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Spontaneous Circulation
Spontaneous Circulation focuses on advanced ECG interpretation, cardiac pharmacology, hemodynamic assessment and resuscitation, and managing acute coronary syndrome. It is devoted to translating the best evidence-based treatments from critical care, resuscitation, and trauma for bedside use in the emergency department.
Friday, October 11, 2013
Take Me Out to the Ballgame

A 31-year-old man presented to the ED with syncope. He was previously healthy, takes no medications, and had run a marathon the day before. He was riding the light rail home from a baseball game when he developed vague 4/10 epigastric abdominal pain associated with nausea and diaphoresis. He remembers feeling lightheaded and flushed before momentarily passing out.

His wife said he became quite pale immediately beforehand. He did not have any headache, chest pain, or shortness of breath before or after the syncopal episode. He has a significant family history of premature coronary artery disease. He had normal vital signs and a normal physical exam in the ED. A 12-lead electrocardiogram was obtained.

The ECG shows sinus rhythm with rSR' pattern in V1 and V2 with borderline prolonged QRS suggestive of incomplete right bundle branch block. Diffuse ST-segment elevation in the precordial leads is suggestive of possible early repolarization or injury pattern. His initial cardiac troponin I was minimally elevated at 0.058 ng/mL. He underwent emergent coronary angiography, which showed normal coronary arteries without significant atherosclerotic changes.

Figure 1.

His ECG demonstrates a Type 2 Brugada pattern (saddleback ST-T wave with >2 mm ST-elevation), which suggests Brugada syndrome, a cause of cardiac syncope in those without structural heart disease. Chemistry panel and blood counts were unremarkable, but his initial cardiac troponin I was minimally elevated at 0.058 ng/mL.

Evaluation of a patient who suffers a transient loss of consciousness can often be a challenge in the emergency department. Syncope is defined as an abrupt and transient loss of consciousness with the loss of postural tone followed by rapid spontaneous and complete recovery without intervention and no residual neurologic deficits. It is precipitated by acute decrease in cerebral perfusion, which then is restored, allowing the patient to regain consciousness.

This definition usually makes it possible to differentiate syncope from mimicking etiologies that cause transient changes in consciousness, such as mechanical falls with head injury, hypoglycemia, seizure, and TIA/stroke. Syncope describes an event, however, not a specific etiology. The differential for syncope is quite large (see table below), and covers the spectrum from benign causes that require no further workup to life-threatening disorders that demand immediate intervention. The evaluation of all patients with syncope should begin with a thorough history including any witnesses to the event, a physical exam focusing on abnormal vital signs, and cardiopulmonary and neurological exams. An ECG should be the only routine test obtained. Further workup should be directed at specific findings.

Common Etiologies of Syncope
• Dysrhythmias
  o Bradyarrhythmias
  o Wolff-Parkinson-White syndrome
  o Long QT syndrome
  o Brugada syndrome
  o Ventricular tachycardia
• Structural heart disease
  o Valvular disorders (e.g., aortic stenosis)
  o Hypertrophic obstructive cardiomyopathy
  o Dilated cardiomyopathy
  o Restrictive cardiomyopathy
  o Arrhythmogenic right ventricular dysplasia
• Pulmonary embolism
• Myocardial infarction
• Orthostatic or postural hypotension (hypovolemia, medications)
• Reflex mediated/situational (micturition, defecation, cough, swallow)
• Carotid sinus hypersensitivity

Findings on history and physical can usually suggest reflex-mediated, orthostatic, cerebrovascular, or syncope mimics. A prodrome is highly suggestive of vasovagal syncope, and the lack of prodrome points toward cardiac causes. The ECG is most useful in evaluating cardiac causes of syncope. The common underlying process in patients with cardiac-related syncope is an acute drop in cardiac output (the product of the stroke volume and heart rate), which leads to a cerebral hypoperfusion and that precipitates the syncopal episode.

It is easiest to divide patients into those who have underlying structural heart disease from those who do not when considering cardiac causes of syncope. The cause is almost universally a dysrhythmia for patients with a normal heart structure who have a cardiac cause of their syncope. Bradydysrhythmias such as sinus bradycardia, sinus arrest, sinus node exit block, or atrioventricular blocks impair the heart from increasing cardiac output. The heart cannot completely compensate for the decreased heart rate despite a larger stroke volume. The tachyarrhythmias, in contrast, provide inadequate filling time during diastole, which decreases stroke volume, and again the cardiac output falls despite a compensatory higher heart rate.

Physicians should evaluate for the primary tachyarrhythmias: Wolff-Parkinson-White (WPW) syndrome, Brugada syndrome, long QT syndrome, and ventricular tachycardia.

The ventricle in WPW syndrome is depolarized earlier than would be expected by normal conduction through the atrioventricular node (described as preexcitation), and usually occurs through an accessory pathway in the fibrous annulus. WPW syndrome has three electrocardiographic features: a shortened PR interval, a widened QRS, and a characteristic slurring of the upward slope of the R wave (referred to as a delta wave). Patients with WPW syndrome suffer episodes of paroxysmal supraventricular tachycardia, atrial fibrillation, or atrial flutter.

Brugada syndrome is a genetic mutation of the cardiac voltage-gated sodium channels that can cause paroxysmal ventricular tachycardia and lead to sudden cardiac death or syncope if the dysrhythmia self-terminates. Prolongation of the QT syndrome can be a congenital or acquired disorder, and is also associated with development of paroxysmal ventricular tachycardia. A wide complex tachycardia can be caused by supraventricular tachycardia with aberrant conduction (either bundle branch block or WPW) or ventricular tachycardia. Either can impair perfusion enough to cause syncope.

Structural defects of the heart such as pericardial tamponade, valvular disorders (e.g., aortic stenosis or mitral regurgitation), hypertrophic obstructive cardiomyopathy, restrictive cardiomyopathy, or arrhythmogenic right ventricular dysplasia limit the ability to increase stroke volume, and the heart rate response may be inadequate to compensate for the increased demand. Unfortunately, the ECG changes are usually nonspecific in structural heart disease, but often history or physical exam findings are usually present that should raise suspicion. Hypertrophic obstructive cardiomyopathy is the exception, and can show left ventricular hypertrophy, left axis deviation, depressed or flipped T-waves, and Q-waves laterally or inferiorly. Bedside echocardiogram can be useful for evaluating a patient with suspected structural heart disease. Unfortunately, most of the causes of structural heart disease also predispose patients to dysrhythmias, which complicate the evaluation.

The emergency physicians were most concerned with our case patient for cardiac ischemia, given the ST-elevation anteriorly, ongoing epigastric pain, and elevation of the initial troponin. He underwent emergent coronary angiography that showed normal coronary arteries without significant atherosclerotic change. No culprit lesion (current of injury) was identified. Serial ECGs did not demonstrate any dynamic changes. A transthoracic echocardiogram demonstrated normal left ventricular size, normal left ventricular ejection fraction, no wall motion abnormality, and no valvular abnormalities. Cardiology consultation was obtained, and a Type 2 Brugada pattern was noted on the ECG.

The Brugada syndrome was first described in 1992, and has been attributed to 40 percent of the deaths from sudden cardiac arrest in those without structural heart disease. It is caused by a missense mutation in the SCN3A gene responsible for cardiac voltage-gated sodium channels, and results in a reduction in fast sodium channel currents in the right ventricular epicardium but not those in the endocardium. The Brugada changes occur largely in the early precordial leads because these leads overlie the right ventricle. These changes predispose the patient to ventricular tachycardia, which can present as syncope if the arrhythmia self-terminates. It can also decompensate into ventricular fibrillation and death.

The Brugada pattern on ECG is not sufficient to make the diagnosis. Formal diagnosis requires one of the following in addition to the ECG pattern:

• Documented ventricular fibrillation
• Self-terminating polymorphic ventricular tachycardia
• Family history of sudden cardiac death under age 45
• Type 1 ST-segment elevation in family members
• Electrophysiologic inducibility of ventricular tachycardia
• Unexplained syncope suggestive of a tachyarrhythmia
• Nocturnal agonal respiration

Patients who have a concern for Brugada syndrome should be evaluated by an electrophysiologist for diagnosis and risk stratification. Treatment usually involves placement of an ICD. The Brugada syndrome can be classified into three characteristic ECG patterns. All involve persistent ST-elevation in leads V1-V3 accompanied by a complete or incomplete right bundle branch block. Type 1 has an elevated ST-segment (≥2 mm) in two precordial leads that descends with an upward convexity to an inverted T-wave (so-called coved pattern). Types 2 and 3 have a saddle-shaped ST-T wave pattern, in which the ST-segment initially declines toward the baseline and then rises to an upright T-wave. The ST-segment is elevated ≥1 mm in Type 2 and <1 mm in Type 3. None of the patterns should manifest reciprocal ST depression in inferior leads or a long QT interval. The saddleback configurations are thought to be less specific for this syndrome.

Moving the right precordial leads (V1 and V2) up one intercostal space (to the third or second intercostal space) may increase the sensitivity of detecting these abnormalities. This was done for this patient, and the ECG is shown below. It demonstrates a clearer Type 2 pattern in V2. (Figure 2.)

Figure 2.

Our patient did well during his hospitalization. (Figure 3.) Given the significant prodrome, his syncope was ultimately attributed to vasovagal syncope from the acute onset of gastritis epigastric pain. His troponin elevation did not show a characteristic rise and fall that would indicate acute coronary syndrome, and was attributed to the marathon he ran the day before. He did not meet the criteria for Brugada syndrome despite the Type 2 Brugada pattern ECG. He is following closely with his cardiologist.

Figure 3.

About the Author

Charles Bruen, MD

Charles Bruen, MD, is a fellow in critical care medicine and emergency cardiology at Hennepin County Medical Center in Minneapolis. He has special interest in stabilization, resuscitation, hemodynamic evaluation, and emergency cardiovascular care. He obtained his undergraduate degree in aerospace engineering at the Massachusetts Institute of Technology, and worked in aerospace for several years, leading the effort at Beal Aerospace Technologies to develop the largest rocket engine since the Apollo program. He earned his medical degree at the University of Texas Southwestern Medical School at Dallas, and completed a combined residency in emergency medicine and internal medicine at Hennepin. Visit his website, http://resusreview.com, and follow him on Twitter: @resusreview.

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