In neurologic patients with normal intracranial pathologic findings, short-termse of nitroglycerin may be tolerated with transient increases in ICP.
map In patientsith suspected or documented elevated ICP (cerebral tumors or hematoma),erfusion in the brain is particularly susceptible to any changes
map in blood pressure;herefore, great caution should be exercised when using nitroglycerin in patientsith compromised intracranial compliance. Patients with concomitant myocardialnfarction
map may be candidates for nitroglycerin; however, the risk versus benefithould be weighted before administering this agent. In addition, nitroglycerinerebral circulation
map vasoactive therapy 231aste may not be an optimal antihypertensive agent in patients with strokeecause it is not easy to titrate
map and may have residual effects.-receptor antagonistsardiovascular effectsmolol and labetalol are the two most commonly used parenteral badrenergicntagonists. Esmolol is a
map b1-selective antagonist with a rapid onsetf action and short half-life. It is metabolized by blood esterases; therefore, thelearance of the
map drug is independent of liver and renal function. Esmolol isrimarily used for supraventricular tachycardia as well as for intraoperative orostoperative
map hypertension. The major concern with this medication is that severeradycardia can develop before lowering of blood pressure is observed;herefore, it
map is not routinely used for the treatment of a hypertensive crisis.nlike esmolol or other pure b-adrenergic antagonists, labetalol is a
map mixed a1-,1-, and b2-antagonist. Its beta-blockade activity is approximately seven timeshat of alpha-blockade after intravenous administration. Because labetalol hasn effect
map on both adrenergic receptors, it possesses less of an effect on heartate and cardiac output compared with other beta-blockers. The
map onset of action ofabetalol is approximately 5 minutes. The duration of action is between 3 and hours, which makes it
map difficult to titrate as a continuous infusion. Similar tother b-antagonists, labetalol should be avoided in patients with first-degree heartlock, severe
map bradycardia, and asthma.erebrovascular effecthe cerebrovascular effect of labetalol is primarily drawn from healthyolunteers and chronic hypertensive patients. In 1979, Griffith
map and coworkers53] reported the effects of chronic use of four beta-blockers (labetalol,etoprolol, oxprenolol, and sotalol) on blood pressure and CBF.
map A universaleduction in blood pressure was observed as expected; however, no change inBF was observed before or after treatment. These
map authors concluded that betablockersave little impact on cerebral circulation in the chronic setting but thatore research was warranted because their
map effects may vary during acutedministration. Another study [54] conducted in eight healthy normotensiveolunteers examined the effects of labetalol on blood
map pressure, global CBF andCBF, CMRO2, and cerebral autoregulation. Similar to previous findings, nohange in global CBF and rCBF or CMRO2
map was detected. The autoregulatoryurve was successfully plotted in all participants, and there was no difference inAP before and after drug
map infusion. Results from this study indicated thatabetalol has little effect on cerebral circulation in the normal brain.espite a lack of
map data on cerebrovascular effects in patients with neurologicnjuries, labetalol has been widely used for blood pressure management inhese patients. Patel
map and colleagues [55] examined the efficacy (blood pressureesponse) of labetalol in patients with hemorrhagic stroke. A moderate loweringn blood pressure
map (3%–26 was observed with doses ranging from 5 to 25 mg.32 rhoney & liu-deryken addition, no worsening of neurologic deficits
map occurred after administration ofhe drug. Powers and coworkers [26] further examined the effect of systemiclood pressure lowering on CBF using
map nicardipine or labetalol in patients withCH within 6 to 22 hours after onset. Fourteen patients were included in the study7
map were given nicardipine and 7 were given labetalol); MAP and global andericlot CBF were measured and compared with the patients’
map own baseline. Theajor conclusions were that a reduction in MAP, up to 20% from baseline,eemed to be safe and that
map nicardipine and labetalol preserved autoregulation ofBF in patients with ICH.herapeutic implicationn the basis of available data, labetalol seems to be
map a suitable antihypertensivegent in patients with neurologic injuries because it did not demonstrate anyegative impact on CBF or autoregulation in
map healthy patients and patients withCH. Larger studies are needed to delineate the impact of labetalol on cerebralirculation when autoregulation is
map impaired. A retrospective study [56] noted thatrequent boluses of labetalol were needed to achieve goal blood pressure,equiring more nursing time
map and frequent monitoring. Further investigationvaluating the effective labetalol dose and time to blood pressure response mayave an economic impact on
map clinical practice.alcium channel antagonistsardiovascular effectublingual nifedipine was frequently given in the past for hypertensivemergencies; however, reports of increased ischemic events
map and mortality curtailedts use, primarily because of an unpredictable drop in blood pressure [29].icardipine has gained popularity as a parenteral
map antihypertensive agent foranaging postoperative hypertension and hypertensive crisis in the past decade,articularly in patients with brain injury. Nicardipine, a second-generationihydropyridine
map calcium channel blocker, is structurally similar to nifedipine.ith the addition of a tertiary amine, nicardipine is highly lipophilic and readilyrosses
map the blood-brain barrier (BBB). Because of its chemical structure, the saltorm of nicardipine is more water-soluble than nifedipine, which makes the intravenousreparation possible. Like other calcium channel blockers, nicardipine
