Heart Failure and Cardiomyopathies

Ventricular dysfunction and myocardial disease represent a spectrum of conditions affecting cardiac performance, ranging from impaired contractility to structural remodeling. Heart failure emerges when the ventricles cannot adequately fill or eject blood, resulting in systemic hypoperfusion and characteristic symptoms including fatigue, dyspnea, and peripheral edema. The condition stratifies into two major phenotypes based on ejection fraction: reduced ejection fraction presents with depressed systolic function, myocardial contractile impairment, and compensatory chamber dilation, whereas preserved ejection fraction involves diastolic dysfunction with abnormal relaxation and increased myocardial stiffness, particularly in older patients with hypertension or metabolic disease. Diagnosis integrates clinical presentation, echocardiographic assessment, and natriuretic peptide biomarkers reflecting ventricular wall stress, with severity graded through functional and structural classification systems. Pharmacologic management diverges significantly between phenotypes; reduced ejection fraction benefits from beta-blockers and renin-angiotensin-aldosterone inhibitors that improve survival, while preserved ejection fraction management emphasizes symptom relief through diuretics and aggressive comorbidity control. Acute decompensation requires immediate diuretic therapy and vasodilators, with advanced cases necessitating mechanical circulatory support or transplantation. Cardiomyopathies constitute a diverse group of primary myocardial disorders with genetic or acquired etiologies. Hypertrophic cardiomyopathy features severe left ventricular thickening with outflow tract obstruction, demanding preservation of preload and afterload while avoiding increased contractility. Dilated cardiomyopathy involves biventricular enlargement with systolic dysfunction and elevated thromboembolism risk. Stress-induced cardiomyopathy causes reversible apical dysfunction mimicking acute infarction despite patent coronaries. Peripartum variants emerge during pregnancy or the immediate postpartum period, while restrictive forms stem from infiltrative diseases producing fixed stroke volume with severe diastolic impairment. Cor pulmonale develops when chronic pulmonary disease and hypoxia cause right ventricular dysfunction, requiring oxygen therapy and pulmonary vasodilators while avoiding maneuvers that elevate pulmonary resistance. Perioperative management across these conditions demands meticulous optimization of preload, afterload, contractility, and rhythm maintenance, with specific drug selection and monitoring strategies tailored to the underlying pathophysiology and surgical requirements.