I. Scope of the problem

Syncope, from the old Greek sy[n]gkope meaning “a cutting into pieces”, is defined as a sudden, temporary loss of consciousness and postural tone with spontaneous recovery, which results from insufficient oxygen delivery to the brain. While other names are often used to describe syncope (fainting, swooning or blacking out), this definition excludes seizures, coma, shock and other causes of altered consciousness.

Syncope is usually short in duration (20-30 seconds) and in the majority of cases, patients rarely seek medical attention. Although extremely common in the general adult population (lifetime incidence of nearly 40%), syncope is responsible for a substantial portion of emergency room visits (up to 3%) and hospital admissions (up to 6%). However, despite its relative frequency, many studies have suggested that up to 40% of patients admitted with syncope will be discharged without a clear and conclusive etiology of their syncopal event.

More prevalent among women than men, the incidence of syncope increases with age, number of comorbidities, and medication use. With our aging population, presentations for syncope are expected to increase, as the incidence of syncope increases significantly over the age of 70. While the majority of syncopal episodes among the younger population can be ascribed to benign conditions, more dangerous and potentially fatal causes are likely to be found amongst those who suffer from their first fainting spell at a later age.

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Perhaps the most important factor to be established when evaluating a patient with syncope is whether the likely cause is benign or if it may be graver, and requires immediate clinical attention. To establish this, a thorough history and a well-performed physical exam are required and will dictate subsequent work-up and evaluation.

II. Diagnostic Approach

A. General approach

Given the large number of potential causes of syncope, a systematic and organized approach is essential. . As it is the case with other clinical situation, the most important information to be obtained from a patient presenting with syncope is the history (or better yet, the
story) surrounding the event itself. Some estimates indicate that up to 75% of all diagnoses of confirmed causes of syncope are made with the information gathered from the history alone, and further diagnostic testing is often unnecessary.

In addition to the history, a thorough physical examination may add valuable information and increase the probability of reaching a diagnosis (up to 85%). It has been argued that if the clinician is unable to make a clear diagnosis for the cause of syncope after obtaining a detailed history and physical exam, the likelihood of making such diagnoses by adding further testing to the evaluation (labs, imaging, etc.) is low (less than 20%).

B. What is the differential diagnosis for this problem?

As stated above, a complete list of possible causes of syncope (loss of consciousness and postural tone) is long and beyond the scope of this practical review. A practical approach to the evaluation of a seemingly overwhelming number of etiologies should begin by excluding those obvious causes that may need immediate further evaluation (head trauma, cardiac arrest) or no evaluation at all (breath-holding).

It is important to remember that there are some presentations that mimic syncope but do not fit strict definitions of loss of consciousness and postural tone. These include, among others, vertigo, transient ischemic attack, stroke, seizure, hypoglycemia, lightheadedness/presyncope, and simple falls.

The clinician should employ a systematic methodology to help him/her recall the numerous etiological links to syncope. While the great majority of syncopal episodes are of neurocardiogenic (neurological reflexes responding to emotional or situational stimuli), causes of transient loss of consciousness and postural tone can be classified into four major categories based on the pathogenesis (mechanism) that results in oxygen deprivation to the brain:

  • Orthostatic, approximately 10-20% of cases

    Caused by positional/orthostatic hypotension either due to hypovolemia (low blood volume) or inability of the body’s neurogenic mechanisms to mount an appropriate cardiac response to change in posture.

  • Cardiogenic (cardiovascular in origin), approximately 20% of cases

    Valvular heart disease (e.g., severe aortic stenosis)

    Structural heart disease

    Dysrhythmias (tachyarrhythmias, bradyarrhythmias & conduction abnormalities)

    Vascular abnormalities (e.g., pulmonary embolus, severe subclavian steal)

  • Neurocardiogenic (also known as neurally-mediated or reflex syncope resulting in vasodilation and/or bradycardia),approximately 30-40% of cases

    Vasovagal, situational, micturition, coughing, postprandial, carotid sinus hypersensitivity, etc.

  • Neurogenic (often NOT considered true syncope, as they are caused by focal brain disturbances that result in impaired blood flow to the posterior circulation of the brain)

    Vertebrobasilar insufficiency

    Seizure-related loss of consciousness

    Transient ischemic attacks (TIA) or strokes (CVA)

Unfortunately, it has been estimated that approximately 20-40% of causes of syncope go undiagnosed despite efforts to reach a cogent diagnosis. When the diagnosis is based on physical exam alone (due to patient inability or unwillingness to communicate verbally), a broader differential must be entertained (to include psychogenic causes, drop-attacks, trauma and metabolic derangements).

C. Describe a diagnostic approach/method to the patient with this problem

In order to evaluate the myriad of potential causes of syncope listed above, it is imperative to first obtain a detailed history and physical exam, which will subsequently guide any necessary diagnostic workup. Outlined below is a systematic approach to the diagnosis and evaluation of syncope.

1. Historical information important in the diagnosis of this problem.

In identifying potential causes of syncope, one should start with a detailed analysis of the information obtained from interviewing the patient and/or those who may have witnessed the event. Although there are innumerable possible questions that can be asked regarding the circumstances that surround a syncopal event, the following questions (although not exhaustive) follow a traditional strategy that represents a good foundation for formulating a diagnosis that will minimize unnecessary testing:

What happened?
  • Detailed description of the event (including onset, timing and duration)

  • Was there loss of consciousness and muscular tone?

  • If witnessed, was there associated body movements, tongue biting, incontinence, transient disorientation/amnesia, white/blue appearance, were their eyes open/closed, or were there any other notable physical markers surrounding the event?

  • What was the patient like after regaining consciousness?

When did it happen?
  • Was this the first time?

  • When was the first time it happened?

  • At what time of the day/month/year did it happen?

  • Is the timing always similar (if recurrent)?

Where did it happen?
  • Description of locale where event took place.

  • Was it cold/hot, crowded, or in public?

Why did it happen?
  • What was the patient doing just prior to the event?

  • What was the patient’s position (were they standing, walking, did they suddenly change position, was is associated with head turning)?

  • Was the patient exerting themselves prior to loss of consciousness?

How did it feel?
  • Describe the patient’s physical experience before, during, and after the event.

  • Were there any prodromal symptoms (palpitations, nausea/vomiting, sweating, chest pain, shortness of breath, lightheadedness/dizziness, etc.)?

  • Did the event take place “out of the blue” without any preceding symptoms?

  • Was there something different about this episode, as compared to similar situations in the past?

To whom did it happen?

Explicit information about the patient including:

  • Past medical history (particularly cardiac and neurological history) and medications (e.g. diuretics and anti-hypertensive medications).

  • Family history of syncope, heart disease, or sudden cardiac death.

2. Physical Examination maneuvers that are likely to be useful in diagnosing the cause of this problem.

A thorough physical exam is imperative when approaching a patient with suspected syncope. Measurement of vital signs and in particular, appropriate recording of postural heart rate and blood pressure (both while lying and standing) is critical in the evaluation of syncope.

Although much has been written about the correct way to measure postural (orthostatic) vital signs, the following method yields the highest rate of abnormal recording in patients with true orthostatic hypotension:

  • Record blood pressure (and heart rate) while supine after at least 10 minutes recumbent.

  • Ask patient to stand (or sit with legs down if unable to stand) and record blood pressure (and heart rate) immediately after standing, and then repeat measurements after standing for 2-3 minutes. Remember to ask patient about symptoms of dizziness/lightheadedness while doing the maneuver. By adding the recorded blood pressure immediately upon standing, you will maximize your chances of capturing true orthostatic hypotension due to hypovolemia as opposed to autonomic dysfunction.

In addition to a thorough evaluation of the patient’s vital signs, the following parts of the exam are of particular importance when assessing possible causes of syncope.

  • Assess for volume: examine skin turgor, jugular venous pressure, mucosal membranes and capillary refill.

  • Neurologic exam: perform a detailed motor, sensory, cerebellar and cranial nerve exam. Also test reflexes, gait and balance. If there is suspicion for a particular disorder that requires more specialized neurological evaluation and/or neuropsychiatric testing, it should be pursued.

  • Cardiovascular exam: a detailed exam of the vascular beds (pulses, bruits, capillary refill, and color) and a cardiac exam should always be included in the evaluation of syncope. Of particular interest are the heart tones and rhythm, along with cardiac murmurs and heart size by exam (PMI).

  • The portions of the exam that yield the highest proportion of the evidence contributing to the diagnostic work-up of syncope have been represented above. The rest of the physical exam will in many cases yield important corroborating or refuting information to guide the work-up of syncope (e.g. pulmonary, abdominal, musculoskeletal exam, etc.).

3. Laboratory, radiographic and other tests that are likely to be useful in diagnosing the cause of this problem.

In addition to a complete history (from the patient and/or witnesses) and a thorough physical examination, there are a few studies that may be useful in the evaluation of syncope. Testing should be determined by what factors in the history and exam might need further clarification or supporting evidence.

As part of initial evaluation, consider obtaining a basic metabolic panel (including renal function test with blood urea nitrogen and creatinine) to ascertain volume status and the possibility of metabolic abnormalities. A complete blood cell count may add information regarding anemia and inflammation. An electrocardiogram and cardiac studies are only indicated if the story is suggestive of cardiac causes of syncope. Further specialized imaging studies are rarely indicated in the initial evaluation.

Guided by history and exam, the clinical evaluation of syncope may require further testing only if suspicion is high enough to warrant a study that would be capable of discriminating among diagnoses. Depending on the suspected pathogenesis of the syncope, the following studies may aid in reaching a diagnosis:

  • Orthostatic hypotension: No further testing is typically necessary.

  • Neurocardiogenic: In cases where the story and basic studies are insufficient to clearly diagnose neurally-mediated causes of syncope (vasovagal, situational, etc.), a tilt-table test and/or response of vital signs and symptoms to carotid massage may be helpful. Although the sensitivity of these tests is low (~60% for tilt table testing in neurocardiogenic syncope), these maneuvers may help exclude positional syncope and carotid hypersensitivity syndrome as potential causes offainting.

  • Cardiogenic: Most often, cardiogenic syncope is heralded by a significant clinical history of structural and/or ischemic/vascular heart disease, all of which can be obtained from clinical history, exam and an electrocardiogram. For specialized cardiac testing options,

  • Consider the following:

    Echocardiography in patients with suspected structural/functional or valvular heart disease severe enough to cause syncope (e.g. severe dilated cardiomyopathy, hypertrophic obstructive cardiomyopathy, severe aortic stenosis).

    Holter monitors, event monitors, or loop recorders when screening for dysrhythmias. Further electrophysiological studies (i.e. pharmacological stimulation and testing) may be indicated if the baseline electrocardiogram or cardiac monitoring suggests a cause of syncope (e.g. ventricular tachyarrythmias, high-degree heart blocks, sick sinus syndrome).

  • Neurologic causes: although much rarer and often not considered true syncope, there are a number of neurological conditions that may result in the loss of consciousness and which may require further testing. If the neurological exam or story is suggestive of cerebrovascular disease, CT or MRI of the brain imaging of the brain (vascular, parenchymal). Carotid or transcranial ultrasonography may be helpful in cases where vascular insufficiency to certain vessels (carotid or posterior cerebral) is suspected. An electroencephalograms is indicated if seizure activity is evoked as a potential cause for loss of consciousness.

C. Criteria for Diagnosing Each Diagnosis in the Method Above.

There are no standardized, validated criteria for the diagnosis of many of the conditions described in previous sections; therefore, when evaluating patients with syncope, the history, physical exam and a few supporting studies, should guide the diagnostic work-up.

Ultimately, the diagnosis for the cause of syncope is based on the pre-determined probability of the suspected condition, bolstered by corroborating or refuting information obtained. Once completed, the evaluation may point toward a diagnosis which may require further testing (i.e. advanced electrophysiological studies in sick sinus syndrome). However, since a large portion of syncope has its origins in benign conditions (neurocardiogenic), the majority of diagnoses will be made purely based on story/history and exam, with little need for further testing.

D. Over-utilized or “wasted” diagnostic tests associated with the evaluation of this problem.

See above.

III. Management while the Diagnostic Process is Proceeding

A. Management of Clinical Problem.

From an evolutionary perspective, the adaptive response to syncope is one of great value. As perfusion to the brain decreases, a person loses consciousness and the body loses postural tone so that the person falls to the ground and perfusion can be restored to the brain without having to defy gravitational forces. Although this may seem primitive, it highlights the fundamental maneuver that the clinician must remember when attending to a patient with syncope – attempt to first and foremost regain cerebral perfusion.

Further clinical management, including fluid resuscitation, attention to cardiovascular problems and interventions should be directed by the suspected etiologic diagnosis and is beyond the scope of this chapter.

What's the evidence?

Brignole, M. “Guidelines on management (diagnosis and treatment) of syncope–update 2004”. Europace. vol. 6. 2004. pp. 467-537.

Kapoor, WN. “Syncope”. N Engl J Med. vol. 343. 2000. pp. 1856-62.

Puig, A. “Measuring Orthostatic Hypotension…Wait a Minute, or Should You”. SGIM Forum. vol. 34. March 2011. pp. 10-12.

Serrano, LA. “Accuracy and quality of clinical decision rules for syncope in the emergency department: a systematic review and meta-analysis”. Ann Emerg Med. vol. 56. 2010. pp. 362-373.

Soteriades, ES. N Engl J Med. vol. 347. 2002. pp. 878-85.

Williamson, C, Reed, JM. “Syncope: the emergency department and beyond”. Intern Emerg Med. vol. 10. 2015. pp. 843-950.