Stroke management is a race against two clocks simultaneously: the clock measuring how long brain tissue has been ischemic, and the clock measuring how long the clinician has before the treatment window closes. Understanding the physiology behind each time target — and the reasoning behind the decisions made at each step — is what separates clinicians who use the protocols from clinicians who understand them.

Ischemic versus hemorrhagic: the decision that cannot wait.

Stroke presents as focal neurological deficit of sudden onset. The mechanism is either ischemic (87% of cases) or hemorrhagic (13%). The treatment for each is opposite in critical ways: ischemic stroke may benefit from thrombolytics; hemorrhagic stroke is made catastrophically worse by them. Non-contrast CT is the test that makes this distinction. It is rapid, available, and reliable for ruling out hemorrhage. Treatment decisions are made on the back of that CT, and they cannot be made before it.

CT cannot reliably identify ischemic infarction in the first hours. A normal CT in the setting of focal deficit does not mean no stroke — it means no hemorrhage is visible. MRI with DWI sequences will show ischemic change within minutes of onset but takes longer to acquire. CT angiography (CTA) identifies large vessel occlusion and guides mechanical thrombectomy decisions.

The clinical assessment: NIHSS and what it measures.

The National Institutes of Health Stroke Scale (NIHSS) is the standardized assessment tool for stroke severity. It evaluates 11 items: level of consciousness, gaze, visual fields, facial palsy, motor function (arms and legs separately), limb ataxia, sensory, language, dysarthria, and extinction/inattention. Scores range from 0 to 42. A score above 15 suggests a major hemispheric stroke; above 20 suggests a severe stroke with poor prognosis without revascularization.

The NIHSS serves two functions: it quantifies the deficit for documentation and communication, and it helps determine whether the patient is a candidate for intervention. A very low NIHSS (rapidly improving symptoms) or a very high NIHSS (profound deficit suggesting large territory infarct with likely futility) both influence the risk-benefit calculus for thrombolytics.

The Cincinnati Prehospital Stroke Scale (facial droop, arm drift, speech abnormality) is the field screen — fast, teachable, useful for early activation. Any positive finding should trigger immediate stroke team activation and priority transport. Time begins at symptom onset or last known well.

tPA: the criteria that determine eligibility.

Alteplase (tPA) at 0.9 mg/kg (maximum 90 mg, 10% IV bolus over 1 minute, remainder over 60 minutes) is indicated for ischemic stroke within 3 hours of symptom onset in patients meeting eligibility criteria. The window extends to 4.5 hours for select patients without additional risk factors. These time windows are not administrative targets — they reflect the point at which the risk of hemorrhagic transformation begins to exceed the benefit of revascularization in average-risk patients.

Key absolute contraindications to tPA: hemorrhage on CT, rapidly improving symptoms, SBP >185/DBP >110 that cannot be controlled prior to treatment, prior intracranial hemorrhage, recent major surgery within 14 days, platelets <100,000, active bleeding, and recent ischemic stroke or head trauma within 3 months. The full exclusion list is longer; certification exams test the highest-yield contraindications with the clearest physiologic rationale.

Blood pressure management before tPA: aggressive antihypertensive treatment is required to bring BP below 185/110 before administration. After tPA, maintain BP below 180/105 for 24 hours — elevated BP after thrombolysis increases hemorrhagic transformation risk. Labetalol or nicardipine are commonly used agents.

Mechanical thrombectomy: the extended window.

For large vessel occlusion (LVO) strokes, mechanical thrombectomy extends the treatment window substantially beyond tPA. Current evidence supports thrombectomy up to 24 hours from last known well in carefully selected patients with significant penumbra (tissue that is ischemic but not yet infarcted) on advanced imaging. CT perfusion or MRI perfusion imaging identifies the mismatch between infarcted core and salvageable penumbra that defines candidacy.

Thrombectomy is performed regardless of whether tPA was given — tPA is not a prerequisite, and delay for tPA should not occur if thrombectomy can be performed immediately. These decisions require neurological expertise and imaging; the bedside clinician’s role is rapid recognition, appropriate BP management, time documentation, and transfer to a thrombectomy-capable center if necessary.

Hemorrhagic stroke: a different problem entirely.

Intracerebral hemorrhage (ICH) management is primarily supportive and neuroprotective. Anticoagulation must be reversed urgently. BP control is more aggressive than in ischemic stroke — target SBP <140 mmHg within the first hour (evidence for benefit in reducing hematoma expansion). Glucose management, temperature control, and seizure prophylaxis (in some patients) are active interventions. Neurosurgical consultation is immediate for posterior fossa hemorrhage, obstructive hydrocephalus, or rapid deterioration.

Subarachnoid hemorrhage (SAH) presents as thunderclap headache — the worst headache of the patient’s life — often with neck stiffness. Non-contrast CT is diagnostic in the first 6 hours with high sensitivity; lumbar puncture for xanthochromia is the next step when CT is negative but clinical suspicion remains high. LP should be performed at least 6–12 hours after symptom onset to allow sufficient red cell lysis for reliable xanthochromia detection — an LP performed too soon after onset may yield a false negative. SAH management focuses on preventing rebleeding (blood pressure control, early aneurysm securing), preventing vasospasm (nimodipine is standard), and managing complications (hydrocephalus, elevated ICP).

The transport dimension.

For flight and transport clinicians, the critical stroke decision is destination: a comprehensive stroke center with thrombectomy capability versus the nearest facility. A patient with suspected LVO within the thrombectomy window benefits from bypass of closer facilities to reach a thrombectomy center. En route monitoring includes BP management, glucose control, and neurological reassessment. Deterioration in transport may indicate hemorrhagic transformation or hematoma expansion in hemorrhagic stroke — both require immediate escalation of destination decision-making.

The exam relevance.

Stroke questions on CCRN, CEN, and CFRN consistently test tPA eligibility decisions, BP management targets (before tPA, after tPA, in hemorrhagic stroke), and appropriate response to a patient who deteriorates after thrombolysis. The deteriorating tPA patient who develops new focal deficit or decreased consciousness has hemorrhagic transformation until proven otherwise — stop tPA if still infusing, obtain emergency CT, and reverse anticoagulation if indicated. This sequence, and the reasoning behind it, is what earns points on the exam and keeps the patient from dying from the treatment.