BP Targets in Stroke
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High blood pressure is the primary modifiable risk factor for stroke, affecting a significant portion of stroke patients, and requires careful management to prevent poor outcomes. Recommendations include specific blood pressure targets and treatment protocols for both acute ischemic and hemorrhagic strokes, emphasizing the need for controlled lowering or maintenance of blood pressure within defined limits. Additionally, fluctuations in blood pressure may negatively impact clinical outcomes, highlighting the importance of stabilizing blood pressure in stroke patients.
![• 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](https://image.slidesharecdn.com/bpgoalsinaisppt-230808151131-a2f76a79/85/BP-Targets-in-Stroke-28-320.jpg)
BP Targets in Stroke
- 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
- 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