Bradycardia and hypertension in anticipation of, and exacerbated by, peribulbar block: a prospective audit.

Abstract

Changes in heart rate (HR), systolic arterial pressure (SAP) and diastolic arterial pressure (DAP) occur in anticipation of, and following, injection of a peribulbar local analgesic agent. We examined these changes in two groups of awake patients given a pre-medication of either hydroxyzine 1.0 mg/kg alone (control) or hydroxyzine 1.0 mg/kg with morphine 0.05 mg/kg. HR, SAP and DAP of 100 patients per group were monitored the day before surgery (baseline), every 5 min in the anesthesia holding room before peribulbar injection, every minute for the first 5 min after peribulbar injection and then every 5 min until transfer to the operating room. Within and between pre-medication group values of HR, SAP and DAP before and after peribulbar injection were compared with baseline. The two groups of patients were similar. Before peribulbar injection, HR was unchanged in the hydroxyzine group, but 6% slower in those given morphine (P<0.01). After injection, HR slowed in both groups, by 5% and 7% (P<0.01, both comparisons), respectively. In anticipation of injection, SAP increased in both groups to 20% and 16% above baseline, respectively, and increased further after injection to 26% and 24% above baseline, respectively (P<0.001, all comparisons). In both groups, maximum SAP following injection exceeded maximum SAP before injection (P<0.02, both comparisons). DAP increased by 4% (P<0.05) in the hydroxyzine group before injection, and by 5% and 4%, respectively (P<0.005 and P<0.05, respectively) after peribulbar injection. The audit reveals pronounced increases in SAP accompanied by lesser increases in DAP and a tendency to slowing of HR in awake patients in anticipation of peribulbar injections. Peribulbar injections cause further increases in blood pressure and mild bradycardia. These changes occur similarly in patients pre-medicated with hydroxyzine or hydroxyzine plus morphine. A mix of neuro-humoral influences (anxiety/catecholamine/baroreceptor/trigemino-vagal) are postulated as etiological.