Arterial dilator drugs are commonly used to treat systemic and pulmonary hypertension, heart failure and angina. They reduce arterial pressure by decreasing systemic vascular resistance. This benefits patients in heart failure by reducing the afterload on the left ventricle, which enhances stroke volume and cardiac output and leads to secondary decreases in ventricular preload and venous pressures. Anginal patients benefit from arterial dilators because by reducing afterload on the heart, vasodilators decrease the oxygen demand of the heart, and thereby improve the oxygen supply/demand ratio. Oxygen demand is reduced because ventricular wall stress is reduced when aortic pressure is decreased. Some vasodilators can also reverse or prevent arterial vasospasm (transient contraction of arteries), which can precipitate anginal attacks.
Most drugs that dilate arteries also dilate veins; however, hydralazine, a direct acting vasodilator, is highly selective for arterial resistance vessels.
The effects of arterial dilators on overall cardiovascular function as depicted graphically using a cardiac and systemic vascular function curve
The effects of arterial dilators on overall cardiovascular function can be depicted graphically using cardiac and systemic vascular function curves as shown to the right. Selective arterial dilation decreases systemic vascular resistance, which increases the slope of the systemic vascular function curve (red line) without appreciably changing the x-intercept (mean circulatory filling pressure). This alone causes the operating point to shift from A to B, resulting in an increase in cardiac output (CO) with a small increase in right atrial pressure (PRA). The reason for the increase in PRA is that arterial dilation increases blood flow from the arterial vasculature into the venous vasculature, thereby increasing venous volume and pressure. However, arterial dilators also reduce afterload on the left ventricle and therefore unload the heart, which enhances the pumping ability of the heart. This causes the cardiac function curve to shift up and to the left (not shown in figure). Adding to this afterload effect is the influence of enhanced sympathetic stimulation due to a baroreceptor reflex in response to the fall in arterial pressure, which increases heart rate and inotropy. Because of these compensatory cardiac responses, arterial dilators increase cardiac output with little or no change in right atrial pressure (cardiac preload). Although cardiac output is increased, systemic vascular resistance is reduced relatively more causing arterial pressure to fall. The effect of reducing afterload on enhancing cardiac output is even greater in failing hearts because stroke volume more sensitive to the influence of elevated afterload in hearts with impaired contractility.
Arterial dilator drugs are commonly used to treat systemic and pulmonary hypertension, heart failure and angina. They reduce arterial pressure by decreasing systemic vascular resistance. This benefits patients in heart failure by reducing the afterload on the left ventricle, which enhances stroke volume and cardiac output and leads to secondary decreases in ventricular preload and venous pressures. Anginal patients benefit from arterial dilators because by reducing afterload on the heart, vasodilators decrease the oxygen demand of the heart, and thereby improve the oxygen supply/demand ratio. Oxygen demand is reduced because ventricular wall stress is reduced when aortic pressure is decreased. Some vasodilators can also reverse or prevent arterial vasospasm (transient contraction of arteries), which can precipitate anginal attacks.Most drugs that dilate arteries also dilate veins; however, hydralazine, a direct acting vasodilator, is highly selective for arterial resistance vessels.The effects of arterial dilators on overall cardiovascular function as depicted graphically using a cardiac and systemic vascular function curveThe effects of arterial dilators on overall cardiovascular function can be depicted graphically using cardiac and systemic vascular function curves as shown to the right. Selective arterial dilation decreases systemic vascular resistance, which increases the slope of the systemic vascular function curve (red line) without appreciably changing the x-intercept (mean circulatory filling pressure). This alone causes the operating point to shift from A to B, resulting in an increase in cardiac output (CO) with a small increase in right atrial pressure (PRA). The reason for the increase in PRA is that arterial dilation increases blood flow from the arterial vasculature into the venous vasculature, thereby increasing venous volume and pressure. However, arterial dilators also reduce afterload on the left ventricle and therefore unload the heart, which enhances the pumping ability of the heart. This causes the cardiac function curve to shift up and to the left (not shown in figure). Adding to this afterload effect is the influence of enhanced sympathetic stimulation due to a baroreceptor reflex in response to the fall in arterial pressure, which increases heart rate and inotropy. Because of these compensatory cardiac responses, arterial dilators increase cardiac output with little or no change in right atrial pressure (cardiac preload). Although cardiac output is increased, systemic vascular resistance is reduced relatively more causing arterial pressure to fall. The effect of reducing afterload on enhancing cardiac output is even greater in failing hearts because stroke volume more sensitive to the influence of elevated afterload in hearts with impaired contractility.
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