Current therapeutic principles in the acute management of severe congestive heart failure.

The phrase "heart failure" encompasses many clinical entities. The therapeutic principles determining the treatment of these entities vary according to the etiology of congestive heart failure (CHF), the existing hemodynamics, and the mode of action of different drugs. In acute CHF due to myocardial ischemia, intracellular acidosis and the accumulation of phosphate may be the initial underlying causes of contractile failure while, minutes later, lack of high-energy compounds may be an important contributory factor. The cause of contractile failure in chronic syndromes is less well understood. There is evidence for the desensitization of beta receptors on the cell surface but the precise location of the defect is unclear. The receptors may be down-regulated but, in addition, abnormalities have been reported in several other parts of the contractile pathway including the contractile proteins and the sarcoplasmic reticulum. Deficiency of cyclic adenosine monophosphate has also been suggested as a mechanism of contractile failure. In both acute and chronic CHF, there is a redistribution of blood flow to the body organs. Of particular significance is the reduction of blood flow to the kidneys, and a reversal of this defect is one of the major therapeutic objectives. Positive inotropic drugs, vasodilators and drugs altering relaxation of the heart, have been evaluated in the treatment of CHF. Pure inotropic drugs can cause tachycardia, ischemia and "metabolic exhaustion" of the myocardium. The most advantageous profile for an "inotropic" drug in many patients with CHF would be a drug combining systemic vasodilatation, renal vasodilatation, increased relaxation of the myocardium only a mild positive inotropic effect and no chronotropic effect.