Cardiac output, decreased compensatory responses

Fluid retention A fall in cardiac output decreases blood flow to the kidney, prompting the release of renin, with a resulting increase in the synthesis of angiotensin II and aldosterone (see p. 181). This results in increased peripheral resistance and retention of sodium and water. Blood volume increases, and more blood is returned to the heart. If the heart is unable to pump this extra volume, venous pressure increases and peripheral edema and pulmonary edema occur (Figure 16.4). These compensatory responses increase the work of the heart and, therefore, can contribute to the further decline in cardiac function. 

Propranolol—but not prazosin—may decrease cardiac output. Prazosin may increase renin output (a compensatory response), but beta-blockers inhibit its release by the kidney. By reducing blood pressure, both may increase central sympathetic outflow (a compensatory response). Propranolol does not cause orthostatic hypotension. The answer is (D). 

Vasoconstriction Maintain blood pressure and perfusion in the face of reduced cardiac output Increased MV02 Increased afterload decreases stroke volume and further activates the compensatory responses... 

Acutely, diuretics lower BP by causing diuresis. The reduction in plasma volume and stroke volume associated with diuresis decreases cardiac output and, consequently, BP. The initial drop in cardiac output causes a compensatory increase in peripheral vascular resistance. With chronic diuretic therapy, the extracellular fluid volume and plasma volume return almost to pretreatment levels, and peripheral vascular resistance falls below its pretreatment baseline. The reduction in peripheral vascular resistance is responsible for the long-term hypotensive effects. Thiazides lower BP by mobilizing sodium and water from arteriolar walls, which may contribute to decreased peripheral vascular resistance. 

Neurohumoral (extrinsic) compensation involves two major mechanisms (previously presented in Figure 6-7)—the sympathetic nervous system and the renin-angiotensin-aldosterone hormonal response—plus several others. Some of the pathologic as well as beneficial features of these compensatory responses are illustrated in Figure 13-2. The baroreceptor reflex appears to be reset, with a lower sensitivity to arterial pressure, in patients with heart failure. As a result, baroreceptor sensory input to the vasomotor center is reduced even at normal pressures sympathetic outflow is increased, and parasympathetic outflow is decreased. Increased sympathetic outflow causes tachycardia, increased cardiac contractility, and increased vascular tone. Vascular tone is further increased by angiotensin II and endothelin, a potent vasoconstrictor released by vascular endothelial cells. The result is a vicious cycle that is characteristic of heart failure (Figure 13-3). Vasoconstriction increases afterload, which further reduces ejection fraction and cardiac output. Neurohumoral antagonists and vasodilators... 

For example, because an adequate dose of hydralazine causes a significant decrease in peripheral vascular resistance, there will initially be a drop in mean arterial blood pressure, evoking a strong response in the form of compensatory tachycardia and salt and water retention (Figure 11-5). The result is an increase in cardiac output that is capable of almost completely reversing the effect of hydralazine. The addition of a B-blocker prevents the tachycardia addition of a diuretic (eg, hydrochlorothiazide) prevents the salt and water retention. In effect, all three drugs increase the sensitivity of the cardiovascular system to each other s actions. 

Baroreflexes involving the sympathetic nervous system are responsible for the rapid moment-to-moment regulation of blood pressure. A fall in blood pressure causes pressure-sensitive neurons (baroreceptors in the aortic arch and carotid sinuses) to send fewer impulses to cardiovascular centers in the spinal cord. This prompts a reflex response of increased sympathetic and decreased parasympathetic output to the heart and vasculature, resulting in vasoconstriction and increased cardiac output. These changes result in a compensatory rise in blood pressure (Figure 19.3, and Figure 3.5, see p. 31). 

Barbiturates are associated with dose-dependent cardiovascular depression. However, because of preservation of the baroreceptor reflex, the hemo-d3mamic response to an induction dose of thiopental is mild. Heart rate generally increases to compensate for a brief fall in arterial blood pressure. As a result of this reflex response, blood pressure remains unchanged and cardiac output may increase slightly with the elevation in heart rate (Ilkiw et al 1991). Without the compensatory heart rate response, or if the change in heart rate is small, a decrease in systemic blood pressure and cardiac output would predominate. 

Heart failure is due to defects in cardiac contractility (the vigor of heart muscle), leading to inadequate cardiac output. Signs and symptoms include decreased exercise tolerance and muscle fatigue, coupled with the results of compensatory responses (neural and humoral) evoked by decreases in mean BP. Increased SANS activity leads to tachycardia, increased arteriolar tone T afterload, 4- output, 4 renal perfusion), and increased venous tone (T preload, T fiber stretch). Activation of the renin-angiotensin system results in edema, dyspnea, and pulmonary congestion. Intrinsic compensation results in myocardial hypertrophy. These effects are summarized in Figure IH-4-1. 

Cardiovascular System Isoflurane produces a concentration-dependent decrease in arterial blood pressure cardiac output is maintained and hypotension is the result of decreased systemic vascular resistance. Vasodilation occurs in most vascular beds, particularly in skin and muscle. Isoflurane is a potent coronary vasodilator, simultaneously producing increased coronary blood flow and decreased myocardial consumption. Patients anesthetized with isoflurane generally have mildly elevated heart rates as a compensatory response to reduced blood pressure however, rapid changes in isoflurane concentration can produce both transient tachycardia and hypertension due to isoflurane-induced sympathetic stimulation. 

Mechanical effects The increase in contractility evoked by digitalis results in increased ventricular ejection, decreased end-systolic and end-diastolic size, increased cardiac output, and increased renal perfusion. These beneficial effects permit a decrease in the compensatory sympathetic and renal responses previously de.scribed. The decrease in sympathetic... 

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