Pharmacologic Enhancement Of Cardiac Output

In addition to the normalization of preload and metabolic parameters, patients with severe heart failure or cardiogenic shock require aggressive pharmacologic support with vasoactive infusions to enhance contractility and output. From a historical perspective, dopamine hydrochloride has served as the first-line treatment of low cardiac output. In lower dosages of 2 to 5 pg/kg/min, blood flow to the kidney and bowel is increased, and a paradoxical fall in blood pressure is noted. Midrange dosages of 6 to 10 p/kg/min result in b-adrenergic effect, and heart rate and contractility are improved. In dosages in excess of 10 p/kg/min, a effects predominate, and vasoconstriction results in correction of hypotension.

Epinephrine has replaced dopamine as the initial infusion of choice in hypotensive states. Predominant b-adrenergic effects are noted at lower dosages of 0.05 to 0.5 p/kg/min, whereas a-adrenergic effects are noted at higher dosages, which can result in rapid reversal of hypotension. Dobutamine is another useful drug that increases contractility without increasing heart rate or systemic vascular resistance. Its vasodilatory effects and lack of a effect at higher dosage ranges limit its usefulness as a single agent to counteract extremely low cardiac output with normal blood pressure. Nitroprusside can be useful in increasing stroke volume by the mechanism of afterload reduction. It is administered by continuous infusion with arterial and central venous pressure monitoring to detect hypotension and the need for volume expansion. Its use, in doses of 0.5 to 5 p/kg/min, is always reserved for intensive care situations.

Isoproterenol administration produces a marked decrease in total peripheral vascular resistance predominantly due to vasodilation in skeletal muscle vascular sites. Diastolic and mean blood pressures fall. The effects on the heart are similar to those with epinephrine, but with enhanced heart rate and stroke volume due to the decrease in mean blood pressure and reflexively decreased vagal tone.

Norepinephrine causes marked vasoconstriction of all vascular beds on both the venous side and the arterial side. Consequently, there is a net increase in total peripheral vascular resistance that results in a marked rise in both systolic and diastolic blood pressure. Due to complex actions on the heart, which depend in part on the amount of parasympathetic activity, the overall contribution to chronotropy is negligible and the inotropic response is only minimally increased.

Phenylephrine, which is not a naturally occurring catecholamine, has actions similar to those of norepinephrine, with minimal activity on chronotropic or inotropic function. Like norepinephrine, it causes marked increase in systemic vascular resistance due to direct vasoconstriction of all vascular beds. The difference between this drug and norepinephrine is predominantly in its metabolism. Overall, it has activity that is two to three times the duration of norepinephrine, making it highly effective in situations in which blood pressure elevation is likely to be depressed for long intervals. It is seldom used today, because of its narrow therapeutic window of benefit and its toxicity.

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