[Pathophysiologic mechanisms of cardiac decompensation]

Heart failure is a complex clinical syndrome in whose manifestations and prognosis compensatory mechanisms have a prominent role as a response of the organism to an elementary disturbance. There are five basic compensatory mechanisms: the Frank-Starling mechanism, structural changes of the heart, activation of neuroendocrine mechanism, adaptation to hypoxia and anaerobic metabolism. The interaction between the two main neurohumoral mechanisms, namely vasodilatation and vasoconstriction, has been drawing much of the attention recently. Vasoconstriction which evolved into maintaining cardiac output in hypovolemic state, leads to a number of deleterious hemodynamic and metabolic disturbances in heart failure. The organism tends to diminish this negative effects by changing beta adrenergic pathway and by activating vasodilative mechanisms. Once heart failure becomes severe, vasoconstriction predominates due to a loss of normal baroreceptor activity. It is considered that too marked activity of neurohumoral mechanisms is a significant cause of disease progression. By use of contemporary drugs (ACE inhibitors, beta blockers, digitalis), excessive vasoconstrictive mechanisms are tried to be diminished and prognosis of the disease improved.