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PY5.1-16 | Cardiovascular Physiology — Part 5

Heart Failure — When the Pump Weakens (PY5.16)

Heart failure (HF) is a clinical syndrome where the heart cannot pump enough blood to meet the body's metabolic demands, OR can only do so at elevated filling pressures.

Figure: Heart Failure — When the Pump Weakens (PY5.16)

Causes:
• Systolic failure (reduced ejection fraction, HFrEF) — weakened contraction. Causes: ischaemic heart disease (most common in India), dilated cardiomyopathy, myocarditis, chronic alcoholism.
• Diastolic failure (preserved ejection fraction, HFpEF) — impaired filling. Causes: hypertensive heart disease (LVH), hypertrophic cardiomyopathy, constrictive pericarditis.

Pathophysiology — the vicious cycle:

1. Decreased cardiac output -> inadequate tissue perfusion
2. Compensatory mechanisms activate (initially helpful, ultimately harmful):
- Frank-Starling mechanism: increased preload -> increased stretch -> more forceful contraction. But excessive stretch leads to ventricular dilation and worsening function.
- Sympathetic activation: increased HR and contractility. But chronically increased catecholamines are toxic to cardiac myocytes.
- RAAS activation: Na+ and water retention -> increased blood volume -> increased preload. But fluid overload causes pulmonary oedema (left heart failure) and peripheral oedema (right heart failure).
- Ventricular remodelling: the heart dilates and hypertrophies. But a dilated heart is less efficient (Laplace's law: wall stress = pressure x radius / 2 x wall thickness).

1. The compensatory mechanisms themselves worsen the disease -> vicious cycle -> progressive deterioration.

Clinical features:
• Left heart failure -> pulmonary congestion: dyspnoea (breathlessness), orthopnoea (breathlessness lying flat), paroxysmal nocturnal dyspnoea (PND), pulmonary crackles, S3 gallop.
• Right heart failure -> systemic congestion: raised JVP, hepatomegaly, peripheral oedema (ankle swelling), ascites.
• Biventricular failure -> features of both. This is the most common presentation because left heart failure eventually causes pulmonary hypertension -> right heart failure.

Key concept: Treatment of heart failure targets the harmful compensatory mechanisms — ACE inhibitors (block RAAS), beta-blockers (block sympathetic overdrive), diuretics (reduce fluid overload). This is why understanding the pathophysiology matters for treatment.