Acute Decompensated Heart Failure

John A. Galdo, PharmD, BCPS; Ashlee Rickard Riggs, PharmD; Amy L. Morris, PharmD Candidate

Disclosures

US Pharmacist. 2013;38(2):HS-2-HS-8. 

In This Article

Pathophysiology

ADHF is defined as a sudden worsening of HF symptoms and is usually caused by cardiogenic pulmonary edema with rapid fluid accumulation in the lungs, although it can occur without pulmonary edema.[7] Hypertension, ischemia, and/or ventricular dysfunction causes a decrease in cardiac output, which leads to an activation of the neurohormonal pathway. The sympathetic system increases norepinephrine to improve peripheral perfusion via vasoconstriction and activates the renin-angiotensin-aldosterone system to increase renal perfusion through water retention.[8] An acute increase in left ventricular filling pressure causes protein-poor fluid to leak into the lung alveoli and interstitium, but no compromise of pulmonary membrane integrity occurs. Compensatory mechanisms increase heart rate and systemic vascular resistance in an attempt to improve cardiac output, and a vicious cycle ensues.[7,8]

Common causes of ADHF include left ventricular or diastolic dysfunction with or without coronary artery disease (CAD) or valvular abnormalities. Although most patients hospitalized with ADHF have a worsening of preexisting HF, up to 20% of patients have no prior diagnosis of HF.[9]

ADHF can also occur in patients without any preexisting cardiac disease, including conditions such as severe hypertension, fluid overload, severe renal disease, or renal artery stenosis. Factors precipitating an event involve a change in the flow of blood through the heart; ADHF can be induced by hypertensive crisis, MI or ischemia, atrial obstruction, acute mitral regurgitation, fluid overload, or nonadherence to HF medications. Certain medications, such as beta-blockers, nondihydropyridine calcium channel blockers, and nonsteroidal anti-inflammatory drugs (NSAIDs), can also precipitate ADHF.[7,10]

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