AHF occurs as a result of injury to the heart tissues and often occurs as the bodies compensation systems fail in the case of CHF or as a result of acute injury. Whatever the cause, the heart's CO decreases. As decreased perfusion is detected release of epi, NE and vasopressin occurs. This leads to vasoconstriction of the vasculature, increased contractility and HR. However, the heart, already unable to produce the necessary CO is further damaged by the increased pressure resulting in decreased CO. At the same time the kidneys activate the RAAS system ultimately increasing fluid retention, raising BP and further increasing the workload of the heart, further stressing it, causing additional damage and decreased CO. As the heart continues to fail dysrhythmias can develop and cause sudden death
As the heart's CO decreases blood begins to congest in the lungs in the case of left sided heart failure. This results in cardiogenic pulmonary edema as the increased fluid pressure in the lungs causes the alveoli to become filled with liquids. This impairs gas exchange leading to cyanosis, impaired mental status, development of crackles and a cough. Untreated, the lungs continue to fill and multiple organ damage occurs as gas exchange is further impaired and various tissues become ischemic.