Stroke nursing: assessment, interventions, and care priorities

Stroke is the fifth leading cause of death in the United States and the leading cause of long-term disability. Every 40 seconds, someone in the U.S. has a stroke — and every 3.5 minutes, someone dies from one. For nurses, stroke care is defined by urgency: roughly 1.9 million neurons are lost for every minute a large-vessel ischemic stroke goes untreated. Whether you work in the ED, on a neuro floor, or in the ICU, you will care for stroke patients, and the speed and quality of your assessments directly affect outcomes.

Key facts at a glance

This reference covers pathophysiology, stroke recognition tools, time-critical interventions, post-thrombolysis management, hemorrhagic stroke protocols, dysphagia screening, secondary prevention, rehabilitation, and NCLEX-style questions. Pair it with the Glasgow Coma Scale guide and the ICP nursing reference for a complete neurological assessment foundation.

Ischemic vs hemorrhagic stroke: key differences

Pathophysiology: what is happening in the brain

Ischemic stroke: the penumbra and ischemic cascade

Ischemic stroke begins when blood flow to a region of the brain is interrupted by arterial occlusion. Within seconds of flow cessation, neurons in the core infarct zone lose their ATP supply. Membrane ion pumps fail, sodium and calcium flood into cells, and irreversible cell death begins within minutes.

Surrounding this core is the ischemic penumbra — tissue that is hypoperfused and electrically silent but structurally intact. Penumbral cells survive for hours when some collateral flow persists. The entire rationale for rapid reperfusion therapy is to rescue this penumbra before it converts to infarcted tissue. This is what “time is brain” means at the cellular level.

The ischemic cascade unfolds in sequence:

1. Failure of ion pumps → cellular depolarization, excitotoxic glutamate release
2. Calcium influx → activation of destructive enzymes (proteases, lipases, nucleases)
3. Mitochondrial dysfunction → free radical production, oxidative stress
4. Inflammatory cascade → cytokine release, leukocyte infiltration
5. Cerebral edema → peaks at 3–5 days post-infarct; major cause of secondary injury

Three main mechanisms cause ischemic stroke:

• Thrombotic stroke. A thrombus forms at an atherosclerotic plaque within a cerebral artery, progressively narrowing and occluding the vessel. Large-vessel thrombosis typically involves the internal carotid or middle cerebral arteries. Symptoms may stutter over hours as the clot builds.
• Embolic stroke. A clot or debris forms elsewhere (most commonly the left atrium in atrial fibrillation) and travels to the cerebral vasculature. Onset is abrupt. Embolic strokes carry higher risk of hemorrhagic transformation because when the embolus fragments and flow returns, damaged vessel walls may bleed.
• Lacunar infarct. Occlusion of a single small perforating artery due to chronic hypertension-related lipohyalinosis. These produce small (<1.5 cm) deep infarcts in the basal ganglia, thalamus, internal capsule, or pons. Prognosis is generally better than large-vessel strokes.

Hemorrhagic stroke: hemorrhage expansion and secondary injury

Hemorrhagic stroke results from rupture of a cerebral blood vessel. The bleeding causes direct tissue destruction, and the expanding hematoma raises intracranial pressure, compresses adjacent structures, and can cause herniation.

• Intracerebral hemorrhage (ICH). Rupture of a small artery within the brain parenchyma, most commonly from hypertension-related Charcot-Bouchard microaneurysms. Common locations: basal ganglia, thalamus, pons, cerebellum. ICH accounts for ~10% of strokes but carries 30–50% 30-day mortality. Hematoma expansion occurs in roughly 30% of patients within the first 3 hours — the strongest predictor of early deterioration.
• Subarachnoid hemorrhage (SAH). Bleeding into the subarachnoid space, most often from rupture of a berry aneurysm at the circle of Willis. Classic presentation: sudden “thunderclap” headache described as the worst headache of the patient’s life, with nuchal rigidity, photophobia, and rapid LOC decline. SAH’s unique complication is vasospasm, which peaks at days 4–14 after the initial bleed.

Stroke recognition: FAST, BE-FAST, and stroke mimics

The FAST mnemonic is the most widely taught prehospital and nursing stroke screen. BE-FAST adds two components that capture posterior circulation strokes, which FAST alone misses.

BE-FAST stroke screen

B — Balance. Sudden loss of balance or coordination, trouble walking, dizziness.

E — Eyes. Sudden vision changes — blurred or double vision, visual field loss.

F — Face drooping. Ask the patient to smile. Is one side drooping or numb?

A — Arm weakness. Ask the patient to raise both arms. Does one drift downward?

S — Speech difficulty. Ask the patient to repeat a simple sentence. Is it slurred or garbled?

T — Time to call 911. Note the time symptoms began. Activate the stroke team immediately. Last-known-well time drives every treatment decision that follows.

The B and E additions matter because posterior circulation strokes (vertebrobasilar territory) present with vertigo, ataxia, diplopia, and visual field cuts rather than classic hemiparesis. Posterior strokes account for roughly 20% of ischemic strokes and are frequently missed when only FAST is used.

Stroke mimics to rule out first: Hypoglycemia is the most critical — check a fingerstick glucose immediately on every suspected stroke patient. Other mimics include Todd’s paralysis (post-seizure focal deficit), complex migraine, Bell’s palsy, and hypertensive encephalopathy. BE-FAST positive findings initiate the stroke alert; they do not confirm stroke.

NIH Stroke Scale (NIHSS): what it measures and how to use it

The NIHSS is a systematic, quantitative tool for measuring stroke-related neurological deficit. You will use it at admission, at regular intervals throughout the acute phase, and before and after any intervention. Changes over time tell you whether the patient is improving, stable, or deteriorating, and they guide treatment decisions.

NIHSS assessment items

Total score range: 0–42.

Interpreting the score

Nursing tips for NIHSS administration:

• Score what the patient does, not what you think they can do. If the patient does not attempt a task, score the deficit.
• Repeat the NIHSS at consistent intervals — typically every 1–2 hours in the acute phase. A change of 2 or more points warrants immediate physician notification.
• Document the exact time of each assessment. Trending NIHSS scores is as important as trending vital signs.
• The NIHSS is certified training — most facilities require nursing staff to complete the online NIHSS certification before independently administering the scale.

Time-critical interventions: the treatment windows

Every treatment decision in ischemic stroke is anchored to the last-known-well (LKW) time — the last moment when someone confirmed the patient was at their neurological baseline. For wake-up strokes, LKW is when the patient went to sleep. This is not when symptoms were found — it is when the patient was last confirmed normal.

Thrombolytic therapy (tPA)

Intravenous thrombolytic therapy dissolves the occlusive clot and restores blood flow to the penumbra.

Alteplase remains the established standard: 0.9 mg/kg IV (max 90 mg), with 10% given as a bolus over 1 minute and the remaining 90% infused over 60 minutes.

Tenecteplase is increasingly used as a single IV bolus at 0.25 mg/kg. Current guidelines give it a Class 1 recommendation alongside alteplase for patients presenting within 4.5 hours, based on equivalent efficacy and simpler administration.

Treatment windows:

• Within 3 hours: Strongest evidence of benefit; standard eligibility criteria apply.
• 3–4.5 hours: Benefit persists but is smaller. Additional exclusion criteria apply: age >80, NIHSS >25, history of both diabetes and prior stroke, oral anticoagulant use regardless of INR.
• 4.5–9 hours (selected patients): May be reasonable when advanced imaging (CT perfusion or MRI diffusion-perfusion mismatch) confirms salvageable penumbra.

Absolute contraindications to tPA:

• Active internal bleeding (excluding menses)
• Recent intracranial surgery, serious head trauma, or prior stroke within 3 months
• History of intracranial hemorrhage
• Intracranial neoplasm, AVM, or aneurysm
• Platelets <100,000/mm³
• INR >1.7 or PT >15 seconds
• Heparin use within 48 hours with elevated aPTT
• Systolic BP that cannot be lowered below 185 mmHg or diastolic below 110 mmHg
• Blood glucose <50 or >400 mg/dL (unresponsive to treatment)
• CT evidence of hemorrhage or major acute infarct (>1/3 of a cerebral hemisphere)

Hospital target: door-to-needle time <60 minutes.

Mechanical thrombectomy

For large-vessel occlusion (LVO) ischemic strokes, mechanical thrombectomy using a stent retriever or aspiration catheter is standard of care.

• Treatment window: Up to 24 hours for selected patients with favorable imaging (mismatch between infarct core and salvageable tissue on CT perfusion or MRI).
• Eligible vessels: Internal carotid artery (ICA), M1 segment of the middle cerebral artery (MCA), and in some cases the basilar artery.
• Typical NIHSS: ≥6, indicating moderate-to-severe deficit.
• Thrombectomy can be performed in conjunction with IV tPA (bridging therapy) or as standalone treatment when tPA is contraindicated.

Acute nursing care: first 24 hours

The table below organizes nursing priorities by time phase during the acute stroke admission.

Post-thrombolysis nursing management

Post-tPA care is a defined nursing protocol with specific BP targets, monitoring frequencies, and bleeding precautions. This is high-yield NCLEX content.

Blood pressure management

Why permissive hypertension matters in ischemic stroke without tPA: The elevated pressure is the brain’s compensatory response to perfuse the penumbra through collateral vessels. Lowering it aggressively removes the driving force for collateral flow and can extend the infarct. This is counterintuitive — and frequently tested on NCLEX.

Neurological monitoring schedule

• During tPA infusion: NIHSS and full vital signs every 15 minutes
• Hours 1–6 post-tPA: Every 30 minutes
• Hours 6–24 post-tPA: Every 1 hour

Any NIHSS change of ≥2 points: notify provider immediately.

Hemorrhagic transformation: recognizing and responding

Hemorrhagic transformation occurs when reperfusion occurs through damaged vessels. Signs:

• Sudden, severe headache (not present at admission)
• Acute worsening of NIHSS score (especially LOC decline)
• New vomiting
• Acute hypertension after a period of stability
• Sudden decrease in SpO₂ or altered breathing pattern

Response protocol:

1. Stop the tPA infusion immediately
2. Call the provider — stat CT head required
3. Keep the patient still; reduce stimulation
4. Have cryoprecipitate (containing fibrinogen) and fresh frozen plasma available per facility protocol
5. Do not restart infusion — even if CT later shows no large bleed

Bleeding precautions for 24 hours post-tPA

• No arterial punctures (femoral, radial, brachial)
• No central venous line insertion
• No nasogastric tube placement
• No Foley catheter insertion (place before tPA if anticipated, or use external collection device)
• No antiplatelet agents, anticoagulants, or NSAIDs for at least 24 hours (until 24-hour CT is reviewed)
• Soft toothbrush; no invasive oral care
• Apply direct pressure for at least 10 minutes to any venipuncture site
• Monitor all existing IV sites for oozing

Hemorrhagic stroke management

Management of hemorrhagic stroke differs fundamentally from ischemic stroke. The priorities are stopping the bleed, controlling pressure, and preventing secondary injury from hematoma expansion and elevated ICP.

Blood pressure control in ICH

Rapid reduction to a systolic target of 140 mmHg (range 130–150 mmHg) within the first few hours is recommended. IV nicardipine (5–15 mg/h infusion) and clevidipine allow precise, titratable control. The goal is to limit ongoing hematoma expansion, which occurs in approximately 30% of ICH patients within the first 3 hours.

Anticoagulation reversal agents

Time to reversal correlates directly with hematoma expansion and outcome. The correct reversal agent depends on which anticoagulant the patient was taking.

Surgical considerations in hemorrhagic stroke

• External ventricular drain (EVD): Placed for obstructive hydrocephalus caused by intraventricular extension of blood. Also used for ICP monitoring. See the ICP nursing reference for EVD management principles.
• Craniotomy for cerebellar ICH: Large cerebellar hemorrhages (>3 cm) causing brainstem compression or hydrocephalus are surgical emergencies. Cerebellar herniation can cause respiratory arrest with little warning.
• Minimally invasive surgical evacuation: An evolving option for selected supratentorial ICH.
• SAH aneurysm securing: The ruptured aneurysm must be secured (surgical clipping or endovascular coiling) as early as possible to prevent rebleeding — which carries mortality exceeding 70%.

SAH-specific nursing monitoring

Subarachnoid hemorrhage has a unique complication timeline. After initial stabilization, the primary threat shifts to vasospasm — arterial narrowing from blood breakdown products in the subarachnoid space.

• Vasospasm peaks at days 4–14 after the initial bleed
• Nimodipine 60 mg every 4 hours orally for 21 days is standard prophylaxis
• Transcranial Doppler (TCD) ultrasound monitors cerebral blood flow velocities — elevated velocities signal developing vasospasm
• A patient who appeared stable on day 2 may deteriorate on day 8 — serial neurological assessments through the vasospasm window are essential

Also monitor closely for cerebral salt wasting (CSW): hyponatremia with volume depletion and high urine sodium. CSW is common in SAH and is frequently confused with SIADH (which causes hyponatremia with euvolemia). The distinction matters because treatment differs: CSW requires sodium and volume replacement; SIADH requires fluid restriction.

Dysphagia screening: why it matters and how to do it

Dysphagia screening must be completed before the patient takes anything by mouth — including medications, water, and ice chips. Up to 50% of acute stroke patients have some degree of swallowing dysfunction, and aspiration pneumonia is one of the most common, preventable, and potentially fatal complications of stroke hospitalization.

When to screen

• Immediately upon arrival for any patient with suspected stroke
• Before any oral medications, oral nutrition, or fluids
• Repeat after any change in neurological status (NIHSS change ≥2, new LOC change, new facial palsy)
• Before removing NPO status if the patient was sedated or had a procedure

Nursing dysphagia screen

Most facilities use a validated bedside screening protocol (Yale Swallow Protocol, water swallow test, or similar). A basic bedside approach involves:

1. Level of consciousness: Patient must be alert enough to follow commands
2. Oral motor assessment: Check for facial symmetry, lip closure, tongue movement, and voice quality (“wet” or gurgly voice suggests pooling in pharynx)
3. 3-oz water swallow test (if applicable per facility protocol): Give 3 oz of water in continuous sips; any coughing, choking, wet voice, or change in SpO₂ = failed screen
4. If the patient fails any step, maintain NPO and place a speech-language pathology (SLP) referral for formal swallowing evaluation

What to document

• Date and time of screen
• Patient’s level of alertness
• Presence or absence of cough reflex
• Presence of wet/gurgly voice after swallow
• Pass or fail outcome
• NPO status maintained or oral diet ordered (with texture modification if applicable)
• SLP referral placed (if failed)

While NPO

• Essential medications: administer IV or discuss with pharmacy about crushing and suspending medications in thickened liquid per SLP guidance
• Oral care every 2 hours to reduce bacterial colonization — micro-aspiration of oral secretions is a major driver of aspiration pneumonia even when the patient is NPO
• Document last oral intake

Secondary prevention and discharge planning

Once the acute phase is managed, the focus shifts to preventing recurrent stroke. Stroke recurrence risk is highest in the first 90 days — up to 15% after a TIA.

Antiplatelet therapy

For non-cardioembolic ischemic stroke:

• Minor stroke or TIA: Dual antiplatelet therapy — aspirin plus clopidogrel — started within 24 hours of symptom onset (or at least 24 hours after tPA if given). Transition to single antiplatelet after 21–90 days.
• Moderate-to-severe stroke: Single antiplatelet therapy (aspirin 81–325 mg/day) once 24-hour CT confirms no hemorrhagic transformation.

Anticoagulation for atrial fibrillation

AF-related cardioembolic stroke requires long-term anticoagulation:

• First choice: Direct oral anticoagulants (DOACs) — apixaban, rivaroxaban, dabigatran, or edoxaban
• When DOACs are contraindicated: Warfarin (INR target 2.0–3.0)
• Timing after acute stroke: Typically 4–14 days after the event, depending on infarct size (small infarct = earlier; large infarct = later, to reduce hemorrhagic transformation risk)

Educate patients on adherence, bleeding warning signs, drug interactions, and lab monitoring (INR for warfarin).

Statin therapy

High-intensity statin therapy (atorvastatin 40–80 mg or rosuvastatin 20–40 mg) is recommended for all patients with atherosclerotic ischemic stroke regardless of baseline LDL. Statins stabilize atherosclerotic plaques, reduce inflammation, and improve endothelial function beyond lipid lowering.

Blood pressure control

Long-term BP target is generally <130/80 mmHg once the acute phase resolves (typically after 48–72 hours for ischemic stroke). Thiazide diuretics, ACE inhibitors, and ARBs have the strongest evidence for stroke recurrence prevention.

Lifestyle modification

Rehabilitation priorities: starting early

Stroke rehabilitation begins in the acute phase — not after discharge. Early mobilization within 24–48 hours of admission (when medically stable) reduces complications including DVT, pneumonia, deconditioning, and depression.

Mobilization timeline

Important exception: Patients receiving tPA or who are hemodynamically unstable should not be mobilized until the physician clears them. Post-tPA, no active mobilization for at least 24 hours in most protocols.

Rehabilitation team roles

Physical therapy (PT): Mobility, gait training, balance and fall prevention, strengthening of affected extremities, assistive device selection.

Occupational therapy (OT): Activities of daily living (ADLs) — dressing, bathing, grooming; adaptive equipment; upper extremity function; cognitive rehabilitation for spatial neglect.

Speech-language pathology (SLP): Formal swallowing evaluation and dysphagia management; aphasia treatment (expressive and receptive); cognitive-communication deficits; augmentative communication devices.

Nursing role in rehabilitation:

• Reinforce therapy gains between PT/OT/SLP sessions — use mealtimes, ADLs, and repositioning as therapeutic opportunities
• Consistently approach the patient from the affected side to encourage awareness and reduce neglect
• Encourage independence — allow the patient time to attempt tasks rather than doing everything for them
• Document functional changes in response to therapy

Complications that impair rehabilitation

• Shoulder pain and subluxation: Common in flaccid hemiplegia. Use arm slings, proper positioning, and support during transfers. Never pull on the affected arm.
• Spasticity: Develops weeks after stroke; treated with stretching, positioning, and medications (baclofen, botulinum toxin).
• Depression: Occurs in 30–40% of stroke survivors and directly impairs rehabilitation participation. Screen with PHQ-9 or similar tool. Early treatment (SSRIs) improves both mood and functional outcomes.
• Cognitive impairment: Executive function, attention, and memory deficits affect up to 30% of stroke survivors beyond physical deficits. Involves OT cognitive rehabilitation and environmental modifications.

Nursing interventions by system: reference table

NCLEX-style questions

Test your knowledge with these 6 questions. Each reflects a high-frequency NCLEX stroke concept.

Question 1

A nurse is preparing to administer alteplase to a patient with acute ischemic stroke. The patient’s BP is 192/108 mmHg. What is the priority nursing action?

A) Administer the alteplase immediately and then treat the hypertension B) Hold the alteplase and administer IV labetalol or nicardipine as ordered C) Notify the provider that the patient cannot receive alteplase D) Recheck the BP in 30 minutes before making any decision

Answer: B

Rationale: Blood pressure must be <185/110 mmHg before alteplase can be administered. The correct approach is to hold the medication and promptly reduce BP with IV antihypertensives (labetalol 10–20 mg IV over 1–2 min, or nicardipine infusion) to bring it into the eligible range. Option A is incorrect — administering tPA with BP above threshold increases hemorrhagic transformation risk. Option C is premature — eligibility is not permanently lost if BP can be lowered. Option D is incorrect because a 30-minute delay risks irreversible penumbral damage (“time is brain”).

Question 2

A patient who received IV alteplase 45 minutes ago reports a sudden, severe headache and the nurse notes an acute increase in blood pressure and new vomiting. What is the priority action?

A) Increase the rate of the alteplase infusion to complete it faster B) Reassure the patient that headache is a common side effect of tPA C) Stop the tPA infusion immediately and notify the provider D) Administer IV acetaminophen for headache and continue monitoring

Answer: C

Rationale: Sudden severe headache, acute hypertension, and new vomiting during or after tPA infusion are warning signs of intracranial hemorrhage (hemorrhagic transformation). The infusion must be stopped immediately, the provider notified, and a stat CT head arranged. Continuing the infusion (A) would worsen the bleed. Reassurance (B) is inappropriate — these are not expected side effects; headache plus vomiting plus BP spike is an emergency presentation. Treating headache symptomatically (D) delays critical intervention.

Question 3

A patient with a history of atrial fibrillation who takes warfarin presents with acute intracerebral hemorrhage. The INR is 3.2. Which combination of reversal agents should the nurse anticipate administering?

A) Protamine sulfate and fresh frozen plasma B) Idarucizumab and vitamin K C) Andexanet alfa and 4F-PCC D) IV vitamin K and four-factor prothrombin complex concentrate (4F-PCC)

Answer: D

Rationale: Warfarin is reversed with IV vitamin K (phytonadione) plus 4F-PCC. Vitamin K alone takes 12–24 hours to reduce INR; 4F-PCC provides immediate replacement of clotting factors II, VII, IX, and X. Using both together achieves rapid reversal and sustained effect. Option A (protamine) is used for heparin, not warfarin. Option B (idarucizumab) reverses dabigatran specifically. Option C (andexanet alfa) reverses factor Xa inhibitors (rivaroxaban, apixaban). Recognizing which reversal agent matches which anticoagulant class is a key NCLEX pharmacology concept.

Question 4

A nurse is caring for a patient admitted 36 hours ago for subarachnoid hemorrhage who initially had a Glasgow Coma Scale score of 14 and was conversational. Today the patient is confused, has new left arm weakness, and a transcranial Doppler shows elevated blood flow velocities. What complication does the nurse recognize?

A) Rebleeding from the aneurysm B) Cerebral salt wasting C) Vasospasm causing delayed cerebral ischemia D) Hydrocephalus from CSF outflow obstruction

Answer: C

Rationale: Vasospasm is the most feared complication of SAH and classically presents with new focal neurological deficits and declining LOC developing days after the initial bleed — typically peaking at days 4–14. Elevated TCD velocities confirm developing vasospasm. Rebleeding (A) typically presents acutely with sudden severe headache and rapid LOC deterioration — not a gradual new focal deficit. Cerebral salt wasting (B) would present with hyponatremia and volume depletion, not focal motor deficits. Hydrocephalus (D) typically presents with LOC decline and gait instability rather than focal arm weakness. Understanding the SAH complication timeline is high-yield NCLEX content.

Question 5

A patient with an ischemic stroke is not receiving tPA. The patient’s blood pressure is 210/100 mmHg. The nurse is reviewing the orders. Which order would the nurse question?

A) Continuous cardiac monitoring B) IV labetalol 20 mg now and every 10 minutes PRN for SBP >220 C) IV nicardipine infusion titrate to keep SBP 160–170 mmHg D) Sequential compression devices to bilateral lower extremities

Answer: C

Rationale: In ischemic stroke patients not receiving tPA, permissive hypertension is the correct approach — the standard recommendation is to allow BP up to 220/120 mmHg without treatment. The elevated BP supports collateral perfusion of the ischemic penumbra. Actively lowering BP to 160–170 mmHg with a nicardipine infusion can reduce collateral flow and extend the infarct. Option B (treating only if SBP >220) is appropriate — it allows permissive hypertension while setting a safety ceiling. Cardiac monitoring (A) and SCDs for VTE prophylaxis (D) are both correct standard orders for acute stroke patients.

Question 6

A patient with acute ischemic stroke cannot swallow safely on bedside dysphagia screening. The patient has a prescribed oral statin and aspirin ordered. What is the correct nursing action?

A) Hold both medications until the patient passes the dysphagia screen B) Crush the aspirin, dissolve in water, and administer orally in small sips C) Hold the aspirin, consult pharmacy about IV or alternative formulation for the statin D) Notify the provider that the medications cannot be administered until discharge

Answer: A — with clinical nuance

Rationale: When a patient fails dysphagia screening, the correct nursing action is to maintain strict NPO status and hold all oral medications. No oral intake — including “small sips” of crushed medications — is permitted until the patient either passes the screen or receives formal SLP evaluation and dietary modification orders. For medications considered medically urgent (not the case for a statin on day 1), the nurse should contact the provider to discuss IV alternatives or nasogastric administration. Giving the aspirin in small sips (B) violates the NPO order and creates aspiration risk. Option C is partially correct in approach but incorrect in holding only aspirin — both oral medications are held. Option D misrepresents the situation — the provider should be notified for a treatment plan, but administration may resume as soon as the patient is cleared, not only at discharge.

Key takeaways for nursing students

• Time is brain. Know the treatment windows: tPA within 4.5 hours, thrombectomy up to 24 hours for selected patients. Every minute of delay costs ~1.9 million neurons.
• CT rules the decision tree. Hemorrhagic or ischemic? tPA is absolutely contraindicated in hemorrhagic stroke. All treatment planning flows from this single finding.
• Blood pressure management is stroke-type and treatment-dependent. Permissive hypertension (up to 220/120) in ischemic stroke without tPA; <185/110 before tPA; <180/105 after tPA; <140 systolic in ICH. Getting this wrong extends the injury.
• NIHSS is your trending tool. Change of ≥2 points = call the provider. Serial assessments matter as much as the initial score.
• Screen swallowing before anything by mouth. Dysphagia affects half of acute stroke patients. Aspiration pneumonia is common, preventable, and potentially fatal.
• Know your reversal agents by drug class. Warfarin → vitamin K + 4F-PCC. Dabigatran → idarucizumab. Factor Xa inhibitors → andexanet alfa.
• SAH has its own complication timeline. Vasospasm peaks at days 4–14. A stable day-2 patient can deteriorate on day 8.
• Rehabilitation starts in the acute phase. Early mobilization within 24–48 hours reduces DVT, pneumonia, and deconditioning when the patient is medically stable.
• Secondary prevention starts before discharge. Antiplatelets or anticoagulants (based on stroke mechanism), high-intensity statins, BP control, and lifestyle counseling are nursing education responsibilities.

For related neurological content, review the TBI nursing reference for traumatic brain injury comparisons, the meningitis nursing guide for infectious neurological emergencies, and the seizure nursing reference — post-stroke seizures and management overlap frequently in clinical practice. The head-to-toe assessment guide covers the full neurological exam that anchors stroke assessment at every phase of care.