MANAGEMENT OF HYPERTENSION IN STROKE PATIENT

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Dr. Shahin Akter NipaMD (Phase A) Resident , Internal

Medicine Chittagong Medical College &

Hospital

GOALS OF BP MANAGEMENT:

1. Ensure adequate cerebral perfusion2. Prevent intracranial bleeding3. Avoid exacerbation of cerebral edema

ACUTE ISCHEMIC STROKE

Acute transient blood pressure elevation occurs after stroke that lasts days to weeks.

Autoregulation of cerebral circulation is impaired in ischemic

cerebral tissue

Higher arterial pressure may be required to

maintain cerebral blood flow.

Sudden and profound

reduction of BP

Insufficient perfusion in

areas already affected

Neurological decline

Unless there is heart failure, MI, renal failure, evidence of hypertensive encephalopathy or aortic dissection blood pressure should not be lowered in first week.

BP often returns towards patient’s normal level within first few days.

WHEN TO START ANTIHYPERTENSIVE?

IF PATIENT IS INELIGIBLE FOR THROMBOLYSIS:

Antihypertensive is only recommended if systolic BP>220 mmHg or diastolic BP >120 mmHg

IF ELIGIBLE FOR THROMBOLYSIS:BP should be <185/110 mmHg before starting thrombolysis

After administration of fibrinolytic drug BP must be strictly

maintained <180/105mmHg

IF FAILURE TO CONTROL BP:

Increased chance of

intracranial haemorrha

ge

Poor functional outcome

DRUGS: IV Labetalol or esmolol

Nicardipine –continuous infusion

Sodium nitroprusside(when diastolic BP >

140mmHg)

Nicardipine

•Initial 5 mg /hour.•Titrate by 2.5 mg/h 5 min -15 interval.

Labetalol

• 2 mg/min up to 300 mg or

• 20 mg over 2 min, then 40-80 mg at 10 min interval upto 300 mg total

• Initial: 0.3 microgm/kg/min

• Maximum:10microgram/kg/min

• Usually 2-4 microgram/kg/min

Nitropruside

• Initial 80-500 mcg/kg over 1 min then,

• 50-300 mcg /kg/min

Esmolol

OBJECTIVES OF TREATMENT:

Reduction of BP 10 -

15%

After stroke, combination therapy with an

ACEI and

a diuretic reduce recurrent stroke.Target BP <130/80mmHg

Intracerebral Haemorrhage

Elevated BP is very common in intracerebral haemorrhage.

Because variety of factors including stress, pain, increased ICP and premorbid acute or persistant elevation in BP

High SBP (MAP >110 mmHg or systolic >160mmHg) is associated with -greater haematoma expansion, -exaggerate cerebral edema, -neurologic deterioration and -death.

Areas of hypoperfusion are frequently present around parenchymal haematoma.

Aggressive BP reduction could precipitate ischemia in these regions.

IF Systolic BP >180 and Diastolic BP >130 mmhg

WHEN TO START ANTIHYPERTENSIVES:

I

TARGET:

SBP<160 mmHg , MAP <110 mmHg

Current evidence indicates :

Early intensive BP lowering (systolic BP target < 140 mmhg) is safe and surviving patients show modestly better functional recovery

Observational studies with advanced neuroimaging have shown no significant ischemic penumbra in ICH with perihematomal rim of low attenuation seen on CT being related to extravasated plasma.

The major CCB drugs are used less often because of reports of adverse effects on intracranial pressure.

SUBARACHNOID HAEMORRHAGE

ACUTE ANEURYSMAL SAH

Target systolic BP<160mmHg, until ruptured aneurysm is secured in order to prevent rebleeding

After aneurysm is secured BP should not be lowered as increased risk for delayed ischemia from vasospasm

REFERENCES:1. Bradley’s Neurology in Clinical Practice 7th Edition

2. Adam’s &Victor’s Principles of Neurology 10th Edition

3. Harrison’s Principles of Internal Medicine 19th Edition

4. AHA/ASA Guideline for the Management of Spontaneous Intracranial Hemorrhage , July 2015

5. AHA/ASA Guideline for the Early Management of Patients with Acute Ischemic Stroke , 2013