PreambleIt is becoming more apparent each day that despite a strong national commitment to excellence in health care, the resources and personnel are finite. It is, therefore, appropriate that the medical profession examine the impact of developing technology on the practice and cost of medical care. Such analysis, carefully conducted, could potentially impact on the cost of medical care without diminishing the effectiveness of that care.

The acute hemodynamic effects of dobutamine and nitroprusside were compared in 19 patients with low output cardiac failure. At dosage levels yielding similar increases in cardiac index (12 patients), nitroprusside resulted in significantly lower arterial systolic and wedge pressures and did not increase heart rate suggesting advantages over dobutamine when reduction in myocardial oxygen requirement or pulmonary congestion is a major goal. Systemic arterial mean and diastolic pressures were minimally changed with dobutamine, but fell significantly with nitroprusside suggesting advantages of dobutamine over nitroprusside in patients where hypotension could limit coronary blood flow or perfusion of other vital organs. Reduction in pulmonary arteriolar resistance occurred only with nitroprusside. Arterial hypoxemia developed in three patients during nitroprusside infusion suggesting the possibility of increased right-to-left intrapulmonary shunting resulting from a direct vasodilating effect of nitroprusside on pulmonary arteriole smooth muscle. Although both inotropic and vasodilator drugs can result in hemodynamic improvement when administered to patients with chronic low output cardiac failure, significant differences of potential clinical importance exist between these two modes of therapy.

Fourteen patients with coronary artery disease and normal or near-normal left ventricular function were studied at rest and during atrial pacing until the occurrence of angina (12 patients) before and during infusion of dobutamine (3.80 + 0.45 ,ug/kg/min). At rest, during the infusion, three patients developed chest pain, mean ST segment depression increased from 0.02 to 0.08 mV (p < .001), and myocardial lactate extraction fell from + 17.5% to -1.4% (p < .05). These ischemic changes were associated with significant increases in arterial systolic pressure (134 to 149 mm Hg), heart rate (79 to 91 beats/min), coronary sinus flow (89 to 113 ml/min) and myocardial oxygen consumption (10.8 to 13.5 cc/min). In contrast, during atrial pacing, dobutamine did not reduce the pacing threshold or further increase myocardial oxygen consumption or ST segment changes; however, arterial mean and diastolic pressures were significantly lower with pacing during dobutamine infusion compared with control pacing. In the absence of heart failure, dobutamine in low doses can cause myocardial ischemia in patients with coronary artery disease. The absence of increased ischemia from dobutamine during pacing may reflect reversal of pacing-induced ventricular dysfunction. Circulation 68, No. 5, 1044-1050, 1983. BECAUSE of its relative lack of direct chronotropic and peripheral-vascular effects, dobutamine has become a popular inotropic agent for temporary support of cardiac patients with acute hypotension and lowoutput states, even when left ventricular function is only modestly impaired. Such patients frequently have had recent myocardial infarction or coronary artery surgery. Thus the effects of dobutamine on the balance between myocardial oxygen supply and demand in patients with coronary artery disease are of clinical importance. The purpose of our study was to evaluate the effects of dobutamine infusion on coronary hemodynamics and myocardial metabolism both at rest and during rapid atrial pacing in a group of patients with significant coronary disease who nevertheless had normal or only modest impairment of left ventricular function. MethodsPatients were selected for the study on the basis of a clinical diagnosis of angina pectoris and angiographic demonstration of 1044significant coronary obstruction (>50% transluminal diameter) of at least one major coronary artery. Patients with unstable angina, significant left main coronary artery obstruction, myocardial infarction within the preceeding 6 weeks, severe heart failure (New York Heart Association class III or IV), or significant valvular heart disease were excluded. The study group was selected from the patients with angina pectoris who were referred to our cardiac catheterization laboratory for coronary angiography. The study group consisted of 14 patients who met all the inclusion criteria and who consented to participate in the study. The study was done 1 to 21 days (mean 8 days) after coronary angiography. f3-Adrenoreceptor blocking agents were discontinued for 48 h...

Fifteen patients with midsystolic clicks associated with mitral valve prolapse were studied in order to assess changed in ausculatatory findings produced by pacing-induced variations in cardiac rate, rhythm, and conduction. As the heart rate was increased in stepwise intervals to the maximum possible extent by right atrial pacing (RAP) in 14 patients, the interval between the Q wave and the click (Q-C) decreased in all cases (21 plus or minus msec/10 beats/min; P smaller than 0.001). In two patients, RAP at rates of and above 118 and 159 per minute, respectively, resulted in disappearance of the click. During right ventricular pacing (RVP) without evidence of atrioventricular (A-V) dissociation on the surface ECG in ten patients, the click was inaudible at all pacing rates in three instances. In all seven of the cases in which the click was audible at the lowest rate of RVP with VA conduction, Q-C was greater and C-S2 less than that in sinus rhythm. As the rate of RVP was increased, Q-C was noted to decrease (26 plus or minus 4 msec/10 beats/min) and C-S2 to increase (19 plus or minus 7 msec/10 beats/min) in all patients. In three patients in whom RVP induced atrioventricular dissociation, the click was seen only in beats closely preceded by a P wave. In ten of 11 patients the click occurred earlier in systole with a postextrasystolic or post tachycardia beat as compared to its appearance after a sinus beat when a shorter preceding diastolic filling period was present (P smaller than 0.001). In the eleventh patient a loud systolic murmur was present during a postextrasystolic cycles. It is concluded that pacing-induced rhythm disturbances can result in disappearance of a midsystolic click or can alter its timing and cause it to mimic sonic phenomena seen in other disease states. The possibility of similar changes taking place as a result of spontaneously occurring disturbances of rate, rhythm, and conduction should be recognized in order that the possible diagnosis of mitral valve prolapse not be overlooked.

Hemodynamic effects of dopamine and intravenous nitroglycerin alone, and in combination, were studied in 27 patients with severe left ventricular failure. Dopamine alone increased cardiac index from 1.8 to 2.5 1/min/m2 but also increased wedge pressure from 24 to 30 mm Hg and heart rate from 88 to 101 beats/min. Arterial oxygen saturation fell from 92% to 87% (p < .001). Nitroglycerin alone had a lesser effect on cardiac index (1.8 to 2.2 1/min/m2) but decreased wedge pressure from 26 to 16 mm Hg and heart rate from 91 to 86 beats/min. Arterial oxygen saturation fell from 91% to 90% (NS). Combined dopamine and nitroglycerin administration resulted in optimal hemodynamics, with cardiac index of 2.9 1/min/m2, wedge pressure of 17 mm Hg, and heart rate of 96 beats/min. Arterial oxygen saturation remained low at 88% in spite of the reduction in left ventricular filling pressure, which probably reflects increased intrapulmonary right-to-left shunting coupled with increased pulmonary blood flow. These results suggest that the combination of dopamine with intravenous nitroglycerin should be considered for patients with severe left ventricular dysfunction who require temporary pharmacologic support. Circulation 68, No. 4, 813-820, 1983. TEMPORARY pharmacologic support of patients with chronic severe left ventricular dysfunction is frequently required either during episodes of deterioration or before definitive diagnostic or therapeutic procedures. Although a variety of intravenous inotropic and vasodilator drugs are available for this purpose, the selection of a specific drug or combination of drugs remains largely empiric.Dopamine, a catecholamine with significant inotropic activity, has potential advantages for use in patients with advanced low-output cardiac failure because of its selective effect on promoting blood flow to renal and splanchnic beds via stimulation of nonadrenergic vasodilator receptors in these areas.1 Although dopamine infusion may reduce an elevated left ventricular filling pressure in some patients with heart failure, other patients may show a significant increase in filling pressure associated with the development of pulmonary