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 O2 (PbtO2) 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 PbtO2 and intracranial pressure bolt inserted following resuscitation. Using a critical care guide, PbtO2 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 mm Hg, and PbtO2 > 20 mm Hg. Physiological parameters—intracranial pressure, PbtO2, central venous pressure, systolic BP, diastolic BP, MABP, fraction of inspired O2, 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, respectively; arteriovenous malformation in 1; and hypoxic brain injury in 1). Nicardipine was effective in 87% of the patients (with intravenous β 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 PbtO2 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 on normobaric hyperoxia was achieved at 8 hours (0.72 ± 0.289 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 PbtO2 (10.30 ± 6.49 mm Hg), with higher CPP (p < 0.001) requiring hyperoxia (p = 0.02). In this group, intravenous nicardipine resulted in an 83% improvement in 4- and 8-hour PbtO2 levels (18.1 ± 11.33 and 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 PbtO2.
Abbreviations used in this paper:
ACVS = acute cerebrovascular syndrome; BP = blood pressure; CBF = cerebral blood flow; CPP = cerebral perfusion pressure; FiO2 = fraction of inspired O2,; ICH = intracerebral hemorrhage; ICP = intracranial pressure; MABP = mean arterial BP; PbtO2 = regional brain tissue O2; SAH = subarachnoid hemorrhage; TBI = traumatic brain injury.
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