HYPERTENSION MANAGEMENT IN - EMCREG-International
HYPERTENSION MANAGEMENT IN - EMCREG-International HYPERTENSION MANAGEMENT IN - EMCREG-International
ADVANCING THE STANDARD OF CARE:Cardiovascular and Neurovascular Emergenciesduration being 5 minutes), depending upon thedesired response, the maintenance infusion may becontinued at 0.05 mg/kg/min or increased step-wiseto a maximum of 0.2 mg/kg/min with each step beingmaintained for 4 or more minutes.Esmolol is contraindicated in patients with sinusbradycardia, heart block greater than first degree,cardiogenic shock or overt heart failure. 22EnalaprilatEnalaprilat, an angiotensin-converting enzyme (ACE)inhibitor when administered intravenously, is theactive metabolite of the orally administered pro-drug,enalapril maleate. Enalaprilat intravenous results inthe reduction of both supine and standing systolic anddiastolic blood pressure. The onset of action usuallyoccurs within fifteen minutes of administration withthe maximum effect occurring within one to fourhours. The duration of hemodynamic effects appearsto be dose-related. Enalaprilat is indicated for thetreatment of hypertension when oral therapy is notpractical.makes this drug very attractive in the facilitation ofblood pressure reduction. It is exactly this property,however, which makes the drug potentially lessattractive for cases of hypertensive neurologicalemergencies. Of great concern in this setting is thesignificant potential for this agent to not only reducesystemic blood pressure via relaxation of vascularsmooth muscle, but also to cause significant increasesin intracranial pressure due to dilatation of intracranialvasculature via the same mechanism. This increaseis nicely illustrated in Figure 4 adapted from AnileThe dose in hypertension is 1.25 mg every six hoursadministered intravenously over a five minute period.A clinical response is usually seen within 15 minutes.Peak effects after the first dose may not occur for up tofour hours after dosing. The peak effects of the secondand subsequent doses may exceed those of the first.Enalaprilat is contraindicated in patients with a historyof angioedema related to previous treatment withan angiotensin converting enzyme inhibitor and inpatients with hereditary or idiopathic angioedema. Aswith all vasodilators, enalapril should be given withcaution to patients with obstruction in the outflowtract of the left ventricle. 23Why Not Sodium Nitroprusside?Sodium nitroprusside is used frequently in manyEDs for rapid titratable blood pressure control inseverely hypertensive patients. Sodium nitroprussideis a potent vascular smooth muscle relaxant, whichFigure 4. Changes in intracranial pressure withnitroprusside therapy. MICP = mean intracranialpressure. Adapted with permission from Anile et al.Acta Neurochir 1981;58:203-211.68w w w . e m c r e g . o r g
HYPERTENSION MANAGEMENT INACUTE NEUROVASCULAR EMERGENCIESet al. in which preoperative neurosurgical patientswith intraventricular catheters were treated withsodium nitroprusside for blood pressure reduction.The observed increase in intracranial pressure in 9out of 10 patients was both rapid and concerning.Notably, after an initial period of steady incrementalincrease in intracranial pressure, there does appearto be a phenomenon of return toward pre-treatmentintracranial blood pressures. In the majority of cases,however the ICP did not return to normal and, in fact,in some cases remained markedly elevated. Thus, withmultiple other powerful, titratable agents available forblood pressure control in the setting of neurovascularemergencies, the use of sodium nitroprusside isgenerally not recommended. 24-27SUMMARYBlood pressure management in acute neurovascularemergencies has potential for therapeutic benefit aswell as the potential to cause harm if not performedwith great care. The indications for management areas yet not clearly defined and the exact degree ofmanagement is highly dependent on the individualpatient and their pathology. Fortunately, highlyeffective and easily titratable agents exist for use withthese complicated patients.REFERENCES1. Baron JC. Perfusion thresholds in human cerebral ischemia:Historical perspective and therapeutic implications. CerebrovascDis. 2001;11 Suppl 1:2-82. Powers WJ. Acute hypertension after stroke: The scientific basisfor treatment decisions. Neurology. 1993;43:461-4673. Paulson OB, Waldemar G, Schmidt JF, Strandgaard S. Cerebralcirculation under normal and pathologic conditions. Am J Cardiol.1989;63:2C-5C4. Zivin JA. Factors determining the therapeutic window for stroke.Neurology. 1998;50:599-6035. Adams HP, Jr., Adams RJ, Brott T, del Zoppo GJ, Furlan A,Goldstein LB, Grubb RL, Higashida R, Kidwell C, KwiatkowskiTG, Marler JR, Hademenos GJ. Guidelines for the earlymanagement of patients with ischemic stroke: A scientificstatement from the stroke council of the American StrokeAssociation. Stroke. 2003;34:1056-10836. Grossman E, Messerli FH, Grodzicki T, Kowey P. Should amoratorium be placed on sublingual nifedipine capsules givenfor hypertensive emergencies and pseudoemergencies? JAMA.1996;276:1328-13317. Brott T, Lu M, Kothari R, Fagan SC, Frankel M, Grotta JC,Broderick J, Kwiatkowski T, Lewandowski C, Haley EC, MarlerJR, Tilley BC. Hypertension and its treatment in the NINDS rt-PAstroke trial. Stroke. 1998;29:1504-15098. Fogelholm R, Avikainen S, Murros K. Prognostic value anddeterminants of first-day mean arterial pressure in spontaneoussupratentorial intracerebral hemorrhage. Stroke. 1997;28:1396-14009. Hemphill JC, 3rd, Bonovich DC, Besmertis L, Manley GT,Johnston SC. The ICH score: A simple, reliable grading scale forintracerebral hemorrhage. Stroke. 2001;32:891-89710. Qureshi AI, Bliwise DL, Bliwise NG, Akbar MS, Uzen G,Frankel MR. Rate of 24-hour blood pressure decline and mortalityafter spontaneous intracerebral hemorrhage: A retrospectiveanalysis with a random effects regression model. Crit Care Med.1999;27:480-48511. Broderick JP, Adams HP, Jr., Barsan W, Feinberg W, FeldmannE, Grotta J, Kase C, Krieger D, Mayberg M, Tilley B, ZabramskiJM, Zuccarello M. Guidelines for the management of spontaneousintracerebral hemorrhage: A statement for healthcare professionalsfrom a special writing group of the Stroke Council, AmericanHeart Association. Stroke. 1999;30:905-91512. Jauch EC, Lindsell CJ, Adeoye O, Khoury J, Barsan W, BroderickJ, Pancioli A, Brott T. Lack of evidence for an association betweenhemodynamic variables and hematoma growth in spontaneousintracerebral hemorrhage. Stroke. 2006;37:2061-206513. Becker KJ, Baxter AB, Bybee HM, Tirschwell DL, AbouelsaadT, Cohen WA. Extravasation of radiographic contrast isan independent predictor of death in primary intracerebralhemorrhage. Stroke. 1999;30:2025-203214. Powers WJ, Zazulia AR, Videen TO, Adams RE, Yundt KD,Aiyagari V, Grubb RL, Jr., Diringer MN. Autoregulation ofcerebral blood flow surrounding acute (6 to 22 hours) intracerebralhemorrhage. Neurology. 2001;57:18-2415. Bullock RM, Chesnut R, Clifton GL, al. e. Management andprognosis of severe traumatic brain injury, part 1. Guidelines forthe management of severe traumatic brain injury. J Neurotrauma.2000;17:451-55316. Schellinger PD, Fiebach JB, Hoffmann K, Becker K, OrakciogluB, Kollmar R, Juttler E, Schramm P, Schwab S, Sartor K,Hacke W. Stroke MRI in intracerebral hemorrhage: Is there aperihemorrhagic penumbra? Stroke. 2003;34:1674-167917. Ohkuma H, Tsurutani H, Suzuki S. Incidence and significance ofearly aneurysmal rebleeding before neurosurgical or neurologicalmanagement. Stroke. 2001;32:1176-118018. Treggiari MM, Walder B, Suter PM, Romand JA. Systematicreview of the prevention of delayed ischemic neurological deficitswith hypertension, hypervolemia, and hemodilution therapyfollowing subarachnoid hemorrhage. J Neurosurg. 2003;98:978-984w w w . e m c r e g . o r g69
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ADVANC<strong>IN</strong>G THE STANDARD OF CARE:Cardiovascular and Neurovascular Emergenciesduration being 5 minutes), depending upon thedesired response, the maintenance infusion may becontinued at 0.05 mg/kg/min or increased step-wiseto a maximum of 0.2 mg/kg/min with each step beingmaintained for 4 or more minutes.Esmolol is contraindicated in patients with sinusbradycardia, heart block greater than first degree,cardiogenic shock or overt heart failure. 22EnalaprilatEnalaprilat, an angiotensin-converting enzyme (ACE)inhibitor when administered intravenously, is theactive metabolite of the orally administered pro-drug,enalapril maleate. Enalaprilat intravenous results inthe reduction of both supine and standing systolic anddiastolic blood pressure. The onset of action usuallyoccurs within fifteen minutes of administration withthe maximum effect occurring within one to fourhours. The duration of hemodynamic effects appearsto be dose-related. Enalaprilat is indicated for thetreatment of hypertension when oral therapy is notpractical.makes this drug very attractive in the facilitation ofblood pressure reduction. It is exactly this property,however, which makes the drug potentially lessattractive for cases of hypertensive neurologicalemergencies. Of great concern in this setting is thesignificant potential for this agent to not only reducesystemic blood pressure via relaxation of vascularsmooth muscle, but also to cause significant increasesin intracranial pressure due to dilatation of intracranialvasculature via the same mechanism. This increaseis nicely illustrated in Figure 4 adapted from AnileThe dose in hypertension is 1.25 mg every six hoursadministered intravenously over a five minute period.A clinical response is usually seen within 15 minutes.Peak effects after the first dose may not occur for up tofour hours after dosing. The peak effects of the secondand subsequent doses may exceed those of the first.Enalaprilat is contraindicated in patients with a historyof angioedema related to previous treatment withan angiotensin converting enzyme inhibitor and inpatients with hereditary or idiopathic angioedema. Aswith all vasodilators, enalapril should be given withcaution to patients with obstruction in the outflowtract of the left ventricle. 23Why Not Sodium Nitroprusside?Sodium nitroprusside is used frequently in manyEDs for rapid titratable blood pressure control inseverely hypertensive patients. Sodium nitroprussideis a potent vascular smooth muscle relaxant, whichFigure 4. Changes in intracranial pressure withnitroprusside therapy. MICP = mean intracranialpressure. Adapted with permission from Anile et al.Acta Neurochir 1981;58:203-211.68w w w . e m c r e g . o r g
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