Described the BP targets in Ischemic stroke with and without IV thrombolysis, with and without mechanic thrombectomy, Intra cerebral Heamorrhage, SAH and other Neurological emergencies with revised AHA/ ASA upated guidelines ALSO showed different journal evidence of work on blood pressure management in acute ischemic and heamorrhagic stroke, BP tergets in SAH, PRES

1. BP Targets in Stroke

2. • Stroke has a global incidence of 15 million people per year, is the
third leading cause of death and is the most common cause of
disability in the world.1
• High-blood pressure (BP) is the leading modifiable risk factor for
both ischaemic and haemorrhagic stroke2 affecting 1 billion people
worldwide.3
• In acute stroke, 75% of patients have high BP and 50% of those
have a prior history of hypertension.4 ,5
• Although BP spontaneously falls in two-thirds of patients in the first
week following stroke,4
• One-third remain hypertensive and have an increased risk of a poor
outcome.6
• Appropriate control of blood pressure is required to ensure good
outcome in patients with stroke and to prevent recurrence of stroke.
Introduction

3. • Acute stroke impairs the autoregulation of the cerebral circulation so that
the blood flow in the ischemic area becomes passively dependent on
MAP.
• The acute hypertensive response seen in stroke has numerous potential
causes including:
• fluctuations in, or elevation of, pre-existing hypertension; DM, S.Creat.
• infection; pain, for example, due to urinary retention;
• stress related to hospitalisation;
• activation of cortisol, natriuretic peptide, renin–angiotensin–aldosterone
and sympathetic neuroendocrine systems;
• impaired cardiac baroreceptor sensitivity; and
• raised intracranial pressure (Cushing's reflex).12–15
Pathophysiology

4. • Although low BP is far less common in acute stroke, it is
associated with a poor outcome.7
• Potential causes include sepsis, cardiac arrhythmias, heart failure
and ischaemia, hypovolaemia and aortic dissection.16
• A higher BP may be beneficial for the penumbra, which is viable
but under-perfused, by increasing collateral flow.
• On the other hand, a higher BP may increase the risk of
hemorrhagic transformation and cerebral edema

5. • Data from the first International Stroke Trial demonstrated a U-
shaped relationship between presenting BP and outcome after
ischaemic stroke.
• Both low and high extremes of BP are associated with a poor
outcome.
• For every 10mmHg of SBP below 150mmHg the risk of death and
dependency increased by 17.9%
• For every 10mmHg increase in SBP above 180mmHg the risk of
early death increased by 3.8%.
Blood Pressure

7. • Elevated BP is present in >80% of patients with AIS.
• Aggressive lowering of BP may lower cerebral perfusion
pressure (CPP), thereby aggravating brain ischemia.
• Very high BP, can worsen cerebral edema, resulting in
poorer outcomes.
• Best outcomes are observed at SBP between 140-180
mmHg.
Management of BP in AIS

8. ASA
AHA
Stroke
Guidelines

9. • Patients who have elevated BP and are otherwise
eligible for treatment with IV rtPA should have their
blood pressure carefully lowered so that their SBP is
<185 mm Hg and DBP is <110 mm Hg (Class I; Level of
Evidence B) before fibrinolytic therapy is initiated.
• If medications are given to lower BP, the clinician should
be sure that the BP is stabilized at the lower level before
beginning treatment with IV rtPA and maintained below
180/105 mm Hg for at least the first 24 hours after IV
rtPA treatment.
ASA Guidelines

11. • In patients with markedly elevated blood pressure
who do not receive fibrinolysis, a reasonable goal
is to lower blood pressure by 15% during the first
24 hours after onset of stroke.
• The level of blood pressure that would mandate
such treatment is not known, but consensus exists
that medications should be withheld unless the
systolic blood pressure is >220 mm Hg or the
diastolic blood pressure is >120 mm Hg (Class I;
Level of Evidence C).

12. • Antihypertensive medications are withheld, as
long as SBP is 220 mmHg or lower and DBP is
120 mmHg or lower
(Class I; Level of Evidence C).
• In stroke patients undergoing IV thrombolysis with
alteplase or tenecteplase, anti-hypertensive
drugs are not used if the SBP is 185 mmHg or
lower and DBP is 110 mmHg or lower.
(Class I; Level of Evidence B)
BP targets in AIS

14. ◾1. Goal SBP<180 mmHg, DBP<105
◾2. SBP 180-230 OR DBP 105-120:
Labetalol 10 mg IV given over 1-2 minutes; may repeat or
double labetalol every 10-20 minutes to maximum dose of 300
mg
or
give initial labetalol dose, then start Nicardipine 5 mg/hour IV
infusion as initial dose and titrate to desired effect by increasing
rate by 2.5 mg/hour every 5 minutes to maximum of 15 mg/hour
or
consider a labetalol drip at
2-8 mg/min.
BP management in first 24 hrs after ivtpa

15. ◾3. Systolic >230 OR Diastolic 121-140:
Labetalol or give initial labetalol dose, then start
Nicardipine or
consider a labetalol drip at 2-8 mg/min.
◾If blood pressure Is not controlled by labetalol or
nicardipine, consider sodium nitroprusside.
◾4. Diastolic >140:
Sodium nitroprusside

16. ◾• Systolic >220 OR Diastolic 121–140:
Labetalol or Nicardipine
◾- Aim for a 10% to 15% reduction of blood pressure
◾• Diastolic >140
Nitroprusside
◾- Aim for a 10% to 15% reduction of blood pressure
BP management in non eligible IVtpa candidates

17. Non eligible for IVtpa - Plan MT Cases

19. No IVtpa - No MT cases

20. • HTN in the first 24 hours may be beneficial as it improves
CPP
• Small studies have used phenylephrine or norepinephrine
in the first 24 hours to keep the BP high normal or mildly
high
• Studies showed improvement in ischemic deficits including
aphasia
• Improved perfusion was also noted on MR perfusion studies
• Treatment appears promising, however further larger trials
are needed. (Class IIb; Level of Evidence B).
Induced HTN as a Strategy in AIS

24. • Primary prevention :<140/90 mmHg for
uncomplicated hypertensive patients, <130/80
mmHg for those with diabetes mellitus or chronic
kidney disease
• Secondary prevention :<130/80 mmHg for those
with recent lacunar stroke. (Class IIb; Level of
Evidence B).
Acute Ischemic Stroke

28. • Increased BP is very common in ICH, which may stem from
premorbid hypertension or secondary increase due to ICP,
stress, or pain [9].
• 30% of patients with ICH may have hematoma expansion
within the first 6 hours of ICH occurrence, whereas up to 12%
may have hematoma expansion between 1-hour and 20-hour
noncontrast head CTs.
• Elevated BP during the acute phase of ICH has been found to
be associated with hematoma expansion, perihematomal
edema, rebleeding, neurological deterioration, and death
[10,11].
• However, there are concerns about decreasing BP too far,
which may cause cerebral ischemia around the hematoma.
BP Target in ICH

30. BP management in ICH

31. • The current recommendation for SBP goal in ICH is
<140 mm Hg for patients presenting with SBP between
150 mm Hg and 220 mm Hg without contraindication
to intensive blood pressure control.
• No recommendation has been made on the specific
medication to be used to control blood pressure.
• Considerations in selection of medication are usually
dependent on potential side effects, patient
comorbidity, allergy history, refractoriness of the blood
pressure, and availability of the medication.

32. • In addition to absolute SBP levels, BP variability may
predict poor clinical outcomes in ICH, although the exact
mechanism not fully understood.
• Recurrent BP fluctuations may increase oncotic and
hydrostatic pressure gradients in the perihematomal region
and perihematomal edema.
• These fluctuations may be associated with autonomic
dysfunction that promotes proinflammatory cytokine
production, hyperglycemia, disruption of the blood-brain
barrier, and vasogenic edema, all of which may contribute
to worse outcomes.
BP variability in acute ICH

33. • Rebleeding in patients with SAH leads to an extremely poor
prognosis.
• The AHA/ASA recommends maintaining a SBP < 160 mmHg to
balance the risks of ischemia and rebleeding.
• The Neurocritical Care Society states that extreme hypertension
in SAH should be avoided, and suggests maintaining a mean
arterial pressure (MAP) < 110 mmHg.
• European guidelines recommend a MAP above 90
BP Targets in SAH

34. • Experts agree that severe hypertension should be treated, and
fluctuations of blood pressure avoided.
• The choice of antihypertensive agent has not been investigated,
although most clinicians favour CCB’s because of their
vasodilatory effects.
• Blood pressure should be reduced gradually by approximately
25% every 3 to 4 hours.
• Arterial line monitoring of blood pressure and IV infusion of
antihypertensive agents are often necessary.
• Care should be taken to avoid hypotension and worsening
cerebral ischemia.
PRES Posterior Reversible Encephalopathy
Syndrome

35. Take Home Message