PA26.3 | Heart Failure — Summary & Reflection

REFLECT

Think about the patient described in the opening hook: hypertension → concentric LV hypertrophy → diastolic dysfunction → LHF → pulmonary congestion → pulmonary hypertension → RHF → biventricular failure.

1. At what point in this progression would a BNP test first become significantly elevated?
2. Why does this patient have hepatomegaly and basal pulmonary haziness — which ventricle has failed on each side?
3. If you were to biopsy this patient's liver, what microscopic features would you expect to find in the centrilobular zone?
4. The patient is given a loop diuretic. Which specific symptoms and signs would you expect to improve first, and which would lag?

KEY TAKEAWAYS

Heart failure is the inability of the heart to meet metabolic demand, or to do so only at elevated filling pressures.

Three compensatory mechanisms temporarily restore output — Frank-Starling (preload utilisation), neurohormonal activation (RAAS + SNS), and myocardial hypertrophy/remodelling — but each eventually maladapts, driving progressive deterioration.

Left heart failure backs up into the pulmonary circulation → dyspnoea, orthopnoea, PND, pulmonary oedema, and the hallmark microscopic finding of heart failure cells (haemosiderin-laden macrophages, Perl's stain positive).

Right heart failure (usually secondary to LHF or cor pulmonale) backs up into the systemic circulation → raised JVP, dependent oedema, nutmeg liver (centrilobular congestion/necrosis), ascites, splenomegaly.

Systolic HF: reduced EF (< 40%), dilated ventricle. Diastolic HF: preserved EF (≥ 50%), stiff ventricle — cannot fill.

Complications: arrhythmia, sudden death, thromboembolism (stroke), cardiorenal syndrome, cardiac cachexia, cardiac cirrhosis.

BNP rises with ventricular wall stretch; a level < 100 pg/mL effectively rules out HF as a cause of dyspnoea.

NYHA Classes I-IV describe functional limitation; ACC/AHA Stages A-D describe structural progression (unidirectional).