Blood Pressure And Stroke

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The most important risk factor for stroke is hypertension, and aggressive treatment of hypertension can significantly reduce the risk of stroke (2-4). In the setting of acute ischemic stroke, however, interventions that reduce blood pressure (BP) can be detrimental (5-7). Spontaneous BP fluctuations are also predictive of outcome; both extreme hypotension and extreme hypertension after stroke onset are associated with worse outcome (8-14). Marked hypertension is associated with severe stroke, and appears to contribute to the development of cerebral edema (13,14). Whether treatment of extreme hypertension will improve outcome or limit the formation of cerebral edema has not been rigorously studied in prospective randomized, controlled trials.

Given the tight regulation of CBF, the relationship between BP and stroke outcome might seem difficult to reconcile. Blood flow to the brain is independent of mean arterial blood pressure and cerebral perfusion pressure (CPP) within the normal physiologic range, a phenomenon known as cerebral autoregulation (Fig. 1). In normotensive individuals, CBF in gray matter is maintained at approximately 50 mL/100 g tissue/min at CPP between 50 and 150 mmHg; patients with chronic hypertension autoregulate CBF at a higher CPP range. In ischemic brain, however, the ability to autoregulate is lost, and CBF becomes passively dependent on BP (15). It is this loss of cerebral autoregulation following stroke that likely accounts for the relationship between BP extremes and outcome from stroke. The loss of autoregulation also suggests that lowering BP in patients with acute stroke might further decrease CBF to already ischemic tissue (e.g., tissue in the penumbra) and threaten its survival. Given that BP directly influences CBF in ischemic tissue, BP should not be lowered in acute stroke unless signs indicate hypertensive urgency or the patient is to be treated with a thrombolytic. Failure to adequately treat hypertension prior to thrombolysis is associated with an increased risk of hemorrhagic transformation (16-19).

Figure 1 Cerebral autoregulation to pressure. Patients with chronic hypertension autoregulate CBF at higher cerebral perfusion pressure than normotensive individuals; the ability to autoregulate is lost in ischemic brain tissue. Source: From Refs. 159, 160. Abbreviation: CBF, cerebral blood flow.

The loss of autoregulation in ischemic brain also suggests that increasing BP could improve CBF and help salvage tissue within the ischemic penumbra. In experimental models of stroke, elevating BP decreases infarct volume; clinical data from small pilot trials also suggest that neurologic symptoms can be improved in patients by pharmacologically elevating BP (20-23). The benefits of induced hypertension, however, have not yet been proven in prospective, randomized, controlled trials; the decision to raise the BP, therefore, must be weighed against the possibility that hypertension will induce cerebral hemorrhage and exacerbate cerebral edema. Therefore, until further data are available, prudence dictates that BP not be lowered following acute stroke unless there are extenuating circumstances (i.e., desire to give thrombolytics or signs/symptoms of hypertensive urgency/emergency). However, it may be very difficult to clinically differentiate worsening ischemia (requiring maintenance of elevated BP) from hypertension-induced cerebral edema (requiring aggressive lowering of BP). If BP is to be lowered, intravenous drugs with a short half-life that do not directly affect the cerebral vas-culature are preferred because the response to these drugs is predictable and easy to titrate. In general, labetalol, an a > P blocker, is the antihypertensive of choice for patients with stroke and other intracranial pathologies (24). Intravenous nicardipine can be used to lower BP in patients who are unresponsive to, or intolerant of, labetalol. For patients with relative hypotension, intravascular volume should be optimized with isotonic fluids; the use of vasopressors (e.g., phenylephrine) can be considered if BP goals cannot be met in volume-replete individuals.

Vascular tone, and thus CBF, are also regulated by the arterial content of carbon dioxide (PaCO2) and oxygen (PaO2). Reduction in PaCO2 leads to vasoconstriction and decreased CBF, whereas reduction in PaO2 leads to vasodilatation and increased CBF (Fig. 2). The response to PaCO2 is much more robust than that to PaO2; CBF increases 1 to 2 mL/100 g/min for 1 mmHg increase in PaCOi and decreases 1 to 2 mL/100 g/min for 1 mmHg decrease in PaCO2 (25). In ischemic brain, the ability to autoregulate blood flow in response to changes in perfusion pressure is clearly impaired; whether an appropriate response to CO2 occurs in ischemic brain is less clear. Within the ischemic core, CBF does not change normally in response to changes in COii the response to CO2 within the penumbra, however, may be preserved (26,27). If the CBF response to changes in PaCO2 is impaired in ischemic tissue, but maintained in normal brain, the vasodilatory response to hypercapnia in the nonischemic tissue could lead to a "steal phenomenon" and exacerbate ischemia where blood flow is already impaired. Given that a significant decrease in PaCO2 leads to vasoconstriction and thus decreases blood flow, hyperventilation can exacerbate ischemia in already ischemic tissue and even precipitate ischemia in previously nonischemic tissue. Hyperventilation should, therefore, be avoided in stroke patients unless it is being used as a temporizing measure in patients experiencing transtentorial herniation. The vascular response to PaO2 is relatively weak in comparison to that for PaCO2,

Figure 2 Changes in CBF in response to PaCO2 and PaO2. Patients with chronic hypertension autoregulate CBF at higher CPP than normotensive individuals; the ability to autoregulate is lost in ischemic brain tissue. Source: From Refs. 160. Abbreviations: CBF, cerebral blood flow; CPP, cerebral perfusion pressure.

Figure 2 Changes in CBF in response to PaCO2 and PaO2. Patients with chronic hypertension autoregulate CBF at higher CPP than normotensive individuals; the ability to autoregulate is lost in ischemic brain tissue. Source: From Refs. 160. Abbreviations: CBF, cerebral blood flow; CPP, cerebral perfusion pressure.

and no data suggest that oxygen supplementation in adequately oxygenated patients improves outcome from stroke (28). Similarly, no convincing evidence supports a role for hyperbaric oxygen in the treatment of patients with acute stroke (29).

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Blood Pressure Health

Your heart pumps blood throughout your body using a network of tubing called arteries and capillaries which return the blood back to your heart via your veins. Blood pressure is the force of the blood pushing against the walls of your arteries as your heart beats.Learn more...

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