be an independent risk factor for rupture in AAA. Women make up ~20% of AAAs compared to men but
constitute approximately ~30% of all AAA ruptures.45
C. Clinical Presentation
TAA and AAA are typically clinically silent, however, patients who are symptomatic can present with symptoms due to
compression of surrounding structures. 46 Patients with
● Ascending aorta/aortic arch
o Heart failure due to aortic regurgitation
o Myocardial ischemia or infarction due to compression of a coronary artery
o Dysphagia due to esophageal compression
o Hoarseness due to left recurrent laryngeal nerve compression
o Hemidiaphragmatic paralysis due to phrenic nerve compression
o Wheezing, cough, dyspnea due to compression of the tracheobronchial tree
o SVC syndrome
● Descending aorta: Back pain from erosion into the adjacent spine
● Abdominal: Pulsatile abdominal mass, Constant abdominal pain or back pain
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D. Diagnosis
Typically, an incidental finding on imaging studies (e.g., CT, CXR, echo)
TAA:
1. CTA or MRA: Helpful in determining size and extent of the aneurysm. Patients with known connective tissue
disease syndromes or first-degree relatives with TAA should undergo complete aortic imaging.39
2. TTE: Indicated when aortic root or ascending aortic aneurysm is present to evaluate for the presence of a
bicuspid aortic valve and aortic regurgitation.
AAA:
1. Transabdominal US: Preferred for screening and surveillance of infra-renal AAA. Initial test if suspect AAA. High
sensitivity at 98% and specificity of 99%42.
2. CT imaging: Preferred for supra-renal AAA, stable symptomatic patients, preop planning and often post-op
surveillance.
E. Management
TAA: The decision point for management rests on whether there is any indication for surgical repair. Repair options
include open surgery or endovascular repair.
Indications for repair 47 Conservative Management 46
1. Symptomatic TAA Risk factor modification

2. Asymptomatic ascending TAA with end- 1. Smoking cessation
diastolic aortic diameter (EDAD) >5.5 cm or aortic 2. Statin therapy for HLD
3. Aggressive blood pressure control
size index ≥2.75 cm/m2 ● Goal SBP 105-120 mm Hg
3. Asymptomatic ascending TAA with (EDAD) ● Beta blockers are preferred give decreases
>4.5 cm if undergoing aortic valve surgery decreasing aortic shear stress.
4. Asymptomatic descending TAA if Aortic *Avoid fluoroquinolones as they have been linked
diameter >5.5 cm to an increased risk of aortic aneurysm or
5. Asymptomatic TAA with growth rate >0.5 dissection.48
cm/year
6. Asymptomatic TAA in hereditary conditions
AAA: Options for repair include open surgical repair or endovascular repair (EVAR) if indicated. EVAR 1, DREAM, OVER
all show initial survival benefit with EVAR but similar long-term mortality at 8-10 years. Patients who undergo EVAR
require long-term surveillance with CT for development of endoleaks 49,50.
Indications for Repair 42 Conservative Management 49,50
1. Symptomatic AAA Medical management is focused on preventing

2. Asymptomatic AAA if further enlargement.
● Smoking cessation (only intervention
- Diameter ≥5.5 cm
proven to reduce rate of AAA growth
- Saccular abdominal aneurysms may be repaired ● Aggressive HTN and HLD treatment
at smaller diameters. ● No clear evidence that pharmacotherapy
- Rapid growth rate reduce AAA growth (statins, beta blockers,
- Distal embolization of aneurysm material (mural ACE inhibitors)
thrombus)
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F. Surveillance
TAA: Asymptomatic patients with thoracic aortic aneurysm who do not meet indications for repair should undergo long-
term monitoring. Imaging modalities used for surveillance include TTE, CTA, or MRA.
Surveillance Recommendations for TAA47
Type of Aneurysm Size Surveillance timing

Aortic root or ascending aorta
Sporadic 3.5-4.4 cm Annual
4.5-5.4 cm Every 6 months
Genetically mediated 3.5-4.4 cm Annual
Descending aorta 4.0-5.0 cm Annual
AAA: The U.S. Preventive Services Task Force (USPSTF) recommends a one-time screening by abdominal
ultrasound for men aged 65 to 75 years who have ever smoked Society guidelines also recommend ultrasound
screening for AAA in first-degree relatives of patients with AAA who are >65 years of age.43,51 Once detected, it is
recommended that monitoring continue until aneurysm diameter exceeds 5.5 cm.
Surveillance Recommendations for AAA43
Aneurysm size Surveillance timing

3.0-3.9 cm Every 2-3 years
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Aortic Dissection
A. Definition
Tearing of the aortic intima resulting in separation of the arterial wall into
two layers forming a false lumen that can propagate both distally and
less commonly in a retrograde fashion. The Stanford system is the most
widely used classification system that guide management decisions.
Type A: Dissection involves the ascending +/- descending aorta.

Type B: Dissection involves only the descending aorta.
Duration: acute (<2 weeks) vs chronic (>2 weeks)
B. Risk Factors
Hypertension, collagen disorders (Marfan Syndrome, Ehlers-Danlos
Syndrome type IV, Loeys-Dietz Syndrome, aortic surgery/
instrumentation (CABG, coronary cath, TAVR), preexisting aortic Stanford Type A Type B
aneurysm, congenital heart defects (bicuspid aortic valve, aortic DeBakey I II III
coarctation), and pregnancy.
Aortic dissection classifications. Adapted from Ital J
C. Clinical Presentation Vasc End Surg 2015;22:141.
● Symptoms: Ripping/ tearing chest pain, inter-scapular back pain,
abdominal or per umbilical pain (may be migratory as dissection
propagates caudally), hypertension, hypotension, syncope, AMS.
● Physical exam: Asymmetric BP (SBP variation >20 mm Hg between arms) or pulse deficit
● Image findings: CXR with mediastinal widening on CXR (60-90% of cases). EKG findings are 31% normal, 42%
nonspecific ST-T changes, 15% ischemia, and 5% acute MI
Complications of aortic dissection are mainly from propagation and include aortic valve regurgitation, cardiac tamponade,
obstruction of coronary artery ostia, coronary artery dissection, and end-organ failure due to abdominal aortic branch
vessel obstruction.
End organ complications Presentation
Acute MI (RCA most common53) Chest pain; ST-T changes, + trop
Acute stroke Focal neurologic deficits, headache
Spinal cord ischemia Acute paraplegia
Mesenteric ischemia Abdominal pain, bloody diarrhea,
Limb ischemia 6 P’s (pallor, paresthesia, pain etc.)
D. Diagnostics
Imaging remains the mainstay of diagnosis. Diagnostic tools have been developed to better predict likelihood of aortic
dissection given variable nature of presentation.
D-dimer: Recent studies have demonstrated that a D-dimer <500ng/mL can effectively identify patients who do not have
acute aortic dissection. (97% sn, 56% sp, 96% NPV).54
Imaging: CTA most common initial test. If the patient is hemodynamically unstable, TEE. (98% sn & 63-96% sp).
Study Sens (%) Spec (%) Comment
CXR 68-90 n/a Mediastinal widening (64%), displaced intimal calcification (9%),
pleural effusion (16%), abnl aortic contour (76%), normal (12%)
TTE 30-80 83-96 Pros: Useful for complications: AI, tamponade, LV, valves
Cons: Only proximal aorta is visualized
Chest 97-100 83-100 Pros: Available, fast and holistic evaluation of chest
CTA* Cons: IV contrast, cannot evaluate coronaries or aortic valve
reliably, site of tear often not defined
MRA 98-100 87-100 Pros: Test of choice for following chronic dissection
Cons: Long image acquisition time
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TEE 97-100 98-100 If high pretest probability and chest CTA contraindicated.
Evaluate LV, AV, prox coronaries, and pericardial effusion
*Consider ordering CTA chest with neck, abdomen, pelvis w/ leg run offs
**Surveillance imaging should be obtained at 3, 6, 12 months and annually thereafter.
E. Management
Acute management consists of the following:
● Access: A-line in arm with highest pressure. Frequent BP checks of both sides; CVC; intubate
o Rule out tamponade / CHF, then volume resus 🡪 take emergently to the OR.
● Goal HR <60: IV BB (e.g., labetalol, esmolol). Reduce HR before blood pressure to prevent reflex tachycardia/
inotropy and minimize shear stress. CCB may be used as an alternative
o Caveat: reducing HR in the setting of acute severe AI will increase the diastole/systole ratio, may precipitate
cardiogenic shock.
● Goal SBP 100-120 mmHg: If SBP remains elevated after appropriate HR control, antihypertensive drip should be
started (nitroprusside or nicardipine)
o Avoid use of hydralazine - can increase hydraulic shear
● Urgent surgical consultation should be considered for all patients
o Type A Dissection: Stat page CT surgery. Typically treated surgically with sternotomy, aortic root
replacement with graft +/- valve repair/replacement since they are at high risk for complications.
▪ If untreated, mortality is 1-2%/hour for the 48hrs in acute proximal dissections.
▪ Surgery: mortality is 10-20%; medical therapy only: mortality is >50%.55
o Type B Dissection: usually treated medically. Surgical interventions are reserved for patients who develop
complications related to the dissection.
Agents used in the acute management of aortic dissection
Agent Initial Dose Comment

Labetalol 20-80 mg IV bolus Can be used as a single agent
0.5-2 mg/min gtt Preferred PO agent
Propranolol 1-10 mg IV load May be a more potent beta-blocker than esmolol
3 mg/h gtt
Esmolol 250-500 mcg/kg IV Preferable in acute setting due to short half-life
25-200 mcg/kg/min gtt Better tolerated in pts with asthma or CHF
Diltiazem 20 mg bolus Useful when BB contraindicated
5-15 mg/h gtt Avoid if reduced LVEF (can precipitate shock)
Nitroprusside 0.25-0.5 mcg/kg/min gtt Use after BB to prevent reflex tachycardia minimize
Nicardipine 2.5-15 mg/hr gtt shear stress
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Quick Reference Guide: Vascular Medicine
Deep Vein Thrombosis (DVT)

● Therapeutic anticoagulation is indicated in all patients with proximal lower-extremity DVT (arising in the popliteal,
femoral, or iliac veins) and in some cases of distal DVT, in the absence of contraindications
● Therapeutic AC should also be considered in cases of upper extremity DVT. Most of these cases are secondary
to indwelling catheters
● DOACs are considered first-line agents for VTE in the majority of patients
o Warfarin is favored in patients with APLAS
o DOACs and Lovenox preferred in malignancy
o When possible, prefer LMWH over UFH
● Regarding duration of therapy:
o Most patients with a first episode of provoked VTE should receive at least 3 months of therapeutic AC
o Patients with low risk of bleeding and persistent risk factors (e.g., immobility or hormone replacement
therapy) should be treated with an extended course (i.e., 6-12 months)
o Long-term AC should be considered in select populations (Patients with unprovoked DVT/PE, Recurrent
provoked DVT/PE, or Active malignancy)
● The only widely accepted indication for catheter-directed thrombolysis (CDT) for lower extremity DVT is proximal
(typically ilio-femoral) clot leading to compromised lower extremity perfusion and risk of limb ischemia (i.e.,
phlegmasia cerulea dolens)
● IVC filters are indicated for patients with DVT who have an absolute contraindication to AC in order to decrease
risk of PE.
Pulmonary Embolism (PE)

● Risk stratification of PE depends on the presence or absence of hemodynamic instability and right heart strain
o RV strain can be assessed via multiple modalities including cardiac biomarkers (NT-proBNP, hsTnT),
EKG (RBBB, anterior T wave inversions, S1Q3T3), CT-PE (RV/LV ratio >0.9), or TTE (RV dilation,
hypokinesis, or McConnell’s sign, in which there is diffuse RV wall hypokinesis with apical sparing)
● Based on the above, PE is generally classified as low-risk, intermediate-risk (e.g., submassive), and high-risk
(e.g., massive)
● The MGH Pulmonary Embolism Response Team (PERT, x47378) is a multidisciplinary team that can be activated
for prompt assessment and management of PE
o Consult PERT in all cases of massive and select cases of submassive PE
● Intermediate-risk or submassive PE is characterized by right heart strain without hemodynamic instability. Prompt
initiation of AC and ongoing monitoring is imperative.
● High-risk or massive PE is characterized by the presence of hemodynamic instability and carries significant risk of
mortality. CONSULT PERT for consideration of tPA, thrombectomy, catheter directed thrombolysis, surgical
embolectomy and ECMO
o Administration of systemic thrombolytics (alteplase [t-PA] and Tenecteplase) is associated with decreased
all-cause mortality
Peripheral Artery Disease

● The diagnosis of PAD can be suspected clinically based on history of symptoms, risk factors for PAD, and
physical exam findings
● Diagnosis should be confirmed with ankle-brachial index (ABI)
o ABI < 1 indicates PAD,
● Stable PAD is generally managed with exercise and risk-factor modification
● ASA 81 or clopidogrel 75 mg daily are often used as first-line agents in PAD
● Statins provide a reduction in systemic and limb arterial events and may also improve symptoms
● Medications such as cilostazol are used for lifestyle-limiting claudication
● Revascularization is an option for patients with significant or disabling symptoms unresponsive to other treatment
options
Acute Critical Limb Ischemia

● This is defined as a sudden decrease in limb perfusion presenting within 2 weeks of an inciting event. Etiologies
of arterial occlusion include thrombosis at site of atherosclerotic plaque in native artery (most common cause),
thromboembolism, thrombosis of stent/graft, thrombosis of aneurysm, arterial dissection, and iatrogenic from
arterial access sites
● Management involves immediate anticoagulation with a heparin gtt and revascularization (either endovascular or
surgical)
● If irreversible ischemia (non-salvageable), amputation is recommended
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Chronic Critical Limb Ischemia

● Clinically presents as rest pain and / or non-healing wound and / or gangrene
● Typically corresponds to ABI <0.4 and is defined as ischemia of >2 weeks duration sufficient to threaten the
limb
● Most patients will require revascularization with either endovascular therapy (percutaneous transluminal
angioplasty) or bypass surgery
● Adjunctive measures include aggressive wound care, pain control, and medical management
● Amputation may be indicated in patients with sepsis, uncontrolled pain or as a result of a multidisciplinary decision
for patients who are otherwise debilitated.
Renal Artery Stenosis

● Renal artery stenosis (RAS) is characterized by narrowing of one or both renal arteries and accounts for an
important cause of secondary HTN.)
● Atherosclerotic RAS (ARAS) accounts for 90% of all RAS
● Fibromuscular Dysplasia (FMD), a non-inflammatory, non-atherosclerotic vascular disease, commonly affects the
renal arteries (66% of patients)
● Testing for RAS should only be pursued in patients thought to have a high likelihood of benefitting from
revascularization
● Diagnostic/imaging modalities include: US, CTA, MRA, and arteriography
● Medical therapy and risk modification remains the mainstay of treatment for RAS
o Choice of anti-HTN medication should follow published guidelines as if for non-RAS patients. Importantly,
ACE and ARB are not contraindicated
● Options for revascularization include percutaneous angioplasty +/- stenting and surgical revascularization.
Thoracic Aortic Aneurysm

● Aneurysms are classified by their location (ascending aorta, aortic arch, descending thoracic aorta) and
morphology (fusiform vs saccular)
● The majority of TAAs are sporadic (degenerative) and are associated with risk factors for atherosclerosis
● The natural history of TAA is characterized by slow expansion with progressive increase in risk of dissection as
the aortic size increases
o The risk of rupture or dissection increases abruptly as thoracic aneurysms approach 6 cm
o The annual risk of rupture is 2% for TAAs <5 cm and 7% for TAAs >6 cm
● TAA is typically incidental diagnosed on imaging (CXR or TTE)
o Further evaluation using CTA/ MRA is recommended to determine the size and extent of the aneurysm
o When aortic root or ascending aortic aneurysm is present, TTE should be performed to evaluate for the
presence of a bicuspid aortic valve
● Indications for repair include:
o Symptomatic ascending and descending TAA (MI, CHF, back pain, paresthesia)
o Asymptomatic ascending TAA
▪ End-diastolic aortic diameter >5.5 cm or aortic size index ≥2.75 cm/m 2
▪ End-diastolic aortic diameter >4.5 cm if undergoing aortic valve surgery
o Asymptomatic descending TAA
▪ Aortic diameter >5.5 cm or Aortic diameter ≥6 cm if high surgical risk
o Asymptomatic TAA with growth rate >0.5 cm/year
o Asymptomatic TAA associated with genetically mediated conditions
● Repair options include open surgery or endovascular repair
● For asymptomatic patients without an indication for repair, conservative management and surveillance is
recommended to prevent rupture or dissection.
o Risk factor modification (smoking cessation, statin therapy)
o Blood pressure control with goal SBP 105-120 mm Hg
o Surveillance (Frequency depends on etiology, location, size, and growth rate)
Abdominal Aortic Aneurysm
● The natural history is marked by progressive dilation over time
o Risk of rupture increases with aneurysm size with <1% annual rupture risk for AAA <4 cm in diameter and
>10% annual rupture risk for AAA >6 cm in diameter
o Rupture is often lethal with mortality cited as high as 85-90%
● AAA are often detected incidentally on imaging studies performed for an alternative indication or through
screening initiatives
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o The USPSTF recommends one-time screening by abdominal ultrasound for men aged 65 to 75 years
who have ever smoked (i.e., 100 or more lifetime cigarettes)
● Patients with AAA are often asymptomatic but may present with a sensation of pulsation near the umbilicus,
constant abdominal or back pain.
o The classic triad of ruptured AAA (severe acute pain, pulsatile abdominal mass, and hypotension) is
present in only 50% of cases
● In stable patients with a high suspicion for ruptured AAA, CT aortography is the initial test of choice
● In patients who presents with abdominal or back pain and some suspicion for AAA, abdominal ultrasound is the
initial test of choice
● Indications for repair include:
o Symptomatic AAA regardless of diameter
o Asymptomatic AAA if Diameter ≥5.5 cm, Saccular abdominal aneurysms, Rapid growth rate
● Repair options include open surgical repair or endovascular repair (EVAR)
● Medical management is focused on risk modification
o There is no clear evidence that pharmacotherapy (statins, beta blockers, ACE inhibitors) reduce AAA
growth
● Surveillance imaging should be performed using transabdominal ultrasound
Aortic Dissection
● Aortic dissection occurs when a tear in the aortic intima exposes the medial layer to the systemic pressure of
intraluminal blood
o Type A dissections involve the ascending +/- descending aorta. Type B dissections involve only the
descending aorta
● Risk factors for aortic dissection include HTN (most common), cocaine, heavy lifting, pregnancy, collagen
disorders (Marfans/ Ehlers Danlos type IV), and prior aorta surgery/ minimally invasive intervention.
● Most patients with aortic dissection present with abrupt-onset severe, sharp chest pain that
can radiate to the back
o Exam findings include a pulse deficit, SBP variation >20 mm Hg between arms, and findings associated
with complications/distal propagation
o Complications include: Acute AI, tamponade, and end-organ ischemia secondary to branch-vessel
involvement
● CTA is the most commonly performed imaging modality available
o If hemodynamically unstable, TEE is the preferred diagnostic test given its high sensitivity and specificity
o The addition of a negative D-dimer <500ng/mL can help to effectively rule-out dissection in addition to low
ADD-RS score (<1)
● Type A dissections require emergent surgical evaluation for consideration of sternotomy and
aortic root replacement with graft +/- valve repair/replacement. PAGE CT SURGERY
● In contrast, Type B dissections are typically managed medically with surgical intervention
reserved for patients who develop critical complications
o Use IV beta blockers first to aggressively reduce HR to goal <60 (reduces reflex tachycardia and
decreases shear stress)
o Once HR goal achieved, use vasodilators (nitroprusside, nicardipine) to reduce SBP (goal SBP 100-120
mm Hg)
● Longer-term management of Type B dissection involves ongoing therapy with anti-hypertensives (goal BP
<120/80) to reduce incidence of late complications
o Beta blockers or nondihydropyridine CCB and ACE are preferred over hydralazine
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Anatomic and Physiologic Classification System
The 2018 ACC/AHA Adult Congenital Heart Disease (ACHD) guidelines presented a new classification system (1).
The ACHD anatomic and physiological (ACHD AP) classification system uses both anatomic complexity and
physiologic/functional status.
● Anatomic classification:
o Class I (simple)
o Class II (moderate complexity)
o Class III (great complexity)
● Physiological classification:
o stages A-D (similar to the NYHA heart failure classification system)
o considers patient’s functional status and presence of valve disease, pulmonary hypertension,
arrhythmias, aortic dilatation, end-organ function, or cyanosis.
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PATENT FORAMEN OVALE (PFO)
PFO is defined as failure of the foramen ovale (opening between the atria in fetal circulation that allows blood to bypass the
pulmonary vasculature) to close in the first few months of life, allowing a flap-like communication between the RA and LA
Epidemiology/Presentation
● PFOs are common (25-30% of the general population) and generally asymptomatic
● PFOs are more common (~40%)2 in patients presenting with cryptogenic stroke, especially in those who
suffer strokes before age 55
● Very rarely do PFOs result in right-to-left shunting and hypoxia, or orthodeoxia (positional desaturation)
● PFOs should be screened for in the setting of a cerebral ischemic event in young patients or hypoxemia of
uncertain origin
o Associated atrial septal aneurysms (ASA) confer highest risk for recurrent PFO-related stroke5
Exam: Typically normal

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Imaging: Echocardiogram with color flow Doppler or agitated saline contrast (a “bubble study”) is the diagnostic test
of choice.
● TEE has higher sensitivity than TTE for the detection of PFO
Management
● Primary prevention of stroke in patients with a PFO is not indicated3
● Secondary prevention in patients with ischemic stroke/TIA and found to have PFOs and without alternative
explanation for stroke despite thorough evaluation:
o For patients aged ≤60 yrs: percutaneous PFO device closure in addition to
antiplatelet therapy, rather than antiplatelet therapy alone4
o For patients > 60 yrs: data less clear, as the risks of intervention must be balanced with changing
technology (including percutaneous suture options)6
▪ This does not apply to selected patients with strong clinical evidence of paradoxical
embolus (ex: pts with acute DVT, PE, or other VTE)
References:
Cardiol. 2018;73(12):1494-1563.
2. Lechat et al. Prevalence of patent foramen ovale in patients with stroke. N Engl J Med. 1988; 318:1148-1152.
3. Messé et al. Practice advisory update summary: Patient foramen Ovale and secondary stroke prevention: Report of the
Guideline Subcommittee of the American Academy of Neurology. Neurology. 2020; 94 (20).
4. Mojadidi et al. Cryptogenic Stroke and Patent Foramen Ovale. J Am Coll Cardiol. 2018; 71:1035-1043.
5. Turc et al. Atrial septal aneurysm, shunt size, and recurrent stroke risk in patients with patent foramen ovale. J Am Coll
Cardiol. 2020; 75(18):2312-2320.
6. Gaspardone and Sgueglia. Cryptogenic stroke over 60 years of age: should patent foramen ovale be closed? Eur
Heart J Supplements. 2020; 22: E82-E86
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ATRIAL SEPTAL DEFECT

ASDs represent a persistent communication between the RA and LA due to abnormalities of atrial septal
development and tissue regression.
There are four main types:
● Primum defect (15-20%): Also known as partial or complete AV canal defects or endocardial cushion
defects. Often associated with AV valve anomalies (cleft mitral valve)
● Secundum defect (70-75%): The most common ASD. They vary in size and are usually isolated lesions
but can be associated with other ASDs
● Sinus Venosus defect (5-10%): Occurs at the juncture of great veins to atrial septal tissue due to failure
of correct insertion of the IVC or SVC
● Coronary sinus defect (very rare): Caused by absence (full or partial) of the wall between the coronary
sinus and the LA
● Most common type of congenital heart lesion
● 2:1 female to male predominance
● Typically, left-to-right atrial shunt (due to RV compliance)
o Can eventually lead to R-sided volume overload, RV enlargement and pHTN (rarely with large
defects, right-to-left shunting and Eisenmenger Syndrome)
▪ In right-to-left shunting, increased risk of paradoxical embolization and stroke
Exam: Large ASDs may result in a fixed and split S2 that does not vary with inspiration. A soft systolic crescendo-
decrescendo systolic pulmonary flow murmur may be heard due to increased flow over the pulmonary valve.
Precordial lift may be felt in cases or RV enlargement. Prominent P2 may be present at the apex if resting
pulmonary hypertension has developed.
Imaging:
● TTE generally first step, sinus venosus defects can be difficult to diagnose by TTE but RV enlargement
without other explanation should prompt additional imaging
● TEE, cardiac CT, or MRI may additionally be performed to help define the margins of the defect (an
important consideration for device closure of secundum ASD) and to identify associated pulmonary
venous anomalies
Management
ASD repair (primum or secundum, either transcatheter or surgical) is indicated (Class I recommendation),1 if:
● The patient exhibits impaired functional capacity, has RA and/or RV enlargement, and net left-to-right
shunting large enough to cause physiologic sequelae
ASD closure is NOT recommended (Class III: Harm) if:
● PA systolic pressure > 2/3 systemic pressure and PVR >2/3 SVR
● There is net right-to-left shunt
Note: All sinus venosus, primum, and coronary sinus defects must be repaired surgically. For isolated secundum
defects, percutaneous closure is the most common approach for repair, with extremely high success rates (surgical
repair reserved for very large defects or patients with deficient septal rims).
References:
Cardiol. 2019;73(12):1494-1563.
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VENTRICULAR SEPTAL DEFECT
VSDs results from the failure of septal development. There are four main types:
● Supracristal (5%): Result from deficiency of the septum inferior to the aortic and pulmonary valves. Aortic
valve cusp can prolapse into the VSD, leading to progressive AR and occasionally aortic sinus dilatation
● Perimembraneous (60-70%): Most common, located near the membranous septum below the AV
● Muscular (10%): Can be small or large, single or multiple, and may spontaneously close. In adults, they
are generally small
● Inlet (rare): Results from deficiency of the inlet septum located beneath both mitral and tricuspid valves.
Does not result in mitral or tricuspid regurgitation unless associated with an AV canal defect and septum
primum defect (often seen with Down’s syndrome)
● VSDs are among the most common congenital heart entities in early childhood, but only account for 10% of
ACHD. Most close spontaneously.
● Small restrictive VSDs rarely cause chamber enlargement
● Moderate VSDs result in left heart volume loads (via L to R shunting)
● Large VSDs can lead to L-to-R shunting—enough to cause biventricular failure, RV volume overload,
pHTN, and even reversal of flow (R-to-L shunting, i.e. Eisenmenger Syndrome)
● Note: Congenital VSDs differ from post-infarct VSDs; which typically are muscular, large, and impact RV
function primarily.
Exam: Small VSDs may be associated with a high-pitched pansystolic murmur. Larger VSDs tend to cause lower-
frequency murmurs or may not be audible. These should augment with hand-grip (due to increased left ventricular
afterload and increased shunt fraction).
**The presence of a diastolic murmur in a patient with known restrictive VSD must be further evaluated (aortic
regurgitation or aortic fistula).
Imaging: TTE is generally sufficient to define the lesion and assess for biventricular size and function.
Management
● Class I indication for repair1:
o Evidence of LV volume overload and hemodynamically significant shunt AND PA systolic pressure < ½
systemic systolic pressure and PVR < 1/3 SVR
● Class II indication for repair1:
o Worsening aortic regurgitation due to VSD (Class IIa)
o History of infective endocarditis caused by VSD (if not otherwise contraindicated) (Class IIb)
o There is net L-to-R shunt when PA systolic pressure > ½ systemic systolic pressure and/or PVR >
1/3 SVR
● Repair contraindicated (Class III: Harm)1:
o PA systolic pressure > 2/3 systemic pressure, PVR > 2/3 SVR, and/or there is net R to L shunt
References:
Cardiol. 2018;73(12):1494-1563.
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COARCTATION OF THE AORTA
Coarctation of the Aorta (CoA) is characterized by discrete or diffuse narrowing of the aorta. The typical location is in
the region of the ligamentum arteriosum, adjacent to the origin of the L subclavian artery.
Epidemiology/Presentation2
● Accounts for ~5% all congenital heart defects
● Occurs more commonly in males
● Can be associated with other congenital cardiac lesions
o In children, CoA is often associated with complex congenital heart lesions
o In adults, bicuspid aortic valve is the most common associated defect
● Obstruction to blood flow causes increased afterload on the LV leading to LV hypertrophy
● There is also differential hypertension, with higher BP in vessels proximal to the obstruction and relative
hypotension distally (patients may suffer from claudication).
● Patients are at increased risk of aortic dissection, particularly with pregnancy. 10% of CoA cases have
aneurysms along the Circle of Willis (as below, should be screened with a one-time MR/CTA).
Exam: Differential hypertension can be pressure (> 20mmHg BP difference between arm and leg). Lower extremities
may have diminished or late pulses (brachiofemoral delay). Systolic bruit may be heard along the scapular region.
Systolic click of a bicuspid aortic valve may be heard if present (about 50-60%)
Imaging:
● CXR may show aortic indentation at the CoA site “3 sign,” (see Figure)
and notching on the underside of the ribs from collateral vessels
● TTE views from the suprasternal notch can demonstrate a narrowed
aortic lumen as well as measure pressure gradient across the CoA
segment
● CT/MRI preferred for screening for late complications (aneurysm, focal
dissection, re-stenosis) and for helping guide interventional approach
Management1
● Class I indication for surgical repair:
o Adults with native or recurrent CoA who have hypertension and significant native/recurrent
coarctation
● Type of repair varies based on anatomy
o Percutaneous stent implantation or surgical repair is procedure of choice, though balloon
angioplasty can be considered if stent/surgical repair not feasible
References:
Cardiol. 2019;73(12):1494-1563
2. Baumgartner H et al. ESC guidelines for the management of grown-up congenital heart disease.
Eur Heart J 2010;31:2915–57
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Tetralogy of Fallot
Tetralogy of Fallot (TOF) is a constellation of four
abnormalities: pulmonic stenosis, VSD, overriding
aorta, and right ventricular hypertrophy
● Initial diagnosis and management
typically occurs by early childhood
o Most patients in the current era will
have undergone surgical repair in
early infancy
o Some older adult patients may
have undergone palliative
shunting prior to surgical repair
● It is the most common palliated complex
CHD in adults
Exam:
● Findings in adults are variable and will
depend on prior management (e.g. repair
versus palliative shunt).
● Scar anatomy is important (thoracotomy
and/or sternotomy) Figure 1. Native anatomy in
● Many patients will have systolic RVOT murmur and patients with PR will have a TOF (Adult Congenital Heart short
diastolic murmur. Disease in Clinic Practice
● Diminished radial pulse may indicate prior BT shunt. 2018)
● Right heart failure exam is critical (JVP, ascites, leg edema, right heart gallops)
Imaging:
● TTE is first line imaging and used to assess the degree of pulmonary regurgitation and other associated residual defects
(VSD, pulmonic stenosis, aortic dilation)
● Cardiac MRI is the gold standard for following RV size and function and pulmonic regurgitation quantification and to assess for
indications for pulmonary valve replacement (performed once RV volumes reach a certain size).
Management1
● Management in adulthood is primarily aimed at addressing late complications after childhood surgical repair including
pulmonic insufficiency, recurrent pulmonary stenosis, complications of prior shunts, and arrhythmia
o Many patients require repeat pulmonary valve intervention during adulthood (either surgical or transcatheter). Note:
the origins and proximal courses of coronary arteries must be mapped prior.
o Even after repair, adult pts with TOF are at increased risk of heart failure and sudden cardiac death (~2% per decade
of life), which may require ICD for primary or secondary prevention as well as targeted anti-arrhythmics and/or
ablation
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TRANSPOSITION OF THE GREAT ARTERIES
There are 2 types of Transposition of the Great Arteries (TGA): D-TGA and L-TGA
● D-TGA (“dextra-TGA”): aorta arises from anterior of the RV and the PA arises from the LV such that the RV is the systemic
ventricle (deoxygenated blood is in systemic circulation, oxygenated blood is in the pulmonary circulation). Thus, systemic and
pulmonary circulations are in parallel
● L-TGA (“levo-TGA”): in this “congenitally corrected” type of TGA, the morphologic RV is on the left and the morphologic LV is
on the right, the pulmonary artery arises from the right sided LV and the aorta from the left sided RV, such that pulmonary and
systemic circulation still occur in series
D-TGA
● Most common type

● Leads to neonatal cyanosis hence is typically corrected in childhood
o Short-term survival is dependent on mixing of these circuits via PFO, ASD, VSDs, and/or a patent ductus arteriosus
● Adults who survive have generally undergone one of these surgeries in early life:
o Atrial switch (Senning/Mustard procedure; see Figure 2)
▪ Residual complications include baffle leak/obstruction or progressive systemic RV dilation/dysfunction after
years of pumping against a systemic circulation.
o Arterial switch (Jatene procedure, see figure 3 below)
▪ Residual complications from this procedure include pulmonary branch stenosis (due to tension from anterior
surgical translocation of the main PA), aortic regurgitation of the neo-aortic valve, and coronary artery
stenosis as a result of surgical translocation
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From Adult Congenital Heart Disease in Clinic Practice (DeFaria Yeh & Bhatt)
Figure 3: Jatene
Procedure for D-TGA
correction
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L-TGA
● Because this is a “congenitally corrected” anomaly (ie systemic and
pulmonary circulation are in series), patients may present in adulthood
o Some adult patients will have undergone surgical correction in
childhood
o May be picked up earlier in life if associated PS/VSD where
murmurs may lead to TTE
● L-TGA can be associated with other congenital anomalies such as VSD,
pulmonary stenosis, apical displacement of systemic tricuspid valve, and
displacement of the AV node with accessory AV node pathways (this often
leads to complete heart block and/or re-entrant SVTs).
● Heart block is common: 2% development per year
Exam: In both D-TGA and L-TGA the exams will be highly variable based on prior
surgical corrections and/or associated congenital anomalies
Imaging: In both D-TGA and L-TGA, cardiac MRI generally provides the best
assessment of structural and functional complications. Cardiopulmonary exercise
testing is important to assess peak VO2 which is highly prognostic. From Adult Congenital Heart Disease
in Clinic Practice (DeFaria Yeh &
Management Bhatt)
● Management of the adult patient with D-TGA involves managing
complications of prior intervention
o Arrhythmia: Ambulatory monitoring for bradycardia or sinus node dysfunction (especially true of pts treated with beta
blockers/other rate-slowing medications).1 Otherwise, standard targeted anti-arrhythmics and ablation procedures
advised.
o Baffle obstruction/leak: May present as edema of the face and upper extremities with superior baffle limb obstruction.
If the inferior baffle limb is obstructed, cirrhosis and ascites may develop. These patients may also exhibit
desaturation or paradoxical embolization if baffle leaks occur. Leaks/obstruction can be corrected percutaneously or
surgically. Cardiac MRI provides the best assessment of structural and functional complications.
o Progressive systemic RV dysfunction: Manage as per any other pt with RV dysfunction
● Management of the adult patient with L-TGA involves management of complications including arrhythmia and hemodynamic
effects
o Arrhythmia: As a result of AV nodal displacement, patients are at high risk for CHB. Many will require pacemaker
implantation (in subpulmonary LV). Ablation may also be necessary for accessory pathways contributing to AVRTs
o Progressive systemic right ventricular dysfunction: Pts are at risk of severe systemic TR due to anterior leaflet
dislocation, and TV repair can be considered in rare situations. In many cases, if systemic RV failure develops then
transplantation must be entertained.
References:
1. Stout KK et al. 2018 AHA/ACC Guideline for the management of adults with congenital heart disease. J am Coll Cardiol.
2019;73(12):1494-1563
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SYSTEMIC VENTRICLE PHYSIOLOGY/FONTAN PALLIATION:

see diagrams at the end of this section
Hypoplastic Left Ventricle
● Single ventricle physiology can result from many underlying congenital heart defects that
necessitate mixing.
● The four most common are tricuspid atresia, hypoplastic left heart syndrome,
double inlet LV, and unbalanced AV canal defect.
● In all these native anatomies, the myocardial mass receives cardiac
inflow, mixes oxygenated and deoxygenated blood, and distributes
moderately oxygenated blood to both pulmonary and systemic circulations.
Having moderately oxygenated blood perfusing the systemic circulation
has long term consequences
● Surgical correction with the Fontan procedure aims to separate oxygenated
from deoxygenated blood by routing the systemic veins directly to the
pulmonary artery, the pulmonic valve is ligated and the systemic ventricular
mass pumps oxygenated blood out the aorta.
Clinical Presentation in Adults:

● Several surgeries may occur in early childhood:
(see below for diagram)
o 1) correcting pulmonary blood flow with pulmonary artery band
or BT shunt
o 2.) connection of the SVC to pulmonary artery (Glenn or superior
cavopulmonary anastomosis)
o 3) diversion of the IVC blood to the pulmonary artery (Fontan
completion, most common in modern era is lateral
tunnel) From Adult Congenital Heart Disease
● Careful understanding of all operative anatomy and procedures is in Clinic Practice (DeFaria Yeh &
critical to appropriate management Bhatt)
● After Fontan palliation, the patient lacks sub pulmonary pump to drive blood into the
pulmonary arteries causing cardiac output to be limited by 1) the downstream
systemic ventricle’s ability to pull blood through the pulmonary bed and 2) the passive return from the systemic veins to the
pulmonary artery through the Fontan circuit
o Limited cardiac output results in exercise limitation and fatigue
o Venous collaterals may develop between the systemic (blue) and pulmonary (red) veins, bypassing the pulmonary bed
and resulting in systemic cyanosis
● Atrial arrhythmias are common
● Pts with morphologic RV pumping systemically develop early progressive ventricular dysfunction
● Patients can also develop Congestive Fontan hepatopathy leading to progressive Fontan Associated Liver Disease (FALD) and
HCC
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Fontan Procedure: (a) RA to PA connection (b) lateral tunnel, intracardial (c) extracardiac Fontan
Management
● Patients with
Fontan circulation
must be managed in
conjunction with
specialists in ACHD
● Fenestrations
(between the Fontan
lateral tunnel and
systemic circuit) can
be created which
allow a small right-
to-left shunt to
From Adult Congenital Heart Disease in Clinic Practice (DeFaria Yeh & Bhatt) persist
o Benefits include
increased cardiac output due to increased systemic preload and decreased central venous pressures
o Downside is that fenestration is associated with increased risk of paradoxical thromboembolism
o Hypoxemia/cyanosis may also occur in cases of excessive right greater than left shunting
● Common complications:
o Arrhythmia: Atrial dysrhythmias are common and poorly tolerated. Targeted antiarrhythmics, ablation procedures, and
ultimately conversion to extra-cardiac conduit may be indicated
o Cyanosis: Cross sectional imaging (CTA or MRI) plus RHC should be performed to look for systemic to pulmonary
venous connections, which may be treated by transcatheter occlusion
o Thrombosis: Fontan physiology represents a low-flow state, and the degree of right-to-left shunting in these patients
makes systemic thromboembolism a very high risk. Anticoagulation is indicated if there is history of atrial arrhythmia,
fenestration, or EF <40% (even in patients without history of thromboembolism)
o Protein-losing enteropathy: Though the pathophysiology is poorly understood, this is a complication occurring in 3-18% of
patients. Mortality is very high with only ~50% 5-year survival. Therapy is empiric and includes optimizing Fontan
hemodynamics, considering fenestration, optimizing cardiac output, and reducing pulmonary vascular resistance
o Spontaneous fenestration closure: This occurs frequently and may be a silent event. However, in patients with poor
cardiac output who were dependent on fenestration to augment ventricular preload, cardiac output may drop, systemic
venous pressures may rise, and protein-losing enteropathy may ensue
o Heart failure: Symptoms may progress such that transplantation may be the only therapeutic option. Of note, early post
procedure transplant outcomes within this population are poor relative to those with biventricular circulation due to
anastomotic challenges and bleeding. However, if patients survive, early post procedure window survival is on par with
other age-matched patients
o NAFLD: regular screening is imperative with liver ultrasound or MRI, HCC screening
LEFT-TO-RIGHT SHUNTING AND EISENMENGER SYNDROME
There are several congenital abnormalities that cause blood to flow from the systemic to pulmonary circulation (left-to-right shunt).
Rarely, large uncorrected shunts may progress to Eisenmenger physiology in which the excess flow across the pulmonary arteries from
the shunt leads to pulmonary vascular remodeling and increased pulmonary vascular resistance (PVR), which results in shunt reversal
(right-to-left shunting) and cyanosis.
Epidemiology and Presentation

● Adults presenting with the Eisenmenger syndrome typically have progressive dyspnea, chronic exercise intolerance, and
symptoms of right heart failure
o Even rarer: presenting with arrhythmia, syncope, hemoptysis, or cyanosis
● Systemic to pulmonary (left-to-right) shunt lesions result in volume overload, with resulting chamber enlargement (the chamber and
degree of enlargement is dependent on shunt size and location)
o Pre-tricuspid valve shunts (ASD, anomalous pulmonary venous returns) typically result in RA/RV volume overload
o Post-tricuspid valve shunts (VSD, PDA) result in LA/LV volume overload (LV systemic output decreased by shunt ->
compensatory increase in intravascular volume until LVEDV is sufficient to produce normal CO -> LV volume overload)
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● In progression to Eisenmenger Syndrome, R-sided pressure overload results from both direct transmission of pressure from the
higher-pressure LV as well as increased afterload due to pulmonary arterial remodeling
o Overtime, increased PVR causes elevated right-sided pressures as the RV aims to maintain cardiac output. If right-sided
pressures approximate and then exceed left-sided pressures, the shunt direction can reverse, resulting in systemic
desaturation
● Rate of progression of pulmonary hypertension is dependent on the type and size of the anatomic defect, as well as the magnitude
of shunt flow
o Patients with ventricular (i.e. VSD, AVSD) or arterial shunts (i.e. PDA, truncus arteriosus) are at higher risk of progressing
rapidly to Eisenmenger syndrome compared to patients with pre-tricuspid shunt lesions
Exam: Examination may reveal signs of PH and RV failure (RV heave, loud P2 that extends to apex, prominent venous a wave);
chronic hypoxemia (cyanosis, clubbing); and/or TR/PR and murmur of the causative lesion (will become progressively more quiet as
pulmonary and systemic pressures equalize).
Imaging: TTE should be initial diagnostic imaging (as well as CT or cardiac MR in certain cases)
Management
Eisenmenger syndrome patients must be managed in conjunction with an ACHD specialist
● Care of patients with Eisenmenger syndrome includes avoidance of the following (Class I recommendations)1:
o Significant volume shifts (dehydration, or volume overload)
o Chronic exposure to high altitude
o Iron deficiency
o Strenuous activity (in particular, isometric exercise)
o Excessive heat (i.e. sauna, hot tub) due to risks associated with dehydration as well as worsening of right-to-left
shunting through systemic vasodilation
o Unnecessary surgery or anesthesia
o Pregnancy (high maternal mortality)
● These pts require prompt workup and treatment for infection, as they may not have the cardiac reserve to support septic
physiology
o Systemic vasodilation will worsen right-to left shunt flow
● Any degree of pulmonary hypertension should be appropriately managed

o See AHA/ACC 2018 ACHD guidelines for full recommendations and specific therapies. Mortality benefit is conferred
with pulmonary vasodilator therapy
▪ Bosentan is Class I recommendation for Eisenmenger + ASD or VSD
▪ PDE-5 inhibitors have Class IIa recommendation to treat for Eisenmenger + ASD or VSD
● The only surgical option for patients who have progressed to Eisenmenger physiology is heart-lung transplant. Bilateral lung
transplant with intracardiac repair is less common.
● Additional management considerations relate to various complications. Common complications in these patients include:
o Arrhythmia/SCD: Patients are at increased risk of both atrial and ventricular tachyarrhythmia. Endocardial pacing, if
necessary, is not recommended in intravascular shunting due to risk of paradoxical emboli and infection
o Hypoxemia: Due right-to-left shunting. Generally, avoid intubation due to temporary hypoxemia in the setting of
anesthesia
o Hemoptysis: Secondary to pulmonary vascular hypertension (risk of bronchial artery rupture)
o Thrombosis: Pulmonary arterial thrombi are often seen and are associated with worse disease. However, the use of oral
anticoagulants is controversial given the risk of hemoptysis as above. In the absence of reliable data, oral anticoagulant
therapy may be carefully considered in patients with severe disease and no prior episodes of hemoptysis.
o Paradoxical embolism: Filtering of all IVs is essential to prevent strokes. Avoidance of central lines and endocardial pacer
leads is also encouraged to reduced risk of VTE and paradoxical embolism
o Erythrocytosis/Hyperviscosity: Secondary erythrocytosis is common given physiologic response to chronic hypoxemia.
Resulting hyperviscosity may contribute to the increased risk of neurovascular events. Therapeutic phlebotomy should be
performed only when neurologic symptoms are attributed to hyperviscocity and hemoglobin is > 20 g/dL or hematocrit is >
65%.
▪ Iron deficiency and dehydration must be excluded before phlebotomy is considered. Iron deficiency
worsens intravascular sludging and increases risk of stroke. CBC and iron stores should be checked at
least yearly and repleted as necessary
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o Hyperuricemia: Increased uric acid levels are common in patients with cyanotic congenital heart disease and are due to
increased production and decreased renal clearance. Serum uric acid increases in proportion to hemodynamic severity in
adults with Eisenmenger syndrome and is associated with long-term mortality. Uric acid levels should be assessed
annually, and treatment of hyperuricemia should be initiated in patients who develop gout.
References:
1. Stout KK et al. 2018 AHA/ACC Guideline for the management of adults with congenital heart disease. J am Coll Cardiol.
2019;73(12):1494-1563
2. DeFaria Yeh et al. 2018. Adult Congenital Heart Disease in Clinic Practice
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CARDIO-OBSTETRICS
Basic Physiology of Pregnancy
ANTEPARTUM
Hemodynamic changes in normal pregnancy (source: AHA)
SVR: ↓ (nadir 2T)
HR: ↑ (peaks in late 3T)
Total Blood Volume: ↑ “physiologic anemia
and ↑EPO”
CO: ↑ to 30-50% above baseline (peaks in
early 3T; increases due to (1) increased
preload, (2) reduced afterload and (3)
increased HR)
MAP: Mild ↓ in 1+2T, returns to pre-pregnancy
baseline in 3T (balanced ↓ SVR reduction with
concomitant ↑ in CO)
INTRAPARTUM
CO ↑ by ~15% in early labor, ~25% in active
phase of labor, ~50% during pushing in second stage. Note: Epidural anesthesia attenuates some of this increase.
Uterine contraction contributes 300-500cc blood/contraction into maternal circulation.
POSTPARTUM
Immediately post-partum CO ↑ to 80% above pre-labor value due to autotransfusion from aortocaval
decompression/uterine involution (blood auto-transfused usually > blood lost during labor). BP should remain constant
during this phase, hypotension is abnormal. Returns to baseline over ~ 3 months.
NOTE: hypotension in third trimester may be due to positioning or volume depletion
Supine Positioning 🡪 hypotension 2/2 compression of aorta and vena cava due to gravid uterus (reduced CO and SV,
increases HR) 🡪 place in left lateral decubitus shifts uterus off major vessels 🡪 restoration of venous return, CO 🡪
improved BP
Risk stratification of women with pre-existing cardiovascular disease interested in pregnancy
1. Modified WHO classification (most commonly used; 2018 ESC guidelines). Population specific: CARPREG, ZAHARA,
ROPAC (Regitz-Zagrosek et al. EHJ 2018, 39(34): 2165-3241)
Cardiac Diagnosis in Pregnant Women

Manual Uterine Displacement Techniques:
Exam
Normal: Higher basal heart rate; JVP normal to mildly 1-handed from right side of pt:
elevated, loud heart sounds, S3 and venous hum/mammary INCLUDEPICTURE
flow, splitting of S1 or S2 in 3T "https://www.ahajournals.org/cms/asset/7c6e
Abnormal: S4, diastolic murmurs, signs of CHF, loud P2 or bcf8-3c15-41ee-bf59-
RV heave dff5bbf36a79/1747fig03.jpg" \*
MERGEFORMATINET
Studies
Echo: Normal: physiologic multivalvular regurgitation (R>L)
during late gestation, can persist into early postpartum.
2-handed from left side of pt:
Chamber enlargement, annular dilatation, small physiologic
pericardial effusions are frequent incidental findings during
pregnancy. Abnormal: AR, large effusion, symptoms of Figures 3&4 (Circulation 2015; 132:1747-
pericarditis 1773)
EKG: Normal: 15-20 degree LAD, enlarged chamber
volumes. Q waves in III and aVF, TWI in III, V1-V3. PACs and
PVCs common.
Labs: NT-proBNP doubles but remains within normal limits.
Low NT-proBNP has strong NPV for CV complications
(Tanous et al. JACC 2010; 56(16);1247-53)
If imaging is required for workup during gestation, talk with

our OB colleagues to help engage your patient in an
informed risk/benefits conversation. Most imaging studies
do not carry significant risk to mom or fetus, and it is very
important to make the correct diagnosis in a pregnant
women (i.e. etiology of troponin elevation should be
determined, PE should be evaluated with CT when clinical
suspicion is high).
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ACLS in Pregnancy
See 2015 AHA Statement on cardiac arrest in pregnancy for more details (Circulation 2015;132:1747-1773)
o At onset of arrest PAGE MATERNAL CARDIAC ARREST TEAM (see ACLS algorithm below)
o MATERNAL interventions and OBSTETRIC interventions should be performed IN TANDEM
Maternal interventions
o Place IV above diaphragm
o If receiving IV mag, STOP mag and give calcium chloride or gluconate
o Defibrillation and epinephrine should be given when indicated according to the standard ACLS algorithm
o If you suspect PE as a cause of arrest, treat it and get PERT involved; Alteplase is not strictly contraindicated in
pregnancy; heparin and LMWH are safe
Obstetric Interventions
o While performing compressions relieve aortocaval compression with lateral uterine displacement
o If no ROSC within 4-5 minutes, consider immediate perimortem cesarean delivery. Goal is to improve both
maternal and fetal outcomes
Potential Etiologies of Maternal Cardiac Arrest: ABCDEFGH
▪ Anesthetic ▪ Embolic
complications ▪ Fever
▪ Bleeding ▪ General non-OB causes (Hs
▪ Cardiovascular & Ts)
▪ Drugs ▪ Hypertension
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Cardiac Medications during pregnancy

Pharmacokinetic Changes during Pregnancy: Drug distribution and clearance may be affected. Important factors
include delayed gastric emptying and motility; increased plasma volume and fat accumulation 🡪 increased volume of
distribution; decreased albumin and plasma binding proteins; increased hepatic and renal clearance; cytochrome P450
enzymes mostly upregulated
Pregnancy and Lactation Labeling Rule (PLLR): In 2015, PLLR replaced previous FDA scoring system of medications
(used to be ABCDX). Incorporates consideration that baseline rate of major birth defects and miscarriage, and includes
recommendations for pregnancy, labor, delivery and lactation all on the same label. New system more descriptive than
prior ABCDX approach.
Guiding principles: Consider necessity, urgency, timing during gestation, fetal adverse effect of drug. Use lowest
effective dose. Counsel re: limited availability of data, when pertinent. MFM should help guide intrapartum and post-
partum medications.
Summary of safety during pregnancy for the most commonly used cardiac medications (adaptation of central
illustration from Halperin et al, see original paper for further discussion as well as FDA categorization and lactation safety)
(Jeejeebhoy et al. Circulation 2015; 132(18); 1747-73)
● Arrythmias Heart Failure/Shock HTN/PHTN Heme
Aldosterone
Atenolol
antagonists Statins
Contraindicated Amiodarone ACEi, ARB
Atenolol DOAC
Endothelin-R antag
ACEi, ARB
Metoprolol
Adenosine
Carvedilol Labetalol
Digoxin
Furosemide Nifedipine UFH
Considered Safe Lidocaine
Dopamine Alpha-methyldopa (PO) Enoxaparin
Metoprolol
Dobutamine
Propranolol
Norepinephrine
Verapamil Hydralazine
Amlodipine Epoprostenol Alteplase Bivalirudin
Diltiazem Isosorbide dinitrate
Limited data/ Hydralazine Nitroglycerin ASA 81mg Fondaparinux
Procainamide Nitroglycerin
to be used with Iso dinitrate Nitroprusside Clopidogrel Prasugrel
Sotalol Metolazone
caution Iloprost Sildenafil Warfarin Streptokinase
Flecainide Torsemide
Argatroban Ticagrelor
Propafenone
Peripartum Cardiomyopathy (PPCM)

Definition: (1) cardiomyopathy presenting with HF secondary to LV systolic dysfunction (EF<45%) (2) towards the end of
pregnancy or in the months following delivery (3) with no other evident cause (diagnosis of exclusion) (Silwa et al. Eur J
Heart Failure 2010; 12:767-778).
Incidence: PPCM seen in ~103/100k births in the United States with marked regional variation across the world, maternal
mortality rate ~ 14/100k of live births (Kolte et al. JAHA 2014; 3(3):e001056)
Risk factors: Age > 30 y.o, African descent, pregnancy with multiple fetuses, hx of PEC, eclampsia or postpartum HTN,
longterm tocolysis (Lee et al. Circ Heart Fail 2018; 11(4):e004134)
Pathophysiology: dysregulated metabolic pathways and angiogenic imbalance. Prolactin regulation (via STAT pathway)
and VEGF (in PGC-1a KO murine models and via sFlt1 antagonism) regulation implicated (Hoes et al. Nat Rev Cardiol
2022; doi: 10.1038/s41569-021-00664-8).
Diagnosis: Most often first month postpartum. S/Sx: dyspnea, pedal edema, orthopnea, PND, chest tightness. Note: do
not dismiss pedal edema and SOB symptom of pregnancy, especially post-partum (Arany et al. Circulation 2016;
133(14):1397-409). Work-up: NTproBNP, TTE, can obtain cMR but avoid gadolinium during pregnancy, no EMB unless
high suspicion for other etiology.
Management: Similar to other forms of HFrEF (see position statement from HF Association of the ESC for details) i.e.
GDMT; continue if EF remains depressed, however no data to support duration of tx after EF recovery (see figure below).
Important points: Anticoagulation: Consider when LVEF<30-35% during late pregnancy and 6-8 weeks postpartum.
Favor LMWH over warfarin (unless mechanical heart valves), both safe with lactation. No data for DOACs, avoid (Davis et
al. JACC 2020; 75(2) 207-221). Experimental: Bromocriptine in addition to standard therapy is associated with a higher
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rate of EF improvement, although no difference in overall rates of recovery in several small trials. (Silwa et al. Circulation
2010; 121:1465-1473; Yaméogo et al. J Cardiol Clin Res 2017; 5:1098-1106; Hilfiker-Kleiner et al. Eur Heart J 2017;
38:2671-2679). Ongoing REBIRTH trial of 200 women with PPCM to further evaluate bromocriptine in PPCM on
myocardial recovery. ESC 2018 guidelines include Class IIb recommendation for bromocriptine; if used, must also
consider therapeutic AC in conjunction due to elevated thrombotic complication risk. Advanced therapies: 60% of
cardiogenic shock during or after pregnancy are related to PPCM (Banavan et al. Hypertens Pregnancy 2017; 36:117-
123). tMCS and ECMO should be considered early. Lactation: Current data suggest breastfeeding safe in PPCM, in
spite of stimulation of prolactin secretion (Koczo et al. JACC Basic Trans Science 2019; 4:291-300). Primary PPX for
sudden cardiac death: Because PPCM has higher likelihood of recovery of EF, important to avoid premature ICD;
consider wearable vest in severely reduced LVEF until recovery or ICD placement. Subsequent pregnancy: as
illustrated below, risk is stratified by recovery of EF; persistent systolic dysfunction portends high risk pregnancy.
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(illustrations from JACC State-of-the-Art Review - Davis et al. JACC 2020; 75(2) 207-221)
Prognosis: 46% of patients have LVEF recovery within 6 months of diagnosis (Hoes et al. Nat Rev Cardiol 2022; doi:
10.1038/s41569-021-00664-8). If LVEF normalizes post-partum, women still carry an increased risk of clinical HF, further
deterioration in LVEF and persistent LV dysfunction with a subsequent pregnancy. If LVEF does not normalize post-
partum, risks of HF, further deterioration of LVEF, persistent LV dysfunction are further increased, and importantly
maternal mortality is increased with subsequent pregnancy (Elkayam JACC 2011; 58 (7) 659–670). Women should be
carefully counseled about very high risks of further pregnancies (Davis et al. JACC 2020; 75(2) 207-221)
Hypertensive Disorders of Pregnancy
Disease Diagnostic Criteria

Gestational HTN ● New onset HTN after 20w gestation, SBP >=140 or DBP >=90 on at least 2 occasions 4
hours apart
● No proteinuria, no severe features of pre-eclampsia (see below)
Preeclampsia ● New onset HTN after 20w gestation, SBP >=140 or DBP >=90 on at least 2 occasions 4
(PEC) +/- hours apart
severe features ● Must have proteinuria OR in the absence of proteinuria one of the symptoms/labs below
o + Proteinuria: Spot UPro:Cr >=0.3, >=300 mg per 24h urine collection or urine dip
>=1 (if no other methods available) OR
o In the absence of proteinuria, one of the following: Plt <100k, Cr > 1.1 or 2x baseline
w/o other renal disease, ALT/AST> 2x ULN, pulmonary edema, persistent cerebral
or visual symptoms
● With severe features: SBP >=160 or DBP >110 on 2 occasions at least 4 hours apart
while patient on bed rest OR any of the above symptoms/labs (besides proteinuria)
Eclampsia ● PEC + generalized seizures that cannot be explained by other causes
HELLP ● HTN can be seen in patients with HELLP (hemolysis, elevated liver enzymes, low
syndrome platelets), but not always present nor required for diagnosis
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Chronic (pre- ● HTN diagnosed or present before 20w gestation (also if first diagnosed during
existing) HTN pregnancy and present for >12w post-partum)
Chronic HTN + ● Chronic HTN with sudden increase in BP that was previously well controlled, or
superimposed requiring escalation of anti-HTN regiment to control BP
PEC +/- severe ● New onset proteinuria or sudden increase in proteinuria if had prior to pregnancy
features ● See severe features above
Adapted from UTD Hypertensive Disorders of Pregnancy
Risk factors: personal history of PEC, chronic HTN, age, multiple gestation, obesity, race, diabetes, renal disease,
autoimmune disease.
Management:
Acute severe hypertension: reduce MAP by no more than 25% over 2h using IV labetalol 20 mg over 2 minutes
(hydralazine also OK but labetalol preferred), followed at 10 min interval doses of 20 to 80 mg up to max total cumulative
dose of 300 mg if BP remains above target, constant infusion can be used instead of intermittent therapy. If labetalol
alone ineffective ACOG recommends switching to hydralazine (and vice versa). Alternative options include nicardipine
and nifedipine. If PEC or Eclampsia 🡪 give IV mag sulfate in addition to anti-hypertensive medication. Call OB.
Chronic HTN 🡪 target is less than 140/90 mmHg (CHAP Trial Consortium, NEJM 2022; prior CHIPS 2015 trial suggested
strict versus lax BP control were equal, but underpowered for clinical outcomes). Meds: First line: labetalol and nifedipine.
Second line: hydralazine. Methyldopa less effective. If already on amlodipine or HCTZ, ok to continue. STOP ACEi, ARBs,
MRA for teratogenicity.
Risk reduction: ASA 81mg daily during 2T and 3T reduces PEC risk. USPTF Grade B recommendation for ASA after 12
weeks gestation (similar to ACOG recommendation for ASA).
Arrhythmias in Pregnancy
Incidence: Significant ectopy (PVC, paroxysmal SVT) common. In addition, variation of SVT most common, followed by
AF/AFL, VF/VT (overall 70 per 100,000) (Vaidya et al. Circulation 2017; 135(6):619-621).
Pathophysiology: hypothesized to be related to atrial stretch leading to irritated tissue and re-entrant arrhythmias.
Important to control arrhythmias due to risk of impaired fetal perfusion. Sustained tachycardia not well tolerated, especially
AFL.
Diagnosis and Management: diagnosis and treatment for arrhythmias in pregnancy follows same principles as in non-
pregnant patients. Pregnancy may reveal index case of underlying structural heart disease or inborn arrhythmia (e.g.
WPW, ARVC, HCM, etc.) Notable points: adenosine and cardioversion are safe. Catheter ablation is safe, better to delay
until late pregnancy or postpartum. Metoprolol, propranolol, verapamil, digoxin, lidocaine (fetal bradycardia), procainamide
are preferred agents; AVOID atenolol (fetal bradycardia, IUGR, highest risk among BB although risk is shared),
amiodarone (consider after 1T), dronedarone. Lactation: All passed into breast milk. Anticoagulation: Use CHAD2S2-
VASc. Unclear risk of stroke with limited data (ESC Guidelines On Management of Cardiovascular Diseases During
Pregnancy Eur Heart J 2011; 32(34):3147-97).
Pregnancy and Acute Coronary Syndrome
Key principle: The fundamentals of diagnosing ACS in pregnant patient are the same as in non-pregnant patient
There are some baseline EKG changes in pregnancy (ex: LAD 2/2 diaphragm elevation, TWI III and aVF, small Q in III)
but ST changes are never normal (Kealey et al. Can J Cardiology 2010; 26(6): 185-9)
Management of acute MI in pregnancy: See diagram below. Adapted from: Ismail et al Clinical Cardiology 2017;40:
399-406
In addition, low-dose ASA (81mg), Beta Blocker (Metoprolol preferred) is safe. NB: Despite the appropriate role of PCI in
early mgmt. of MI in pregnancy, coronary catheterization rates during pregnancy are lower than expected in ACS
(Cauldwell et al Heart 2019;105(3):189-195).
Special case: Spontaneous coronary artery dissection (SCAD): See 2018 2018 AHA Scientific Statement on
management of SCAD for further details
Most common cause of acute MI in pregnancy and most commonly occurs first week after delivery. Dx: Coronary
angiogram is recommended. Management: medical management may be preferred over invasive given risk of
propagating the dissection22 especially if there is only minimal distal coronary ischemia or preserved coronary flow. PCI v
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Cardio-Obstetrics
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CABG should be considered in patients with ongoing ischemia, hemodynamic instability, or LM disease (Hayes et al,
Circulation 2018; 137: e523-e557). Obtain arterial imaging from head to pelvis as there is an association between SCAD
and fibromuscular dysplasia. Prognosis: SCAD treated conservatively 95% of the time will heal in one month (JACC
State-of-the-Art Review. J Am Coll Cardiol 2020;76:961-984).
Troponin elevation (> 1 ng/ml highly suggestive of MI)

Diagnosis of AMI in CKMB elevation (>4x normal highly suggestive of MI
Pregnancy ECG with ST changes
TTE w/ regional wall motion abnormalities
Clopidogrel
Anti-Thrombin Low dose ASA (continue throughout delivery)
Therapy UFH (Argatroban for patients with history of HIT)
Peri-procedural GP IIb/IIa inhibitors in patients with prior MI,
high thrombus burden, complex PCI
Coronary angiography via

radial access for all pregnant
patients presenting with
STEMI
DES or BMS in the first two

Revascularization per standard clinical trimester
practice in those found to have BMS in the final trimester
atherosclerotic disease or coronary POBA with provisional stent
artery dissection in select cases* placement (less preferable)
188
TOC
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The Red Book

Housestaff Manual for Cardiology

Kevin Heist Rahul Sakhuja

Peyton Hanson, Erik Dove ACS and Ischemic Heart Disease

ARRHYTHMIAS AND ELECTROPHYSIOLOGY 62

INTRODUCTION TO INPATIENT CARDIOLOGY

Introduction to the Ellison 9 CCU:

Staffing Team Cap Case Mix

CCU Blue Team Roles:

Codes in the CCU:

Codes outside the CCU:

Tips for CCU Admission/ Presentation:

Tips for daily CCU rounds:

Admitting Team roles:

Rounding Team roles:

Overview of Cardiac Procedures Relevant to CCU/SDU Patients:

Coronary angiography +/- PCI:

Right Heart/Pulmonary Artery Catheterization

TAVR (Transcatheter aortic valve replacement):

Pulmonary vein isolation:

ACUTE CORONARY SYNDROMES AND ISCHEMIC HEART DISEASE

Joint Task Force Classification of Myocardial Infarction JACC 2018;72(18):2231-2264:

Erik Dove, Peyton Hanson

B. 12-lead ECG: 50% of patients with MI have a normal or non-

NSTEMI ECG Criteria: (Left) Right-sided leads, (Right) Posterior leads

STEMI ECG Criteria: (≥1 of the following)

Sgarbossa Criteria: Used to diagnose AMI in LBBB/Paced Rhythm

Localization of Injury (Zimetbaum et al. NEJM 2003;348)

STE >1 mm in aVR AND STE in aVR > V1

Other Notable ECG patterns:

B. Stable Ischemic Heart Disease

Glycoprotein IIb/IIIa inhibitors

B. Lipid Lowering Therapy

PCSK-9 inhibitors (evolocumab, alirocumab)

E. ACE-I and ARBs

● MOA: Reduction in pain decreases sympathetic activity

Coronary Angiography and Percutaneous Coronary Intervention (PCI)

B. Angiographic Nomenclature and Anatomy

Erik Dove, Peyton Hanson

Imaging the LCA:

RAO Caudal (LCA): RAO Cranial (LCA):

LAO Cranial (LCA): LAO Caudal (LCA,

LAO Cranial (RCA): Spine and catheter

C. Identifying Significant Lesions

PCI of Non-culprit Lesions

Assessment of Blood Flow Before & After Intervention:

Post-Cath Orders/Vascular Access Questions:

Sheaths and Removal:

Vascular Closure Devices (VCD):

Access Site Complications

Cardiopulmonary Bypass Grafting (CABG)

C. Concomitant Medical Therapy

Mechanical Complications (JACC 2013;61:e78, JACC 2019;12(18):1825-1836.)

Myocardial Infarction with Non-obstructive Coronary Arteries (MINOCA):

Spontaneous Coronary Artery Dissection (SCAD):

Cocaine-induced myocardial infarction

Discharge planning and outpatient management:

C. Lipid Lowering For Secondary Prevention

E. Adjunctive Medications on discharge

KEY PHYSIOLOGY CONCEPTS

Afterload: describes the force opposing LV ejection

HISTORY & INITIAL ASSESSMENT

Orthopnea Sensitivity: 22-50% Tachycardia Sensitivity: 7%