Acute Heart Failure (AHF) is a critical cardiovascular condition that leads to a sudden decline in cardiac function, often requiring urgent medical intervention. Unlike chronic heart failure, AHF develops rapidly and is triggered by underlying conditions such as myocardial infarction, hypertension, arrhythmias, or valvular disease. The high morbidity and mortality associated with AHF highlight the importance of timely diagnosis and effective treatment strategies. AHF arises due to various precipitating factors, including myocardial infarction, hypertension, arrhythmias, valvular disease, pulmonary embolism, sepsis, and non-compliance with medications. Myocardial infarction (heart attack) results in ischemic injury, impairing contractility and reducing cardiac output. Hypertension causes chronic pressure overload, leading to left ventricular hypertrophy and heart failure. Arrhythmias, such as atrial fibrillation, disrupt efficient cardiac output, while valvular diseases, including stenosis and regurgitation, increase cardiac workload. Pulmonary embolism obstructs blood flow to the lungs, straining the right heart, whereas sepsis induces systemic inflammation and myocardial dysfunction. Additionally, non-compliance with heart failure medications can precipitate acute decompensation. The pathophysiology of AHF involves structural and functional changes in the heart. Reduced stroke volume results from weakened myocardial contractility, leading to inadequate cardiac output. Increased filling pressure occurs due to blood accumulation in the heart chambers, causing congestion and pulmonary edema. Elevated afterload, characterized by higher vascular resistance, further impairs the heart’s ability to pump efficiently. These disruptions in the cardiac cycle contribute to the worsening of symptoms and disease progression. The primary goal of AHF treatment is to alleviate symptoms, optimize cardiac function, and prevent deterioration. Pharmacological interventions are the cornerstone of management, with various drug classes playing crucial roles. Diuretics, such as furosemide and bumetanide, reduce fluid overload by increasing urine output, alleviating pulmonary and systemic congestion. However, they may cause hypokalemia, hypotension, and renal dysfunction. Vasodilators, including nitroglycerin and nitroprusside, decrease preload and afterload to improve cardiac efficiency and relieve congestion, but they carry risks of hypotension and reflex tachycardia. Inotropic agents, such as dobutamine, milrinone, and levosimendan, enhance myocardial contractility in severe AHF cases, improving cardiac output. However, they can increase the

risk of arrhythmias, hypotension, and myocardial oxygen demand. Angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor blockers (ARBs) help reduce afterload and prevent cardiac remodeling, improving long-term survival. Despite their benefits, these drugs can cause hyperkalemia, hypotension, and a persistent cough (in the case of ACE inhibitors). Aldosterone antagonists, including spironolactone and eplerenone, counteract fluid retention and cardiac fibrosis, further improving patient outcomes. However, they pose a risk of hyperkalemia and, in the case of spironolactone, gynecomastia. Beta-blockers, such as carvedilol (also α1-blocker), metoprolol, and bisoprolol, reduce sympathetic overactivity, decreasing heart rate and myocardial oxygen demand. These agents prevent cardiac remodeling and reduce hospitalizations but may cause bradycardia, fatigue, and hypotension. Vasopressors, including norepinephrine and dopamine, are essential in cardiogenic shock, maintaining blood pressure and organ perfusion. However, their vasoconstrictive effects can lead to arrhythmias, ischemia, and renal hypoperfusion. Potential drug interactions must be carefully managed in AHF treatment. Loop diuretics combined with NSAIDs can reduce diuretic efficacy and worsen fluid retention. ACE inhibitors or ARBs, when used with potassium-sparing diuretics, significantly increase the risk of hyperkalemia. Beta-blockers combined with calcium channel blockers can cause severe bradycardia, while aldosterone antagonists used alongside NSAIDs can increase the likelihood of renal dysfunction and hyperkalemia. These interactions highlight the importance of individualized therapy and close patient monitoring.