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

Uploaded by

Copyright:

Available Formats

Heart Failure

Uploaded by

Document Information

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Heart Failure

Uploaded by

Copyright:

Available Formats

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

You might also like