© 2002 European Society of Cardiology
Acute heart failure: a novel approach to its pathogenesis and treatment
Clinical Pharmacology Research Unit, The Cardiology Institute, Assaf-Harofeh Medical Center, Zerifin, Sackler Faculty of Medicine Tel-Aviv University, Tel-Aviv, Israel
* Corresponding author. The Cardiology Institute, Assaf-Harofeh Medical Center, 70300 Zerifin, Israel. Tel.: +972-8-9779778; fax: +972-8-9779779. E-mail address: cotterg{at}hotmail.com
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Abstract |
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Acute heart failure (HF) is one of the most common syndromes in emergency medicine, however, its exact pathogenesis has remained largely unknown. Based on clinical and hemodynamic data we have sub-divided acute HF into four syndromes: cardiogenic shock, pulmonary edema, hypertensive crisis and exacerbated HF. Cardiogenic shock is caused by a severe reduction in cardiac power which is not met by an adequate increase in peripheral vascular resistance leading to significant decrease in blood pressure and end organ perfusion. Hence the treatment of cardiogenic shock should be directed at improving cardiac performance (by optimizing filling pressure, intra-aortic balloon pump and immediate revascularization) and administration of peripheral vasoconstrictors. The other acute HF syndromes (pulmonary edema, HTN crisis and exacerbated HF) are caused by a combination of progressive excessive vasoconstriction superimposed on reduced left ventricular functional reserve. The impaired cardiac power and extreme vasoconstriction induce a vicious cycle of afterload mismatch resulting in a dramatic reduction of CO and elevated left ventricular end diastolic pressure, which is transferred backwards to the pulmonary capillaries yielding pulmonary edema. Therefore, the immediate treatment of these acute HF syndromes should be based on the administration of strong, fast-acting intravenous vasodilators such as nitrates or nitroprusside. After initial stabilization, therapy should be directed at reducing recurrent episodes of acute HF, by prevention of repeated episodes of excessive vasoconstriction along with efforts to optimize cardiac function.
Received June 4, 2001; Revised September 3, 2001; Accepted November 26, 2001
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