Clinical Review

4 EKG Abnormalities: What Are the Lifesaving Diagnoses?

Clinician Reviews. 2014 July;24(7):368-375

References

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Etiology and epidemiology. Hypertrophic cardiomyopathy is an autosomal dominant intrinsic myocardial disorder resulting in LVH that is commonly associated with SCD during extreme physical activity.^26,27 The prevalence of HCM is approximately 1 in 500.²⁶ Although it can present at any age, it is the most common cause of SCD in young people (under age 30), responsible for 33% of deaths during athletic events.²⁸

TABLE 3
4 diagnoses and what you'll see on EKG

Diagnosis	EKG finding
Prolonged QT interval	QTc interval >.450 sec (men) or >.470 sec (women)
Brugada syndrome	Partial or complete RBBB, and ST segment elevation in right precordial leads V1-V3
Wolff-Parkinson-White syndrome	Delta wave, widened QRS, short PR interval, ST segment and T-wave changes
Hypertrophic cardiomyopathy	No definitive finding; may have left ventricular hypertrophy or abnormal Q-waves

^{EKG, electrocardiogram; RBBB, right bundle branch block.}

Clinical features. The severity of HCM ranges from asymptomatic to fatal. Symptoms of HCM include chest pain, dyspnea, and syncope. The disorder causes morbidity and mortality in at least one of 3 ways: ventricular tachyarrhythmias (often in younger patients), heart failure (from left ventricular outflow obstruction), and/or thromboembolism.²⁷

Although classically associated with syncope, hypertrophic cardiomyopathy often presents similarly to acute coronary syndromes.Although echocardiography typically is used to make the diagnosis,²⁷ an EKG often is the initial screening tool. EKG changes are seen in 75% to 95% of affected patients and include the presence of Q-waves and increased voltages related to LVH.^27,29 Infarct-like patterns may be present before wall thickening on echocardiogram. Abnormal Q-waves are found in 20% to 50% of HCM patients, and are more common in younger patients. Konno et al³⁰ have shown that Q-waves >3 mm in depth and/or >.040 seconds in duration in at least 2 leads other than aVR is specific (90%) in identifying carriers of HCM genes before they develop clinical symptoms.

Ambulatory monitoring may be useful for risk stratifying HCM patients; those with nonsustained ventricular tachycardia (NSVT) are at higher risk of SCD. Holter monitoring is recommended in initial evaluation because evidence of ventricular tachyarrhythmias may warrant AICD placement.²⁶

Treatment. The risk of SCD in HCM is approximately 1%, but higher in those with a family history of SCD, syncope, NSVT, hypotension during exercise, or severe LVH (left ventricle thickness >30 mm).²⁶ AICDs are recommended for HCM patients with prior cardiac arrest, patients with ≥2 of these risk factors, or patients with one risk factor who have experienced syncope related to arrhythmia.²⁶

For patients who are symptomatic but have <2 risk factors, beta-blockers are firstline therapy.²⁶ Verapamil is used as a second line treatment. Both beta-blockers and calcium channel blockers reduce dyspnea, palpitations, and chest pain.²⁷

For hypertrophic cardiomyopathy patients who are symptomatic but have <2 risk factors, beta-blockers are first-line therapy.For patients who don’t respond to medical therapy, septal reduction therapy may be performed, either by septal myectomy or alcohol septal ablation.²⁷ It is also important to consider genetic screening and counseling for the family.

A summary of all 4 diagnoses described in this article, their associated EKG findings, and their pathophysiology appears in TABLE 3.

CORRESPONDENCE
Samir Haydar, DO, MPH, FACEP, Tufts University School of Medicine, Maine Medical Center, Department of Emergency Medicine, 47 Bramhall St., Portland, ME 04103; haydas@mmc.org