STEMI Treatment Quiz

Acute Coronary Syndrome (ACS)

• ACS encompasses syndromes associated with acute myocardial ischemia, arising from an imbalance between myocardial oxygen demand and supply.
• Classification is based on electrocardiographic (ECG) changes:
  • ST-segment elevation myocardial infarction (STEMI):
    • Characterized by ST-segment elevation in at least two contiguous leads on the 12-lead ECG.
  • Non-ST-segment-elevation acute coronary syndrome (NSTE-ACS):
    • Includes:
      • Non-ST-segment-elevation myocardial infarction (NSTEMI):
        • Characterized by ST-segment depression or T-wave inversion, possibly with elevated cardiac biomarkers.
      • Unstable angina (UA):
        • Characterized by chest pain or discomfort, and may or may not have elevated cardiac biomarkers.

Learning Outcomes (Acute Coronary Syndrome)

• Explain the pathophysiology of ACS.
• Identify factors inducing and potentiating ACS.
• Discuss the clinical presentation, diagnosis, and laboratory evaluation of ACS.
• Evaluate therapeutic outcomes of ACS treatment.

Coronary Artery Structure

• The artery wall consists of several layers:
  • Tunica intima: innermost layer, contains endothelium and elastic membrane
  • Tunica media: middle layer, composed of smooth muscle and elastic fibers
  • Tunica adventitia: outermost layer, composed of connective tissue

Pathophysiology of ACS

• Endothelial dysfunction, inflammation, and fatty streak formation contribute to atherosclerotic plaque development.
• Plaque rupture leads to collagen and tissue factor exposure, thus inducing platelet adhesion and activation.
• Platelet activation promotes the release of adenosine diphosphate (ADP) and thromboxane A2, which results in vasoconstriction.
• Platelet aggregation through fibrinogen bridges occurs.
• Exposure of blood to the thrombogenic lipid core and endothelium activates the extrinsic coagulation cascade and forms a fibrin clot.

Learning Outcomes (Arrhythmia)

• Explain the pathophysiology of arrhythmias.
• Identify factors inducing and potentiating arrhythmias
• Discuss clinical presentation, diagnosis, and laboratory evaluation of arrhythmias.
• Evaluate therapeutic outcomes for arrhythmia treatment

Arrhythmia

• Arrhythmia is the irregular heartbeat abnormality, including:
  • Ventricular arrhythmias: occur in the lower chambers (ventricles) of the heart.
  • Supraventricular arrhythmias: occur in the upper chambers (atria) of the heart.

Atrial Fibrillation (AF)

• Extremely rapid (400–600 beats/min) and disorganized atrial activation.
• Irregular ventricular rate, often not visible P waves in the ECG.

Atrial Flutter

• Rapid (270–330 beats/min) but regular atrial activation.
• Regular ventricular response pattern (often 2:1, 3:1, or 4:1 conduction).

Paroxysmal Supraventricular Tachycardia (PSVT)

• Caused by re-entry mechanisms, including AV nodal re-entry, AV re-entry incorporating an anomalous AV path, sinoatrial (SA) nodal re-entry, and intra-atrial re-entry..
• Characterized by a regular, narrow complex tachycardia.

Ventricular Tachycardia (VT)

• Three or more repetitive ventricular premature complexes (PVCs) at a rate above 100 beats per minute.
• Can be monomorphic (consistent QRS) or polymorphic (varying QRS morphology), with torsades de pointes as a specific polymorphic form.

Ventricular Proarrhythmia

• Development of new or worsening ventricular arrhythmias due to antiarrhythmic agents.
• Torsades de pointes (TdP) is a rapid, polymorphic VT associated with delayed ventricular repolarization.

Ventricular Fibrillation (VF)

• Chaotic irregular deflections without identifiable P-QRS-T waves.
• Usually associated with no cardiac output and sudden cardiac arrest in patients with left ventricular dysfunction or coronary artery disease.

Cardiac Arrest

• Cessation of cardiac mechanical activity, confirmed by the absence of signs of circulation (e.g., pulse, responsiveness, and breathing).

Pathophysiology of Cardiac Arrest

• Two primary causes:
  • Primary: arterial blood is typically fully oxygenated.
  • Secondary: occurs from respiratory failure as a result of absent or inadequate ventilation.
  • Coronary artery disease as a possible underlying contributor in adults.

Clinical Presentation of Cardiac Arrest

• Cardiac arrest may be preceded by symptoms like anxiety, shortness of breath, chest pain, nausea, vomiting, and diaphoresis.
• After arrest, patients are unresponsive, apneic, and hypotensive, lacking a detectable pulse.

Diagnosis of Cardiac Arrest

• Clinical manifestations consistent with cardiac arrest.
• Vital signs (heart rate, respirations) confirm the diagnosis
• ECG identifies the rhythm, guiding the determination of drug therapy.

Treatment of Cardiac Arrest

• CPR; Return of Spontaneous Circulation (ROSC) with early ventilation.
• Immediately address precipitating cause(s) of arrest..
• Optimize tissue oxygenation and prevent subsequent episodes.

Chain of Survival Approach

• Out-of-hospital arrests:
  • Recognition and activation of the emergency response system.
  • Immediate high-quality CPR.
  • Rapid defibrillation.
  • Basic and advanced emergency medical services.
  • Advanced life support and post-arrest care.
• In-hospital arrests: same as above, with added surveillance and prevention steps.

Treatment of Ventricular Fibrillation and Pulseless Ventricular Tachycardia

• Administer electrical defibrillation (360 J monophasic or 120-200 J biphasic).
• Restart CPR until rhythm analysis, then repeat defibrillation or consider pharmacologic therapy.
• Establish airway and IV access when feasible.
• Provide 100% oxygen.

Pharmacologic Therapy (Cardiac Arrest)

• Epinephrine: first-line treatment.
• Amiodarone: second-line treatment if epinephrine ineffective or unavailable.
• Lidocaine: alternative to amiodarone

Treatment of Pulseless Electrical Activity (PEA) and Asystole

- CPR, airway control, and IV access.
- Avoid defibrillation in asystole.
- Transcutaneous pacing if available.

Acid-Base Management (Cardiac Arrest)

• Acidosis typically occurs due to decreased blood flow or inadequate ventilation.
• Sodium bicarbonate is sometimes used in special circumstances (e.g., preexisting metabolic acidosis, hyperkalemia, TCA overdose).

Postresuscitation Care

• Ensure adequate airway and oxygenation.
• Evaluate for myocardial infarction (MI) and consider revascularization.
• Therapeutic hypothermia (32-36°C) is usually used.
• Monitor for and address complications, including electrolyte imbalances, infections, and dysrhythmias.
• Gradually rewarm the patient at a controlled rate.

Test your knowledge on the treatment protocols for STEMI, including medication administration and contraindications. This quiz covers critical scenarios in which fibrinolytics may be used, as well as the management approaches when primary PCI is unavailable. It's essential for healthcare professionals involved in cardiology and emergency medicine.