STEMI Clinical Overview

I. The "On-Call" Snapshot

Clinical Significance in Malaysia: This is a time-critical diagnosis and a leading cause of death in our wards. Your immediate actions in the Emergency Department directly impact patient survival and morbidity. "Time is muscle."

High-Yield Definition: "STEMI is a clinical syndrome defined by characteristic symptoms of myocardial ischemia in association with persistent ST-segment elevation and subsequent release of biomarkers of myocardial necrosis." (Source: Malaysian CPG for Management of Acute STEMI, 4th Ed., 2019).

Clinical One-Liner: Basically, a major coronary artery is completely blocked by a thrombus, and the heart muscle it supplies is actively dying. Your job is to get that artery opened, fast.

II. Etiology & Risk Factors

Etiology: The overwhelming cause is acute coronary thrombosis, typically from the rupture of an atherosclerotic plaque in a coronary artery.

Risk Factors (What we see in our population):

• Non-Modifiable:

  • Age (>45 for men, >55 for women)

  • Male gender

  • Family history of premature coronary artery disease

• Modifiable (Very common in Malaysia):

  • Smoking (Ask about this specifically)

  • Diabetes Mellitus (T2DM)

  • Hypertension (HTN)

  • Dyslipidemia (High LDL)

  • Obesity & Sedentary lifestyle

III. Quick Pathophysiology

It's straightforward: An atherosclerotic plaque becomes unstable and ruptures. This exposes thrombogenic material, leading to platelet activation and the formation of an occlusive thrombus. This complete occlusion stops blood flow downstream, causing transmural ischemia of the myocardium. The ECG reflects this with ST-segment elevation. If flow isn't restored, irreversible necrosis (infarction) occurs within hours.

IV. Clinical Assessment

Red Flags & Immediate Actions:

• Hypotension (SBP <90 mmHg) or signs of shock (cold, clammy, altered mental state): Alert senior immediately. This is likely cardiogenic shock. Secure IV access, start a gentle fluid challenge if no signs of fluid overload, and prepare for inotropes.

• Acute Pulmonary Edema (Pink, frothy sputum; widespread crepitations): Sit the patient up, give high-flow oxygen, administer IV Furosemide 40mg, and alert your senior.

• Ventricular Arrhythmias (VT/VF): Immediate defibrillation as per ALS protocol. This is a common cause of death in the first hour.

• Persistent Bradycardia or High-Degree Heart Block: Alert senior. May require temporary pacing.

History:

• Common (>50%):

  • Chest Pain: Central, crushing, pressure-like. Radiation to the left arm, jaw, or neck. Lasts >20 minutes, not relieved by GTN.

  • Diaphoresis (profuse sweating)

  • Nausea, vomiting

• Less Common (10-50%):

  • Dyspnea (especially in heart failure)

  • Syncope or pre-syncope

  • Epigastric pain (often mistaken for gastritis)

• Pertinent Negatives: Ask if the pain is sharp, stabbing, positional, or pleuritic to help rule out differentials like pericarditis or PE.

Physical Examination:

• General: Patient is often anxious, distressed, pale, and sweaty.

• Vitals: Can be hypertensive (sympathetic surge), hypotensive (cardiogenic shock), tachycardic, or bradycardic (e.g., inferior STEMI).

• Cardiovascular:

  • Listen for a new S4 gallop (common).

  • A new pansystolic murmur could indicate acute mitral regurgitation from papillary muscle rupture – this is a surgical emergency.

• Respiratory: Check for bilateral basal crepitations, suggesting left ventricular failure.

Clinical Pearl: In diabetic, elderly, or female patients, the presentation can be atypical. Think of STEMI in any of these patients presenting with shortness of breath, sudden weakness, confusion, or epigastric discomfort, even without classic chest pain.

V. Diagnostic Workflow

Differential Diagnosis:

• Acute Pericarditis:

  • Points For: Central chest pain.

  • Points Against: Pain is often sharp, pleuritic, and relieved by sitting forward. Widespread "saddle-shaped" ST elevation without reciprocal changes.

  • How to Differentiate: ECG is key. Look for PR depression. Cardiac enzymes are typically normal or only mildly elevated.

• Pulmonary Embolism (PE):

  • Points For: Acute dyspnea, chest pain, tachycardia.

  • Points Against: Pain is usually pleuritic. Look for signs of DVT.

  • How to Differentiate: ECG may show S1Q3T3 pattern, but CT Pulmonary Angiogram (CTPA) is the gold standard.

• Aortic Dissection:

  • Points For: Severe, sudden chest pain.

  • Points Against: Pain is tearing/ripping, often radiating to the back. Look for unequal blood pressure between arms or pulse deficits.

  • How to Differentiate: Widened mediastinum on CXR. CT aortogram is definitive. This is a "can't miss" diagnosis because thrombolysis is fatal.

Investigations Plan:

• Bedside / Initial (First 10 Mins):

  • 12-Lead ECG: This is the most important test. Perform immediately. Look for new ST elevation ≥1 mm in two contiguous limb leads or ≥2 mm in two contiguous chest leads, or a new Left Bundle Branch Block (LBBB). Repeat every 15-30 mins if initial ECG is non-diagnostic but suspicion is high.

• First-Line Labs & Imaging:

  • Cardiac Troponins (T or I): Will be elevated, confirming myocardial injury. Send it off, but DO NOT wait for the result to activate the STEMI pathway if the ECG is diagnostic.

  • FBC, RP, Coagulation Profile, GXM: Baseline labs needed before starting antithrombotics and for potential procedures.

  • Portable CXR: Look for cardiomegaly, signs of heart failure (pulmonary edema), or a widened mediastinum.

• Confirmatory / Gold Standard:

  • Coronary Angiography: This is both diagnostic and therapeutic. It is the gold standard to visualize the coronary anatomy and perform Percutaneous Coronary Intervention (PCI).

VI. Staging & Severity Assessment

We use the Killip Classification at the bedside to assess the severity of cardiac dysfunction.

• Killip Class I: No clinical signs of heart failure. (Management: Standard STEMI care).

• Killip Class II: Rales or crepitations in the lungs (<50% of lung fields), S3 gallop. (Management: Add IV diuretics).

• Killip Class III: Frank pulmonary edema (crepitations >50% of lung fields). (Management: Aggressive diuresis, nitrates, ventilatory support if needed).

• Killip Class IV: Cardiogenic shock (Hypotension SBP <90 mmHg, evidence of hypoperfusion). (Management: Urgent senior review, inotropes/vasopressors, likely requires IABP/mechanical support and immediate revascularization).

VII. Management Plan

Our goal is reperfusion. The strategy depends on the time from symptom onset and the availability of a cath lab.

Immediate Stabilisation (The ABCDE & MONA Plan):

• A, B, C: Secure airway, give Oxygen if SpO2 < 94%. Secure IV access (x2 large bore). Attach cardiac monitor.

• Morphine: IV Morphine 2.5-5mg slowly. For pain relief and anxiolysis.

• Oxygen: As above.

• Nitrates: Sublingual GTN tablet/spray unless hypotensive (SBP<90), bradycardic, or suspected right ventricular infarct.

• Antiplatelets: Aspirin 300mg and Ticagrelor 180mg (or Clopidogrel 600mg) to be chewed and swallowed immediately. This is critical.

Definitive Treatment (Reperfusion):

• Primary Percutaneous Coronary Intervention (PCI): This is the gold standard.

  • Goal: Door-to-balloon time <90 minutes in a PCI-capable hospital.

  • If the patient is at a district hospital, the goal is FMC-to-device time <120 minutes. Activate the STEMI network immediately for transfer.

  • Patient will also need an anticoagulant, usually IV Unfractionated Heparin.

• Fibrinolysis (Thrombolysis): Used if timely PCI is not available (>120 minutes).

  • Goal: Door-to-needle time <30 minutes.

  • Agent: Typically Tenecteplase (TNK), given as a weight-adjusted IV bolus.

  • Contraindications: You MUST screen for these. Absolute contraindications include any prior intracranial hemorrhage, known cerebral vascular lesion, ischemic stroke within 3 months, suspected aortic dissection, or active bleeding.

  • After lysis, the patient should be transferred to a PCI-capable center for angiography within 3-24 hours (pharmaco-invasive strategy).

Long-Term & Discharge Plan (The Ward Round Plan):

• Dual Antiplatelet Therapy (DAPT): Aspirin + Ticagrelor/Clopidogrel for at least 12 months.

• Statins: High-intensity statin (e.g., Atorvastatin 80mg ON) for all patients.

• Beta-blockers: (e.g., Bisoprolol) to be started within 24 hours if no signs of heart failure or risk of shock.

• ACE Inhibitors / ARBs: (e.g., Perindopril) especially if anterior MI, LVEF <40%, or heart failure.

• Lifestyle Advice: Smoking cessation, diet, exercise. Document this.

• Follow-up: Cardiac rehabilitation referral and cardiology clinic appointment.

VIII. Complications

• Immediate (First 24 hours):

  • Arrhythmias (VF/VT): Management: Defibrillation (as per ALS).

  • Cardiogenic Shock: Management: Inotropes, mechanical support, urgent revascularization.

  • Acute LVF/Pulmonary Edema: Management: Diuretics, nitrates, oxygen/ventilation.

• Short-Term (Days to weeks):

  • Pericarditis: Management: High-dose Aspirin.

  • Left Ventricular Thrombus: Management: Anticoagulation (e.g., Warfarin).

  • Mechanical Complications (e.g., VSD, papillary muscle rupture): Management: Surgical emergency, requires urgent echo and cardiac surgery review.

• Long-Term (Months to years):

  • Chronic Heart Failure: Management: Guideline-directed medical therapy.

  • Ventricular Aneurysm: Management: Medical therapy, anticoagulation if thrombus present.

IX. Prognosis

Prognosis is highly dependent on the "Total Ischemic Time" - the time from symptom onset to reperfusion. Shorter times lead to better outcomes.

• Key Negative Prognostic Factors:

  1. Killip Class > I on admission.

  2. Delayed reperfusion (>12 hours from onset).

  3. Post-MI Left Ventricular Ejection Faction (LVEF) < 40%.

X. How to Present to Your Senior

Use the SBAR format. Be concise and clear.

"Dr., for review, STEMI alert in Resus Bay 1. This is Mr. [Name], a [Age]-year-old man with a background of [risk factors], who presented with an hour of crushing central chest pain.

His vitals are [BP, HR, RR, SpO2]. On exam, he is diaphoretic with clear lungs.

The ECG shows a [e.g., 3mm ST-elevation in leads II, III, and aVF], consistent with an acute inferior STEMI.

I have already given Aspirin 300mg and Ticagrelor 180mg. His pain is ongoing. I am activating the primary PCI pathway now and have sent the initial bloods. I would like to ask about giving a dose of IV morphine."

XI. Summary & Further Reading

Top 3 Takeaways:

1. ECG within 10 minutes. This is your primary diagnostic tool. Time is muscle.

2. Load with Aspirin and a P2Y12 inhibitor immediately once STEMI is confirmed. Do not delay.

3. Activate the reperfusion pathway immediately. Your primary goal is Primary PCI. If not available in a timely manner, proceed with Fibrinolysis after checking contraindications.

Key Resources:

• Primary Guideline: Clinical Practice Guidelines: Management of Acute ST Segment Elevation Myocardial Infarction (STEMI), 4th Edition, 2019

• UpToDate: Overview of the acute management of ST-elevation myocardial infarction

• Review Article: NEJM - Myocardial Infarction (This is a good overview of the pathophysiology and treatment principles).