Congestive heart failure

Clinical syndrome of the heart's inability to pump blood effectively, leading to inadequate perfusion and congestion of tissues; can be left-sided (pulmonary edema) or right-sided (systemic edema), and classified as HFrEF (systolic dysfunction, reduced ejection fraction) or HFpEF (diastolic dysfunction, preserved ejection fraction).

• Extremely common (≈6 million adults in the US) and a leading cause of hospitalization in older adults. Despite modern therapies, HF carries high morbidity and mortality (≈20% one-year and ~50% five-year mortality for advanced HF) and significantly impacts quality of life, making it a major public health challenge and frequent exam topic.

• Key symptoms include dyspnea (shortness of breath on exertion, progressing to at rest), orthopnea (difficulty breathing lying flat, relieved by sitting up), paroxysmal nocturnal dyspnea (PND) (waking up gasping for air), fatigue, and edema (leg swelling). Exam may show jugular venous distension (JVD), pulmonary crackles at lung bases, displaced apical impulse (cardiomegaly), and an S3 gallop (in HFrEF).
• Left-sided HF causes pulmonary congestion (dyspnea, orthopnea, crackles, PND) due to fluid backing up into the lungs. Right-sided HF causes systemic congestion (JVD, hepatomegaly, ascites, peripheral edema) due to blood backing up in systemic veins. Longstanding left HF can lead to right HF (biventricular failure).
• Common causes: Coronary artery disease (post-MI ischemic cardiomyopathy) is the leading cause of HFrEF. Other causes include chronic hypertension (causing LV hypertrophy, often leading to HFpEF), valvular diseases (e.g., aortic stenosis, mitral regurgitation), myocarditis, dilated cardiomyopathy (alcohol, chemotherapy, viral), and arrhythmias (chronic tachycardia). HFpEF typically occurs in older patients with hypertension, obesity, or diabetes (stiff LV with an S4 gallop).

1. Confirm the diagnosis: obtain a B-type natriuretic peptide (BNP) level (elevated in HF from ventricular stretch) and perform a transthoracic echocardiogram to assess ejection fraction and cardiac structure (chamber sizes, wall motion, valves). Also get a chest X-ray (cardiomegaly, pulmonary edema) and ECG (prior MI, arrhythmia) as part of initial evaluation.
2. Evaluate the cause: check for ischemia (if angina or history suggests, do stress test or coronary angiography), review medications (e.g., chemo drugs) and toxins (alcohol), and screen for contributing conditions (TSH for thyroid disease, iron studies for hemochromatosis, etc.).
3. Assess severity and type: determine if HFrEF (EF ≤40%) vs HFpEF (EF ≥50%, with 41–49% = HFmrEF) and classify the functional severity by NYHA class I–IV (I = no symptoms, IV = symptoms at rest) and disease progression by ACC/AHA Stage A–D (A = risk factors only, B = structural heart disease no symptoms, C = symptomatic HF, D = refractory HF).
4. Monitor for complications: check renal function (for cardiorenal syndrome), liver enzymes (congestion can cause hepatopathy), and watch for arrhythmias (e.g., atrial fibrillation or ventricular tachycardia) that commonly occur in HF patients.

1. Lifestyle: HF patients should follow a low-salt diet (<2g/day), restrict fluids (especially if hyponatremic), monitor daily weight, and exercise as tolerated. Educate on recognizing symptoms of fluid overload early and medication compliance.
2. Medications (HFrEF): Start ACE inhibitor (or ARB, or ideally an ARNI) plus a beta blocker (bisoprolol, metoprolol succinate, or carvedilol) and an MRA (mineralocorticoid receptor antagonist like spironolactone) – these improve survival. Add an SGLT2 inhibitor (e.g., dapagliflozin) for additional morbidity/mortality benefit. Use loop diuretics as needed for symptomatic relief of congestion (reduces edema and dyspnea).
3. Additional therapies: In HFrEF, hydralazine + isosorbide dinitrate is recommended for African-American patients with persistent Class III–IV symptoms despite the above, or if ACEi/ARB can't be used. If LVEF ≤35% (and NYHA II–III) despite optimal meds, add an ICD to prevent sudden cardiac death. If LVEF is low and QRS is prolonged (LBBB), consider CRT (biventricular pacing) to improve synchronization.
4. Advanced HF (Stage D): Refractory symptoms at rest despite therapy may require intravenous inotropes (e.g., dobutamine) for short-term stabilization. Evaluate for heart transplant in eligible patients or consider a durable LVAD (left ventricular assist device) as a bridge or destination therapy. Discuss palliative care for symptom management in end-stage HF.
5. HFpEF management: There is no proven mortality-reducing therapy yet for HFpEF, so focus on treating contributors: strict blood pressure control (e.g., with ACEi/ARBs), manage atrial fibrillation or ischemia if present, use diuretics to control edema, and encourage lifestyle changes (weight loss, exercise). SGLT2 inhibitors have shown some benefit in reducing HF hospitalizations in HFpEF.

• Sleeping upright on multiple pillows (to relieve orthopnea) and episodes of PND are classic for HF; lying flat increases venous return, worsening pulmonary edema.
• An S3 gallop ("kentucky") is a classic sign of systolic HF (volume overload, dilated ventricle), whereas an S4 ("tennessee") suggests a stiff LV (diastolic HF, e.g., LV hypertrophy).
• BNP is released by stretched ventricles in HF; a normal BNP level essentially rules out significant HF as the cause of dyspnea.

• Acute pulmonary edema: rapid onset of severe dyspnea, anxiety, and pink frothy sputum – indicates flash pulmonary edema (acute left HF) requiring emergency treatment (high-flow oxygen, IV diuretics, possibly nitrates and ventilatory support).
• Signs of cardiogenic shock in HF (hypotension, cool clammy skin, altered mental status, very low urine output) – indicates end-stage pump failure; requires immediate inotropic support and consideration of mechanical support (e.g., intra-aortic balloon pump, LVAD) or transplant.

1. Patient with risk factors (CAD, hypertension) + symptoms of HF (dyspnea, edema) → suspect HF.
2. If HF suspected → order BNP and perform echocardiography to confirm diagnosis (assess EF and cardiac function); evaluate for precipitating factors (ECG, troponin to rule out MI, etc.) and start diuresis if volume overloaded.
3. If HF confirmed → categorize HFrEF vs HFpEF by EF and assess severity (assign NYHA class I–IV for symptoms, and ACC/AHA Stage A–D for disease stage).
4. Initiate guideline-directed medical therapy (GDMT) for HFrEF: ACEi/ARNI + beta-blocker + MRA + SGLT2i (if not contraindicated) to improve survival; add diuretics for symptom relief. Treat underlying causes (revascularize if ischemic, control BP, manage AF, etc.) and optimize comorbid conditions (e.g., diabetes).
5. Follow-up: Titrate medications to target doses. If LVEF remains ≤35% on optimal therapy → consider ICD placement (and CRT if indicated). Advanced Stage D HF → refer for specialized therapies (inotropes, transplant evaluation, or mechanical support).

• Older male with prior MI who has exertional dyspnea, orthopnea, leg edema, and an S3 heart sound on exam → chronic systolic HF (HFrEF due to ischemic cardiomyopathy).
• Elderly hypertensive woman with LV hypertrophy who develops acute flash pulmonary edema (severe dyspnea, pink frothy sputum) despite a normal EF on echo → diastolic HF (HFpEF crisis).
• Patient with longstanding COPD (cor pulmonale) presenting with elevated JVP, hepatomegaly, and bilateral ankle edema but clear lungs → isolated right-sided heart failure.