Intravenous nifedipine for control of hypertension in patients after coronary artery bypass graft surgery.
A study was undertaken to assess the use of intravenous nifedipine in controlling hypertension in patients following coronary artery surgery. A combined hemodynamic and metabolic assessment was carried out in 15 patients on data recorded at six sequential time intervals: (1) baseline, (2) control of blood pressure, (3) 30 minutes after control of blood pressure, (4) 1.5 hours after control of blood pressure, (5) 3.5 hours after control of blood pressure, and (6) 30 minutes after discontinuing nifedipine. Coronary sinus and great cardiac vein blood flows were measured by the continuous thermodilution technique using the Baim coronary sinus flow catheter. Intravenous nifedipine was run initially at an average rate of 1.82 microg/kg/min. It took an average time of 12 minutes to lower the blood pressure to less than 130 mmHg systolic. There were highly significant decreases in systolic, mean, and diastolic blood pressures (P < .001), associated with significant decreases in systemic vascular resistance (P < .001) and left ventricular stroke work index (P < .05). There was an increase in cardiac output at 30 and 90 minutes of infusion (P < .05), and the stroke volume was increased 90 minutes after starting nifedipine (P < .05). The increase in heart rate was not significant. There was no significant effect on conduction times as measured by PR and QRS intervals on the ECG. However, the QTc interval was decreased after 3.5 hours (P < .05). There was an increase in right atrial pressure at 90 minutes and again 30 minutes after stopping nifedipine. (P < .05). The pulmonary artery pressure also was increased after stopping the infusion (P < .05). The pulmonary capillary wedge pressure, pulmonary vascular resistance, and right ventricular stroke work index remained unchanged. Coronary sinus and great cardiac vein flows were maintained despite a decrease in perfusion pressure, suggesting that nifedipine is a potent coronary vasodilator. Indeed, coronary vascular resistance was significantly decreased (P < .05). Myocardial oxygen consumption remained unchanged. The lactate extraction indicated that myocardial metabolism remained aerobic regionally and globally. Thus, the results suggest that blood pressure was easy to control and that there were no adverse effects on atrioventricular conduction, cardiac performance, regional and global myocardial oxygen utilization, or lactate extraction.
Davis
M E
ME
Department of Anaesthetia, The London Chest Hospital.
Jones
C J
CJ
Feneck
R O
RO
Walesby
R K
RK
D000328:Adult; D000368:Aged; D001794:Blood Pressure / Q000187:drug effects; D002302:Cardiac Output / Q000187:drug effects; D001026:Coronary Artery Bypass; D003326:Coronary Circulation / Q000187:drug effects; D004305:Dose-Response Relationship, Drug; D005260:Female; D006801:Humans; D006973:Hypertension / Q000188:drug therapy*; D007262:Infusions, Intravenous / Q000379:methods; D008297:Male; D008875:Middle Aged; D009206:Myocardium / Q000378:metabolism; D009543:Nifedipine / Q000008:administration & dosage*; D011183:Postoperative Complications / Q000517:prevention & control*; D013318:Stroke Volume / Q000187:drug effects; D013815:Thermodilution / Q000379:methods; D013997:Time Factors; D016896:Treatment Outcome; D014655:Vascular Resistance / Q000187:drug effects; D014665:Vasodilator Agents / Q000008:administration & dosage*
D014665:Vasodilator Agents; D009543:Nifedipine