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- Syncope is a transient loss of consciousness, associated with loss of postural tone, with spontaneous return to baseline neurologic function requiring no resuscitative efforts.
- The underlying mechanism is global hypoperfusion of both the cerebral cortices or focal hypoperfusion of the reticular activating system.
Syncope Life-threatening conditions
- The most important causes to consider are: cardiac syncope, blood loss, pulmonary embolism, and subarachnoid hemorrhage.
- Other conditions, such as seizure, stroke, and head injury, do not meet the technical definition of syncope but should be considered during the initial assessment.
- Cardiac causes are the most common life-threatening conditions associated with syncope.
- They include arrhythmia, ischemia, structural/valvular abnormalities (eg, aortic stenosis), cardiac tamponade, and pacemaker malfunction.
- Studies of short term and one year outcomes following syncope found patients with cardiac syncope to be at significant risk for sudden death.
- Patients with syncope and a history of heart failure are at even greater risk.
- Large blood loss, particularly acute severe hemorrhage, can manifest as syncope.
- Important potential causes include: trauma, gastrointestinal bleeding, ruptured aortic aneurysm, ruptured ovarian cyst, ruptured ectopic pregnancy, and ruptured spleen.
Hemodynamically significant pulmonary embolism is an uncommon but well documented cause of syncope.
Patients presenting with syncope following a headache require evaluation for a possible subarachnoid hemorrhage.
Common Causes of Syncope
- Neurocardiogenic syncope: Micturition, Defecation, Cough mediated, Deglutition, Glossopharyngeal nerve, Situational
- Carotid sinus hypersensitivity: Head turning, Circumferential neck compression (neck tie), Shaving
- Orthostatic syncope: Volume loss, Autonomic dysfunction, Deconditioning, prolonged bed rest
- Medication related syncope: Vaso active medications (Alpha and beta blockers, calcium channel blockers, nitrates, antihypertensive medications, diuretics, erectile dysfunction medications). Medications affecting conduction (Antiarrhythmics, calcium channel and beta blockers, digoxin). Medications affecting the QT interval (Antiarrhythmics, antiemetics, antipsychotics/depressants). Diuretics
- Often referred to as vasovagal or vasodepressor syncope, neurocardiogenic syncope is the most common cause of syncope, accounting for 25 to 65 percent of cases. Patients diagnosed with neurocardiogenic syncope have an excellent prognosis with no increase in mortality or morbidity.
- Autonomic activation causes neurocardiogenic syncope.
- Three types of responses are seen: a cardioinhibitory response, a vasodepressor response, and a mixed response with features of both.
- Significant bradycardia and/or hypotension accompany the acute loss of consciousness.
- Potential triggers are numerous and often determination of the underlying cause is made in the outpatient setting.
- Most patients with neurocardiogenic syncope experience a prodrome, which may include dizziness or lightheadedness, a sense of warmth, pallor, nausea/vomiting, abdominal pain, and diaphoresis, prior to their loss of consciousness.
- Examples include micturition or defecation syncope, situational syncope (eg, while having blood drawn), or cough-mediated syncope.
Carotid sinus hypersensitivity
Carotid sinus hypersensitivity is a variant of neurocardiogenic syncope, resulting from pressure at the carotid sinus. External pressure to the neck can induce this reflex response. Common causes include shaving, a tight collar, and turning of the head.
- Orthostatic syncope comprises between 5 and 24 percent of syncope cases and can be defined by a drop in blood pressure of more than 20 mmHg, or a reflex tachycardia of more than 20 beats per minute.
- Orthostasis is most often caused by a loss of intravascular volume, from any number of causes, or by failure or instability of the autonomic nervous system. Nevertheless, clinicians should remain cautious because orthostasis can occur with cardiac syncope.
- Syncope from orthostatic hypotension is a diagnosis of exclusion in the emergency department, reserved for low risk patients who have symptoms consistent with the diagnosis.
- Orthostatic vital signs are neither sensitive nor specific in assessing volume status or diagnosing syncope.
- Many patients become symptomatic if their systolic blood pressure drops below 90 mmHg, but a large portion of the population who meet the definition of orthostasis do not have syncope.
- Elders, pregnant women, and patients taking drugs with vasodilating effects are predisposed to develop symptomatic orthostasis.
- The effects of medications account for 5 to 15 percent of syncopal events. The mechanism can be orthostasis or cardiotoxicity.
- Medications often implicated include calcium channel blockers, beta blockers, alpha blockers, nitrates, antiarrhythmics, diuretics (affecting volume status and electrolyte concentrations), and medications affecting the QTc interval (eg, antipsychotics and antiemetics).
Syncope Other conditions
- Neurologic syncope
- Psychiatric syncope
- Rare causes
- True syncope is defined by an immediate, spontaneous return to baseline function following loss of consciousness, without new focal neurologic findings. Therefore, true neurologic causes, representing underlying neurovascular disease and not transient autonomic dysfunction, are rare.
- Examples of neurologic syncope include: subarachnoid hemorrhage, transient ischemic attack, subclavian steal syndrome, and complex migraine headache. Stroke and transient ischemic attacks generally cause focal neurologic deficits that do not recover rapidly or completely. Often, patients with cerebrovascular disease convey a history of nonsyncopal episodes featuring neurologic deficits. Syncope may be misconstrued as seizure because many patients with transient loss of consciousness have brief convulsive episodes, particularly if bystanders or objects keep them upright. Syncope can usually be differentiated from seizure by the brevity of the convulsions and the lack a true postictal phase.
- Anxiety and panic disorders can cause situational syncope.
- Patients with hypoxia, inadequate cerebral perfusion, or other medical conditions may appear confused or anxious.
- Patients with psychiatric syncope are generally young, without cardiac disease, and complain of multiple episodes.
Drug induced loss of consciousness
- Drugs of abuse and alcohol may cause a transient loss of consciousness, but generally these patients manifest signs of toxicity, and do not spontaneously return to normal neurologic function immediately after regaining consciousness.
- Alcohol can also cause symptomatic orthostasis by impairing vasoconstriction.
Metabolic causes of syncope include hypoglycemia and hypoxia.
Rare causes of syncope include atrial myxoma, Takayasu's arteritis, systemic mastocytosis, and carcinoid.
Syncope hx: Age
- Young patients more often experience neurocardiogenic syncope. Nevertheless, the emergency clinician must consider the possibility of dysrhythmia, particularly if other concerning factors exist (eg, exertional syncope, family history of sudden death).
- Electrocardiogram findings consistent with dysrhythmia include a prolonged QTc or short PR interval.
- Elderly patients appear to be at greater risk for adverse outcomes following syncope.
- Elderly patients are more likely to have autonomic dysfunction, orthostasis, and multiple medications, increasing the risk for syncope.
Syncope hx: Associated symptoms and triggers
- Concomitant symptoms can provide important diagnostic clues.
- As an example, chest pain may indicate an acute coronary syndrome or pulmonary embolism. Palpitations suggest an arrhythmia. Dyspnea raises concern for pulmonary embolism or heart failure. Headache raises the possibility of subarachnoid hemorrhage. Symptoms such as headache, paresthesias, or weakness may suggest a neurologic cause.
- The emergency clinician should seek a history consistent with neurocardiogenic syncope, as these patients are low risk. A prodrome generally precedes neurocardiogenic syncope, and often includes a sense of warmth, nausea and vomiting, diaphoresis, and pallor, either just prior to or shortly after the event. Inquiring about potential neurocardiogenic triggers is also helpful. Triggers commonly associated with neurocardiogenic syncope include strong physical or emotional stress, micturition, defecation, coughing, swallowing, and prolonged standing in a warm environment.
Syncope hx: Position
- Patients who lose consciousness with prolonged standing (ie, minimum of 15 to 20 minutes) are more likely to have neurocardiogenic syncope.
- Patients who lose consciousness while moving from a lying to a standing position are more likely to have orthostasis.
- Syncope while sitting or supine is suspicious for arrhythmia.
Syncope hx: Onset
- Sudden loss of consciousness without warning or prodrome suggests arrhythmia.
- Patients with prodromes are more likely to have neurocardiogenic syncope and have repeatedly been shown to be low risk.
Syncope hx: Duration of symptoms
- The duration of a syncopal event is difficult to quantify. Patients are generally unaware of the duration of their loss of unconsciousness and events are often unwitnessed or poorly quantified if they are witnessed.
- As a rough guide, an "event" or loss of consciousness persisting for more than four or five minutes should raise concerns for seizure or other causes of altered mental status.
Syncope hx: Exertional syncope — Syncope with exertion raises the possibility of arrhythmia or cardiac outflow obstruction (eg, aortic stenosis, hypertrophic cardiomyopathy, or pericardial tamponade). These patients warrant a thorough cardiac evaluation, including chest x-ray, electrocardiogram and echocardiography.
Syncope hx: Seizure versus syncope
- Often clinicians have difficulty determining whether their patient suffered a seizure or syncope.
- Patients with certain seizure disorders do not manifest generalized convulsions; patients with syncope may have brief tonic/clonic episodes.
- Approximately 5 to 15 percent of patients thought to have syncope have a seizure disorder.
Factors suggestive of seizure include
- Prodrome (aura) different from that described for vasodepressor syncope
- Episode of abrupt onset associated with injury
- Presence of a tonic phase before the onset of rhythmic clonic activity
- Head deviation or unusual posturing during the episode
- Tongue biting (particularly involving the lateral aspect of the tongue)
- Loss of bladder or bowel control
- Prolonged postevent (postictal) phase during which the patient is confused and disoriented.
Syncope hx: Medications
- A review of the patient's medications may reveal the cause of syncope.
- This is particularly important with elderly patients.
- Medications often implicated include calcium channel blockers, beta blockers, alpha blockers, nitrates, antiarrhythmics, diuretics (affecting volume status and electrolyte concentrations), and medications affecting the QTc interval (eg, antipsychotics and antiemetics)
Syncope hx: Prior episodes
- A history of syncopal episodes may be of value. A single episode or multiple episodes over many years suggests a benign etiology.
- Several episodes over a short period of time in someone with no history of syncope suggest a more significant cause, such as dysrhythmia.
Syncope hx: Family history
A family history of unexplained sudden death or early cardiovascular disease (ie, in close relatives less than 50 years old) places patients at increased risk for cardiac syncope.
Syncope hx: Associated injury
- Acute loss of consciousness may result in significant injury or events that predispose to injury.
- Motor vehicle accidents, hip fractures, and subdural hematomas can result.
- Emergency clinicians should assess the patient for potential injuries.
- Although patients with prodromal symptoms have less risk of death and other adverse outcomes following syncope, there is no evidence they have less risk of acute injury from syncope (eg, from falls). Such patients may ignore warning signs and may be just as likely to incur injury as patients without a prodrome.
The physical exam should focus on vital signs and a focused cardiac and neurologic exam, as well as any specific complaints.
- Transient hypotension or bradycardia occur during most syncopal events.
- Abnormal vital signs generally normalize by the time of evaluation in the emergency department (ED).
- Persistently abnormal vital signs are concerning and must be investigated.
- Discrepancies between upper extremities in pulse or blood pressure may reflect aortic dissection or subclavian steal syndrome, and should be investigated.
- Low patient oxygen saturation or tachypnea may be a sign of heart failure or pulmonary embolism.
Orthostatic vital signs
- The patient should be supine for five minutes before the initial set is obtained.
- Vital signs are retaken after the patient has been standing for three minutes and compared with initial measurements.
- The following changes are considered abnormal and may reflect hypovolemia or autonomic dysfunction: Drop in systolic blood pressure of 20 mmHg or more. Increase in heart rate of 20 beats per minute or more
- Many asymptomatic patients meet these criteria for orthostasis, but a drop of blood pressure below 90 mmHg associated with symptoms can be diagnostic.
- Clinicians should keep in mind that syncope from orthostatic hypotension is a diagnosis of exclusion in the emergency department, reserved for low risk patients who have symptoms consistent with the diagnosis.
- Auscultation of the heart may reveal a rate that is either abnormal or irregular (eg, atrial fibrillation).
- The clinician should listen for murmurs, specifically for aortic and mitral stenosis.
- Extra heart sounds, either an S3 or S4, can often be heard in patients with heart failure.
- Findings on cardiac exam suggesting structural heart disease should be investigated.
Auscultation of the lungs may reveal abnormal sounds (eg, crackles, wheezes) consistent with heart failure or other pathology (eg, pulmonary embolus, cardiac ischemia).
- Patients with syncope by definition return to baseline neurologic function.
- A thorough exam should be done to identify any subtle focal abnormality suggestive of stroke
- Clinicians should listen for a carotid bruit.
- Murmurs of aortic stenosis may also radiate to the neck. Examine the neck for elevated jugular venous pressure, a possible sign of heart failure.
A rectal exam with a stool guaiac test can identify some patients with gastrointestinal hemorrhage, which may present with syncope.
Lacerations to the lateral aspect of the tongue are suggestive of seizure.
Injury assessment and general examination
- The emergency clinician should perform a head to toe exam (ie, secondary survey) looking for evidence of trauma.
- Common injuries associated with falls following syncope include facial fractures, hips fractures, wrist fractures, and subdural hematomas.
- A general examination, guided by patient complaints, may reveal important findings, such as papilledema or a pulsatile abdominal mass.
- Several practice guidelines suggest that all patients presenting with syncope receive an electrocardiogram (ECG).
- Though the diagnostic yield of the ECG is low (approximately 2 to 7 percent reveal a significant abnormality), the test is inexpensive and easy to perform, and an abnormal ECG suggests an underlying cardiac problem, which should be investigated further.
- The clinician should assess the ECG looking for evidence of cardiac arrhythmia or ischemia as the cause of syncope.
- Some variation exists about what constitutes significant ECG findings
- A consensus group from the European Society of Cardiology lists several factors thought to be suggestive of arrhythmia-induced syncope. Significant findings include: prolonged intervals (QRS, QTc), severe bradycardia, preexcitation, and evidence of myocardial infarction. Other notable findings include low voltage in the standard limb leads, suggesting pericardial effusion, and abnormal conduction syndromes (eg, Wolf-Parkinson-White and Brugada).
- While in the ED, patients suspicious for abnormal cardiac rhythms should be placed on a cardiac monitor.
- In one prospective observational study of 95 consecutive syncope patients, major abnormalities identified by Holter monitoring included significant bradycardia (heart rate <30 beats/minute), sinus pauses (particularly those >2 seconds), Mobitz II block, complete heart block, ventricular tachycardia, and frequent premature ventricular contractions (PVC's). Such findings alert the clinician to an arrhythmogenic cause of syncope. Atrial tachydysrhythmias may cause a syncopal event, but usually do not in patients with structurally normal hearts.
- Routine laboratory screening in patients with syncope is not supported by evidence and seldom aids in management.
- Hypoglycemia may rarely explain an acute syncopal event, but should be performed on all patients with altered mental status.
- Clinicians should obtain other tests based on clinical circumstance.
- Electrolytes may be beneficial in critically ill patients or patients thought to have electrolyte abnormalities from volume loss or diuretic use.
- In patients with active bleeding or suspected anemia, a hematocrit should be obtained, and coagulation studies may be useful.
- A hematocrit less than 30 increases the risk of adverse short-term events in patients with syncope.
- A urine pregnancy test should be performed in any female of child-bearing age.
- Some researchers are evaluating brain natriuretic peptide (BNP) as a predictor of risk in patients with syncope, but further study is needed before the test can be recommended for this purpose. In particular, in remains unclear whether a single BNP measurement is sufficient, how the timing of the blood draw in relationship to the syncopal event affects the usefulness of the result, and whether BNP testing provides value beyond what is learned from taking a good history and performing a careful examination.
- Patients with a history or physical exam suspicious for a transient ischemic attack, stroke, or new onset seizure need further evaluation.
- Patients without historical or examination features suggestive of neurologic disease need no further neurologic studies.
- Despite the low diagnostic yield of brain imaging, clinicians overutilize head CT and magnetic resonance imaging (MRI) in the evaluation of syncope patients.
- An electroencephalogram may be useful in ruling out epilepsy.
- Although not readily available in many emergency departments, echocardiography is helpful in determining the presence of structural heart disease.
- Echocardiography can show valvular anomalies, wall motion abnormalities, elevated pulmonary pressure (seen with pulmonary embolism), and pericardial effusions. It is most useful in patients with a history of cardiac disease or abnormal electrocardiogram findings.
- Emergency clinicians are becoming more proficient with limited bedside echocardiography, but its value in the patient with syncope is unclear.
- History appears to be as valuable a screening tool in determining risk and the need for further investigation.
Syncope Risk Stratification
- Short-term high risk criteria which require prompt hospitalization or intensive evaluation
- Severe structural or coronary artery disease (heart failure, low LVEF, or previous myocardial infarction)
- Clinical or ECG features suggesting arrhythmic syncope: Syncope during exertion or supine, Palpitations at the time of syncope, Family history of SCD, Non-sustained VT, Bifascicular-block (LBBB or RBBB combined with left anterior or left posterior fascicular block) or other intraventricular conduction abnormalities with QRS duration ≥120 ms, Inadequate sinus bradycardia (<50 bpm) or sinoartrial block in absence of negative chronotropic medications or physical training, Pre-excited QRS complex, Prolonged or short QT interval, RBBB pattern with ST-elevation in leads V1-V3 (Brugada pattern), Negative T waves in right precordial leads, epsilon waves, and ventricular late potentials suggestive of ARVC (arrhythmogenic right ventricular cardiomyopathy)
- Important co-morbidities: Severe anaemia, Electrolyte disturbance
High Risk for Adverse Outcome
- Abnormal ECG (acute ischemia, dysrhythmias, or significant conduction abnormalities)
- History of cardiac disease, especially presence of heart failure
- Persistently low blood pressure (systolic <90 mmHg)
- Shortness of breath with event or during evaluation
- Hematocrit <30 (if obtained)
- Older age and associated comorbidities
- Family history of sudden cardiac death
- Patients with obvious cardiac or neurologic causes of syncope, as well as those with concerning symptoms or signs, should be investigated thoroughly in the emergency department (ED) and likely admitted for further in-hospital testing or treatment.
- To some degree, clinician judgment determines which symptoms or signs are "concerning,” but such findings may include: Syncope accompanied by chest pain or shortness of breath, Exertional syncope, Abnormal vital signs, Abnormal findings on cardiac, pulmonary, or neurologic examination
- For well-appearing asymptomatic patients with an unclear cause, clinicians should determine the risk for adverse outcome. Clinicians determine risk on the basis of patient history, examination and electrocardiogram (ECG) findings, and evidence-based guidelines.
- The presence of any of the following features determines high risk: Abnormal ECG, History of structural heart disease or clinical findings suggestive of heart failure, Persistently low blood pressure (systolic <90 mmHg), Shortness of breath with event or during evaluation, Hematocrit <30 (if obtained), Older age and associated comorbidities, Family history of sudden cardiac death
- High-risk patients should be investigated in the ED and likely admitted. Low risk asymptomatic patients may be discharged, provided out-patient follow-up can be arranged and the clinician has no other concerns. Patients with obvious neurocardiogenic syncope who have returned to baseline and are asymptomatic without injury should be discharged.
- In some emergency departments, patients identified as intermediate risk are managed in a syncope observation unit.
- One prospective randomized multicenter study found that instructing patients diagnosed with vasovagal syncope in the use of physical counterpressure maneuvers (PCM) decreased the incidence of recurrent episodes of syncope from 51 percent to 32 percent, compared with conventional therapy.
- Conventional therapy consisted of explaining the mechanism underlying fainting and providing advice about lifestyle modifications (eg, avoiding known triggers, increasing fluid and salt intake, lying down when symptoms occur).
- PCM consisted of one or more of the following: (1) leg crossing combined with tensing of the muscles of the legs, abdomen, and buttocks; (2) arm tensing by grasping one hand with the other and forcibly abducting the arms; or, (3) squeezing an object clasped in the dominant hand.
Syncope SUMMARY AND RECOMMENDATIONS
- When evaluating the patient with syncope, the primary responsibility of the emergency clinician is to assess whether a life-threatening cause is present, and to provide appropriate management and disposition. The most important causes to consider are: cardiac syncope, blood loss, pulmonary embolism, and subarachnoid hemorrhage. Other conditions, such as seizure, stroke, and head injury, do not meet the technical definition of syncope but should be considered during the initial assessment. An algorithm outlining emergency department management and a table listing dangerous causes of syncope are provided.
- Common but less dangerous causes of syncope include: neurocardiogenic, carotid sinus sensitivity, orthostasis, and medication-related.
- Historical features that reflect increased risk of a dangerous cause of syncope include: concomitant symptoms (eg, shortness of breath, headache, chest pain), sudden loss of consciousness without prodrome, exertional syncope, older age, and family history of sudden death. The clinician should carefully review the patient's medications. Medication reactions account for a significant percentage of syncopal episodes.
- Syncope and seizure can be difficult to differentiate. Characteristics to help clinicians make this distinction are described in the text.
- Perform a careful physical examination focusing on vital signs and the neurologic and cardiac examination. Patients with syncope often fall and sustain secondary injuries, which may include the head (eg, subdural hemorrhage), wrist, or hip. Perform a symptom-guided examination looking for injuries.
- Obtain an electrocardiogram (ECG) on all syncope patients. Significant findings include: prolonged intervals (QRS, QTc), severe bradycardia, preexcitation, and evidence of myocardial infarction. Other notable findings include low voltage in the standard limb leads, suggesting pericardial effusion, and abnormal conduction syndromes (eg, Wolf-Parkinson-White and Brugada).
- Emergency clinicians rely on information garnered from the history, examination, and ECG to assess the patient with syncope. While performing their assessment, they should keep in mind three questions:
- Is this true syncope or does some other serious condition account for the patient's loss of consciousness (eg, stroke, seizure, head injury)?
- If this is true syncope, is there a clear life-threatening cause?
- If this is true syncope and the cause is not clear, is the patient at high risk?
- Patients with obvious cardiac or neurologic causes of syncope, as well as those with concerning symptoms or signs, should be investigated thoroughly in the ED and likely admitted. Patients with obvious neurocardiogenic syncope who have returned to baseline and are asymptomatic without injury should be discharged.
- For well-appearing asymptomatic patients with an unclear cause, clinicians should determine the risk for adverse outcome. Clinicians determine risk on the basis of patient history, examination and electrocardiogram (ECG) findings, and evidence-based guidelines.