Manipulation of blood pressure becomes necessary in many ischemic stroke patients, as patients with ongoing ischemia and fixed stenotic arterial lesion(s) may require blood pressure management to feed the ischemic penumbra. Conversely, patients with cerebral edema may require blood pressure lowering to reduce the detrimental effect of increased cerebral blood flow (CBF). In the normal human brain, CBF is kept relatively constant by the mechanism of cerebral autoregulation. This applies throughout a range of CPP from approximately 40 to 140 mm Hg. Beyond this range, the autoregulatory capacity is overwhelmed, and at pressures below 40 mm Hg further ischemia ensues. At pressures above 140 mm Hg, cerebral edema often worsens. Both of these circumstances assume an intact autoregulatory capacity, which may be significantly impaired in acute stroke patients. Older patients, or patients with chronic hypertension, often have poor vasoreactivity of the cerebral resistance vessels, perhaps secondary to morphometric changes with sympathetic denervation within the vessels themselves.40 Consequently, they may be more susceptible to worsening ischemia due to an impaired ability to vasodilate, even in the setting of diminished cerebral perfusion. Alternatively, patients with a large ischemic stroke, by definition, have an impaired BBB, and with relatively higher blood pressures they may lose their ability to appropriately vasoconstrict, leading to more profound cerebral edema.
Blood pressure lowering in the setting of an acute ischemic stroke can be detrimental. Oliveira-Filho et al.41 found that the degree of systolic blood pressure reduction in the first 24 hours strongly correlated with poor outcome at 3 months in acute stroke patients (odds ratio (OR) 1.89 per 10% decrease, 95% CI 1.02-3.52, p = 0.047). In contrast, there is much debate regarding the efficacy of induced hypertension in stroke patients. In a pilot study by Rordorf et al.,42 controlled augmentation of the systolic blood pressure by 20% in the acute setting resulted in significant clinical improvement in 7 out of 13 acute stroke patients. Marzan et al.43 retrospectively evaluated 34 acute stroke patients who underwent induced hypertension (10-20% of the initial value) for a median of 26 hours, and found that cardiac arrhythmias occurred in one patient, and intracerebral hemorrhage in two patients (one fatal). They concluded that the process is feasible and safe in patients with acute stroke. Koenig et al.44 performed a retrospective analysis of 100 acute stroke patients, 46 of whom underwent induced hypertension, aiming for a mean arterial pressure (MAP) target of 10-20% higher than the patient's baseline value. There was no difference in adverse events between the induced hypertension group and the group that received standard medical therapy, although the length of stay was significantly increased in patients who underwent induced hypertension.
The most commonly used intravenous vasopressor agent is phenylephrine, which is a preferential a-1 agonist, with little or no activity on the intracranial cerebral vasculature. Its use must be weighed against the potential risks, including the possibility for exacerbating underlying coronary artery disease (CAD) or causing hemorrhagic conversion of an ischemic stroke. Induced hypertension therapy for acute ischemic stroke is discussed further in Chapter 5. Table 8.2 provides a summary of the commonly used vasopressor agents and their side effects.
For patients with massive cerebral infarction, induced hypertension is relatively contraindicated, as this may exacerbate cerebral edema. However, the clinician must also be wary of reducing the blood pressure too aggressively, as relative hypotension may induce a reflexive increase in the CBF by cerebral vasodilation and thereby exacerbate cerebral edema. Multiple intravenous antihypertensive agents are available for use, the most common being beta-blockers, calcium channel blockers, and nitrates. Labetolol is typically well tolerated, and may be protective against cardiac ischemia. However, it may also exacerbate asthma/COPD and may be ineffective in treating refractory, severe hypertension. Nicardipine is a recommended alternative; it is a potent vasodilator that is well tolerated, but more costly. It does have negative inotropic effects and may cause left ventricular dysfunction. Nitroprusside should be used with great caution, as it can cause cerebral vasodila-tion and impair autoregulation, thereby increasing ICP. It can also cause excessive
TABLE 8.2 Vasopressor Medications.
Onset of Action
2-lGG mg/minute l-l2
50 mg/kg over
10 minute bolus then 0.375-0.75 mg/kg/minute
Seconds to minutes
Up to 5 minutes
Bradycardia, coronary vasoconstriction, decreased renal perfusion, metabolic acidosis
Increased myocardial demand, flushing, arrhythmia, decreased renal perfusion
Ectopy, tachycardia, headache
1-10 minutes Tachycardia, hypotension, nausea, dyspnea
Arrhythmia, headache, hyperglycemia, hypokalemia
Arrhythmia, chest pain, headache, nausea,
H2O retention, seizures
5-15 minutes Arrhythmia, headache
Alpha-1, increased cardiac output (CO), decreased systemic vascular resistance (SVR)
Alpha-1, beta-1, increased CO, decreased SVR Alpha-1, beta-1, beta-2, increased CO, variable SVR
Alpha-1, beta-1, dopamine, increased CO, SVR
Beta-1, beta-2, increased CO, decreased SVR Beta-1, beta-2, increased CO, decreased SVR
Increased CO, decreased SVR
hypotension in elderly or hypovolemic patients, and can be associated with rebound hypertension upon withdrawal. It also carries the potential for cyanide and thiocya-nate toxicity with prolonged use. Table 8.3 provides an explanation of different available IV antihypertensive agents.
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