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Cardiovascular Summary Saunders Comprehensive Review For The Nclex RN Examination
Cardiovascular Summary Saunders Comprehensive Review For The Nclex RN Examination
Cardiovascular
Diagnostic Tests
Cardiac Markers
CK-MB - an elevation in value indicates
(creatinine myocardial damage
kinase, - an elevation occurs within hours and
myocardial peaks at 18 hours following an acute
muscle) ischemic attack
Normal value male: 2-6ng/mL
Normal value female: 2 to 5ng/mL
Troponin Values are low, any rise can indicate
myocardial cell damage
- troponin I: rises within 3 hours and
persists for up to 7-10 days (this one
is especially related to myocardial
injury) … less than 0.3ng/mL
- troponin T less than 0.2ng/mL
- serum levels of troponin T and I
increase 4-6 hours after the onset of
the MI, peak at 10-24 hours, and
return to baseline after 10-14 days
Myoglobin - myoglonin is an oxygen-binding
protein found in cardiac and skeletal
muscle
- the level rises within 2 hours after
cell death, with a rapid decline in the
level after 7 hours
- may not be cardiac specific
Hemocysteine
- elevated levels may increase the risk of cardiovascular disease
- normal value: 0.54 to 1.9 mg/L
Serum Lipids
- the lipid profile measures serum cholesterol, triglyceride, and lipoprotein levels
- lipid profile is used to assess the risk of developing coronary artery disease
- lipoprotein-a or Lp(a) increases atherosclerotic plaques and increases clots…. Normal
value should be less than 30mg/dl
Electrolytes
* electrolyte and mineral imbalances can cause cardiac electrical instability that
can result in life-threatening dysrhythmias
Potassium Hypokalemia
- causes increased cardiac electrical instability,
ventricular dysrhythmias, and increased risk of
digoxin toxicity
- ECG shows flattening and inversion of the T wave,
the appearance of a U wave, and ST depression
Hyperkalemia
- causes asystole and ventricular dysrhythmias
- ECG shows tall, peaked T waves, widened QRS,
or flat P waves
Sodium - the serum sodium level decreases with the use of
diuretics
- the serum sodium level decreases in heart failure,
indicating water excess
Calcium Hypocalcaemia
- can cause ventricular dysrhythmias, prolonged ST
and QT intervals, and cardiac arrest
Hypercalcemia
- can cause atrioventricular block, tachycardia or
bradycardia, digitalis hypersensitivity, cardiac arrest
Phosphorus - should be interpreted with calcium levels because
the kidneys retain or excrete one electrolyte in an
inverse relationship to the other
Magnesium - low level can cause ventricular tachycardia and
fibrillation
Diagnostic Procedures
Chest X-Ray
- done to determine anatomical changes such as size, silhouette, and position of the
heart
Holter Monitoring
- noninvasive test where the client wears a monitor and an electrocardiographic tracing
is recorded over 24 or more hours while the client performs their activities of daily living
- the monitor identifies dysrhythmias and evaluates the effectiveness of anti-dysrhythmic
or pacemaker therapy
Echocardiography
- non-invasive procedure that evaluates structural and functional changes in the heart
- used to detect vulvar abnormalities, congenital heart defects, cardiac function
Cardiac Catheterization
- an invasive test involving the insertion of a catheter into the heart and surrounding
vessels
- obtains information about the structure and performance of the heart chambers and
valves and the coronary circulation
Pre-procedure interventions:
- obtain informed consent
Post-procedure interventions:
- asses vitals and cardiac rhythms every 30 minutes for at least 2 hours
- assess peripheral pulses
- monitor chest pain
- notify HCP if patient complains of numbness and tingling, cool pale or cyanotic
extremities, or loss of peripheral pulses… emergency; could be a clot formation
- maintain strict bed rest for 6 to 12 hours
NOTE: Metformin must be held for 24 hours before any procedure involving iodine dye
because of the risk of lactic acidosis and the medication is not returned until prescribed
by the HCP
Cardiac Dysrhythmias
Management of Dysrhythmias
1. Vagal Maneuvers
Carotid sinus massage
- turn head away from the side
- massage over 1 carotid artery for a few seconds to determine whether a change in
cardiac rhythm occurs
- the client must be on a cardiac monitor (ECG) and get a rhythm strip before, during,
and after the procedure
Valsalva Maneuver
- HCP instructs the client to bear down or induces a gag reflex to stimulate a vagal
response
- monitor HR, rhythm, and BP
- rhythm strip before, during, and after
- provide an emesis basin if the gag reflex is stimulated
- have a defibrillator and resuscitative equipment available
2. Cardioversion
- cardioversion is a synchronized countershock to convert an undesirable rhythm to a
desirable one
Pre-procedure:
- if it is elective, ensure that informed consent is obtained
- administer sedation as prescribed
- if elective, hold digoxin for 48 hours
- if elective for atrial fibrillation or flutter, the client should receive anticoagulant therapy
for 4 to 6 week pre-procedure
During procedure:
- ensure skin is clean and dry in the area where the electrode pads/hands-off pads will
be placed
- stop oxygen during procedure to avoid fire hazard
- ensure that no one is touching the bed or client when delivering the countershock
Post-procedure:
- priority assessment includes ability of the client to maintain the airway and breathing
- resume oxygen administration
- assess vitals and level of consciousness
- monitor cardiac rhythm
- monitor for indications of successful response, such as conversion to a normal sinus
rhythm, strong peripheral pulses, adequate BP, and adequate urine output
3. Defibrillation
- used for pulseless ventricular tachycardia or fibrillation
- the defibrillator is charged to 360 joules for 1 countershock, then CPR is resumed
immediately and continued for about 2 minutes
- reassess the rhythm after 2 minutes, and if VF or VT continues, the defibrillator is
charged to give a second shock
NOTE: it is very important to ensure that oxygen is shut off before defibrillating and that
no one is touching the bed or the client
Until the defibrillator is attached and charged, the client is resuscitated with CPR. Once
the defibrillator has been attached:
check the ECG to ensure the proper rhythm is there (ventricular fibrillation or pulseless
ventricular tachycardia)
leads are checked for loose connections
nitroglycerin patch is removed from patient
patient does NOT have to be intubated
Pacemakers
Temporary or permanent device that provides electrical stimulation and maintains the
heart rate when the client’s intrinsic pacemaker fails to provide a perfusing rhythm
Synchronous (demand): senses the client’s rhythm and paces only if the client’s intrinsic
rate falls below the set pacemaker rate
Asynchronous (fixed): paces at a pre-set rate regardless of the client’s intrinsic rhythm
and is used when the client is asystolic or profoundly bradycardic
Temporary
Non-invasive transcutaneous pacing: used as a temporary emergency measure in the
profoundly asystolic or bradycardic paitent
- large electrode pads are placed on the chest and back and connected to an external
pulse generator
- wash skin with soap and water beforehand (no need to shave)
- place the posterior electrode between the spine and left scapula behind the heart
- place the anterior electrode between V2 and V5 over the heart
- do not place over breast tissue, but below it
- do not take pulse or BP on the left side... will not be accurate
Permanent
- pulse generator is internal and surgically implanted in a subcutaneous pocket below
the clavicle
- may be powered by a lithium battery with an average lifespan of 10 years or nuclear
powered with an average lifespan of 20 years
- pacemaker function can be checked in the HCP office by a pacemaker interrogator or
programmer from home, using a special telephone transmitter device
Client Teaching
Signs of battery failure and when to notify the HCP
Report any fever, redness, swelling, or drainage from the insertion site
Report signs of dizziness, weakness, fatigue, swelling of the ankles and legs,
chest pain, or shortness of breath
Keep a pacemaker identification card in the wallet and wear a MedicAlert
bracelet
Instruct patient how to take pulse, to take the pulse daily, and to maintain a
diary of daily pulse rates
Wear loose-fitting clothing over the pulse generator site
Inform airport security
Most electrical appliances can be used without any interference, however, do
not operate electrical appliances directly over the site
Avoid contact sports
Avoid transmitter towers and anti-theft devices in stores
If any unusual feeling occurs when near any electrical devices, move 5 to 10
feet away and check the pulse
Use cellphones on side opposite the pacemaker
It develops over time; many years. When symptomatic, the disease process is usually
well advanced; symptoms occur when the coronary artery is occluded to the point that
inadequate blood supply to the muscle occurs, causing ischemia. Goal of treatment:
alter the atherosclerotic progression.
Risk Factors
Unmodifiable:
age
gender (men > women until 60yr)
ethnicity (African American > Caucasian)
genetic predisposition
family history of heart disease
Modifiable:
increased serum lipids
hypertension
cigarette smoking
obesity
physical inactivity
diabetes mellitus
stressful lifestyle
psychosocial state
homocysteine level
metabolic syndrome
Assessment
possibly normal findings during asymptomatic periods
chest pain
palpitations
dyspnea
syncope
cough or hemoptysis
excessive fatigue
Interventions
assist the client to identify modifiable risk factors and to set goals to reduce the impact
of risk factors
assists to identify barriers to compliance
instruct about low-calorie, low-sodium, low-cholesterol, low-fat diet with increased fiber
stress the importance that dietary changes are not temporary and must be maintained
for life
provide community resources regarding exercise, smoking cessation, and stress
reduction
Medications
nitrates – dilate the coronary arteries and decrease preload and afterload
calcium channel blockers – dilate coronary arteries and reduce vasospasm
cholesterol lowering drugs – reduce the development of atherosclerotic plaque
beta blockers – reduce BP in those who are hypertensive
lipid lowering drugs
Diagnostic Studies
Electrocardiography
- when blood flow is reduced and ischemia occurs: ST depression, T wave inversion, or
both is noted… ST segment returns to normal when the blood flow returns
Cardiac Catheterization
- shows the presence of atherosclerotic lesions
Angina
Types
1. Stable angina – aka exertional angina
- occurs with activities that involve exertion or emotional stress
- relieved with rest or nitroglycerin
- usually has a stable pattern of onset, duration, severity, and relieving factors
4. Intractable angina
- chronic, incapacitating angina unresponsive to treatment
5. Preinfarction angina
- associated with acute coronary insufficiency
- lasts longer than 15 minutes
- symptoms of worsening cardiac ischemia
- characterized by chest pain that occurs days to weeks before an MI
Precipitating Factors
physical activity
temperature extremes
strong emotions
consumption of heavy meal
cigarette smoking
sexual activity
stimulants
circadian rhythm patterns
Assessment
pain
- usually described as mild or moderate
- substernal, crushing, squeezing
- may radiate to the shoulders, arms, jaw, neck, or back
- pain intensity is unaffected by inspiration and expiration
- pain usually lasts less than 5 minutes, but can last up to 15 to 20
- pain is relieved by nitroglycerin
dyspnea
pallor
sweating
palpitations and tachycardia
dizziness and syncope
hypertension
digestive disturbances (indigestion)
Interventions
IMMEDIATE:
assess pain and institute pain relief measures
administer oxygen by nasal cannula
assess vitals and provide continuous cardiac monitoring and nitroglycerin to dilate the
coronary arteries
ensure that bed rest is maintained and that patient is in semi-Fowlers
Diagnostic Studies
Electrocardiography
- readings are normal during rest – ST depression or T wave inversion during acute
episode
Stress Testing
- chest pain or changes in the ECG or vital signs during testing may indicate ischemia
Cardiac Catheterization
- provides a definitive diagnosis by providing information about the patency of the
coronary arteries
Medications
antiplatelets (ASA) – reduces risk of MI
b-adrenergic blockers (Lopressor)
nitrates (nitrostat, isordil)
Causes
thrombus
occlusion
coronary artery spasm
hypoxemia
Risk Factors
atherosclerosis
CAD
high cholesterol
smoking
hypertension
obesity
physical inactivity
Symptoms
severe, immobilizing chest pain not relieved by rest, position change, or nitrates
pain may occur while active, at rest, or sleeping; most common in early am
heaviness, pressure, tightness, burning, constricting, or crushing
substernal, retrosternal, or epigastric locations
radiation to neck, jaw, arms, or back
occasionally fever
pain lasts 30 minutes or longer
nausea and vomiting
diaphoresis
dyspnea
dysrhythmias
feelings of fear/anxiety/impending doom
pallor, cyanosis, grey/ashen, coolness of extremities
OR…. Patient can be asymptomatic, have atypical discomfort, or diabetic clients may
not feel severe pain because cardiac neuropathy
Diagnostic Studies
Troponin: level rises within 3 hours and remains elevated for up to 7-10 days
Total CK: rises within 6 hours after the onset of chest pain and peaks within 18 hours
after death of cardiac tissue
CK-MB: peak elevation occurs 18 hours after the onset of chest pain and returns to
normal 48-72h later
WBC: elevated wbc count appears on the second day following the MI and lasts up to 1
week
ECG: shows either ST elevation, T wave inversion, or non-ST elevation with an
abnormal Q wave
- hours to days afterward, the ST and T wave changes will return to normal, but Q wave
changes are usually permanent
Interventions – ACUTE
1. obtain a description of chest discomfort
2. Administer O2 and institute pain relief measures (morphine and nitroglycerin)
3. Assess vitals and cardiovascular status and maintain cardiac monitoring
4. Assess respiratory rate and breath sounds for signs of HF
5. Ensure bed rest and place in semi-Fowler’s
6. Establish IV access
7. Obtain 12-lead ECG
8. Monitor laboratory values
9. Monitor for cardiac dysrhythmias (particularly tachycardia and PVCs)
10. Administer thrombolytic therapy (within first 6 hours) and monitor for bleeding
11. Assess distal peripheral pulses and skin temperature
12. Monitor BP closely – if systolic is lower than 100 or 25mm lower than last reading,
lower the head of bed and notify the HCP
13. Administer beta blockers
NOTE: Pain relief increases oxygen supply to the myocardium; administer morphine as
a priority in managing pain in the client having an MI
Cardiogenic shock is a complication that can occur following an MI; it occurs with
severe damage to the left ventricle.
Classic signs:
hypotension
rapid pulse that becomes weaker
decreased urine output
cool, clammy skin
increased respiratory rate
NOTE: It is important that the nurse assess the patient developing cardiogenic shock
after an MI for ventricular dysthymias
Heart Failure
The inability of the heart to pump sufficient blood to maintain adequate cardiac output to
meet the metabolic needs of the body. Diminished cardiac output = inadequate
peripheral tissue perfusion. *Congestion of the lungs and periphery may occur; the
client can develop acute pulmonary edema.
Compensatory Mechanisms
act to restore cardiac output to near-normal levels
initially, these mechanisms increase cardiac output, but they eventually have a
damaging effect on pump action
examples:
- increased HR
- improved stroke volume
- arterial vasoconstriction
- sodium and water retention
- myocardial hypertrophy
NOTE: signs of left ventricular failure are evident in the pulmonary system; signs of right
ventricular failure are evident in the systemic circulation
Pulmonary Edema
Clinical Manifestations
severe dyspnea
tachycardia
tachypnea
nasal flaring or use of accessory breathing muscles
wheezing and crackles
gurgling respirations
expectoration of large amounts of blood-tinged frothy sputum
acute anxiety and restlessness
cold, clammy skin
cyanosis
The client is immediately placed in a high Fowler’s position, with legs in a dependent
position, to reduce pulmonary congestion and relieve edema. Oxygen is always
prescribed, usually in high concentration, to improve gas exchange and pulmonary
function.
furosemide, a rapid acting diuretic, will eliminate accumulated fluid
morphine sulfate reduces venous return (preload), decreases anxiety, and also
reduces the work of breathing
Foley measures output accurately
weight measurement will also determine response to treatment
digoxin may increase ventricular contractility and enhance stroke volume
Fluids decreased
Afterload decreased
Sodium restriction
Test (digoxin, ABGs, K+)
Cardiogenic Shock
Failure of the heart to pump adequately, thereby reducing cardiac output and
compromising tissue perfusion; necrosis of more than 40% of the left ventricle occurs
which usually results from occlusion of major coronary vessels.
Early Manifestations
hypotension (lower than 90mm systolic)
tachycardia
narrowed pulse pressure
increased myocardial oxygen consumption
As shock progresses
urine output lower than 30ml/hr
cold, clammy skin
poor peripheral pulses
tachypnea
pulmonary congestion
disorientation
restlessness
confusion
continuing chest discomfort
decreased capillary refill time
Interventions
1. Administer O2
2. Administer morphine sulfate IV (decrease pulmonary congestion and relieve pain)
3. Prepare for intubation and mechanical ventilation
4. Administer diuretics and nitrates while constantly monitoring BP
5. Administer vasopressors and positive inotropes to maintain organ perfusion.
6. Prepare for insertion of an intraaortic balloon pump to improve coronary artery
perfusion and cardiac output
7. Prepare for immediate reperfusion procedures such as PTCA or coronary artery
bypass graft.
8. Monitor urinary output.
11. Monitor distal pulses.
Hemodynamic Monitoring
Central Venous Pressure – the pressure within the superior vena cava
- measured with a central venous line in the superior vena cava
- normal: 3 to 8 mmHg
- high: indicates an increase in blood volume (from sodium and water retention,
excessive IV fluids, kidney failure)
- low: decrease in circulating blood volume (from fluid imbalances, hemorrhage, severe
vasodilation); may see pooling or blood in the extremities
Endocarditis
Inflammation of the inner lining of the heart and valves. Ports of entry for the infecting
organism include the oral cavity (especially if the client had a dental procedure in the
previous 6 months), infections (genitourinary, cutaneous, GI, systemic), and surgery or
invasive procedures, such as IV line placement.
Risk Factors
IV drug users
clients who have had valve replacements or repair of valves with prosthetic materials
other structural cardiac defects
Clinical Manifestations
fever
anorexia and weight loss
cardiac murmurs
heart failure
embolic complications
petechiae
splinter hemorrhages in the nail beds
Osler’s nodes (reddish, tender lesions) on the pads of the fingers, hands, and toes
Janeway lesions (nontender hemorrhagic lesions) on the fingers, toes, nose, or
earlobes
splenomegaly
clubbing of the fingers
Interventions
provide adequate rest balanced with activity to prevent thrombus formation
maintain antiembolism stockings
monitor for signs of heart failure
monitor for splenic emboli (sudden abdominal pain radiating to the left shoulder and
the presence of rebound abdominal tenderness on palpation)
monitor for renal emboli (flank pain radiating to the groin)
monitor for confusion, aphasia, or dysphasia (CNS emboli)
monitor for pulmonary emboli (dyspnea, chest pain, cough)
assess skin, mucous membranes, and conjunctiva for petechiae
Pericarditis
Acute or chronic inflammation of the pericardial sac and the outer fibrous layer. It is
most often idiopathic; coxsackievirus B group most common.
Other causes:
- uremia
- bacterial infection
- acute MI
- tuberculosis
- neoplasm
- trauma
Clinical Manifestations
pericardial friction rub – hallmark finding; heard on auscultation
progressive, severe chest pain (worse with deep inspiration and supine, relieved by
sitting and leaning forward, radiates to trapezius muscle)
dyspnea
fever and chills
fatigue and malaise
elevated WBC
atrial fibrillation is common
signs of right ventricular failure in clients with chronic pericarditis
Interventions
place in high Fowler’s or upright and leaning forward
administer oxygen
administer analgesics, NSAIDs, or corticosteroids for pain
auscultate for pericardial friction rub
check results of blood culture to identify causative organisms
administer antibiotics
administer diuretics and digoxin
monitor for signs of cardiac tamponade and notify HCP if it may occur
Complications
pericardial effusion
- accumulation of excess fluid in the pericardium
- cough, dyspnea, tachypnea
cardiac tamponade
accumulation of fluid in pericardial sac
Cardiac Tamponade
Symptoms
hypotension
narrowed pulse pressure
JVD with clear lung sounds
pulsus paradoxus
muffled heart sounds
decreased cardiac output
Interventions
1. Transfer to critical care unit for hemodynamic monitoring
2. Administer IV fluids to manage decreased cardiac output
3. Prepare for CXR or echocardiography
4. Prepare for pericardiocentesis to withdraw pericardial fluid; monitor for recurrence of
cardiac tamponade
- blood pressure should increase almost immediately after procedure
5. If the client continues to experience recurrent tamponade, a portion or all of the
pericardium may be removed to allow adequate ventricular filling and contraction.
Rheumatic Fever
Rheumatic fever: inflammatory disease that may affect connective tissues of the body.
Rheumatic heart disease: chronic condition resulting from rheumatic fever.
Acute rheumatic fever: complication that occurs as a delayed sequela (2-3 weeks) to
group A streptococcal pharyngitis; found primarily in young adults
Clinical Manifestations
chest pain
excessive fatigue
palpitations
thumping sensation in the chest
SOB
edema
Aschoff’s bodies
extracardiac lesions (connective tissue, joints, skin, and CNS)
Assessment
malaise
anorexia
palpitations
ataxia
chest and abdominal pain
low-grade fever
subcutaneous nodules
chorea
polyarthritis
Interventions
no single diagnostic test
treatment – drug therapy and supportive measures
Valvular heart disease occurs when the heart valves cannot open fully (stenosis) or
close completely (regurgitation).
Cardiomyopathy
A group of diseases that directly affect the structural or functional ability of the
myocardium; can be primary or secondary. Treatment is palliative, not curative, and the
client needs to deal with numerous lifestyle changes and a shortened lifespan.
Symptoms
Non-obstructed Obstructed Restrictive
dyspnea Same as non-obstructed, dyspnea
angina but with mitral regurgitation fatigue
fatigue murmur and atrial right sided HF
syncope fibrillation S3 and S4 gallops
palpitations heart block
S4 gallop Treatment emboli
ventricular dysrhythmias symptomatic
sudden death common beta blockers Treatment
conversion of a fib supportive
Vascular Disorders
Venous Thrombosis
Types
Thrombophlebitis: thrombus associated with inflammation
Phlebothrombosis: thrombus without inflammation
Phlebitis: vein inflammation associated with invasive procedures, such as IV lines
Deep vein thrombophlebitis: more serious than superficial; risk of pulmonary embolism
Phlebitis
red, warm area radiating up the vein and extremity
pain and swelling
apply warm, moist soaks to dilate the vein and promote circulation
assess for signs of complications such as tissue necrosis, infection, or PE
Interventions
provide bed rest
Patient Education
hazards of anticoagulation therapy
signs and symptoms of bleeding
avoid prolonged sitting or standing, constrictive clothing, or crossing the legs when
seated
elevate the legs for 10 to 20 minutes every few hours
plan a progressive walking program
inspect the legs for edema, measure circumference of the legs
wear antiembolism stockings
avoid smoking
avoid medications unless prescribed by HCP
obtain and wear a MedicAlert bracelet
Venous Insufficiency
Results from prolonged venous hypertension, which stretches the veins and damages
the valves. The resultant edema and venous stasis cause venous stasis ulcers,
swelling, and cellulitis. Treatment focuses on decreasing edema and promoting venous
return from the affected extremity. Treatment for venous stasis ulcers focuses on
healing the ulcer and preventing stasis and ulcer recurrence.
Assessment
stasis dermatitis or brown discoloration along the ankles, extending up to the calf
edema
ulcer formation: edges are uneven, ulcer bed is pink, and granulation is present;
usually located on the lateral malleolus
Interventions
NOTE: for venous insufficiency, leg elevation is usually prescribed to assist with the
return of blood to the heart
compression stockings during the day and evening (on awakening before getting out
of bed); may be lifelong
Wound Care
assess the patient’s ability to care for the wound and initiate home care resources as
necessary
if an Unna boot (dressing constructed of gauze with zinc oxide) is prescribed, the HCP
will change it weekly
the wound is cleansed with normal saline before application of the Unna boot (iodine
and hydrogen peroxide are not used because they destroy granulation tissue)
the Unna boot is covered with an elastic wrap that hardens to promote venous return
and prevent stasis
monitor for signs of arterial occlusion from the Unna boot being too tight
keep tape OFF the client’s skin
occlusive dressings such as polyethylene film or a hydrocolloid dressing may be used
to cover the ulcer
Medications
apply topical agents to the wound as prescribed to debride the ulcer, eliminate necrotic
tissue, and promote healing
when applying topical agents, apply an oil-based agent such as petroleum jelly on
surrounding skin, because debriding agents can injure healthy tissue
administer antibiotics if infection of cellulitis occurs
Varicose Veins
Assessment
pain in the legs with dull aching after standing
vein walls weaken and dilate, and valves become incompetent
Trendelenburg Test
place the patient in a supine position with the legs elevated
when the client sits up, if varicosities are present, veins fill from the proximal end;
veins normally fill from the distal end
Interventions
emphasize the importance of antiembolism stockings as prescribed
instruct to elevate the legs as much as possible
instruct to avoid constrictive clothing and pressure on the legs
prepare for sclerotherapy or vein stripping as prescribe
Sclerotherapy
a solution is injected into the vein, followed by the application of a pressure dressing
incision and drainage od the trapped blood in the sclerosed vein is performed 14 to 21
days after the injection, followed by the application of a pressure dressing for 12 to 18
hours
Laser therapy – a laser fiber is used to heat and close the main vessel contributing to
the varicosity
Vein stripping – varicose veins may be removed if they are larger than 4mm in
diameter or if they are in clusters (other treatments are usually attempted before this)
Arterial Disorders
Conditions affecting the arteries in the neck, abdomen, and extremities. Tissue damage
occurs below the level of the arterial occlusion. Atherosclerosis is the most common
cause of PAD.
Assessment
intermittent claudication (pain in the muscles resulting from an inadequate blood
supply) – classic symptom
rest pain, characterized by numbness, burning, or aching in the distal portion of the
lower extremities
- this awakens the patient at night, but is relieved by placing the extremity in the
dependent position (dangling)
lower back or buttock discomfort
loss of hair and dry scaly skin on the lower extremities
thickened toenails
cold and gray-blue colour of skin in the lower extremities
decreased or absent peripheral pulses
elevation pallor and dependent rubor in lower extremities
signs of arterial ulcer formation occurring on or between the toes or on the upper
aspect of the foot that are characterized as painful
BP measurements at the thighs, calf, and ankle are lower than the brachial pressure
(normally these readings are higher than those in upper extremities)
in males, may have some degree of sexual dysfunction
NOTE: Because swelling in the extremities prevents arterial blood flow, the client with
PAD is instructed to elevate the feet at rest but to refrain from elevating them above the
level of the heart, because extreme elevation slows arterial blood flow to the feet. In
severe cases, clients with edema may sleep with the affected limb hanging from the bed
or they may sit upright in a chair for comfort.
Interventions
1. Assess pain
2. Monitor the extremities for color, motion and sensation, and pulses.
3. Obtain BP.
4. Assess for signs of ulcer formation or gangrene
5. Assist with developing an individualized exercise program, which in initiated gradually
and increased slowly, will improve arterial flow
6. Instruct to walk to the point of claudication, stop and rest, then walk a little further
7. Avoid crossing the legs (interferes with blood flow)
8. Avoid exposure to cold (causes vasoconstriction) to the extremities and to wear
socks or insulated shoes for warmth at all times
9. NEVER apply direct heat to the limb (e.g. heating pad or hot water) because the
decreases sensitivity in the limb can cause burning
10. Inspect skin daily and report signs of breakdown
11. Avoid tobacco and caffeine.
Raynaud’s Disease
Episodic vasospastic disorder of small cutaneous arteries, most frequently fingers and
toes. Vasospasm causes constriction of the cutaneous vessels. Attacks are intermittent
and occur with exposure to cold or stress. Cause is unknown. Characterized by
vasospasm-induced colour changes to the fingers, toes, ears, and nose (blue, white, or
red).
Assessment
blanching of extremity, followed by cyanosis during constriction
reddened tissue when the vasospasm is relieved
numbness, tingling, swelling, and a cold temperate at the affected site
Interventions
monitor pulses
administer vasodilators
medication therapy
avoid cold and stress
avoid smoking
wear warm clothing, socks, and gloves in cold weather
avoid injuries to fingers and hands
Buerger’s Disease
Occlusive disease of the median and small arteries and veins. The distal upper and
lower limbs are affected most commonly.
Assessment
intermittent claudication
ischemic pain occurs in the digits while at rest
aching pain that is more severe at night
cool, numb, or tingling sensation
diminished pulses
extremities that are cool and red in the dependent condition
development of ulcerations in the extremities
Interventions
monitor pulses
administer vasodilators
medication therapy
avoid cold and stress
avoid smoking
wear warm clothing, socks, and gloves in cold weather
avoid injuries to fingers and hands
Aortic Aneurysms
Abdominal dilation of the arterial wall caused by localized weakness and stretching in
the medial layer or wall of the aorta. The aneurysm can be located anywhere along the
abdominal aorta. The goal of treatment is to limit the progression of the disease by
modifying risk factors, controlling BP, recognizing symptoms early, and preventing
rupture. Occurs in men more often than women and incidence increases with age. Male
gender and smoking are stronger risk factors than hypertension and diabetes. Most
common cause = atherosclerosis.
Types of Aneurysms
Thoracic pain extending to neck, shoulders,
lower back, or abdomen
syncope
dyspnea
increased pulse
cyanosis
hoarseness
difficulty swallowing
Abdominal prominent, pulsating mass in
abdomen, at or above the umbilicus
bruit may be auscultated over the
aorta
tenderness on deep palpation
abdominal or lower back pain
Diagnostic Testing
Done to confirm the presence, size, and location of the aneurysm:
abdominal ultrasound
CT
arteriography
MRI
ECG – to rule out an MI
chest x-ray – to see mediastinal silhouette and any abnormal widening of thoracic
aorta
Interventions
Goal: prevent aneurysm from rupturing
Early detection and treatment imperative
Small aneurysm: conservative treatment
Greater than 5.5cm is the threshold for repair
monitor vital signs
assess for back or abdominal pain
assess for the sensation of pulsation in the abdomen
check peripheral circulation – pulses, temperature, colour
observe for signs of rupture
note any tenderness over the abdomen
monitor for abdominal distention
administer antihypertensives to maintain the BP within normal limits and to prevent
strain on the aneurysm
if ruptured, emergent surgical intervention is required (33-94% mortality)
NOTE: it is crucial to instruct the client with an aortic aneurysm to report immediately
the occurrence of chest or back pain, shortness of breath, difficulty swallowing, or
hoarseness.
Aortic Dissection
Not a type of aneurysm, occurs most commonly in the thoracic aorta. Acute and life-
threatening; mortality rate of 90% if not surgically repaired. A tear in intimal lining allows
blood to track between intima and media, so as the heart contracts, each systolic
pulsation increases pressure on the damaged area, further increasing dissection. May
occlude major branches of the aorta, cutting off blood supply to the brain, abdominal
organs, kidneys, spinal cord, and extremities.
Clinical Manifestations
Pain
- characterized as sudden, severe pain in the anterior part of the chest
- may also be intrascapular pain radiating down the spine to the abdomen
- described as tearing or ripping
- may mimic that of an MI
- as dissection progresses, pain is felt above and below diaphragm
Cardiovascular, neurological, and respiratory symptoms
- if aortic arch is involved, patient will have neurological deficiencies
Complications
Cardiac Tamponade
- severe life-threatnening complication that occurs when blood escapes from dissection
into the pericardial sac
- symptoms include: hypotension, narrowed pulse pressure, distended neck veins,
muffled heart sounds, pulsus paradoxus
Preoperative
assess all peripheral pulses as a baseline for comparison postoperatively
assess neurological status for comparison
teach deep breathing and coughing exercises
Postoperative
monitor vitals
monitor peripheral pulses distal to the graft site
monitor for signs of graft occlusion – changes in pulses, cool extremities below the
graft, white or blue extremities or flanks, severe pain, abdominal distention
limit elevation of the head of the bed to 45 degrees to prevent flexion of the graft
monitor for hypovolemia and kidney failure resulting from severe blood loss during
surgery
monitor urine output hourly, report urine output less than 30-50ml/hr
monitor serum creatinine and BUN daily
monitor respiratory status and auscultate lung sounds
encourage turning, coughing, and deep breathing while splinting the incision
ambulate as prescribed
do not lift objects heavier than 15 to 20 pounds for 6 to 12 weeks
avoid activities requiring pushing, pulling, or straining
do not drive a vehicle until indicated by HCP
Postoperative
monitor vitals, renal, and neurological status
monitor for signs of hemorrhage – e.g. drop in BP and increase in HR an respirations
monitor chest tube for an increase in chest drainage, which may indicate bleeding or
separation at the graft site
assess sensation and motion of all extremities and notify the HCP immediately if
deficits are noted, which can occur because of a lack of blood supply to the spinal cord
during surgery
monitor respiratory status
do not lift objects heavier than 15 to 20 pounds for 6 to 12 weeks
avoid activities requiring pushing, pulling, or straining
do not drive a vehicle until indicated by HCP
Embolectomy
The removal of an embolus from an artery with the use of a catheter.
Preoperative
obtain baseline vascular assessment
administer anticoagulants and thrombolytics
place a bed cradle on the bed
avoid bumping the bed
place the extremity in a slightly dependent position
Postoperative
monitor affected extremity for colour, temperature, and a pulse
assess sensory and motor function of the affected extremity
monitor for signs of a new thrombi or emboli
administer oxygen
monitor pulse oximetry
monitor for edema, pain on passive movement, poor capillary refill, numbness – signs
of swollen skeletal muscles
avoid prolonged standing or sitting and elevate the legs when sitting
wear antiembolism stockings
ambulate daily
hazards of anticoagulation therapy
CRITICAL THINKING
A. The nurse should suspect a rupture, which is a surgical emergency, and immediately
contact the HCP. The nurse should also obtain information about the back pain, stay
with the client, monitor vital signs and neurological status, and provide support. Other
signs of rupture include severe abdominal pain or fullness, soreness over the umbilicus,
and a sudden development of discolouration in the extremities.
Hypertension
Hypertension is a major risk factor for coronary, cerebral, renal, and peripheral vascular
disease. It is usually asymptomatic initially; since it goes unnoticed, it goes on for longer
periods of time and can ultimately cause damage to target organs. Prevalence
increasese with age, in less educated patients, men > female until age 55, then women
> men.
Primary Hypertension
Elevated BP without an identifying cause; accounts for 90 to 95% of all cases.
Contributing Factors:
increases SNS activity
aging
family history
African American race
obesity
smoking
greater than ideal body weight
diabetes
excessive alcohol intake
increase intake of salt and caffeine
Clinical Manifestations
called the “silent killer” as it is asymptomatic until it becomes severe and target organ
disease has occurred
fatigue
reduced activity tolerance
dizziness
palpitations
angina
dyspnea
flushed face
epistaxis
visual disturbances
Secondary Hypertension
Elevated BP with a specific cause that often can be identifies and corrected; 5 to 10% in
adults and 80% in children.
Interventions
obtain BP 2 or more times on both arms, supine and standing
compare BP with prior documentation
identify current medication therapy
obtain weight
evaluate nietary patterns and sodium intake
assess for visual changes or retinal damage
assess for cardiovascular changes such as JVD or dysrhythmias
periodic monitoring of BP; every 3-6 months once it is stable
Nonpharmacological Interventions
weight reduction if necessary
dietary sodium restriction to 2g daily
moderate to reduced intake of alcohol and caffeine
exercise
smoking cessation
relaxation techniques
biofeedback therapy
elimination of unnecessary medications that may contribute
Client Education
Importance of compliance
Disease process (esp. that symptoms usually do not develop until organs
have suffered damage)
Regular exercise program; avoid heavy weight lifting
Express feelings about daily stress and identify ways to reduce stress
Relaxation techniques
Teach the technique for monitoring BP
Maintain a diary of daily BP readings
Emphasise the importance of lifelong medication
Dietary restrictions – sodium, fat, calories, cholesterol
How to shop for and prepare low-sodium meals
Provide with a lsit of products containing sodium
Read labels to determine sodium content – sodium, NaCl, or MSG
(monosodium glutamate)
Bake, roast, or boil foods; avoid salt in preparation of meals
Fresh foods are the best to consume; avoid canned
Actions, side effects, and scheduling of medications
Avoid OTC medications
Stress the importance of follow-up care
Hypertensive Crisis
A severe and abrupt elevation in blood pressure (diastolic greater than 120-130). Acute
and life-threatening condition requiring immediate emergency treatment because target
organ damage can occur quickly (brain, heart, kidneys, eyes [retina]).
Clinical Manifestations
headache
nausea and vomiting
drowsiness and confusion
seizures
blurred vision
stupor
changes in neurological status
tachycardia and tachypnea
diaphoresis
transient blindness
renal impairment
chest pain
dyspnea
back pain
cyanosis
* may be mistaken for a stroke patient, but unlike with a stroke, the patient does NOT
present with unilateral or focal signs
Interventions
1. Maintain a patent airway.