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12-Lead ECG and Patients with Syncopal Episodes (Case 2)

Posted by Jessica Carmichael on 8/20/12 9:30 AM

This is the second in a series of articles that will explore the cardiac causes of syncope and illustrate the importance of acquiring an ECG on all patients who experience presyncope or syncope.

Emergency Medical Services (EMS) personnel frequently respond to patients experiencing syncopal episodes. Syncope accounts for 3% of emergency department visits and 6% of hospital admissions yearly. Syncope is defined as a brief loss of consciousness caused by transiently inadequate blood flow to the brain. EMS personnel often minimize the syncopal event and dismiss it simply as a sign of anxiety or a vasovagal reaction. Although increased vagal tone is often responsible for inadequate cerebral perfusion and subsequent loss of consciousness, it is critical to exclude the postural, neurological, and cardiac causes first.

Case Study

You are dispatched to a 33-year-old male who experienced a syncopal episode while playing basketball. Upon arrival, you find an awake, alert, and oriented adult male.  He appears anxious and insists that he does not want to be transported to the hospital. He denies having chest pain, abdominal pain, or shortness of breath. His vital signs are: blood pressure 118/72, pulse 53, respirations 18, SpO 2 98%, blood sugar 102 mg/dL. His lung sounds are clear and his skin is cool, wet, and pink. You explain the importance of acquiring an ECG and the patient agrees.


Reading the 12-Lead ECG

  • What is your interpretation?
  • Do you see any threats to the patient’s life?
  • What is your next course of action?
  • Does this patient need to be transported to the hospital?

Case Study Summary

The ECG reveals a bradycardic rhythm originating near the atrioventricular (AV) junction or in the atrial tissue. Huge QRS complexes appear across all leads of the ECG tracing, suggestive of left ventricular hypertrophy. The ST and T wave changes are likely due to ventricular hypertrophy. Deep, narrow Q waves appear in the lateral leads, I, and aVL.

High ventricular voltage coupled with deep, narrow Q waves is virtually diagnostic of hypertrophic cardiomyopathy (HCM). HCM is a genetic disorder that causes inappropriate thickening of the left ventricular wall and often affects the interventricular septum also. HCM can cause self-terminating or sustained ventricular and supraventricular arrhythmias. HCM is the leading cause of sudden cardiac arrest in patients younger than 18 years of age.

This patient should be transported to the emergency department for further evaluation. Prehospital treatment includes 12-lead ECG acquisition and continuous rhythm monitoring. Standard ACLS protocol should be initiated if the patient experiences arrhythmias. Definitive treatment for HCM is centered on the prevention of sudden cardiac arrest by early detection of the disease and implantation of a cardioverter-defibrillator.

Clinical Pearls

  • Never dismiss exertional syncope in the prehospital setting because it may be a symptom of a lethal disease.
  • Acquire a 12-Lead ECG on all patients presenting with exertional syncope and scrutinize the tracing for changes consistent with life-threatening diseases.
  • Hypertrophic cardiomyopathy is characterized by:
    • High ventricular voltage / left ventricular hypertrophy
    • Deep, narrow Q waves in leads I, aVL, and V5-V6
    • Diagnosis of HCM is often made only after the patient experiences sudden cardiac arrest.
    • Consider transmitting any questionable ECG to the local emergency department physician if possible.

Suggested Readings

Hypertrophic Cardiomyopath–

Christopher Touzeau, MS, NREMT-P, RN, caught the EMS bug in 1992 and has been a professional firefighter paramedic in Montgomery County, Maryland since 1995. He developed a passion for teaching early in his career and has developed and taught EMS courses in numerous areas around the country and world.

Mr. Touzeau is the author of ECG Cases for EMS, a Jones & Bartlett Learning title that will be available in August 2012.

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