6.2 Acute Ischemic Stroke, Hemorrhagic Stroke & Subarachnoid Hemorrhage

6.2 Acute Ischemic Stroke, Hemorrhagic Stroke & Subarachnoid Hemorrhage

Cerebrovascular emergencies rank among the most time-sensitive conditions encountered in critical care transport. Rapid neurological assessment, precise blood pressure titration, timely administration of thrombolytic agents, urgent reversal of anticoagulation, and prevention of secondary vasospasm are vital to preserving viable brain tissue and preventing permanent disability.

---

Acute Ischemic Stroke (AIS) & Reperfusion Therapy

Acute Ischemic Stroke accounts for approximately 87% of all strokes. Ischemic tissue surrounding the dense infarcted core is known as the ischemic penumbra—a region of hypoperfused but metabolically active, potentially salvageable brain tissue.

Thrombolytic Time Windows & Dosing

• Intravenous Recombinant Tissue Plasminogen Activator (rtPA / Alteplase):
  • Treatment Window: Within 4.5 hours of "Last Known Normal" (LKN).
  • Dosing: $0.9 \text{ mg/kg}$ IV (maximum total dose $90 \text{ mg}$). Administer $10\%$ of total dose as an initial IV bolus over 1 minute, followed by the remaining $90\%$ as a continuous infusion over 60 minutes.
• Tenecteplase (TNK-tPA):
  • Treatment Window: Within 4.5 hours of LKN (increasingly preferred due to single IV bolus administration).
  • Dosing: $0.25 \text{ mg/kg}$ IV single bolus (maximum total dose $25 \text{ mg}$).
• Endovascular Thrombectomy (EVT): Indicated up to 24 hours from LKN for patients with Large Vessel Occlusions (LVO) in the anterior circulation, determined by CT angiogram and perfusion mismatch.

Blood Pressure Management Thresholds in AIS

Blood pressure management in acute ischemic stroke is tightly regulated based on whether the patient is eligible to receive intravenous thrombolysis.

Rationale for Permissive Hypertension: In non-thrombolytic candidates, elevated blood pressure is a compensatory reflex maintaining collateral arterial perfusion through cerebral vessel networks into the ischemic penumbra. Precipitous lowering of BP collapses collateral flow, enlarging the stroke infarct size.

---

First-Line Anti-Hypertensive Infusions

Use titratable IV agents when urgent BP control is indicated; the agent, bolus or infusion strategy, and target depend on the stroke scenario and local protocol. Clevidipine dosing below follows the Cleviprex prescribing information, section 2.2.

---

Acute Spontaneous Intracerebral Hemorrhage (ICH)

Intracerebral hemorrhage involves primary bleeding into the brain parenchyma, most commonly caused by chronic hypertension, cerebral amyloid angiopathy, or vascular malformations. Hematoma expansion occurs rapidly within the first 3–6 hours.

Blood Pressure Reduction in ICH

• 2025 AHA/ACC guidance: For adults with acute spontaneous ICH and initial SBP $150\text{--}220\text{ mmHg}$, lowering SBP to $130\text{ to }<140\text{ mmHg}$ for at least 7 days can improve outcomes; stop antihypertensive medication if SBP falls below $130\text{ mmHg}$. 2025 guideline, section 5.3.9.1.
• Titrate smoothly under the local stroke protocol. Large/severe hemorrhage, impaired cerebral perfusion, or planned decompression requires an individualized plan with the stroke/neurosurgical team.

Urgent Anticoagulant Reversal Protocols

For patients presenting with acute ICH while on anticoagulant therapy, immediate reversal is paramount prior to or during transport.

---

Subarachnoid Hemorrhage (SAH) & Vasospasm Management

Aneurysmal Subarachnoid Hemorrhage (aSAH) results from the rupture of an intracranial saccular ("berry") aneurysm into the subarachnoid space. Patients present with classic "thunderclap headache" ("worst headache of life"), vomiting, nuchal rigidity, photophobia, and rapid loss of consciousness.

SAH Clinical & Radiographic Grading

Delayed Cerebral Ischemia (DCI) & Vasospasm Prevention

Cerebral vasospasm typically develops between days 4 and 14 post-hemorrhage as blood breakdown products irritate cerebral arteries.

• Enteral Nimodipine: Oral/nasogastric calcium channel blocker administered as $60 \text{ mg}$ PO/NG every 4 hours for 21 consecutive days. Nimodipine improves neurological outcomes through neuroprotective actions. Warning: Nimodipine must NEVER be administered intravenously; IV administration causes severe refractory vasodilation and fatal cardiac arrest.
• Euvolemic Hypertension vs. Historical Triple-H Therapy: Historical "Triple-H Therapy" (Hypervolemia, Arterial Hypertension, Hemodilution) has been abandoned due to high risks of pulmonary edema, myocardial infarction, and hyponatremia. Current critical care standard dictates maintaining strict EUVOLEMIA using isotonic crystalloids ($0.9\%$ NaCl) and initiating induced arterial hypertension (using norepinephrine infusion to target MAP $90 - 110 \text{ mmHg}$) ONLY if symptomatic cerebral vasospasm occurs.