Alterations in vasomotor tone in congestive heart failure

T HE changes that occur in the regional circulations with congestive heart failure depend on a number of variables: (A) the stimulus for heart failure; (B) the severity of heart disease; (C) the stage of development of heart failure; (D) the stress placed on the cardiovascular system (exercise, thermal); and (E) the species in which heart failure is studied.‘,’ These variables interact by means of normal physiologic modulators of cardiocirculatory function (reflexes, hormones) operating normally or in excess, and by nonphysiologic abnormalities characteristic of the heart failure state. The reflexes frequently activated include those stimulated via systemic arterial and atria1 baroreceptars, ventricular mechanoreceptors, and somatic afferent and pulmonary afTerent nerve fibers. The hormonal response to heart failure can include activation of the renin-angiotensinaldosterone system, the release of vasopressin, and the secretion of epinephrine and norepinephrine from adrenal medulary and/or peripheral vascular sites. Moreover, interaction between these neurohumoral modulators occurs frequently. Nonphysiologic modulators of circulatory function include salt and water retention which can alter vascular stiffness and externally compress vessels by deforming the interstitial space, and structural changes in afferent nerve fibers and vascular basement membranes. Perturbation of this complex system is caused by medical therapy (digitalis, diuretics, vasodilatars), which may affect the blood vessels directly or alter the modulators. Drugs may interrupt reflexes at multiple levels in the nervous system and can also interfere with hormonal responses at multiple levels. What generalizations can be made regarding vasomotor tone in heart failure? First, blood vessels are constricted. If not present at rest, an abnormal pattern of vasoconstriction almost invariably results during exercise. Second, this vasoconstriction is part of a total cardiocirculatory response designed to maintain optimal circulatory efficiency.‘,3.4 Two sets of cardiocirculatory compensatory mechanisms are activated in heart failure. The first is designed to maintain a normal cardiac output at rest and under conditions of stress. Both cardiac factors (cardioacceleration, myocardial hypertrophy, ventricular dilatation) and circulatory factors (plasma volume expansion and “endogenous impedance reduction”) contribute toward maintaining an adequate cardiac output. The second mechanism is invoked if total flow of the regional circulations cannot be maintained normally. Vasoconstriction is the hallmark of this second response. initially, the vasoconstriction is minimal and selective. The body strives to redistribute blood flow between and within organs, and circulatory efficiency is enhanced. Later, however, vasoconstriction is excessive in order to maintain blood pressure at a normal level. This results in a marked reduction of flow to nonessential circulations (renal, splanchnic, cutaneous), especially during exercise stress. The vasoconstrictor mechanisms thus activated usually spare the coronary and cerebral circulations, which are the main beneficiaries of the body’s effort to maintain a normal blood pressure.’ Third, at some point, the vasoconstriction of congestive heart failure becomes inappropriate. By increasing aortic impedance, vasoconstriction places a further burden on the already failing heart, and the decline in cardiac function is accelerated.‘~’ It is this vicious cycle of inappropriately high vasoconstriction leading to further cardiac dysfunction that vasodilator therapy is intended to interrupt.‘.’ ’ In the remainder of this review, we will first present some examples to illustrate how the type of heart disease. its severity, and its time course of development can alter the vasomotor response. Next, we will review the normal mechanisms regulating regional blood flow at rest and during __-__