This document discusses blood pressure control in patients with acute cerebrovascular diseases such as ischemic stroke, intracerebral hemorrhage, and subarachnoid hemorrhage. It recommends modest reduction of blood pressure to targets of 160/90 mm Hg for intracerebral hemorrhage and less than or equal to 150/90 mm Hg for subarachnoid hemorrhage to reduce risks of hemorrhage expansion and rebleeding. For ischemic stroke, the document recommends not treating hypertension unless systolic blood pressure exceeds 220 mm Hg or diastolic blood pressure exceeds 120 mm Hg. The preferred drugs for blood pressure control in these patients are nicardipine, labetalol, and esmol

1. Blood Pressure Control in Acute
Cerebrovascular Disease
HAIDER EJAM

2. Blood Pressure Control in Acute Cerebrovascular Disease
Acute ischemic stroke = results in two types of neuronal injury. The
core, or central part of the infarction, consists of cellular necrosis and
irreversibly damaged brain tissue. Unfortunately, this area of the brain is
beyond salvage with current therapies. The second type is the
penumbra, which varies in size and surrounds the core. The penumbra
represents ischemic, but not infarcted, neuronal tissue and is the focus
of most interventions for acute stroke. This area is not usually evident on
computed tomography scanning but can be detected using magnetic
resonance imaging.

3. Blood Pressure Control in Acute Cerebrovascular Disease
• It has been shown that without treatment, the hypertension present at
the time of admission will decline over the next 24 hours and this
decline may continue for up to 7 days after the stroke. The American
Heart Association/American Stroke Association (AMA/ASA) Scientific
Statement on the early treatment of stroke recommends that arterial
hypertension not be treated in the acute phase unless the SBP
exceeds 220 mm Hg, the diastolic BP (DBP) exceeds 120 mm Hg, or if
there is evidence of other acute end-organ damage due to
hypertension, such as cardiac ischemia, pulmonary edema, aortic
dissection, or acute renal failure

4. Blood pressure control
• Severe hypertension is considered a contraindication to the use of
thrombolytics in acute ischemic stroke due to the increased risk of
hemorrhagic conversion. If thrombolytic therapy is given, the BP should
be more tightly controlled than if the patient were treated
conservatively. The SBP should be treated if it exceeds 180 mm Hg,
and the DBP should be treated if it exceeds 105 mm Hg.

5. Blood pressusre controls
• Intracerebral hemorrhage = BP control in the management of ICH can
be more aggressive than with acute ischemic stroke, mainly because
of the lack of an ischemic penumbra with ICH.The rim of the
hematoma may be vulnerable to impaired cerebral perfusion,
however, and any BP reduction should be moderate.Currently, the
AHA/ASA recommendsmodest reduction of BP to a target of 160/90
mm Hg, with a MAP of 110 mm Hg

6. Blood pressure control
• Subarachnoid hemorrhage = Rebleeding of the ruptured
aneurysm has an incidence of 4% in the first 24 hours after SAH.
The incidence falls to 1% each day thereafter until the aneurysm
is secured.. Higher rates of rebleeding have been observed
when the SBP exceeds 160 mm Hg,so a target SBP of < or =
to 150 mm Hg seems prudent. [ SBP spikes above 150 mm
Hg, increase the risk of rerupture of the aneurysm, which
carries a 75% risk of mortality ]

7. Pharmacological therapy
• The ideal drug for managing BP in acute cerebrovascular emergencies
would be rapidly titratable, have a short half-life, and have a minimal
number of side effects. Antihypertensives most commonly used in
cerebrovascular emergencies include nicardipine, labetalol, and
esmolol
• Nicardipine [5- to 15-mg/h infusion] = Calcium channel antagonist
with no suppression of the atrioventricular node; acts as a cerebral
arterial vasodilator. Very titratable with few side effects and preferred
for most neurocritical care patients

8. Pharamacological therapy
• Labetalol [20- to 40-mg intravenous bolus, or 0.5- to 2.0-mg/min
infusio = Combined α- and β-receptor antagonist; especially useful in
hyperadrenergic conditions (cocaine intoxication, subarachnoid
hemorrhage). Can cause bradycardia and bronchospasm.
• Esmolol [500 μg/kg intravenous bolus, followed by a 25- to 300-
μg/kg/min infusion ] = Selective β1-receptor antagonist; has very
short half-life. Effect of the drug is lost 10 to 20 min after the infusion
is stopped.

9. Pharmacological therapy
• Sodium nitroprusside = dilates both arterioles and veins, which
increases cerebral edema and intracranial pressure. It also worsens
cerebral autoregulation and has no place in neurocritical care

10. Conclusion
• Acute cerebrovascular diseases are common events, and physicians
should be comfortable with managing BP derangements in these
patients. Above all, the treating physician should ensure that
hypoxemia and cerebral hypoperfusion are avoided, as this can result
in significant secondary brain injury. When uncontrolled hypertension
is present, the physician must decide two things: one, what is the
optimal BP for this patient; and two, what is the best pharmacologic
agent to reach this goal. Prompt treatment, while avoiding
exacerbating cerebral ischemia, is an integral part of the care of
patients with acute cerebrovascular disease