The pathophysiology of ADHF involves a complex interplay of cardiac dysfunction, fluid overload, and neurohormonal activation. It typically begins with an insult that disrupts the equilibrium of chronic heart failure or triggers a new cardiac event. This can include factors such as dietary indiscretion, medication nonadherence, acute illness, or the development of a new cardiac condition like myocardial infarction or atrial fibrillation.
The underlying cardiac dysfunction, characterized by impaired contractility and ventricular remodeling, leads to reduced cardiac output and inadequate tissue perfusion. This triggers compensatory mechanisms, such as activation of the renin-angiotensin-aldosterone system (RAAS) and sympathetic nervous system, resulting in vasoconstriction, sodium and water retention, and increased preload and afterload. These neurohormonal responses aim to maintain cardiac output, but they can contribute to further cardiac damage and exacerbate fluid overload.
In addition, the elevated ventricular filling pressures caused by fluid overload lead to pulmonary and systemic venous congestion. Symptoms like dyspnea and peripheral edema result from this backward failure. Impaired perfusion to vital organs caused by reduced cardiac output manifests as fatigue, altered mental status, and worsening renal function. Patients may present with signs and symptoms of both fluid overload and hypoperfusion.