HF pathophysiology: cardiac dysfunction triggers compensatory neurohormonal activation (RAAS, sympathetic, vasopressin) that initially preserves perfusion but ultimately drives myocardial remodeling, fibrosis, and progressive dysfunction. HFrEF mechanisms - ischemic, idiopathic dilated, valvular, infiltrative, toxic (chemo, alcohol). HFpEF mechanisms - hypertensive, infiltrative (amyloid), restrictive, diabetic cardiomyopathy. Stages (ACC/AHA): A (at risk), B (pre-HF, structural), C (symptomatic), D (advanced). NYHA functional class I-IV stratifies symptom severity.
Diagnostic workup: 1) NT-proBNP - rule-out <125 pg/mL (chronic), <300 pg/mL (acute); rule-in age-adjusted (>450 if <50 yr, >900 if 50-75, >1800 if >75); 2) Echocardiography - LVEF, structural abnormalities, diastolic function, valvular disease; 3) ECG - ischemia, arrhythmia, LVH, conduction disease; 4) Chest X-ray - pulmonary congestion, cardiomegaly; 5) Labs - CBC, BUN/Cr, electrolytes, TSH, ferritin/TSAT (iron deficiency), HbA1c, liver, lipids; 6) Cardiac MRI - infiltrative disease (amyloid, sarcoid), myocarditis; 7) Coronary angiography - exclude CAD; 8) Genetic testing in select cases (familial cardiomyopathy).
Internal medicine treatment focus: HFrEF four pillars - 1) ARNI (sacubitril/valsartan, PARADIGM-HF) preferred over ACEi/ARB; 2) Beta-blocker (carvedilol, metoprolol succinate, bisoprolol); 3) MRA (spironolactone, eplerenone); 4) SGLT2 inhibitor (dapagliflozin DAPA-HF, empagliflozin EMPEROR-Reduced) - mortality reduction independent of diabetes. Add-on - ivabradine (sinus rhythm, HR ≥70), hydralazine-isosorbide (Black patients), vericiguat (FY worsening HF), iron repletion (TSAT <20%, ferritin <100). HFpEF - SGLT2i (EMPEROR-Preserved, DELIVER), MRA, optimize comorbidities (HTN, AF, OSA, obesity). Comorbidity management - CKD (avoid NSAIDs), AF (anticoagulation, rate/rhythm), DM (GLP-1RA, SGLT2i), iron deficiency, depression.