Stroke volume vasodilators

Nitrates (e.g., ISDN) and hydralazine were combined originally in the treatment of HF because of their complementary hemodynamic actions. Nitrates are primarily venodilators, producing reductions in preload. Hydralazine is a direct vasodilator that acts predominantly on arterial smooth muscle to reduce systemic vascular resistance (SVR) and increase stroke volume and cardiac output. Evidence also suggests that the combination may provide additional benefits by interfering with the biochemical processes associated with HF progression. 

The hemodynamic effects of ritodrine have been assessed in 12 fetuses by cardiac and extracardiac Doppler sonography (1). Ritodrine significantly increased maternal and fetal heart rates, left cardiac stroke volume, and cardiac output. There was also an increase in the pulsatility index of the middle cerebral artery and a fall in the pulsatility index of the umbilical artery during ritodrine infusion. The authors suggested that ritodrine vasodilates fetal vessels in the placenta. 

Minoxidil acts as a direct vasodilator of vascular smooth muscle which decreases peripheral vascular resistance and blood pressure. Veins are affected to a lesser extent than arterioles. The resulting hypotensive effect induces a reflex increase in heart rate, cardiac output, and stroke volume. Sodium and water retention also occur leading to edema plasma renin activity is increased. 

The workload of the heart is modified by using medication that increases or decreases preload and afterload, thereby adjusting stroke volume and cardiac output. Vasodilators decrease the preload and afterload, resulting in a decrease in blood pressure (arterial pressure) and cardiac output. Vasopressors increase the preload and afterload, causing in an increase in blood pressure cardiac output. 

Patients with normal left ventricular function will not have an increase in stroke volume when SVR falls because the normal ventricle is fairly insensitive to small changes in afterload. Consequently, these patients experience a significant decrease in blood pressure after administration of arterial vasodilators. This explains why nitroprusside is a potent antihypertensive agent in patients without heart failure but causes less hypotension and reflex tachycardia in patients with left ventricular dysfunction. Nonetheless, even a modest increase in heart rate could have adverse consequences in patients with underlying ischemic heart disease and/or resting tachycardia, and close monitoring is necessary during therapy. 

In patients with elevated systemic vascular resistance and normal-to-elevated systemic blood pressure, afterload reduction with nitroprusside is logical it should be emphasized that nitroprus-side also increases venous capacitance, thereby also decreasing preload. In the context of myocardial dysfunction, afterload reduction will typically lead to improved forward cardiac output. Nitroprusside may also be effective when the systemic vascular resistance is elevated and systemic blood pressure is reduced the caveat in this more complex hemodynamic setting is that the load reduction produced by nitroprusside must be counterbalanced by an increase in stroke volume. This derivative increase in stroke volume may not occur in the patient with advanced heart failure rather, the result will be a further reduction in mean arterial pressure and the potential risk of peripheral organ hypoperfusion. An alternative approach would be the use of an inotropic-dilator drug such as milrinone, which will provide both preload and afterload reduction its concurrent positive inotropic effect may offset the reduction in mean arterial pressure that can occur from vasodilation alone. 

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