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Fairly strong evidence supports the deleterious effects of rapid reductions in BP in the early period following an acute stroke.48,49,50,51,52 Immediately beyond the area of infarction, the penumbra is at high risk for ischemia and infarct extension.53,54 A number of factors about BP in patients with a stroke are worth emphasizing. First, BP frequently rises immediately following cerebral ischemia.54,55 (Proposed mechanisms for increases in blood pressure after stroke generally include excess sympathoadrenal tone from direct neural injury,54 altered parasympathetic function, catecholamine release, and cytokine activation.56,57,58,59) BP typically begins to fall spontaneously within hours to days after stroke without intervention.56,60 As a result, medication-induced reductions in BP may lead to CPP below a level that allows adequate cerebral perfusion to the penumbra. Exacerbating this tendency, patients with stroke typically have long-standing HTN and, thus, an autoregulatory curve that is shifted to the right.
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Not all studies have shown deleterious effects of lowering BP acutely after stroke.61,62 Small sample size may account for the inconsistent findings in this regard. Furthermore, it is important to recognize that low BP upon presentation may be a surrogate for independent cardiac disease, which may explain, in part, the worse outcomes seen with lower BP in this setting.63 Most consensus guidelines recommend that BP not be treated acutely in the patient with ischemic stroke, except in the case of extreme hypertension (eg, systolic BP > 220 mm Hg or diastolic BP > 120 mm Hg) and end-organ damage. Typical examples of end-organ damage include hypertensive encephalopathy, aortic dissection, acute renal failure, acute pulmonary edema, and acute myocardial infarction. Ongoing studies are evaluating ideal BP control in the setting of acute stroke.64
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When urgent BP reduction is needed in the setting of a stroke, limited data exist to guide selection of the optimal pharmacologic agent. Many agents have been tested without clear superiority.1,65,66 Short-term, parenteral medications have the appeal of a quickly titratable effect. Nicardipine, esmolol, and labetalol are frequently used, and the use of these titratable agents is reasonable rather than the frequent bolus therapy. Alternative agents include enalaprilat or fenoldopam.11 Sodium nitroprusside, a previous favorite in the management of HTN emergencies, may dilate both cerebral arterial and venous systems and lead to increased intracranial pressure.67 When intravenous medications are used, particularly in states of altered consciousness, intra-arterial blood pressure should be continuously measured. When antihypertensive medication is given acutely to patients with ischemic stroke, MAP should be reduced by no more than 15% within the first 24 hours,68,69 and reduction of BP should not occur during the acute phase of ischemic stroke. Parenteral antihypertensive agents and some of their properties are listed in Table 44-1.
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Preliminary evidence suggests that vasopressors may have a role in maintaining CPP and thus limit infarct extension.70,71,72 The use of a vasopressor in this setting is not standard of care, however, and has not yet been incorporated into guidelines. Volume expansion, with the goal of improving cerebral perfusion, does not have a role, unless polycythemia is present.73,74 Many stroke patients are volume depleted on presentation, owing to BP-induced sodium excretion, a phenomenon known as pressure natriuresis. This volume depletion may exacerbate the fall in BP after antihypertensive agents are given.75 Low BP in the setting of obvious hypovolemia warrants volume repletion, especially if it is associated with neurologic deterioration in patients with acute stroke. Apart from volume depletion, other causes of hypotension one should consider include arrhythmias, sepsis, and aortic dissection.
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Strokes qualifying for thrombolytic therapy have different blood pressure goals, in part because of the increased risk of bleeding with higher BP. Guidelines suggest initiating antihypertensive medications in eligible patients when systolic BP is above 185 mm Hg and diastolic BP is above 110 mm Hg. For the immediate 24 hours after thrombolytic agents are given, the target BP is below 180/105 mm Hg.
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The optimal management of BP in hemorrhagic stoke is under active investigation. Initially, BP increases in the setting of intracranial hemorrhage (ICH).76 While most patients with ICH have chronic HTN and a shifted autoregulatory curve, there is less of a concern for the ischemic penumbra seen in ische-mic strokes.77,78 Several clinical studies suggest that it is safe to reduce either the BP to less than 160/90 mm Hg or the MAP to less than 130 mm Hg within 24 hours.79,80 Some studies even show reduction in hematoma growth with reduction in BP.81,82 Current guidelines target a BP of 160/90 mm Hg or a MAP of 110 mm Hg in the acute management of intracerebral hemorrhage; as ICP may be elevated, ICP monitoring may be required to ensure CPP is maintained over 60 mm Hg.83