Continuing Education Activity
Syncope is a transient loss of consciousness and postural tone followed by spontaneous recovery. While there are numerous classification schemes used to further identify and manage underlying conditions that may lead to syncope, syncope ultimately results from decreased cerebral perfusion. Syncopal episodes may occur suddenly and without preceding signs or symptoms or may be preceded by dizziness, lightheadedness, diaphoresis, nausea, visual disturbances, or other signs and symptoms. Patients may describe syncopal events in a wide variety of ways, some of which include fainting, blacking out, falling out, having a spell, or losing consciousness. Syncope is responsible for 1 to 3.5 percent of all emergency department visits and 6 percent of all hospital admissions in the United States. Underlying conditions that may cause decreased brain perfusion and lead to syncope can range from benign to life-threatening. This activity describes the pathophysiology, evaluation, and management of syncope and stresses the role of the interprofessional team in the care of affected patients.
- Describe syncope.
- Explain how to evaluate syncope.
- Review considerations that influence the management of syncope.
- Explain interprofessional team strategies for improving care coordination and communication to enhance outcomes for patients affected by syncope.
Syncope is caused by decreased cerebral blood flow leading to transient loss of consciousness and postural tone, associated with spontaneous recovery. Symptoms like dizziness, lightheadedness, diaphoresis, nausea, and visual disturbances may precede it or occur suddenly with none of the above symptoms. Syncope is a symptom described as fainting, blacking out, falling out, or "having a spell," and represents 1 to 3.5% of all emergency department visits and 6% of all hospital admissions in the United States. This large number of emergency department visits and admissions reflect the varied etiologies of syncope from benign to life-threatening and the high degree of diagnostic uncertainty associated with this symptom.
Syncope is a symptom of an underlying disease process rather than a disease itself. Although syncope mimics a death-like experience eliciting extreme consternation among both patients and their families, most syncopal events have a benign cause. Benign causes of syncope reflect vasovagal (also known as neurocardiogenic), volume depletion, or medication-related etiologies. More ominous causes are related to dysrhythmia and valvular abnormalities such as ventricular tachycardia, atrioventricular (AV) block, or critical aortic stenosis. A history of left ventricular dysfunction (with concomitant degeneration of the conduction system leading toward a propensity for dysrhythmias) has been found to be the most ominous predictor of an adverse etiology of a syncopal event.
Causes of Syncope
1. Cardiovascular disorders
- Cardiac arrhythmias (both tachy and bradyarrhythmias)
- Structural and obstructive disorders (valvular abnormalities, HOCM, MI, PE)
2. Cerebrovascular causes (vertebrobasilar insufficiency)
3. Disorders of blood flow and vascular tone
- Vasovagal (neurocardiogenic)
- Orthostatic hypotension (medications, autonomic failure, peripheral neuropathy, decreased blood flow)
- Situational (cough, micturition, defecation, postprandial, deglutition)
- Carotid sinus syncope
4. Others that mimic syncope
- Metabolic (hypoglycemia, hypoxia, symptomatic anemia)
- Psychogenic (panic attacks)
Vasovagal Syncope (Neurocardiogenic syncope, Common faint)
This accounts for almost 50% of all cases of syncope. When faced with certain situations like prolonged standing, crowded places, hot environment, severe pain, extreme fatigue and stress leads to vasodilatation (sympathetic withdrawal) and bradycardia (parasympathetic activity). This condition is also called common faint as it is the common cause of syncope and can occur even in normal people. Syncope events are preceded by prodromal symptoms like blurred vision, diaphoresis, nausea, dizziness, weakness, and then leads to bradycardia, decreased blood pressure, and then lose consciousness. Patients appear pale to the onlookers. Patients normally regain consciousness in few minutes and may experience generalized weakness. They do not lose sphincter control, rarely have any tonic-clonic activity or confusion after regaining consciousness as in patients with seizures.
Syncope accounts for around 1 to 3.5% of visits to emergency department visits in the US. Syncope is more common in older patients due to multiple comorbidities and multiple medications. Cardiac etiology is more common in older patients and noncardiac etiology (vasovagal) common in young adults. There is no significant difference in incidence between men and women.
The brain needs a constant supply of glucose (through adequate cerebral blood flow) to function and any interruption to this even for few seconds can lead to loss of consciousness or syncope. Cerebral blood flow is maintained by a complex mechanism involving cardiac output, systemic vascular resistance, mean arterial pressure, and intravascular volume. Any defect in one or more of these systems leads to decreased cerebral blood flow. Approximately three-fourths of blood is in the venous bed and any interference in venous return can lead to decreased cardiac output.
Any episode lasting more than a few minutes is not syncope and is more likely to be related to a seizure or other acute neurologic process. Seizures are the most common disease misdiagnosed as syncope. When symptoms overlap too closely, the only way to differentiate seizure from syncope may be with an EEG.
Terms near syncope or presyncope are confusing in that they may convey a different meaning to different practitioners. However, when a practitioner defines near syncope as “a feeling that you were going to pass out but did not” then, near syncope and syncope are both thought to be related to cerebral hypoperfusion, and therefore, any disease process which decreases blood flow can cause syncope and near syncope.
History and Physical
A thorough history and physical examination alone may yield a diagnosis in up to 50% of patients presenting with syncope. History of syncope should focus on duration, preceding events or precipitating events, and post-event findings. The position of the patient at the time of the event is important. Syncope in a standing position can suggest vasovagal and in a supine position can be due to neurocardiac causes. A detailed history of the patient's medical problems and medications must be included. The physical examination in syncope should center around vital sign abnormalities as these can often suggest underlying disease processes such as orthostatic hypotension or cardiovascular compromise. Detailed cardiovascular and neurologic examinations should be included looking for signs of vascular disease, congestive heart failure, or an acute cerebrovascular event masquerading as syncope.
Testing rarely leads to a diagnosis as the most common cause is vasovagal and benign. A thorough physical examination is the most important diagnostic tool as it helps in diagnosing the cause and excluding potential life-threatening causes. Choice of diagnostic studies depends on history and physical examination.
In patients presenting to the Emergency department, routine blood work to include hemoglobin, electrolytes, and glucose is indicated. At the minimum ECG is needed in all patients presenting with syncope.
If cardiovascular etiology suspected, further workup includes cardiac enzymes, continuous cardiac monitoring, and echocardiogram. Holter monitor recommended for outpatients suspected of conduction abnormalities.
If cerebrovascular etiology suspected, further workup includes CT head, carotid Doppler ultrasound, MRI brain, and MRA.
Electroencephalography (EEG) indicated if seizures suspected.
A tilt table test is indicated in:
- Patients with recurrent episodes of syncope of unknown etiology in the absence of cardiac disease.
- Suspected vasovagal syncope but not sure
- Differentiate between suspected reflex syncope and orthostatic hypotension syncope.
The ECG is the most useful diagnostic study, yielding an etiology of syncope in approximately 5% of patients, while routine blood work leads to a diagnosis in only about 2% of cases. Despite widespread and often indiscriminate testing, approximately 45% of patients will leave the emergency department without a diagnosis following their syncopal event. Recent data suggests that a focused management plan may help diagnose an etiology of the syncopal event and reduce the number of patients discharged without a diagnosis. For example, echocardiography before discharge may be useful in uncovering valvular disease in a patient presenting with a murmur and syncope. Similarly, overnight telemetry or discharge with an event monitor may help expose a dysrhythmia in a patient with evidence of conduction disease on their presenting ECG.
Treatment / Management
Treatment of underlying cause is the focus of treatment in syncope. During acute an acute episode, patients should be made to sit or lay down quickly and raising the legs help recovery in patients with reflex postural hypotension event. Placing patients in a horizontal position after the acute event and preventing rising too soon. Treatment of any injuries sustained during a sudden fall from syncope warrants immediate attention.
1. Vasovagal syncope:
- Conservative measure includes avoiding situations or stimuli that have caused them, Tilt training and increasing use of salt and fluid.
- Drug therapy with beta-blockers, SSRIs, hydrofludrocortisone, proamatine, and few other medications might be useful if conservative measures fail.
2. Orthostatic hypotension:
- Rising slowly from supine and sitting position, a gradual change in posture.
- Avoiding medications that can cause orthostatic hypotension (diuretics, vasodilators).
- Use of compression stocking to improve venous return.
- Intravenous fluids in patients who are intravascularly volume depleted.
- Use proamatine in refractory cases.
3. Cardiovascular disorders: Treating underlying condition by Cardiology.
Disposition is often the most difficult task in caring for emergency department patients with syncope. Admission rates vary in patients presenting with syncope. In the United States, about 80% of patients presenting to the emergency department following a syncopal event will be admitted. In Canada and elsewhere, admission rates may be as low as 10%. Rather than reflecting differences in acuity, this discrepancy more likely reflects thresholds for missing rare, potentially clinically relevant causes. Practitioners have published multiple pathways with which to risk-stratify syncope patients to help improve this discrepancy; however, all of them appear comparable to a thorough history and examination. The Boston Syncope Criteria center on risk stratifying patients for admission based on prior history of cardiac disease (left ventricular dysfunction, dysrhythmia or valvular disease); concomitant complaints in emergency department presentations of potential cardiac disease such as associated chest pain, dyspnea, or palpations; ECG abnormalities such as signs of ischemia, dysrhythmia, or conduction disease. These criteria suggest that any patient without associated comorbidities and unrevealing emergency department workup should be safe for discharge.
Costs of evaluating syncope have grown exponentially in recent years. Approximately $ 2 billion is spent in the US on patients hospitalized for syncope. 
Follow-up: Patients with unknown etiology and without underlying heart disease have a good outcome. Patients with syncope and underlying heart disease needs regular follow-up with a primary care physician and cardiologist.
Important differential diagnosis for syncope include
1. Seizure disorder: Seizures associated with aura, tonic-clonic activity, prolonged duration of unconsciousness, urinary and/or bowel incontinence, tongue biting and confusion after regaining consciousness. These differentiate syncope from seizures.
3. Panic attacks: Feeling impending doom, palpitations, air hunger and tingling of perioral region and tips of fingers.
Prognosis depends upon the underlying cause, so identification of the cause is very important. The annual mortality rate can range from 0 to 12% in patients with noncardiac cause and 18 to 33% in patients with a cardiac cause. 
Patients can sustain injuries from fall due to syncope. These injuries can be worse if they were driving during the event.
The most common cause of syncope is vasovagal and is self-limiting. A primary care physician or hospitalist can manage this. Cardiology consultation is needed when cardiac etiology suspected. Neurology consultation is needed when cerebrovascular causes suspected.
Deterrence and Patient Education
Patient education is more important in patients with syncope from vasovagal, orthostatic hypotension, and situational syncope.
After an episode of syncope, patients should be advised not to drive and avoid heights.
Patients with situational syncope should be advised to avoid situations that prompt syncope.
Increased fluid intake in patients with orthostatic hypotension and avoid getting dehydrated.
Pearls and Other Issues
Vasovagal syncope is the most common type of syncope.
Mostly benign but can be life-threatening in patients with underlying cardiac arrhythmia.
ECG is the most useful test in syncope, but its diagnostic yield is only 5%, leaving careful history and physical examination as the most valuable tools in evaluating a syncopal event.
Following a syncopal event, patients should be instructed not to drive or operate heavy machinery at least until the completion of their workup or follow up with their primary care provider.
Mental illness and substance abuse should be considered in syncope patients where the etiology of syncope remains unclear. 
Enhancing Healthcare Team Outcomes
Most of the patients with emergency room visits for syncope do not have a diagnosis at discharge. Even hospitalized patients leave the hospital with unclear etiology for their syncope. The majority of times the cause is benign but patients need close outpatient follow-up to make sure there is a cause identified and does not recur. This needs close follow-up with a primary care physician and cardiology.