Literature DB >> 18606905

Cerebral hemodynamics during treatment with sodium nitroprusside versus labetalol in malignant hypertension.

Rogier V Immink1, Bert-Jan H van den Born, Gert A van Montfrans, Yu-Sok Kim, Markus W Hollmann, Johannes J van Lieshout.   

Abstract

In patients with malignant hypertension, immediate blood pressure reduction is indicated to prevent further organ damage. Because cerebral autoregulatory capacity is impaired in these patients, a pharmacologically induced decline of blood pressure reduces cerebral blood flow with the danger of cerebral hypoperfusion. We compared the reduction in transcranial Doppler-determined middle cerebral artery blood velocity during blood pressure lowering with sodium nitroprusside with that of labetalol. Therefore, in 15 patients, fulfilling World Health Organization criteria for malignant hypertension, beat-to-beat mean arterial pressure, systemic vascular resistance (Modelflow), mean middle cerebral artery blood velocity, and cerebrovascular resistance index (mean blood pressure:mean middle cerebral artery blood flow velocity ratio), were monitored during treatment with sodium nitroprusside (n=8) or labetalol (n=7). The reduction in mean arterial blood pressure with sodium nitroprusside (-28+/-3%; mean+/-SEM) and labetalol (-28+/-4%) was comparable. With labetalol, both systemic and cerebral vascular resistance decreased proportionally (-13+/-10% and -17+/-5%), whereas with sodium nitroprusside, the decline in systemic vascular resistance was larger than that in cerebral vascular resistance (-53+/-4% and -7+/-4%). The rate of reduction in middle cerebral artery blood velocity was smaller with labetalol than with sodium nitroprusside (0.45+/-0.05% versus 0.78+/-0.04% cm.s(-1).%mm Hg(-1); P<0.05). In conclusion, sodium nitroprusside reduced systemic vascular resistance rather than cerebral vascular resistance with a larger rate of reduction in middle cerebral artery blood velocity, suggesting a preferential blood flow to the low resistance systemic vascular bed rather than the cerebral vascular bed.

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Year:  2008        PMID: 18606905     DOI: 10.1161/HYPERTENSIONAHA.108.110395

Source DB:  PubMed          Journal:  Hypertension        ISSN: 0194-911X            Impact factor:   10.190


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