11.2 Acute Coronary Syndromes & Cerebrovascular Accidents (Stroke)

Acute Coronary Syndromes & Cerebrovascular Accidents (Stroke)

Clinical Core: Vascular emergencies affecting the coronary and cerebral circulations represent the leading causes of acute mortality and long-term disability worldwide. Rapid, time-critical clinical decision-making dictates whether threatened tissue in the myocardium or cerebral penumbra can be salvaged. The registered nurse must rapidly identify hallmark presentation patterns, initiate targeted first-line therapies within defined time benchmarks, recognize absolute contraindications to reperfusion modalities, and vigilantly prevent catastrophic complications.

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The Acute Coronary Syndrome (ACS) Spectrum: Pathophysiology and Staging

Acute Coronary Syndrome encompasses a clinical spectrum of acute myocardial ischemia triggered by atherosclerotic plaque rupture or erosion, which exposes thrombogenic subendothelial matrix, promotes platelet adhesion and aggregation, and initiates the coagulation cascade to form an intracoronary thrombus.

Clinical Differentiation of ACS Subtypes

Contiguous Leads and Coronary Vascular Anatomy

Coronary ischemia or injury patterns must be identified across anatomically contiguous leads representing specific myocardial territories:

• Inferior Wall: Leads II, III, and aVF (Right Coronary Artery - RCA).
• Septal Wall: Leads V1 and V2 (Left Anterior Descending - LAD).
• Anterior Wall: Leads V3 and V4 (Left Anterior Descending - LAD).
• Lateral Wall: Leads I, aVL, V5, and V6 (Left Circumflex Artery - LCx).
• Right Ventricle: Leads V3R and V4R (Proximal RCA occlusion; investigated whenever inferior wall STEMI is noted).

Atypical Presentations: High-Risk Populations

While crushing substernal chest pressure radiating to the left jaw or arm represents the classic presentation, the nurse must recognize that women, older adults, and clients with diabetes mellitus frequently present with "atypical" or "silent" ischemia. Atypical presentations include unexplained acute dyspnea, overwhelming diaphoresis, uncharacteristic profound fatigue, nausea, vomiting, dizziness, syncope, or epigastric discomfort mimicking indigestion. Diabetic autonomic neuropathy frequently blunts visceral cardiac pain pathways, eliminating chest discomfort entirely.

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Emergency Nursing Interventions: The First 10 Minutes & MONA/FONA

Upon client presentation with suspected acute coronary syndrome, a 12-lead ECG must be acquired and interpreted within 10 minutes of arrival. Immediate management centers on the targeted MONA / FONA intervention bundle:

1. Oxygen Therapy (Targeted, Not Universal)

• Administer supplemental oxygen only if $SpO_2 < 90\%$, or if the client exhibits signs of hypoxemia, heart failure, or respiratory distress.
• Evidence-Based Rationale: Routine administration of high-flow oxygen to normoxic myocardial infarction clients induces coronary vasoconstriction, increases systemic vascular resistance, and accelerates the production of harmful reactive oxygen species (ROS) upon reperfusion, enlarging infarct size.

2. Aspirin (Antiplatelet Loading)

• Administer 162 to 325 mg of non-enteric-coated aspirin immediately.
• Instruct the client to chew and swallow the tablets. Chewing promotes rapid buccal and gastric mucosal absorption, achieving near-complete cyclooxygenase-1 (COX-1) inhibition and suppression of thromboxane $A_2$-mediated platelet aggregation within 15 to 30 minutes.

3. Nitroglycerin (Vasodilator Therapy)

• Administer Nitroglycerin 0.4 mg sublingual tablet or spray every 5 minutes, up to a maximum of 3 doses, provided blood pressure is continuously re-evaluated before each administration.
• Critical Absolute Contraindications:
  1. Severe Hypotension: Systolic blood pressure $<90\text{ mmHg}$ or $>30\text{ mmHg}$ below baseline.
  2. Severe Bradycardia ($<50\text{ bpm}$) or Marked Tachycardia ($>100\text{ bpm}$).
  3. Phosphodiesterase-5 (PDE-5) Inhibitor Use: Concomitant use of sildenafil or vardenafil within the past 24 hours, or tadalafil within the past 48 hours. Combining nitrates with PDE-5 inhibitors produces severe, irreversible cyclic GMP-mediated vasodilation, resulting in catastrophic refractory shock and death.
  4. Right Ventricular (RV) Infarction: Suspected in inferior wall STEMI (leads II, III, aVF) and confirmed by ST elevation $\ge 1\text{ mm}$ in lead V4R. The infarcted right ventricle loses contractile power and behaves as a passive conduit, becoming strictly dependent on elevated right ventricular preload (venous return) to push blood through the pulmonary circulation. Nitroglycerin causes profound systemic venodilation, completely obliterating preload and causing acute, catastrophic cardiovascular collapse. Treat RV infarction with aggressive IV isotonic fluid boluses, never nitrates or diuretics.

4. Morphine Sulfate (Judicious Analgesia)

• Administer Morphine Sulfate 2 to 4 mg IV push only for severe, refractory ischemic chest pain unresponsive to sublingual nitroglycerin.
• Nursing Precaution: Morphine decreases gastric motility and slows the enteral absorption of oral P2Y12 platelet receptor inhibitors (clopidogrel, ticagrelor, prasugrel), potentially delaying platelet inhibition.

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Reperfusion Strategies and Post-Intervention Nursing Surveillance

In acute STEMI, "Time is Muscle." Reperfusion therapy restores epicardial vessel patency, halts wavefront necrosis, and preserves left ventricular ejection fraction.

Primary Percutaneous Coronary Intervention (PCI)

• Benchmark Door-to-Balloon Time: $<90\text{ minutes}$ from hospital presentation at a PCI-capable facility; or $<120\text{ minutes}$ from First Medical Contact (FMC) if transferring from a non-PCI center.
• Post-PCI Nursing Care:
  • Vascular Access Site Monitoring: Regularly inspect the femoral or radial sheath entry site for acute hematoma, bleeding, or pseudoaneurysm. If bleeding or expanding hematoma occurs at the femoral site, apply firm manual digital pressure 1 inch proximal to the skin puncture site for at least 20 minutes.
  • Retroperitoneal Hemorrhage Surveillance: A life-threatening occult bleed from femoral arterial puncture. Watch for sudden severe lower back/flank pain, unexplained tachycardia, pallor, and profound hypotension refractory to fluid boluses.
  • Distal Neurovascular Assessments: Monitor distal pulses (dorsalis pedis/posterior tibial for femoral access; radial/ulnar pulse and capillary refill for radial access), skin temperature, color, and motor/sensory function every 15 minutes for 1 hour, every 30 minutes for 2 hours, then hourly.
  • Immobilization and Hydration: Enforce strict supine bed rest with the affected extremity extended for 2 to 6 hours following femoral manual sheath pull. Administer IV crystalloids to facilitate renal excretion of radiopaque iodinated contrast and prevent contrast-induced acute kidney injury.

Fibrinolytic (Thrombolytic) Therapy

• Benchmark Door-to-Needle Time: $<30\text{ minutes}$ from hospital arrival.
• Indications: STEMI clients presenting within 12 hours of symptom onset when primary PCI cannot be accomplished within 120 minutes of FMC.
• Pharmacological Agents: Tenecteplase (TNK-tPA) given as a single weight-based IV bolus over 5 seconds, or Alteplase (rtPA) weight-based accelerated infusion over 90 minutes.
• Absolute Contraindications to Fibrinolysis:
  • Any prior history of intracranial hemorrhage.
  • Known structural cerebral vascular lesion (e.g., arteriovenous malformation).
  • Known malignant intracranial neoplasm.
  • Ischemic stroke within the preceding 3 months (excluding acute ischemic stroke within 4.5 hours).
  • Suspected aortic dissection (unequal pulses, tearing chest/back pain).
  • Active internal bleeding or bleeding diathesis (excluding menses).
  • Significant closed-head or facial trauma within the preceding 3 months.

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Cerebrovascular Accidents (Stroke): Etiology, Triage & Diagnostics

Acute stroke is defined as a focal neurological deficit resulting from sudden vascular disruption within the central nervous system.

• Ischemic Stroke (85%): Caused by atherothrombotic arterial occlusion or thromboembolism (predominantly originating from atrial fibrillation or carotid stenosis). The central ischemic core suffers irreversible infarction within minutes, but the surrounding ischemic penumbra remains structurally intact though electrically silent; penumbral salvage is the primary objective of emergency reperfusion.
• Hemorrhagic Stroke (15%): Caused by vascular rupture with extravasation of blood into the brain parenchyma (Intracerebral Hemorrhage [ICH], driven by chronic uncontrolled hypertension or cerebral amyloid angiopathy) or into the subarachnoid space (Subarachnoid Hemorrhage [SAH], driven by rupture of an intracranial berry aneurysm). SAH classically presents with a sudden, catastrophic thunderclap headache ("the worst headache of my life"), nuchal rigidity, vomiting, photophobia, and rapid decline in consciousness.

Prehospital and Emergency Department Triage

Emergency screening tools evaluate focal deficits rapidly:

• FAST Mnemonic: Face drooping (asymmetrical smile); Arm weakness (unilateral pronator drift); Speech difficulty (dysarthria or expressive/receptive aphasia); Time to call emergency services.
• Cincinnati Prehospital Stroke Scale (CPSS): Evaluates facial droop, arm drift, and abnormal speech. The presence of a single abnormal finding confers a 72% probability of acute ischemic stroke.

Critical Diagnostic Step: Non-Contrast Head CT

Upon emergency department arrival, a non-contrast cranial Computed Tomography (CT) scan must be completed within 20 minutes and interpreted by an expert radiologist within 45 minutes.

• Crucial Nursing Principle: While an acute ischemic stroke may appear completely normal on a head CT during the first 6 to 12 hours, the non-contrast CT's immediate, indispensable role is to rule out intracranial hemorrhage.
• The presence of hyperdense (bright white) blood confirms hemorrhagic stroke and constitutes an absolute contraindication to thrombolytics or anticoagulants.

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Emergency Management of Acute Ischemic Stroke

Intravenous Thrombolytic Therapy (Alteplase / Tenecteplase)

• Standard Time Window: Within 3 hours of "last known well" (the exact time the client was last seen at baseline neurological function).
• Extended Time Window (3 to 4.5 Hours): Recommended for eligible clients. The original ECASS III trial excluded people over 80, those taking oral anticoagulants, those with an NIH Stroke Scale above 25, and those with both prior stroke and diabetes. Current AHA/ASA guidance has relaxed several of these exclusions, so eligibility follows the local stroke protocol.
• Alteplase Dosing: $0.9\text{ mg/kg}$ (maximum cumulative dose $90\text{ mg}$). Administer 10% of the calculated total dose as an IV bolus over 1 minute; infuse the remaining 90% continuously over 60 minutes using an electronic infusion pump.

Strict Blood Pressure Thresholds for Thrombolysis

Uncontrolled hypertension during or after thrombolysis drastically increases the risk of fatal intracranial hemorrhagic transformation.

• Pre-Thrombolysis Blood Pressure Target: Blood pressure must be $<185\text{ mmHg}$ systolic and $<110\text{ mmHg}$ diastolic before initiating thrombolytic therapy. If BP exceeds these thresholds, titrate IV Labetalol (10–20 mg IV over 1–2 minutes) or Nicardipine IV infusion (5 mg/hr, titrating up by 2.5 mg/hr every 5–15 minutes). If BP cannot be maintained $<185/110\text{ mmHg}$, the client is ineligible for thrombolysis.
• Post-Thrombolysis Blood Pressure Target: Maintain blood pressure $<180\text{ mmHg}$ systolic and $<105\text{ mmHg}$ diastolic continuously for at least 24 hours post-infusion.

Post-Thrombolysis Nursing Surveillance

• Conduct focused neurological assessments (NIH Stroke Scale) and vital sign measurements every 15 minutes for 2 hours, every 30 minutes for 6 hours, then hourly for 16 hours.
• Emergency Discontinuation Trigger: If the client develops sudden severe headache, acute severe hypertension, nausea, vomiting, or acute neurological deterioration, immediately stop the thrombolytic infusion, notify the physician, and transport the client for an emergency non-contrast head CT.
• Delay insertion of invasive devices (nasogastric tubes, indwelling urinary catheters, arterial lines) for at least 24 hours unless absolutely life-saving.

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Emergency Management of Hemorrhagic Stroke

1. Hemodynamic Management: Rapid, controlled lowering of systolic blood pressure to a target of 130 to 140 mmHg using continuous IV antihypertensive infusions (Nicardipine, Clevidipine, or Labetalol) to halt hematoma expansion while maintaining cerebral perfusion pressure.
2. Emergency Anticoagulant Reversal:
   • Warfarin: Administer 4-Factor Prothrombin Complex Concentrate (4F-PCC) and IV Vitamin K (Phytomenadione 10 mg) to normalize INR within minutes.
   • Dabigatran: Administer the specific monoclonal reversal agent Idarucizumab (5 g IV).
   • Factor Xa Inhibitors (Apixaban, Rivaroxaban): Administer Andexanet alfa or 4F-PCC.
   • Heparin: Administer Protamine sulfate.
3. Elevated Intracranial Pressure (ICP) Control: Maintain head of bed elevated at 30 degrees with head and neck in neutral midline alignment to maximize internal jugular venous drainage. Administer osmotic therapy (Hypertonic 3% Saline or 20% Mannitol IV) as ordered. Avoid hyperthermia, hyperglycemia, Valsalva maneuvers, and noxious stimuli.