In neurologic patients with normal intracranial

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