L-4 Congestive heart failure

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CONGESTIVE HEART FAILURE(CHF) OR HEART FAILURE


1. Definition-
• Heart failure (HF)/CHF is a progressive clinical syndrome caused by inability of the heart to pump
sufficient blood to meet the body’s metabolic needs. HF/CHF can result from any disorder that
reduces ventricular filling (diastolic dysfunction) and/or myocardial contractility (systolic
dysfunction).
• What is meaning of congestive in congestive heart failure?
Fluid builds up in the arms, legs, ankles, feet, lungs, or other organs, the body becomes congested
Heart failure also affects the kidneys' ability to dispose of sodium and water. This retained water also
increases swelling in the body's tissues (edema).
• Heart failure/CHF mean- Heart failure doesn’t mean the heart has stopped working. Rather, it means
that the heart works less efficiently than normal. Due to various possible causes
➢ Types of heart failure

Cardiac output(CO) = heart rate(HR) x stroke volume(SV)

i) There are two types of left-sided heart failure. Drug treatments are different for the two types.
• Heart failure with reduced ejection fraction (HFrEF), also called systolic failure: The left
ventricle loses its ability to contract normally. The heart can't pump with enough force to push
enough blood into circulation.
• Heart failure with preserved ejection fraction (HFpEF), also called diastolic failure (or diastolic
dysfunction): The left ventricle loses its ability to relax normally (because the muscle has
become stiff). The heart can't properly fill with blood during the resting period between each
beat.
ii) Right sided heart failure
• Right-sided or right ventricular (RV) heart failure usually occurs as a result of left-sided failure.
When the left ventricle fails, increased fluid pressure is, in effect, transferred back through the
lungs, ultimately damaging the heart's right side. When the right side loses pumping power,
blood backs up in the body's veins. This usually causes swelling or congestion in the legs, ankles
and swelling within the abdomen such as the GI tract and liver (causing ascites).

Type of heart failure Description


Left sided heart failure Most common form of heart failure
Fluid may back up in your lungs, causing shortness of breathe
Right sided heart failure Often occur with left sided heart failure.
Fluid may back up into your abdomen, legs and feet causing swelling
Systolic heart failure The left ventricle can’t contract vigorously, indicating a pumping
problem
Diastolic heart failure The left ventricle can’t relax or fill fully indicating a filling problem
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➢ Stages of hear failure

1. stage A: This is a patient at risk of developing heart failure but no identified structural or functional
abnormalities of the heart and also no signs or symptoms of heart failure
2. stage B: The patient has developed structural heart disease that is strongly associated with the
development of heart failure but without signs or symptoms of heart failure
3. stage C: This patient has developed symptoms of heart failure with associated structural heart disease
4. stage D: This is advanced structural heart disease and marked symptoms of heart failure at rest despite
maximal medical therapy

These stages of heart failure were made by America College of Cardiology (ACC) and American Heart
Association (AHA) based on structure and damage to heart muscles

➢ Classification of Heart Failure

1. Class 1: No limitation to physical activity. Ordinary physical activity does not cause undue fatigue, palpitation
and dyspnea
2. Class 2: Slight limitation to physical activity, comfortable at rest but ordinary physical activity results in
fatigue, palpitation and dyspnea.
3. Class 3: Marked limitation of physical activity, comfortable at rest, but less than ordinary physical activity
results in fatigue, palpitation and dyspnea
4. Class 4: Unable to carryon any physical activity without discomfort. Symptoms of heart failure still occurs at
rest, if any physical activity is undertaken, discomfort is increased.

This is the New York Heart Association (NYHA) classification of Heart Failure based on symptoms and
physical activity.

2. Etiopathogenesis
A. Etiology
i) Heart failure is caused by systemic hypertension in 75% of cases.
ii) Structural heart changes, such as valvular dysfunction, cause pressure or volume overload
on the heart.
iii) Heart is unable to pump enough blood to meet tissues O 2 requirements
(a) Congenital heart defects
(b) Severe lung disease
(c) Diabetes
(d) Severe anemia
(e) Overactive thyroid gland (hyperthyroidism)
(f) Abnormal heart rhythms
iv) Increase in Pulmonary pressure results fluid in alveoli (pulmonary edema)
v) Increase in Systemic pressure results in fluid in tissues (peripheral edema)
vi) Health conditions that either damage the heart or make it work too hard
(a) Coronary artery disease
(b) Heart attack
(c) Heart muscle diseases (cardiomyopathy)
(d) Heart inflammation (myocarditis)

B. Pathogenesis
i) Myocyte loss
(a) Necrosis – resulting from MI or exposure to cardiotoxic drugs
(b) Apoptosis (programmed cell death) from elevated catecholamines, angiotensin II,
inflammatory cytokines, and mechanical strain from increased wall stress
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ii) Compensatory mechanisms


These mechanisms attempt to maintain sufficient blood pressure to perfuse vital organs by
compensating for the decrease in cardiac output that occurs in heart failure.
(a) Frank-Starling relationship: Ventricular output increases in relation to preload, i.e. with a
greater stretch of myocardial fibers (larger diastolic volume), there will be a greater force
of contraction generated
(b) Myocardial hypertrophy-

(c) Neuro-hormonal mechanisms-


• In the early stages of heart failure, these mechanisms help maintain a near normal
perfusion to vital organs by increasing systemic vascular resistance as a way to
balance the fall in cardiac output
i) Renin-angiotensin-aldosterone system (RAAS): The pathway leads to the
activation of angiotensin II which causes Vasoconstriction and Increases TPR to
maintain BP.
ii) Aldosterone -Increased water retention via increased sodium resorption. This
increases preload, in turn increasing the SV

(d) Adrenergic nervous system


• Decreased cardiac output results in decreased perfusion pressure sensed by baroreceptors in
carotid sinus and the aortic arch. Central and peripheral chemoreflex activation induces
epinephrine, norepinephrine, and vasopressin release. This results in an increased sympathetic
outflow to heart and peripheral circulation
Increased HR and contractility directly increase cardiac output (CO = HR × SV)
• Unfortunately, despite these compensatory mechanisms, there is progressive decline in the
heart’s ability to contract and relax in the face of persistent hemodynamic challenges.
Furthermore, chronic activation of the above mechanisms ultimately becomes maladaptive and
induces further worsening of cardiac performance

➢ Exacerbating factors in compensated heart failure


• Heart failure can be clinically silent (i.e. asymptomatic) if compensatory mechanisms are sufficient
to balance the degree of cardiac dysfunction, or alternatively if it is adequately managed
medically. However, patients can become symptomatic, if decompensation occurs.
MIND NURTURE KRISHNA Page 4 of 4

3. Clinical manifestation
• Backup of blood and fluid
• Dyspnea(Shortness of breath)
• Orthopnea(the sensation of breathlessness in the recumbent position, relieved by sitting or
standing)
• Lethargy
• Fatigue
• Nocturnal cough
• Wheeze
• Ankle swelling
4. Non-pharmacological treatment
• Lifestyle modifications
• Patient education on what is heart failure
• Dietary modifications i.e. low salt intake, more vegetables
• Weight reduction in patients with obesity
• Exercise
• Cessation of smoking
• Reduction/cessation of alcohol consumption
5. Pharmacological treatment
i) Diuretics such as Furosemide, Bumetanide
ii) Angiotensin Converting Enzymes Inhibitors (ACEIs) such as Enalapril, Lisinopril and Captopril
iii) Angiotensin Receptor Blockers (ARBs) such as Losartan
iv) Beta blockers such as Carvedilol and Bisoproplol
v) Alpha antagonists such as Prazosin
vi) Direct acting vasodilators such as Hydralazine
vii) Aldosterone antagonists such as spironolactone
viii) Cardiac glycosides such as Digoxin
ix) Anticoagulants
x) Anti-arrhythmic drugs such as Amiodarone

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