CONGESTIVE HEART FAILURE (CHF) - MBBS Final Year Exam Notes (10 Marks)

DEFINITION

"Heart failure is a clinical syndrome resulting from the inability of the heart to meet the metabolic requirements of the body at normal filling pressures." - Textbook of Family Medicine (9th Ed)

CLASSIFICATION

1. Based on Ejection Fraction (EF)

2. NYHA Functional Classification

3. ACC/AHA Staging System

4. Based on Output

• Low-output HF (common): Reduced CO - ischemia, cardiomyopathy, hypertension
• High-output HF (rare): Demands exceed even elevated CO - hyperthyroidism, severe anemia, beriberi (thiamine deficiency), arteriovenous shunts

ETIOLOGY / CAUSES

• Ischemic heart disease / Myocardial infarction (most common)
• Dilated cardiomyopathy
• Myocarditis (viral)
• Hypertension (chronic pressure overload)
• Valvular heart disease (aortic/mitral regurgitation)
• Alcohol, chemotherapy (cardiotoxic drugs)

• Hypertensive heart disease (most common)
• Hypertrophic cardiomyopathy
• Restrictive cardiomyopathy
• Aortic stenosis
• Diabetes, obesity, aging

• F - Forgot medication / non-compliance
• A - Arrhythmia (especially AF)
• I - Ischemia / Infarction
• L - Lifestyle (high salt/fluid intake)
• U - Uncontrolled hypertension
• R - Renal failure
• E - Embolism (pulmonary), Endocarditis, Emotional stress, anEmiA

PATHOPHYSIOLOGY

Underlying Mechanism

1. Primary cardiac injury (MI, cardiomyopathy, etc.) reduces cardiac output (CO)
2. This activates compensatory neurohormonal mechanisms
3. Short-term compensation becomes long-term maladaptation → ventricular remodeling

Four Major Compensatory Mechanisms (Lippincott Pharmacology)

• Baroreceptors sense ↓BP → ↑sympathetic outflow
• Results in: tachycardia (chronotropy), ↑contractility (inotropy), vasoconstriction
• ↑venous return → ↑preload → ↑stroke volume (Frank-Starling)
• Long-term: increases cardiac workload → further decline

• ↓CO → ↓renal blood flow → ↑renin release
• → ↑Angiotensin II → vasoconstriction (↑afterload) + ↑aldosterone
• → ↑Na⁺ and water retention → ↑preload → congestion
• Angiotensin II also causes: myocyte apoptosis, hypertrophy, ventricular fibrosis

• Increased wall tension → myocyte hypertrophy
• Initially compensatory (↑contractility), later leads to fibrosis and stiffness

• Hypertrophy and stiffening of ventricular wall → impaired relaxation
• Ventricle cannot fill adequately → ↓CO despite normal EF

• Inflammation & oxidative stress: Tissue hypoperfusion → mitochondrial dysfunction → myocyte death and fibrosis
• Resistance to natriuretic peptides (ANP/BNP): Despite release of ANP/BNP (which should cause vasodilation and natriuresis), receptors become desensitized → vasoconstriction and fluid retention persist
• Aldosterone escape: Aldosterone levels rise despite ACE-I therapy → ongoing fibrosis (rationale for spironolactone)

The Vicious Cycle (Katzung Pharmacology)

↓CO → ↑Neurohormones (NE, Ang II, ET-1) → Vasoconstriction
→ ↑Afterload → ↓EF → ↓CO (cycle repeats)

CLINICAL FEATURES

Left Heart Failure (Pulmonary Congestion)

Right Heart Failure (Systemic Congestion)

Common to Both

• Fatigue and exercise intolerance (most direct effect of ↓CO)
• Cardiomegaly
• Tachycardia
• Oliguria (↓renal perfusion)
• Cardiac cachexia (in severe chronic HF)

Most common cause of RHF is LHF (cor pulmonale is the second most common cause).

INVESTIGATIONS

Routine

• ECG: LVH, bundle branch block, arrhythmias, evidence of prior MI
• Chest X-ray: Cardiomegaly (CTR > 0.5), upper lobe diversion, Kerley B lines, bat-wing pulmonary edema, pleural effusion
• Blood tests: CBC, serum electrolytes, BUN/creatinine, LFTs, TFTs, blood glucose, iron studies, ESR, ANA

Key Biomarker

• BNP / NT-proBNP: Elevated - secreted by ventricles in response to ↑wall stress; used for diagnosis and monitoring

Echo (Most Important Investigation)

• Confirms diagnosis, measures EF, identifies etiology (wall motion abnormality, valvular disease, pericardial disease)
• Distinguishes HFrEF from HFpEF

Others

• Coronary angiography: if ischemic etiology suspected
• Cardiac MRI: infiltrative disease, scar
• Endomyocardial biopsy: new-onset HF with hemodynamic compromise, unexplained dilated cardiomyopathy

TREATMENT

Non-Pharmacological

• Fluid restriction: < 1.5-2 L/day
• Salt restriction: 2-3 g/day
• Weight monitoring (daily)
• Moderate aerobic exercise (stable patients)
• Avoid alcohol, smoking, NSAIDs
• Treat precipitating factors

Pharmacological Treatment (HFrEF - Proven Mortality Benefit)

The "Four Pillars" of HFrEF Therapy

Also: ARNI (Sacubitril/Valsartan - neprilysin inhibitor + ARB) - superior to ACE-I alone in reducing mortality

Diuretics (Symptom Relief)

• Loop diuretics (Furosemide): Most effective for congestion - inhibit Na⁺/K⁺/2Cl⁻ cotransporter
• Thiazides: Add-on for resistant edema
• Note: Diuretics do NOT improve mortality but reduce symptoms and hospitalizations

Digoxin

• Positive inotrope (↑intracellular Ca²⁺ via Na⁺/K⁺-ATPase inhibition)
• Reduces hospitalizations, especially in AF with HF
• Does NOT improve mortality; has narrow therapeutic window

Pharmacological Treatment (HFpEF)

• No drug proven to improve mortality in HFpEF
• Goal: symptom control
• Diuretics (for congestion), beta-blockers or non-dihydropyridine CCBs (rate control), RAAS inhibitors (LVH regression), aggressive HTN control
• SGLT2 inhibitors show promising benefit (emerging evidence)

Device Therapy

• ICD (Implantable Cardioverter Defibrillator): EF ≤ 35%, NYHA II-III on optimal therapy (prevents sudden cardiac death)
• CRT (Cardiac Resynchronization Therapy): EF ≤ 35% + LBBB + QRS ≥ 150 ms (resynchronizes ventricular contraction)
• LVAD (Left Ventricular Assist Device): Bridge to transplant or destination therapy

Acute Decompensated Heart Failure (Emergency)

• Sit patient upright
• Oxygen / CPAP/BiPAP for respiratory failure
• IV Furosemide (immediate decongestion)
• IV GTN (nitrates) for vasodilation - reduce preload
• Morphine (reduces anxiety/preload) - controversial
• Inotropes: Dobutamine (↑CO in cardiogenic shock), Dopamine
• Consider IABP (intra-aortic balloon pump) in refractory cases

PROGNOSIS

• 5-year mortality remains ~50% after diagnosis
• Annual mortality: NYHA class I ~ 5%; class IV ~ 50-60%
• Sudden cardiac death accounts for ~50% of deaths in HF patients
• BNP levels correlate with prognosis - persistently elevated = poor prognosis

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