Syncope is an abrupt, transient, spontaneously-resolving loss of consciousness and postural tone caused by cerebral hypoxia. It is not a “chief complaint,” but a descriptive and a partially etiologically-defined medical diagnosis.
The first steps in evaluating syncope should be to try to distinguish it from alternative causes of loss of consciousness and postural tone, including seizures, concussions, sleep (both normal or narcoleptic), migraines and psychogenic conditions. Elicitation of a history from a witness can be extremely helpful and should be pursued whenever possible. Also, loss of postural tone can occur without loss of consciousness. These are called ”drop attacks” and can be seen in patients with cervical subluxation (rheumatoid arthritis) or cataplexy.
The next step should be to look for possible red flags. These may include:
- Exertional syncope; think of obstructive or ischemic causes, including aortic stenosis, pulmonary embolism, hypertrophic obstructive cardiomyopathy, and mitral stenosis. These patients may need an echocardiogram and stress testing.
- Syncope while lying flat
- Chest pain, palpitations, shortness of breath
- Family history of syncope or sudden death at a young age
An electrocardiogram should be performed and should be scrutinized for:
- Ischemia: ST changes, T wave inversions, new or worsening Q waves
- Conduction abnormalities (such as heart blocks)
- Evidence of right ventricular strain/pulmonary hypertension/pulmonary embolism: sinus tachycardia, , new right bundle branch block or incomplete right bundle branch block, T wave inversions, especially in anteroseptal and inferior leads
- Pacemaker malfunction
- Abnormal intervals, particularly short or long QTc (ischemia, hypokalemia, hypocalcemia, drugs)
- Short PR intervals, Delta waves and wide QRS complexes (as in Wolff-Parkinson-White syndrome)
- Brugada Sign
- Hypertrophic obstructive cardiomyopathy: High left ventricular voltage, deep narrow Q-waves in inferior and lateral leads (I, aVL, V5, V6); also seen is left atrial enlargement, tall R wave in V1
- Arrhythmogenic right ventricular dysplasia
Longer range options for rhythm analysis include:
- 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
Additional workup might include (some of which may be of dubious utility):
- Pulse oxymetry (to look for hypoxemia)
- Chest radiograph (to check for pacemaker lead placement, pulmonary hypertension, etc.)
- Hemoglobin level (to look for anemia)
- (to look for dehydration or electrolyte imbalances)
- Blood levels of relevant drugs (e.g. digoxin)
- Pacemaker interrogation (if applicable)
- Telemetry or ambulatory cardiac monitoring (see below)
- Echocardiography (to look for obstructive causes)
- Pregnancy screening in relevant populations.
- Neurovascular imaging (if four vessel disease is suspected)
Syncope can be divided into several categories:
- Cardiac: this category can be further subdivided into electrical, ischemic and obstructive causes:
- Electrical: tachydysrhythmias or bradydysrhythmias
- Obstructive: aortic stenosis, pulmonary hypertension, hypertrophic obstructive cardiomyopathy, and pulmonary embolism
- Orthostatic: a drop in cerebral perfusion that often occurs with standing or sitting up. Causes are dehydration (fasting, heat, diuretics, including ETOH and caffeine), dysautonomia (Parkinsonism, diabetes mellitus) and loss of vascular tone (medications).
- Neurocardiogenic (vasovagal, “fainting”): syncope that is preceded by a vagal or noxious event such stress, bad news, sight of blood, defections, micturition, carotid sinus manipulation, etc.
- Cerebrovascular atherosclerotic disease: a rare cause of syncope that results from atherosclerotic obstructive disease of both carotids and both vertebral arteries (“four vessel disease”). Note that anterior circulation disease alone is likely to cause focal neurological deficits, whereas posterior circulation disease is likely to present with vertigo, etc.; neither in isolation is likely to cause syncope.
- Upon sitting or standing up: orthostatic hypotension
- Coughing, urination, defecation: neurocardiogenic
- After a meal: postprandial syncope
- Preceded by palpitations: arrhythmias
- While shaving, turning head or other forms of carotid sinus manipulation:
- 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
- Marc C. Henderson MD. The Patient History: an Evidence-Based Approach to Differential Diagnosis, 2e. 2012.
- Marc S. Sabatine, MD, MPH, Pocket Medicine: The Massachusetts General Hospital Handbook of Internal Medicine (2010)
- Pediatric EM Morsels.
- Life in the Fast Lane has an excellent page with links to important EKGs listed alphabetically by diagnosis.
- Amal Mattu MD, EKG Videos
[Updated on June 15, 2013. Please read important Disclaimer.]