Heart Failure

Heart failure is not a single disease — it is a clinical syndrome defined by the heart's inability to pump sufficient blood to meet the body's metabolic demands, or to do so only at elevated filling pressures. The result is a constellation of symptoms: dyspnea, fatigue, reduced exercise tolerance, and fluid retention.

The ejection fraction classifies heart failure into subtypes with different pathophysiology and different evidence-based therapies. HFrEF (heart failure with reduced ejection fraction, EF <40%) is characterized by impaired systolic function. HFpEF (heart failure with preserved ejection fraction, EF ≥50%) is characterized by impaired diastolic relaxation and filling. HFmrEF (mildly reduced, EF 41–49%) sits between them.

The diagnosis is clinical — built from the history, the physical examination, and supporting data. The ejection fraction, BNP, and imaging confirm and classify. They do not replace the clinical assessment.

The physical examination in heart failure is organized around two questions: is there evidence of elevated filling pressures (congestion), and is there evidence of reduced cardiac output (low perfusion)?

Signs of congestion include elevated jugular venous pressure, an S3 gallop, pulmonary crackles, peripheral edema, and ascites. The JVP is assessed with the patient at 45 degrees — the highest point of venous pulsation above the sternal angle reflects right atrial pressure. An elevated JVP is one of the most specific physical exam findings for elevated filling pressures.

Signs of reduced perfusion include cool extremities, narrow pulse pressure, altered mental status, and oliguria. The combination of congestion and low perfusion — the "wet and cold" profile — identifies the highest-risk patients and guides the urgency of intervention.

The Stevenson hemodynamic profile (wet/dry, warm/cold) is a practical framework for classifying the acute presentation and directing initial management.

BNP (B-type natriuretic peptide) and NT-proBNP are released by ventricular myocytes in response to wall stress — elevated filling pressures stretch the ventricle and trigger peptide release. They are sensitive markers for heart failure in the appropriate clinical context.

A normal BNP in a patient with acute dyspnea makes heart failure an unlikely cause of the presentation. An elevated BNP requires clinical context to interpret. BNP is also elevated in renal failure (reduced clearance), pulmonary embolism, sepsis, and other conditions that increase wall stress or impair clearance.

BNP is most useful as a rule-out tool and as a trend marker. Serial BNP measurements during hospitalization — a falling BNP with diuresis — confirm adequate decongestion. A BNP that fails to fall despite diuresis suggests inadequate treatment or a non-cardiac contributor.

Do not treat the BNP number. Treat the patient. A patient who is clinically euvolemic with a mildly elevated BNP at baseline does not need additional diuresis to normalize the number.

Guideline-directed medical therapy (GDMT) for HFrEF is one of the most evidence-dense areas in cardiovascular medicine. Four drug classes have demonstrated mortality benefit in large randomized trials: ACE inhibitor/ARB/ARNI, evidence-based beta-blocker, mineralocorticoid receptor antagonist (MRA), and SGLT2 inhibitor.

The goal is to initiate all four classes at the lowest tolerated dose and uptitrate to target doses over weeks to months. The benefit is additive — each class reduces mortality through a different mechanism, and the combination produces greater benefit than any single agent.

Sacubitril-valsartan (Entresto) — an ARNI — is preferred over ACE inhibitor or ARB alone in patients who can tolerate it, based on the PARADIGM-HF trial demonstrating superior mortality reduction. It should not be combined with an ACE inhibitor (risk of angioedema) and requires a 36-hour washout when transitioning from an ACE inhibitor.

SGLT2 inhibitors — dapagliflozin and empagliflozin — reduce cardiovascular death and heart failure hospitalizations in HFrEF regardless of diabetes status. They are now a standard component of GDMT for all patients with HFrEF.

Heart failure presents along a spectrum from gradual exertional dyspnea to acute pulmonary edema. The most common presentation is progressive dyspnea on exertion, orthopnea, and lower extremity edema — but atypical presentations include fatigue, early satiety, abdominal fullness from hepatic congestion, and nocturia.

Classification by ejection fraction guides treatment. HFrEF (EF below 40%) has the most robust evidence base for pharmacologic therapy. HFpEF (EF 50% or above) is increasingly common, particularly in older women with hypertension, obesity, and atrial fibrillation — and has fewer proven disease-modifying therapies. HFmrEF (EF 40–49%) is an intermediate category that may respond to some HFrEF therapies.

The initial workup includes BNP or NT-proBNP, chest X-ray (pulmonary vascular redistribution, Kerley B lines, pleural effusions, cardiomegaly), ECG, basic metabolic panel, and echocardiography. Echo is essential — it establishes EF, identifies structural causes (valvular disease, wall motion abnormalities), and guides therapy selection.

Common precipitants of decompensation include dietary sodium and fluid indiscretion, medication non-adherence, new arrhythmia (particularly atrial fibrillation), infection, uncontrolled hypertension, ACS, and nephrotoxin exposure. Identifying and addressing the precipitant is as important as treating the congestion itself.

Acute decompensated heart failure is managed with IV loop diuretics as the cornerstone of decongestion. The initial IV dose should be at least equivalent to the patient's total daily oral diuretic dose. Urine output, daily weights, and symptom response guide titration.

Adequate decongestion — not just symptom improvement — is the target before discharge. Patients who are discharged with residual volume overload have significantly higher 30-day readmission rates. Clinical markers of adequate decongestion include resolution of orthopnea and dyspnea at rest, reduction in peripheral edema, and a JVP that has normalized.

Every decompensation has a trigger. Identifying and treating the trigger is part of managing the acute presentation. Medication non-adherence, dietary indiscretion, new atrial fibrillation, infection, and ischemia are the most common precipitants. A patient who decompensates from rapid atrial fibrillation needs rate control alongside diuresis.

Beta-blockers should not be initiated during active decompensation with volume overload. They can be continued at a reduced dose in patients already on them who decompensate, but should not be started until the patient is euvolemic and hemodynamically stable.

Most patients with acute decompensated heart failure improve with IV diuresis within 24–48 hours. Reassessment should include daily weights, fluid balance, renal function, and electrolytes — particularly potassium and magnesium, which are depleted by loop diuretics and must be repleted to prevent arrhythmia.

Diuretic resistance — inadequate urine output despite adequate IV dosing — should prompt evaluation for low cardiac output (cardiorenal syndrome), hypoalbuminemia reducing drug delivery, or inadequate dosing. Options include dose escalation, addition of a thiazide diuretic (metolazone or chlorothiazide) for sequential nephron blockade, or continuous infusion.

Worsening renal function during diuresis is common and does not always require stopping diuresis. A modest creatinine rise in the context of improving congestion is often acceptable. Persistent or severe renal deterioration, particularly with oliguria, should prompt nephrology involvement and consideration of cardiorenal syndrome.

Escalation criteria include hemodynamic instability (hypotension, cardiogenic shock), failure to respond to IV diuresis, new or worsening arrhythmia, evidence of end-organ hypoperfusion, or need for inotropic support. Cardiology consultation is appropriate for any patient with new-onset heart failure, refractory decompensation, or consideration of advanced therapies.

Outpatient follow-up within 7–14 days of discharge is associated with reduced readmission. Discharge planning should include medication reconciliation, weight monitoring instructions, a clear threshold for calling or returning (typically 2–3 lb weight gain in 24 hours), and confirmation that GDMT is optimized or a plan is in place to uptitrate.