Heart Failure

Heart Failure Overview
• It is a progressive condition in which the heart is unable to pump enough blood into
circulation to meet the body’s needs
• It is often caused by ineffective contraction and relaxation
• It is frequently a long-term effect of CAD and MI when left ventricular damage is
extensive enough to impair CO
• As a result, CO falls, body’s needs are not met, leading to decreased tissue perfusion
Normal Pathophysiology of Blood Flow Through Heart

• Depends on the following:
Ø Strength & pumping action of cardiac muscle.
Ø Amount of blood pumped from ventricles in 1 minute (CO).
Ø Ability of ventricles to work together relies on adequate functional muscle mass
of each ventricle, which CO depends on.
Ø Amount of blood available to move forward through heart.
Ø Cardiac Reserve – ability of heart to increase amount of cardiac output (CO) as
needed – as oxygen demands increase, so does CO
• HR & SV (volume of blood ejected w each heartbeat) – are influenced by autonomic
nervous system.
• Increased HR, increases CO.
• Ejection fraction - is an important measurement of heart’s effectiveness.
Ø Normal ejection fraction is 50%-70% (average is 60%).
Pathophysiology: when the heart fails…

• Compensatory mechanisms – initially kick in to restore tissue perfusion.
Ø Resulting in vascular congestion (hence the term congestive heart failure).
Ø Once they are exhausted, heart failure occurs, with ↑’ed morbidity & mortality.
• CO, SV, & ejection fraction all decrease.
• Frank-Starling mechanism
Ø ↓’ed CO stimulates aortic baroreceptors, which stimulate SNS.
Ø Norepinephrine is released causing ^HR & ^SV = ^CO
• Neuroendocrine response
Ø ↓’ed renal perfusion causes renin release from kidneys.
Ø Renin angiotensin system releases aldosterone and ADH which are responsible
for further vasoconstriction and sodium and water retention
Ø This results in an increased vascular volume which causes and increased force of
contraction – improving CO
Ø Renin-angiotensin system is counterbalanced by ANP and BNP – promote sodium
and water excretion and inhibit release of norepinephrine, renin and ADH
• Myocardial hypertrophy
Ø Increased muscle mass and cardiac wall thickness.
Ø Heart chambers dilate and stretch.
Ø Ventricular hypertrophy occurs
HF: Classifications:
Systolic Vs. Diastolic
• Systolic Failure:
Ø Ventricles fail to contract to eject enough blood into the arterial system.
Ø Affected by loss of myocardial cells due to ischemia/infarction, cardiomyopathy
and inflammation.
• Diastolic Failure:
Ø The heart can not completely relax in diastole which disrupts normal filling
Ø Coronary arteries can not receive an adequate blood supply.
Left sided vs right sided HF

• Left-sided Failure:
Ø Coronary heart disease (CAD) and hypertension are common causes.
Ø Left-sided can lead to right-sided failure.
Ø Decreased blood ejected from the weakened left ventricle, blood backs up into
pulmonary circulation.
Ø This will force fluids into the alveoli.
Ø Pulmonary congestion leads to pulmonary edema.
• Right-sided Failure:
Ø Caused by conditions that restrict blood flow to the lungs such as pulmonary
disease.
Ø Impaired ability to pump blood into the pulmonary circulation.
Ø The right side of the heart distends, blood accumulates in the systemic venous
system.
Ø Abdominal organs become congested and peripheral tissue edema to develop
(feet/ankles).
Acute vs Chronic
• Acute - the abrupt onset of myocardial injury.
• Chronic - a progressive deterioration of the heart muscle function.
Ø 4 stages of HF: each becomes a little more progressive
Ø Stage 1 – mild - no limitations on physical activity – no sob or other s/s
Ø Stage 2 – mild – some physical limitations – fatigue, mild sob, mild palpitations;
comfortable at rest
Ø Stage 3 – increased physical limitations – cannot do normal activities – sob, easily
fatigued; symptoms subside with rest
Ø Stage 4 – severe - physical activity is extremely limited; often palpitations, severe
sob even at rest
Pulmonary Edema
• Abnormal accumulation of fluid in the interstitial tissue and alveoli of the lungs
• Impairs and interferes with gas exchange
• Common consequence of heart failure, which is a sign of severe cardiac
decompensation.
Ø Decompensation – is failure of compensatory mechanisms to restore tissue
perfusion.
Ø It is a medical emergency.
Ø Onset may be acute, or it can progress gradually to severe respiratory distress.
Ø Immediate treatment is needed.
Etiology/Risk Factors
• 5.7 million people in the US have heart failure.
• At risk populations:
• Over 65 years of age
• African Americans – more at risk because of hypetension
• Obesity
• History of CAD, hypertension, valve disorders, congenital disease, diabetes, MI,
severe lung disease.
• Cigarette smoking, substance abuse
• Sleep apnea
Prevention
• Controlling/avoiding the risk factors is major.
• Engage in health-promoting behaviors – activity, diet, stress
• Take prescribed medications as ordered.
Clinical Manifestations
Left-sided Failure
• Fatigue and activity intolerance
• Dizziness & syncope
• Dyspnea, SOB, & cough
• Orthopnea (difficulty breathing in supine position)
• Elevate HOB, encourage use of 2/3 pillows
• Cyanosis – from impaired gas exchange
• Inspiratory crackles (rales), wheezing
Right-sided Failure:
• Edema of legs and feet
• Edema of sacral area if bedridden
• Nausea or anorexia
• Right upper quadrant abdominal pain
• Neck vein distension
Other Manifestations
• Weight gain – due to increased salt and water retention
• Nocturia – urinating 2-3 times a night
• Paroxysmal nocturnal dyspnea – frightening, abrupt onset of extreme SOB in the night
• Results from fluid overload and pulmonary congestion
• Dyspnea on exertion and rest
Complications
• Hepatomegaly – enlarged liver - diagnosed with liver enzyme/function tests
• Splenomegaly – enlarged spleen
• Pulmonary edema
• Respiratory – tachypnea, labored breathing, dyspnea, nocturnal dyspnea, very
productive frothy pink sputum coughing, crackles, rales, orthopnea
• Cardiovascular – tachycardia, cool, clammy, diaphoretic skin, hypoxemia,
cyanosis, hypotension
• Neurological – restless, impending doom, anxiety, LOC (confused, lethargic)
• Atrial Fibrillation (A-Fib)
Surgeries
• Aortic valve replacement surgery
• Heart transplantation
Complementary Health approaches

• Hawthorn – shrubby tree - help improve heart contractions and helps dilate vessels to a
certain degree
• Coenzyme Q 10, magnesium, & thiamine
End of Life Care

• Chronic heart failure is a terminal disease.
• Discuss disease & treatment options.
• Discuss advanced directives – living will, power of attorney
• Hospice services information should be provided.
• Administration of narcotics &/or diuretics are given as needed.
• Family should be informed of what to expect.
Diet/nutrition
• Weight reduction
• Daily weights – monitor for edema – 3 pounds a day, 5 pounds a week – restrict to
1500mL if needed – monitor I&O – assess respiratory status
• Na-restricted diets – 1.5-2g a day
• Foods to avoid - restricted canned goods, lunchmeat, bacon, sausage, pizza, soy
products, ketchup, frozen meals, cereal, cheese, any food that contains baking
soda/powder
Activity
• Assess for activity intolerance
• Prolonged bedrest is not recommended.
• A moderate, progressive activity program is prescribed to improve myocardial function
• Aerobic activity – start with 10 min. warm up; 20-30 min. activity; cool down
period
• Stage 4 HF – refrain in sexual activity; during periods of activity, they may need
to be put on oxygen
• Valsalva maneuver – straining to have a BM

Heart Failure

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Heart Failure

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Heart Failure Overview

Normal Pathophysiology of Blood Flow Through Heart

Pathophysiology: when the heart fails…

Left sided vs right sided HF

Complementary Health approaches

End of Life Care

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