The physiologic basis upon which cardiac transplantation is grounded is the ability of the denervated heart to support normal circulation. The lack of sympathetic and parasympathetic innervation does, however, induce an altered physiologic state. The denervated heart has a normal sinus rhythm with a heart rate between 90 and 100 beats per minute. Denervation results in the absence of the initial centrally mediated tachycardia in response to stress or exercise. The heart remains responsive to circulating catecholamines of either endogenous or exogenous origin. The cardiac response to stress or exertion is therefore blunted. With the onset of exercise, the heart rate initially remains unchanged, then gradually increases to a level of approximately 80 percent of predicted over 10 to 15 min. After termination of exercise, this exercise-induced tachycardia will persist for approximately 20 to 30 min before slowly returning to the patient's baseline rate. Patients may complain of fatigue or shortness of breath with the onset of exercise that resolves with continued exertion as an appropriate tachycardia develops. In order to accommodate this response, patients are trained to perform warmup exercises prior to vigorous exertion to initiate an increase in their heart rate. They are also cautioned to allow appropriate time for recovery at the end of exertion.
Cardiac hemodynamics after transplantation as measured by cardiac catheterization reveal a normal to mildly depressed cardiac output at rest. With exercise, cardiac output increases in response to increased venous return (preload) and circulating catecholamines. Maximal cardiac outputs of 80 to 100 percent of normal have been measured. Patients are able to resume normal activity levels, including vigorous exercise, following transplantation. A number of posttransplant patients have completed marathons and participated in other rigorous physical activities, and at least one such individual has competed as a professional athlete.
Cardiac denervation results in an altered response to some medications used in emergency resuscitation. 3 In patients with supraventricular tachycardias, the lack of sympathetic innervation obviates the utility of carotid sinus massage. Atropine, which acts by abolishing reflex vagal slowing, will have no effect on heart rate in patients with symptomatic bradyarrhythmias. Conversely, denervated hearts are quite sensitive to the chronotropic effects of b-adrenergic agents such as isoproterenol, dopamine, and dobutamine. Because these are normal hearts, they are resistant to the proarrhythmic effects of these drugs. Isoproterenol is used preferentially to increase donor heart rates because it has the greatest chronotropic effects and can easily be titrated to achieve the desired heart rate. The typical dose range is 1 to 4 pg/min administered by continuous intravenous infusion.
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