Hypertension Management in

Acute Stroke

Mursyid Bustami
Neurology Department
University of Indonesia
Background

•  Hypertension is common following acute stroke.

•  75 % of patients AIS have elevated BP at presentation
(>160/95 mmHg within the first 48 h of the event).
•  Decrease spontaneously in 10–14 days.
•  The benefits and risks of treatment of acute stroke
hypertension are not clear.
•  Potential pros and cons (raising BP ? vs lowering BP ?)
•  Very few trials of either pressor or depressor
interventions in the acute stroke period.

Stroke, 1986;17:861-64 .
Hypertension in Acute Stroke

SBP >140 mmHg; 81,6% (IST,2002) SBP >140 mmHg; 77,8% (BASC,2001)

Ischemic stroke patients have elevated BP at presentation (70-94%)

(30% hypertension crises)
Causes of Elevated BP on Acute
Stroke

Related Caused factors:

factors: •  Lesion of the center of
•  Stress vasomotor modulation
(cortex of insula)
•  Full bladder •  Activation of corticotropic
•  Pain system
•  Nausea •  Activation of sympathetic
•  Hemorrhage system.
stroke •  Activation of RAS.
•  Prior of •  Low of NO level
hypertension •  Increased CO.
•  Intracranial hypertension
 Hypertension in Acute Stroke

Dead
• Every 10 mmHg
decreased in SBP < 150
mmHg; mortality rate
increased by 17.5%
• Every 10 mmHg
increased in SBP > 150
mmHg; mortality rate
increased by 3.8%

International Stroke Trial, 2002.

 Hypertension in Acute Stroke

Dead

Every 10 mmHg
increased in SBP > 180
mmHg:
• Risk of neurological
status deterioration
increased by 40%
• Risk of poor outcome
increased by 23%

International Stroke Trial, 2002.

 Hypertension in Acute Stroke

Recurrent

Every 10 mmHg
decreased in SBP <
150 mmHg; risk of
ischemic stroke
recurrence in 14 days
increased by 14.2 %

International Stroke Trial, 2002.

Concepts of Brain Injury (Stroke)

•  Primary Injury:
area of maximum neuronal
damage.
•  Penumbra:
area of less injured and
potentially recoverable neuronal
tissue
•  Secondary injury:
follows primary injury and
causes further neuronal damage.
Autoregulation

Normal :
– CPP 70 – 100 mmHg.
– CBF remains 50 ml/
100mg tissue/min ~
CPP 40 - 140 mm Hg

AUTOREGULATION
Impaired AUTOREGULATION

•  Loss of autoregulation in ischemic

penumbra.
•  CBF varies directly with CPP.
•  Pathologic state of pressure passive
perfusion.
•  CPP < 70 mmHg  CBF ↓  secondary
insults.
Impaired AUTOREGULATION

Rosner MJ, Becker DP, J Neurosurg 1984;50:312.)

Reasons to treat hypertension

Ischemic Stroke Mechanisms :

•  Recurrent Stroke •  Highly elevated BP will caused
•  Hemorrhage vasodilation, cerebral edema,
transformation capillary vasoconstriction which will
•  Cerebral edema be followed by cerebral
hypoperfusion
•  Elevated BP will induce ICH. In
Hemorrhage stroke
ischemic stroke, it will caused
•  Re-bleeding hemorrhagic transformation.
•  Bleeding In hemorrhagic stroke, it will
extension caused hemorrhagic extension or
re-bleeding
Reasons not to treat hypertension

•  Chronically hypertensive patients require

higher perfusion pressure due to shift of
autoregulatory curve.

CBF
CBF = CPP/CVR
CPP = MAP - ICP

Normal
CPP
Chronic Hypertension
 Reasons not to treat hypertension

•  Decreased of BP will deteriorate

perfusion in ischemic area causing
ischemic area extension

CBF
(ml/100g/min)

Normal flow,
normal neuronal function
50

Low flow, raised Oxygen extraction,

CBF = CPP/CVR
normal neuronal function
CPP = MAP - ICP

20 Reversible
Deficit
Penumbra Irreversible reduced
function, i.e. infarction

0 1 2 3
Time passing (hours)
Reasons not to treat hypertension

•  BP will be decreased after putting the

patient in the calm condition, control the
pain, urinary retention and etc.
•  Decreased in ICP will be followed by
decreased in BP
•  BP in 2/3 of ischemic stroke patients will
decrease spontaneously in the first week.
Reasons not to treat hypertension

The Facts
•  Every 10% decreased of BP in the first
day of stroke attack will increased the
likelihood of poor clinical outcome (OR
1,89)
Oliveira-Filha et al. Neurology 2003:1047-51

•  Administration of antihypertensive drugs

in acute stroke patients with SBP <180
mmHg associated with increased of poor
clinical outcome and mortality.
Castillo et al. Stroke 2004, 35: 520-526
Guidelines
Hypertension in Acute Ischemic
Stroke *

Decreasing BP in certain conditions

1.  Acute ischemic stroke *):
SBP >220 ; MAP > 120 (Class I, Level of evidence C)
2.  rtPA candidate **):
SBP >185 ; DBP > 110 (Class I, Level of evidence B)
3.  Acute Ischemic Stroke with hypertension :
–  Hypertensive encephalopathy
–  Aortic dissection
–  Acute MCI
–  Acute lung edema
–  ARF
* ASA Guideline, Stroke 2007;38:1655-1711
 Hypertension in Hemorrhagic
Stroke*

Decreasing BP in certain conditions

1.  SBP >200 mmHg or MAP >150 mmHg  aggressive
reduction of BP with cont. i.v., BP monitoring every 5’.
2.  SBP >180 mmHg or MAP >130 mmHg and elevated
ICP  monitoring ICP and reducing BP using
intermittent or cont. i.v. to keep CPP > 60 - 80 mmHg.
3.  SBP >180 mmHg or MAP >130 mmHg and no elevated
ICP modest reduction of BP (eg, MAP of 110 mmHg
or target BP of 160/90 mmHg) using intermittent or
cont. i.v. medications to control BP, and clinically
reexamine the patient every 15’.

*ASA Guideline. Stroke. 2007;38: 2001-2023.

Guidance in choosing the drug

•  Choose fast and short-acting parenteral

antihypertensive drugs.
•  Start with low dose.
•  Avoid diuretics except in CHF.
•  Avoid antihypertensive drug which will
decreased CBF.
•  Take the target slowly, constantly and
cautiously (15% during the first 24h after
onset of stroke)
The choice of antihypertensive
drugs *

Drug I.V. Bolus Dose Continous Infus Rate

Labetalol 5 – 20 mg every 15’ 2 mg/min (max 300mg/d)

Nicardipine NA 5-15 mg/h
Esmolol 250 ug/kg IVP loading dose 25-300 ug/kg/m
Enalapril 1,25-5 mg IVP every 6 h NA
Hydralazine 5 – 20 mg IVP every 30’ 1,5-5 ug/kg/m
Nipride NA 0,1-10 ug/kg/m
NTG NA 20-400 ug/m

*AHA/ASA Guideline. Stroke. 2007;38: 2001-2023.

Conclusions

•  Elevated BP is common in acute stroke.

This condition related with high rate of
mortality, disability and recurrence
•  Decreasing BP in acute phase is not
recommended because it will deteriorate
clinical outcome and increasing mortality
Conclusions

•  To recent guideline, decreasing BP in acute

phase of stroke is allowed only if :
– Ischemic Stroke with BP >220/120.
– Candidate of rtPA therapy : BP >185/110.
– Hemorrhage stroke with SBP >180 (MAP>130).
– Acute stroke in hypertensive patients with
hypertensive encephalopathy, aortic dissection,
acute MCI, acute lung edema and ARF.
•  Choose parenteral antihypertensive drugs
and do the BP control cautiously