Abstract

N OREPINEPHRINE, a naturally occurring adrenergic transmitter, has both fl~-receptor and cq-receptor inotropic activity and has been used to treat the low cardiac output (CO) seen following cardiopulmonary bypass (CPB). 1 Its oq-receptor effect can produce increases in systemic vascular resistance (SVR), which can be modified by the concurrent use of a vasodilator. 2'3 Amrinone, a phosphodiesterase F-Ill inhibitor, is a potent vasodilator and a positive inotropic drug. 4 Its effects may counteract the vasoconstrictor effects of norepinephrine and may be synergistic or additive with its inotropic action. 5 Tolerance to the effects of norepinephrine may occur in the failing heart. This may be due to a decrease in the density of beta-receptors in the myocardium or secondary to an uncoupling of the beta-receptor from adenylate cyclase. 6'7 Amrinone exerts its effect independent of the beta-receptor, slowing breakdown of cyclic adenosine monophosphate (cAMP), and for a given degree of beta-adrenergic stimulation, it may increase the amount of intracellular calcium available to troponin-C. A case is reported of a patient, following aortocoronary bypass surgery, who was in severe biventricular failure, unresponsive to treatment with high doses of norepinephrine and phentolamine. The addition of amrinone to the patient's treatment resulted in marked improvement in his clinical condition, cardiac index (CI), and mixed venous oxygen saturation (SVO2).

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call