Neurocritical care · 2008
Pharmacologic elevation of blood pressure for acute brain ischemia.
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Stead Latha G, Bellolio M Fernanda, Gilmore Rachel M, Porter Alyx B, Rabinstein Alejandro A
Аннотация
INTRODUCTION: Several studies demonstrated that patients with low blood pressure upon presentation with acute ischemic stroke have worse outcomes. Elevated mean arterial pressure (MAP) directly improves cerebral perfusion. Phenylephrine is a selective alpha-1 agonist with peripheral vasoconstrictive effect, raising the blood pressure without constricting brain vessels.
METHODS: We report a 63-year-old lady presenting with an acute high carotid T occlusion causing hemispheric ischemia that was completely reversed by implementing blood pressure augmentation with fluids and intravenous phenylephrine.
RESULTS: She arrived 4 h after symptoms onset. At its nadir, the NIHSS was 17. Head CT did not reveal hemorrhage or acute ischemic changes. CT angiogram confirmed the presence of a right internal carotid artery occlusion at the level of the neck. Hemodynamic support in the form of IV normal saline was initiated, followed by a bolus of phenylephrine. The patient responded to blood pressure augmentation with marked improvement in her level of consciousness, therefore an infusion of phenylephrine at 140 mcg/min titrated to a MAP of 110-120 mmHg was begun. There was complete resolution of the left hemiparesis less than an hour later.
CONCLUSION: This case lends support to the growing body of literature that sustains the use of pharmacological blood pressure augmentation to treat acute brain ischemia. Patients with cervical carotid occlusion represent the ideal candidates for hemodynamic augmentation treatment, as collateral flow can recruited from multiple pathways.
METHODS: We report a 63-year-old lady presenting with an acute high carotid T occlusion causing hemispheric ischemia that was completely reversed by implementing blood pressure augmentation with fluids and intravenous phenylephrine.
RESULTS: She arrived 4 h after symptoms onset. At its nadir, the NIHSS was 17. Head CT did not reveal hemorrhage or acute ischemic changes. CT angiogram confirmed the presence of a right internal carotid artery occlusion at the level of the neck. Hemodynamic support in the form of IV normal saline was initiated, followed by a bolus of phenylephrine. The patient responded to blood pressure augmentation with marked improvement in her level of consciousness, therefore an infusion of phenylephrine at 140 mcg/min titrated to a MAP of 110-120 mmHg was begun. There was complete resolution of the left hemiparesis less than an hour later.
CONCLUSION: This case lends support to the growing body of literature that sustains the use of pharmacological blood pressure augmentation to treat acute brain ischemia. Patients with cervical carotid occlusion represent the ideal candidates for hemodynamic augmentation treatment, as collateral flow can recruited from multiple pathways.