Myocardial Infarction

Clinical Orientation

The STEMI patient is in the cath lab. The LAD is 100% occluded. Time from door-to-balloon: 62 minutes. But the damage isn't over — the next 48 hours are critical. Reperfusion itself can cause injury. The stunned myocardium may recover — or it may not. The nurse must watch for arrhythmias, pump failure, and mechanical catastrophe. This chapter answers: What mechanism links myocardial infarction to bedside findings, tests, red flags, and nursing priorities?

What Goes Wrong — The Infarction Process

The ischemic cascade:

1. Coronary occlusion → oxygen deprivation
2. Within seconds: ATP depletion → anaerobic glycolysis → lactic acid
3. Within minutes: Loss of contractility (regional wall motion abnormality)
4. Within 20-40 minutes: Irreversible cell injury begins (subendocardium first — most vulnerable to ischemia)
5. Over hours: Necrosis spreads from subendocardium toward epicardium ("wavefront phenomenon")
6. 6-12 hours: Full-thickness necrosis if no reperfusion
7. Days: Inflammatory cell infiltration, early scar formation
8. Weeks: Collagen deposition → mature scar

Reperfusion injury: Paradoxically, restoring blood flow causes additional damage: calcium overload, free radical generation, inflammation, microvascular obstruction. This is why myocardial stunning can occur — contractile dysfunction that recovers over days to weeks.

ECG Localization

What the Nurse May See

Vital signs: Tachycardia (SNS activation, compensatory for low CO). Hypertension (SNS, pain) or hypotension (pump failure, RV infarct). Tachypnea (pulmonary congestion, anxiety).

Cardiac assessment: S3 gallop = LV dysfunction. S4 = stiff, noncompliant ventricle. New holosystolic murmur = papillary muscle dysfunction/rupture or ventricular septal defect. Pericardial friction rub = pericarditis (Dressler syndrome, days to weeks later).

Signs of pump failure: Crackles, hypoxia, frothy sputum (pulmonary edema). Cool extremities, oliguria, confusion (low CO). JVD with clear lungs suggests RV infarction.

Tests and Monitoring

• Serial troponin: Peak level correlates with infarct size. High-sensitivity troponin enables earlier detection.
• Echocardiogram: Wall motion abnormalities, ejection fraction, mechanical complications (papillary muscle, VSD, free wall rupture, pericardial effusion).
• Continuous rhythm monitoring: VT/VF risk highest in first 24-48 hours.
• Hemodynamic monitoring (if unstable): PA catheter to guide therapy in cardiogenic shock.

Nursing Priorities

1. Rhythm monitoring: VT/VF is the #1 killer in acute MI. Defibrillator immediately available.
2. Limit myocardial oxygen demand: Bed rest (initially), manage pain and anxiety, control hypertension and tachycardia.
3. Complication surveillance:
   • Arrhythmias: PVCs, VT, VF, heart block (inferior MI → AV nodal ischemia → bradycardia/heart block).
   • Pump failure: Crackles, S3, hypotension, oliguria.
   • Mechanical: New murmur, sudden pulmonary edema, cardiogenic shock.
   • Pericarditis: Pleuritic chest pain, friction rub, diffuse ST elevation (different from STEMI).
4. Post-PCI care: Monitor access site for hematoma, bleeding, pseudoaneurysm. Bed rest per protocol. Distal pulses before and after.
5. Medication initiation: Dual antiplatelet therapy, beta-blocker, ACEi/ARB, high-intensity statin (unless contraindicated).

Red Flags

Patient Teaching

• "Part of your heart muscle was damaged from a blocked artery. The heart needs time to heal. Take your medications exactly as prescribed — they prevent another blockage, help your heart pump more efficiently, and prevent further damage. Call 911 immediately for any chest discomfort — don't wait."
• Lifestyle: smoking cessation, heart-healthy diet, cardiac rehabilitation, medication adherence.