16.1 STEMI, Cardiogenic Shock & Pulmonary Edema

16.1 STEMI, Cardiogenic Shock & Pulmonary Edema

The cardiac catheterization laboratory is the definitive treatment venue for ST-elevation myocardial infarction (STEMI) and a critical escalation point when patients deteriorate into cardiogenic shock or acute pulmonary edema. The RCIS must rapidly recognize these presentations, coordinate team activation, maintain hemodynamic monitoring, and support primary percutaneous coronary intervention (PCI) without introducing delays that worsen mortality.

STEMI Recognition and Cath Lab Activation

STEMI is an acute coronary syndrome caused by complete thrombotic occlusion of a major epicardial coronary artery. Time to reperfusion is the dominant determinant of myocardial salvage — "time is muscle." Every minute of delay increases infarct size and mortality.

12-Lead ECG Criteria

The RCIS must be proficient in identifying STEMI patterns on the 12-lead ECG:

• ST-Segment Elevation: New ST elevation at the J point in two or more contiguous leads. Thresholds:
  • ≥1 mm (0.1 mV) in all leads except V2–V3.
  • V2–V3: ≥2 mm in men <40 years and women; ≥2.5 mm in men ≥40 years.
• Reciprocal ST Depression: Often seen in leads opposite the territory of injury (e.g., inferior ST elevation with reciprocal depression in I and aVL).
• New Left Bundle Branch Block (LBBB): Treated as equivalent to STEMI when accompanied by ischemic symptoms and concordant ST changes (Sgarbossa criteria aid interpretation).
• Posterior STEMI: Suspect when anterior ST depression with tall R waves in V1–V2; confirm with posterior leads V7–V9 showing ST elevation ≥0.5 mm.

Anatomic Territory Correlation

Primary PCI Workflow in the Lab

When a STEMI patient arrives in the cath lab, the RCIS supports an door-to-balloon target of ≤90 minutes from first medical contact (institutional targets often aim for ≤60 minutes from cath lab arrival):

1. Immediate Monitoring: Continuous 5-lead or 12-lead telemetry, noninvasive blood pressure at least every 5 minutes, pulse oximetry, and IV access verification.
2. Antiplatelet Loading: Confirm aspirin (162–325 mg chewed or 81 mg if already on daily aspirin) and P2Y12 inhibitor (clopidogrel 600 mg, ticagrelor 180 mg, or prasugrel 60 mg) have been administered unless contraindicated.
3. Anticoagulation: Unfractionated heparin bolus (typically 70–100 units/kg, max 5,000–10,000 units) or bivalirudin per protocol; ACT target commonly 250–300 seconds for PCI.
4. Avoid Delays: Do not defer the case for nonessential imaging, repeat labs, or incomplete consent when the patient is unstable — use emergent consent protocols per institutional policy.
5. Culprit Vessel Identification: Angiography identifies the occluded artery; primary PCI with balloon and stent deployment restores TIMI 3 flow as the goal.
6. Document TIMI Flow: Pre- and post-intervention Thrombolysis In Myocardial Infarction (TIMI) flow grades (0 = no perfusion, 3 = complete perfusion) must be recorded.

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Cardiogenic Shock

Cardiogenic shock is a state of inadequate tissue perfusion due to primary cardiac pump failure. It complicates approximately 5–10% of STEMI cases and carries mortality exceeding 40% even with modern therapy.

Hemodynamic Definition and Monitoring

Cardiogenic shock is characterized by:

• Hypotension: Systolic BP <90 mmHg or mean arterial pressure (MAP) <65 mmHg for >30 minutes, OR requirement for vasopressors/inotropes to maintain BP.
• Hypoperfusion: Cool extremities, altered mental status, oliguria (<0.5 mL/kg/hr), elevated lactate (>2 mmol/L).
• Elevated Filling Pressures: Pulmonary capillary wedge pressure (PCWP) >15 mmHg on right heart catheterization when performed.
• Reduced Cardiac Output: Cardiac index (CI) <2.2 L/min/m².

The RCIS must ensure invasive arterial monitoring (radial or femoral arterial line) is placed early for beat-to-beat pressure tracking during shock management.

Medical Stabilization

• Volume Assessment: Most cardiogenic shock patients are not volume depleted — avoid large fluid boluses that worsen pulmonary edema. A cautious 250 mL crystalloid trial may be given only when PCWP is low or echocardiography shows underfilled ventricles.
• Vasopressors: Norepinephrine is first-line for hypotension with cardiogenic shock when MAP cannot be maintained. Dopamine is an alternative but may increase arrhythmias.
• Inotropes: Dobutamine or milrinone improve contractility when BP is adequate or supported by vasopressors; titrate to perfusion endpoints while monitoring for arrhythmias.
• Revascularization: Emergency PCI of the culprit artery remains the cornerstone — shock without reperfusion has near-universal mortality.

Mechanical Circulatory Support (MCS)

When medical therapy fails, escalate to MCS:

• Intra-Aortic Balloon Pump (IABP): Inflates in diastole to augment coronary perfusion and deflates in systole to reduce afterload. Provides ~0.5 L/min augmentation. Contraindicated in aortic regurgitation, aortic dissection, and severe peripheral vascular disease.
• Impella (Axillary or Femoral): Continuous-flow microaxial pump providing 2.5 to 4.0+ L/min forward flow. The RCIS assists with console setup, purge system monitoring, and P-level (motor current) surveillance.
• VA-ECMO: For refractory shock with biventricular failure — provides full cardiopulmonary support but requires specialized team activation.

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Acute Pulmonary Edema

Acute pulmonary edema — particularly flash pulmonary edema — occurs when sudden left ventricular failure causes rapid transudation of fluid into the alveoli. In the cath lab context, it may present pre-procedure (acute MI with pump failure), intraprocedure (contrast load, ischemia, arrhythmia), or post-procedure (stent thrombosis, perforation with tamponade physiology).

Clinical Presentation

• Severe dyspnea and orthopnea
• Pink, frothy sputum (alveolar edema)
• Audible crackles (rales) on auscultation to the mid-lung fields or higher
• Hypoxemia (SpO₂ often <90% on room air)
• Tachypnea (>25 breaths/min) and diaphoresis
• Hypertension is common (sympathetic surge); hypotension suggests cardiogenic shock overlap

Immediate RCIS Interventions

1. Positioning: Sit the patient upright (high Fowler's, 60–90 degrees) to reduce venous return and improve ventilation-perfusion matching.
2. Supplemental Oxygen: High-flow nasal cannula or non-rebreather mask; escalate to noninvasive positive-pressure ventilation (NIPPV) — BiPAP or CPAP — when SpO₂ remains <90% despite high-flow O₂.
3. Nitroglycerin: IV nitroglycerin drip (start 5–10 mcg/min, titrate every 3–5 minutes) reduces preload and afterload. Hold if SBP <90 mmHg or if phosphodiesterase-5 inhibitors (sildenafil, tadalafil) were taken within 24–48 hours.
4. Loop Diuretics: IV furosemide 40–80 mg (or 1–2× the patient's home dose) promotes diuresis when the patient is volume overloaded.
5. Morphine: Historically used for anxiety and preload reduction; many institutions have reduced routine use due to potential adverse outcomes — follow local protocol.
6. Intubation Readiness: Prepare suction, bag-valve-mask, and crash cart if the patient develops respiratory fatigue, inability to protect airway, or refractory hypoxemia despite NIPPV.

The RCIS bridges these stabilizing measures while the operator completes angiography and PCI of the culprit lesion — treating the underlying ischemia is essential to resolve the pulmonary edema permanently.