title: Cerebral hemodynamics during treatment with sodium nitroprusside versus labetalol in malignant hypertension.
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.
authors.affiliation: Medium Care Unit, Department of Internal Medicine, Academic Medical Center F7-205, University of Amsterdam, PO Box 22700, 1100 DE Amsterdam, The Netherlands.
authors.forename: Rogier V
authors.initials: RV
authors.lastname: Immink
authors.forename: Bert-Jan H
authors.initials: BJ
authors.lastname: van den Born
authors.forename: Gert A
authors.initials: GA
authors.lastname: van Montfrans
authors.forename: Yu-Sok
authors.initials: YS
authors.lastname: Kim
authors.forename: Markus W
authors.initials: MW
authors.lastname: Hollmann
authors.forename: Johannes J
authors.initials: JJ
authors.lastname: van Lieshout
mesh_terms: D000328:Adult; D000704:Analysis of Variance; D000959:Antihypertensive Agents / Q000008:administration & dosage; D001795:Blood Pressure Determination; D002560:Cerebrovascular Circulation / Q000187:drug effects / Q000502:physiology; D004305:Dose-Response Relationship, Drug; D004334:Drug Administration Schedule; D004562:Electrocardiography; D005260:Female; D005500:Follow-Up Studies; D006439:Hemodynamics / Q000187:drug effects / Q000502:physiology; D006801:Humans; D006974:Hypertension, Malignant / Q000175:diagnosis* / Q000188:drug therapy* / Q000401:mortality; D007262:Infusions, Intravenous; D007741:Labetalol / Q000008:administration & dosage*; D008297:Male; D008875:Middle Aged; D009599:Nitroprusside / Q000008:administration & dosage*; D011336:Probability; D011446:Prospective Studies; D018570:Risk Assessment; D012720:Severity of Illness Index; D018709:Statistics, Nonparametric; D015996:Survival Rate; D016896:Treatment Outcome; D017585:Ultrasonography, Doppler, Transcranial; D014655:Vascular Resistance / Q000187:drug effects
chemical_list: D000959:Antihypertensive Agents; D009599:Nitroprusside; D007741:Labetalol