GENERAL THERAPY

Blood pressure management in an acute stroke

Vloženo 25.10.2019, poslední aktualizace 02.05.2022

  • high blood pressure (BP) is a common correlate of an acute stroke
  • except for hypertensive emergency (hypertensive crisis) and hypertonic hemorrhage, high BP is a consequence and not a cause of the acute neurological disorder
  • the cause is multifactorial:
    • autoregulation trying to provide sufficient CPP
    • stress reaction to pain and fear
    • Cushing’s reaction (hypertension, bradycardia, and breathing disturbances) in brainstem lesions or advanced intracranial hypertension with secondary brainstem compression
  • rapid and significant BP lowering (except for hypertensive emergency, SAH, and ICH) may be counterproductive, with a negative effect on outcome (due to a decrease of CPP)
  • preferred antihypertensive drugs in the acute stage: urapidil, labetalol, and enalapril
  • arterial blood pressure (BP) monitoring is a mainstay of hemodynamic monitoring in neurocritical care
  • both hypotension and hypertension can impair vital organ function and worsen the outcome
  • BP monitoring techniques:
    • non-invasive BP measurement (more common)
      • intermittent (inflatable cuff) – the proper cuff size is critical
        • manual (auscultatory, palpatory)
        • automated
      • continuous
        • volume clamp method
        • arterial applanation tonometry
    • invasive BP measurement via arterial cannulation (most commonly automated)
  • choice of blood pressure monitoring needs to be individualized
    • low-risk patients – intermittent oscillometric BP measurement
    • high-risk, hemodynamically unstable patients – continuous BP monitoring (non-invasive or invasive)
    • critically ill patients/hypertensive emergency – continuous invasive BP monitoring via an arterial catheter is preferred

Proper cuff size

  • arm circumference < 33 cm: usually cuff 12 cm
  • arm circumference 33-41 cm: cuff 15 cm
  • arm circumference > 41 cm: cuff 18 cm

Acute ischemic stroke

  • autoregulation is disturbed in the ischemic region (sometimes for weeks), and regional perfusion depends on systemic pressure (regulation of cerebral perfusion)
  • too high or too low BP is a negative prognostic factor in acute stroke patients
    • there is a risk of hypoperfusion or, conversely, HEB damage and progression of edema or hemorrhagic transformation
  • see table for management in the first 24-48 h (as recommended by AHA/ASA 2021 and ESO 2021), especially considering all comorbidities and factors that will require more aggressive BP correction
  • routine blood pressure lowering in the prehospital setting is generally not recommended (ESO 2021
  • prehospital treatment with glyceryl trinitrate should be avoided (potential harm in ICH patients)
  • in neurologically stable patients with BP >140/90 mm Hg, resume PO therapy within 48-72 hours
    • it is unclear whether chronic PO therapy should be discontinued (ESO 2021)
    • in patients with dysphagia, wait for improvement or place NG tube
Mechanical thrombectomy with or without IVT
  • keep BP < 180/105 mmHg  before and during thrombolysis/MT and then for the following 24 h   → see thrombolytic protocols
  • reduction of SBP to ≤ 130 mmHg in the first 72h is not suggested; avoid periods of hypotension
  • induced hypertension is not recommended after successful MT (TICI 3) (ESO 2021)
Conservative therapy
  • patients with BP < 220/110 mmHg without comorbidities requiring BP correction – routine BP correction in the first 24 h is not suggested  (ESO 2021) (AHA/ASA 2019 III/A)
  • patients with BP ≥ 220/110 mmHg without comorbidities requiring BP correction – the benefit of BP correction is unknown; a 15% reduction in the first 24h is reasonable and probably safe  (ESO 2021 expert consensus) (AHA/ASA 2019 IIb/C-EO)
  • in case of neurological deterioration:
    • routine use of vasopressors to increase BP and improve perfusion is not recommended
    • if the deterioration is caused by the hypoperfusion (e.g., low intracranial flow on TCCD), it is suggested:
      • discontinue antihypertensive therapy
      • increase IV fluid intake
      • use non-pharmacological procedures to increase blood pressure
      • finally, consider the use of vasopressors
  • treatment of BP in the acute phase is indicated in case of relevant comorbidity (hypertensive emergency)  (AHA/ASA 2019 I/C-EO)
    • pre-/eclampsia
    • left-sided heart failure
    • acute coronary syndrome (ACS)
    • aortic dissection
    • hypertensive encephalopathy
    • concomitant SAH or cerebral aneurysm

according to AHA/ASA 2019 and ESO 2021

Intracerebral hemorrhage

  • on admission, check BP every 5-10 minutes or start invasive BP monitoring
  • aggressive and rapid treatment of hypertension is an essential therapeutic approach (along with correction of coagulopathy)
    • high BP is associated with an increased risk of hematoma progression with worse clinical outcome
    • initiating treatment within 2 hours of ICH onset and achieving the target within 1 hour may be beneficial to reduce the risk of HE and improve functional outcome (AHA/ASA 2022, 2a/C-LD)
    • ischemia around the hematoma plays a minor role (except perhaps in large hematomas), and BP reduction seems safe
  • continue with chronic PO medication if possible; if dysphagia or decreased LOC is present, use parenteral therapy or insert a nasogastric (NG) tube
  • in patients with known hypertension, the target BP may be higher given altered autoregulation with the risk of decreased CBF
  • nitroprusside is not recommended (the potential to increase ICP)
  • smooth and sustained control of BP is required; avoid sudden drops or peaks in BP and maintain MAP >85 mmHg
  • if the intracranial pressure is monitored, then correct BP to maintain CPP 60-80 mmHg
Initial systolic blood pressure (SBP) 150-220 mm Hg in patients with ICH of mild-to-moderate severity
  • target SBP ≤ 140 mmHg (ESO guidelines 2021)  (AHA/ASA 2022 2b/B-R)
    • lowering SBP to 140mmHg is safe and may reduce hematoma expansion and lead to improved outcomes
    • maintain in the range of 130-150 mm Hg
  • no significant clinical benefit of lowering < 140 mmHg has been demonstrated
    • In the INTERACT2  trial, there were fewer patients with mRS 3-6 in the intensive treatment group (SBP<140 mmHg) compared to standard treatment (SBP <180 mmHg);  the difference was not statistically significant
    • the benefit of lowering SBP <140 mmHg was not demonstrated in the ATACH -2 trial – lowering of SBP <120 mm Hg may even be harmful
  • acute lowering of SBP to <130 mm Hg is potentially harmful (AHA/ASA 2022 3/B-R)
  • start antihypertensive treatment ASAP (ideally within 2h of symptom onset)
  • the decrease of SBP should not exceed 90 mmHg from baseline values  (ESO guidelines 2021)

    • larger BP reduction was significantly associated with acute kidney injury regardless of preexisting chronic kidney disease  (Burgess, 2018)
Initial SBP > 220 mmHg or large hematoma
  • limited data on the safety and effectiveness of a target threshold of SBP ≤ 140 mmHg
  • SBP reduction should not exceed 90 mmHg from baseline values
  • cautious BP lowering is required in these patients;  maintain CPP > 6070 mmHg

Subarachnoid hemorrhage

  • start non-invasive continuous BP monitoring immediately; with severe SAH or fluctuating blood pressure,  invasive monitoring is preferred
  • BP control in SAH is complex because there are rationales for both BP lowering (↓ rebleeding risk ) and elevation (↓ risk of DID)
  • with an untreated source of bleeding, maintain SBP ≤ 130-140 mm Hg
    • postoperatively around 150-175 mm Hg (⇒ ↑ CPP)
  • in the presence of cerebral vasospasms in a patient with a secured aneurysm, the target SBP target is approx. 180-220 mmHg (to improve perfusion)
  • excessive and rapid correction of BP may be harmful (↓CPP ⇒ risk of ischemia due to vasospasm)
  • avoid nitrates if possible (may increase ICP)

 

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Blood pressure management in an acute stroke
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