1. BLOOD PRESSURE MANAGEMENT IN ACUTE STROKE
Pat Melanson, MD
McGill University

2. “Brain Attack” Paradigm shift - End of nihilism
Early effective interventions
Time-sensitive disease
Chain of recovery
Stroke units and stroke centers
- there is a new era concerning the treatment of acute stroke PARADIGM SHIFT over the past 5 years
- the next 5 to 10 years should be quite exciting
- recent advances have given new hope to the idea that we will be able to actively intervene and positively affect the outcome of a patient with an acute stroke
- with the publication of the NINDS tPA study, stroke can now be considered a time-sensitive disease much like AMI or trauma, hence the term BRAIN ATTACK
-At the MUHC we are working to create a chain of recovery for the management of acute stroke to ensure that the patient is passed seamlessly and efficiently from the pre-hospital arena, through the ED, with co-ordination between the EP, lab, radiology, neurology, neurosurgery and others
- our goal is to create a regional center of excellence for acute stroke
- the number of patients who can benefit from tPA or more advanced expertise and technology is small
- it is clear that huge improvements in stroke outcome can be achieved with simple, straightforward therapies that can be given anywhere
- avoidance of infections such as aspiration pneumonia, UTI
-blood glucose and temperature control
- BP control

3. Stroke Protocols Aspiration pneumonia, UTI’s DVT prophylaxis
Glucose control
Fever control
BP management
avoidance of overtreatment

4. Cases Ischemic CVA, BP 225/105 (145)
Hemorrhagic CVA, BP 215 /110 (145)
Would you actively lower the BP?
What target or threshold level?
What drug ?
Which drugs should be avoided?
1) 60 year-old male with atrial fibrillation who is not on coumadin
2) 70 year-old male with chronic hypertension and a large left basal ganglia intracerebral hemorrhage on CT
3) 40 year-old male with proven or suspected SAH
- How would you mange these patients blood pressure?
- What would be your threshold levels for treatment?
-If you would lower the BP with an anti-hypertensive, which one would you choose?
- Which antihypertensives should be avoided?

5. Lowering BP in Acute Stroke: Pros
Chronic hypertension
Rebleed/ increase hematoma size
Cerebral edema, Raised ICP
Hemorrhagic transformation
Decrease bleeding with t-PA

6. Lowering BP in Acute Stroke: Cons
Acute hypertension is self-limited
RISK OF ISCHEMIA
Reflex response to maintain CBF
Ischemic penumbra
Shift in autoregulation curve
More sensitive to BP decreases

7. Cerebral Blood Flow CBF = CPP / CVR CPP = MAP - ICP MAP = DBP + 1/3 PP
Cerebral autoregulation
normal between
70/40 to 200/130

8. Cerebral Autoregulation
CBF
50 ml/100g/min 20 50
150
MAP

9. Cerebral Autoregulation
MAP below lower limit
hypoperfusion with ischemia
MAP above upper limit
“breakthrough” vasodilation
Segmental pseudospasm (“sausage-string”)
fluid extravasation

10. Cerebral Autoregulation
Shift to right
Chronic hypertensives
ICH, SAH, Ischemic infarct
Trauma
Cerebral edema
Age, atherosclerosis
Some hypertensives suffer decrease CBF at MAP higher than 120 (160/100)

11. How far can BP be safely lowered?
Lower limit usually 25% below MAP
50% of chronic hypertensives reached lower autoregulation limit with 11 to 20% reduction in MAP
50% had lower limit above usual mean
Kanaeko et al; J Cereb Blood Flow Metab 3:S51,1983
Most ischemic complications develop with reductions greater than %

12. Initial Lowering of BP : Therapeutic Guidelines
Do not lower BP more than 15 % over the first 1 to 2 hours unless necessary to protect other organs
Decreasing to DBP of 110 or patients “normal” levels may not be safe
Further reductions should be very gradual ( days)
Follow neuro status closely

13. Pharmacologic Therapy

14. Drugs Best Avoided Direct-acting cerebral vasodilators Nitroglycerine
adversely affect CBF
potential to increase ICP
shift autoregulation curve to the right
Nitroglycerine
Nitroprusside
Hydralazine
Calcium Channel Blockers

15. Nifedipine Peripheral, cerebral and coronary arteriolar vasodilation
Rapid onset of antihypertensive effect
5-20 minute onset
peak effect in min
duration 4-5 hr
Potential severe hypotension
Several case reports of cerebral or myocardial ischemia after rapid decrease

16. Sublingual Nifedipine
“Should a Moratorium be Placed on Sublingual Nifedipine capsules given for hypertensive emergencies and pseudoemergencies?”
Grossman, Messerli, Grodzicki, Kowey
JAMA, 276 : ,1996

17. Recommended Antihypertensives
Beta-blockers
Alpha-blockers
ACE inhibitors
Clonidine

18. Labetalol Combined a, b adrenergic blockade
Usual contraindications to b-blockade
Rapidly effective when given IV;
Onset < 5 min, peak 5-10 min, duration 2-6 hr (sometimes longer)
mg iv q10 minutes

19. ACE inhibitors
IV enalaprilat, oral captopril potentially useful for acute BP reduction
Difficult to titrate (sometimes ineffective,sometimes excessive BP ¯)
Positive effects on cerebral autoreg.
Captopril 12.5 mg S/L

20. Recommendations MAP of 140 - 145 (220/120) Max decrease of 15 % MAP
Avoid direct acting vasodilators
Avoid sublingual nifedipine
Labetalol, Captopril
Cautious reduction with frequent neurologic exams
- McGill stroke protocol
- always err on the side of higher rather than lower BP
-don’t just do something, stand there
- avoid NTP, NTG, CCB, hydralazine

21. Pharmacological Elevation of BP in Acute Stroke
Pharmacological elevation of blood pressure in acute stroke: Clinical effects and safety. Rordorf, Stroke 1997; 28:2133
Retrospective review of 63 patients
Ischemic stroke with normal BP
30 received phenylephrine (alpha-agonist)
10 demonstrated a BP threshold
Improved outcome

22. Recommendations MAP of 140 - 145 ( 220/120)
Avoid direct acting vasodilators
Avoid sublingual nifedipine
Alpha or beta blockers, ACEI
Cautious reduction with frequent neurologic exams
- McGill stroke protocol
- always err on the side of higher rather than lower BP
-don’t just do something, stand there
- avoid NTP, NTG, CCB, hydralazine