Chronic Heart Failure
A state in which the heart cannot deliver enough output for the body's needs at normal filling pressures, triggering neurohormonal compensations that relieve symptoms short-term but drive progression, which the key drugs are designed to block.
In a nutshell
A pump that cannot meet demand at normal filling pressures. The body compensates with sympathetic and RAAS activation, which props up output briefly and then drives fibrosis, remodelling and progression. Every prognostic drug blocks that neurohormonal axis; diuretics only relieve congestion.
Classic presentation
A patient with prior myocardial infarction or hypertension, progressive exertional breathlessness, orthopnoea and paroxysmal nocturnal dyspnoea, with a raised JVP, bibasal crackles and ankle oedema.
Key points
- Symptoms map onto where blood backs up: left-sided failure congests the lungs (orthopnoea, PND, crackles), right-sided failure congests the systemic veins (raised JVP, ankle oedema, hepatic congestion).
- Natriuretic peptides rise with ventricular wall stretch, so a normal BNP or NT-proBNP in an untreated patient makes heart failure unlikely. It is the gatekeeper to echocardiography.
- Echocardiography splits heart failure into reduced and preserved ejection fraction and identifies the cause. The prognostic drug evidence sits with reduced ejection fraction.
- Prognostic therapy blocks the neurohormonal axis: an ACE inhibitor (or ARB/ARNI), a beta-blocker, a mineralocorticoid receptor antagonist and an SGLT2 inhibitor.
- Loop diuretics relieve congestion and make patients feel better, but do not improve survival. They are symptomatic, not disease-modifying.
First-line investigation
Natriuretic peptide (BNP or NT-proBNP): it reflects the raised filling pressures central to the mechanism, and decides who needs an echocardiogram.
First-line management
Treat the underlying cause, then start neurohormonal blockade in reduced ejection fraction, an ACE inhibitor (or ARB/ARNI) plus a heart-failure beta-blocker, titrated as tolerated.
Exam traps
- A loop diuretic improves symptoms, not survival. If the stem asks which drug improves prognosis, it is never the diuretic.
- Beta-blockers are started in stable chronic heart failure, not during acute decompensation. The timing in the stem is the discriminator.
- A normal natriuretic peptide in an untreated patient argues against heart failure: do not reach for the echocardiogram first.
- Preserved ejection fraction does not mean mild disease. The ventricle is stiff and cannot fill.
Educational content pending clinical review. Not medical advice.