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

<jats:sec> <jats:title>Object</jats:title> <jats:p> Inappropriate sudden blood pressure (BP) reductions may adversely affect cerebral perfusion. This study explores the effect of nicardipine on regional brain tissue O <jats:sub>2</jats:sub> (PbtO <jats:sub>2</jats:sub> ) during treatment of acute hypertensive emergencies. </jats:p> </jats:sec> <jats:sec> <jats:title>Methods</jats:title> <jats:p> A prospective case–control study was performed in 30 patients with neurological conditions and clinically elevated BP. All patients had a parenchymal PbtO <jats:sub>2</jats:sub> and intracranial pressure bolt inserted following resuscitation. Using a critical care guide, PbtO <jats:sub>2</jats:sub> 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 PbtO <jats:sub>2</jats:sub> > 20 mm Hg. Physiological parameters—intracranial pressure, PbtO <jats:sub>2</jats:sub> , central venous pressure, systolic BP, diastolic BP, MABP, fraction of inspired O <jats:sub>2</jats:sub> , and cerebral perfusion pressure (CPP)—were compared before infusion, at 4 hours, and at 8 hours using a t-test. </jats:p> </jats:sec> <jats:sec> <jats:title>Results</jats:title> <jats:p> 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 PbtO <jats:sub>2</jats:sub> 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 PbtO <jats:sub>2</jats:sub> (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 PbtO <jats:sub>2</jats:sub> 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). </jats:p> </jats:sec> <jats:sec> <jats:title>Conclusions</jats:title> <jats:p> Intravenous nicardipine is effective for the treatment of hypertensive neurological emergencies and has no adverse effect on PbtO <jats:sub>2</jats:sub> . </jats:p> </jats:sec>