Abstracts of Posters Presented at the International Anesthesia Research Society; 72nd Clinical and Scientific Congress; Orlando, FL; March 7-11, 1998: Cardiovascular Anesthesia
Introduction: Fenoldopam is a new specific dopamine-1 receptor agonist with systemic and renal vasodilating activity that is being developed for use in perioperative hypertension (HTN). Like other arterial vasodilators, fenoldopam can cause a dose-dependent reflex increase in heart rate. The objective of this study was to compare the BP and HR in patients who had received a single dose of (mostly oral) B-blockers (BB+) with those who had not received them (BB-) in the 24-hours prior to fenoldopam treatment for post-CABG HTN, defined as a MAP >or=to 105 mmHg for >or=to 5 minutes.
Methods: In a single-blinded German trial of patients with post-CABG HTN within 24 hours of surgery, 64 patients were randomized to intravenous nifedipine and 62 to intravenous fenoldopam. Of the 62 on fenoldopam, 54 (41, BB-; 13, BB+) were analyzable. BP control was defined as a decrease in MAP to 80-90 mmHg or by >or=to 15 mmHg within 30 minutes and maintenance of this BP for another 30 minutes.
Results: BP control was achieved in 76% of the fenoldopam group compared with 30% in the nifedipine group. To achieve similar mean systolic and diastolic BP reductions, much lower doses of fenoldopam were required in the BB+ group (see Figure 1). At 180 minutes, for example, for virtually identical reductions in BP, the mean dose in the BB+ group was 0.55 +/- 0.11 [micro sign]g/Kg/min compared with 0.76 +/- 0.08 [micro sign]g/Kg/min in the BB- group. The maximum mean increase in HR in the corresponding groups was 15.3 +/- 4.4 bpm compared with 12.9 +/- 4.7 bpm.
Conclusions: Fenoldopam was more effective than intravenous nifedipine at treating post-CABG HTN. Pre-treatment with B-blockers decreased the dose of fenoldopam required to achieve blood pressure control, suggesting an additive antihypertensive effect of B-blocker pre-treatment. Heart rate was unaffected by B-blocker pre-treatment, possibly secondary to inadequate B-blockade from a single oral dose or because the heart rate increase was partly parasympathetic in nature.