Management of hypertensive emergencies in acute brain disease: evaluation of the treatment effects of intravenous nicardipine on cerebral oxygenation Clinical article

Object. Inappropriate sudden blood pressure (BP) reductions may adversely affect cerebral perfusion. This study explores the effect of nicardipine on regional brain tissue O-2 (PbtO(2)) during treatment of acute hypertensive emergencies. Methods. A prospective case-control Study was performed in 30 patients with neurological conditions and clinically elevated BP. All patients had a parenchymal PbtO(2) and intracranial pressure bolt inserted following resuscitation. Using a critical care guide, PbtO(2) was optimized. Intravenous nicardipine (5-15 mg/hour) was titrated to systolic BP < 160 mm Hg, diastolic BP < 90 mm Hg, mean arterial BP (MABP) 90-110 mg/Hg, and PbtO(2) > 20 mm Hg. Physiological parameters-intracranial pressure. PbtO(2), central venous pressure, systolic BP. diastolic BP, MABP, fraction of inspired O-2, and cerebral perfusion pressure (CPP)-were compared before infusion, at 4 hours, and at 8 hours using a t-test. Results. Sixty episodes of hypertension were reported in 30 patients (traumatic brain injury in 13 patients: aneurysmal subarachnoid hemorrhage in 11: intracerebral and intraventricular hemorrhage in 3 and 1, respective]),: arteriovenous malformation in 1; and hypoxic brain injury ill 1). Nicardipine was effective in 87%, of the patients (with intravenous (3 blockers in 4 patients). with a 19.7% reduction in mean 4-hour MABP (115.3 +/- 13.1 mm Hg preinfusion vs 92.9 +/- 11.40 mm Hg after 4 hours of therapy. p < 0.001). No deleterious effect on mean PbtO(2) was recorded (26.74 +/- 15.42 mm Hg preinfusion vs 27.68 +/- 12.51 mm Hg after 4 hours of therapy, p = 0.883) despite significant reduction in CPP. Less dependence oil normobaric hyperoxia was achieved at 8 hours (0.72 +/- 0.299 mm Hg preinfusion vs 0.626 +/- 0.286 mm Hg after 8 hours of therapy, p < 0.01). Subgroup analysis revealed that 12 patients had low pretreatment PbtO(2) (10.30 +/- 6.49 mm Hg), with higher CPP (p < 0.001) requiring, hyperoxia (p = 0.02). In this group, intravenous nicardipine resulted in air 83% improvement in 4- and 8-hour PbtO(2) levels (18.1 +/- 11.33 and respectively: p < 0.01) despite significant red 19.59 +/- 23.68 mm Hg, respectively; p < 0.01) despite significant reductions in both mean MABP (120.6 +/- 16.65 vs 95.8 +/- 8.3 mm Hg, p < 0.001) and CPP (105.00 +/- 20.7 vs 81.2 +/- 15.4 mm Hg, p < 0.001). Conclusions. Intravenous nicardipine is effective for the treatment of hypertensive neurological emergencies and has no adverse effect on PbtO(2). (DOI: 10.317.JNS.2008.109.12.1065)