Syncope: Differential Diagnosis and Workup

Syncope is an abrupt, transient, spontaneously-resolving  loss of consciousness and postural tone caused by cerebral circulatory hypoxia. It is neither a “chief complaint” nor a final diagnosis. It is a descriptive and a partially etiologically-defined interim diagnosis which requires further investigation.

The first step in evaluating syncope should be to try to distinguish it from alternative causes of loss of consciousness and postural tone. There are many alternate causes of loss of consciousness, including seizures, concussions, sleep (both normal or narcoleptic), migraines and various psychogenic conditions. History from a witness is almost always the best initial diagnostic step. A good history helps, but does not always conclusively confirm, the diagnosis of syncope.

The next step is to evaluate the patient for possible red flags:

  • The worrisome history of present illness: The following cluster of findings almost always points to a malignant cause: absence of a prodrome, passing out with an appearance (to witness) as if the patient was lifeless, a sudden and prompt restoration of consciousness and of all mental faculties in the absence of psychogenic, vasovagal or orthostatic provocation.
  • The worrisome past medical history: History of structural heart disease, particularly of ischemic cardiomyopathy.
  • The worrisome family history: family history of syncope or of sudden cardiac death at a young age points to something bad, namely hypertrophic obstructive cardiomyopathy (HOCM), long QT syndrome, or Brugada syndrome. The younger the relative at time of death or syncope, the redder the red flag.
  • Exertional syncope: these patients should be assumed to have either an obstructive cause or an effort-induced arrhythmia (commonly ventricular tachycardia). Therefore, these patients should get echocardiogram and possibly an exercise electrocardiogram.

An electrocardiogram, when done, it should be scrutinized for:

  • Ischemia (new or old): look for ST changes, Q waves (especially new or worsening), or T wave inversions.
  • Dysrhythmias:
  • Conduction abnormalities (such as heart blocks)
  • Evidence of right ventricular strain/pulmonary hypertension/pulmonary embolism: sinus tachycardia, S1Q3T3, new right bundle branch block or incomplete right bundle branch block, T wave inversions, especially in anteroseptal and inferior leads. Regardless, “the most important thing to remember about pulmonary emboli is that most of them have no effect on the electrocardiogram (ECG) at all…. The reason is obvious: the lungs have such an abundant blood supply that an embolus must compromise a really major segment of the lung before it has any effect on pressure in the pulmonary artery.” (Phibbs, p. 240)
  • Abnormal intervals, particularly short or long QTc (ischemia, hypokalemia, hypocalcemia, drugs)
  • Evidence of pacemaker malfunction: look for (1) pacer spikes that are not followed by P wave/QRS complex (failure to capture), (2) pacemaker rate, (3) spontaneous complexes that do not inhibit the pacemaker, (4) failure of pacemaker to ‘”take over” when spontaneous rhythm slows down.
  • Preexcitation (Wolff-Parkinson-White) pattern: short PR intervals, Delta waves and wide QRS complexes. Also seen are ST changes and T wave inversions that are discordant with the delta waves. A very rapid (250-300), bizarre, highly irregular polymorphic tachycardia with deformed QRS complexes, delta waves, and pauses as long as two R-R intervals points to atrial fibrillation with rapid conduction down an accessory pathway.
  • Brugada Sign: Look for typical or atypical right bundle branch block pattern in leads V1-V3 with a downsloping, coved, elevated ST segment which begins at the top of R’ and ends with an inverted T wave, and without reciprocal changes (Wang, 2013). Before diagnosis Brugada syndrome, make sure that the patient is not hyperkalemic, as hyperkalemia can cause a Brugada sign. Check serum potassium level and look for tall, narrow, pointed and tented T-waves “as if pinched from above.”
  • High left ventricular voltage: in the setting of syncope, high left ventricular voltage suggests either aortic stenosis or hypertrophic obstructive cardiomyopathy (HOCM). In HOCM, the resting ECG is usually nonspecific and ranges from completely normal (up to 25%) to various degrees of high left ventricular voltage, repolarization abnormalities, and left atrial enlargement. Dramatically high left ventricular voltage with deep narrow Q-waves in inferior and lateral leads (I, aVL, V5, V6) is rather specific for HOCM.
  • Epsilon waves: these are seen in patients with arrhythmogenic right ventricular cardiomyopathy. Cardiac MRI is confirmatory.
  • Giant T-wave inversions:  Giant T-wave inversions, particularly in precordial leads, are sometimes seen in patient’s with subarachnoid hemorrhage.

Patients with a pacemaker should get a chest radiograph (for lead placement) and a pacemaker interrogation.

Longer range options for rhythm analysis include:

  • Telemetry
  • Holter monitor: continuous monitoring for several days. Best for frequent events
  • Event recorder: activated by patient. Best for infrequent events with a prodrome
  • External loop recorder: records continuously in a loop, and a recorded loop is saved retroactively after the event starts. Best for infrequent events without a prodrome
  • Implantable loop recorder: records for years. Best for very rare events.
  • Exercise electrocardiogram: for exercise-induced dysrhythmias

Key associations:

  • Upon sitting or standing up: orthostatic hypotension
  • Coughing, urination, defecation: neurocardiogenic
  • Headache: subarachnoid hemorrhage
  • After a meal: postprandial syncope
  • Preceded by palpitations: sick sinus syndrome, arrhythmias
  • While shaving, turning head or other forms of carotid sinus manipulation: carotid sinus syndrome
  • Vertigo, diplopia, dysarthria, numbness or weakness (neurological prodrome): vertebrobasilar transient ischemic attack.
  • upper extremity exertion and neurological prodrome: subclavian steal syndrome
  • Family history of syncope or sudden death at an early age: hypertrophic obstructive cardiomyopathy, arrhythmias, long QT or Brugada Syndrome.
  • Shortness of breath, hypoxia, hemodynamic instability and/or evidence of right ventricular strain on echocardiogram or EKG: pulmonary embolism
  • Plethoric facies: superior vena cava syndrome
  • Positional syncope or murmur, embolic phenomena: atrial myxoma
  • Breath holding in an infant toddler: breath holding spells

References:

  1. Henderson, Marc C., MD, The Patient History: an Evidence-Based Approach to Differential Diagnosis, 2e (2012)
  2. Sabatine, Marc S., MD, MPH, Pocket Medicine: The Massachusetts General Hospital Handbook of Internal Medicine, 5e (2013)
  3. Wang, K., MD, Atlas of Electrocardiography (2013)
  4. Phibbs, Brendan, MD, Advanced ECG: Boards and Beyond, 2e (2005)
  5. Pediatric EM Morsels.
  6. Davey, Patrick, ECG at a Glance (2008)
  7. Mattu, Amal, MD, Emergency ECG Video of the Week (here, here, here and here)

[Updated November 29, 2013. Please read important Disclaimer.]

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