The relevant aspects of the history include the patient's symptoms experienced prior to and following loss of consciousness, the setting in which syncope occurred, the patient's past medical and psychiatric history, medications, and social history. Prior episodes and frequency of syncope episodes may also potentially help guide diagnosis and/or testing.
Determination if the event is truly syncope, rather than nonsyncope, can help include or exclude items within the differential diagnosis (Table 99-1). This initial evaluation incorporates a careful history of events before and after the LOC, a thorough assessment of past medical history, a complete medication and allergy review, and assessment of family history (including sudden death) and social history (Table 99-4).
Table 99-4 Key Historical Points in the Evaluation of Syncope ||Download (.pdf)
Table 99-4 Key Historical Points in the Evaluation of Syncope
- Sudden standing or sitting (suggests orthostatic etiology)
- Prodrome: palpitations, lightheadedness, anxiety, sweating, piloerection, nausea, warmth (suggests vasovagal syncope)
- Severe pain, fear, instrumentation (suggests vasovagal syncope, unless there is concurrent structural or congenital heart disease, in which case adrenergic-mediated dysrhythmia should be considered)
- Situation: micturition, defecation, coughing (suggests vasomotor syncope)
- During or immediately following exertion (suggests cardiogenic syncope)
- Chest pain, shortness of breath (suggests possible cardiopulmonary etiology)
- Focal neurologic symptoms: headache, diplopia, dysarthria, weakness (suggests a neurological cause of syncope such as intracranial hemorrhage, vertebrobasilar ischemic event, or tumor)
- Symptoms suggestive of seizure rather than syncope: tonic-clonic activity, bowel or bladder incontinence, lateral tongue biting
- Postsyncope symptoms (eg, confusion) and duration of recovery (most true syncope should have recovery duration of less than a few minutes)
- Poor oral intake, dehydration, GI bleed symptoms (suggests hypovolemic etiology)
- Injury from fall
- Family history of sudden death or arrhythmia (consider long QT syndrome or other congenital cardiac disease)
- Past Medical History
- Prior syncopal episodes: number, frequency, and surrounding history
- Coronary heart disease, heart failure, arrhythmias
- Psychiatric disease
- CVA, TIA
- Pulmonary hypertension
- Medications or Drugs
- Antihypertensives, antianginals, antidepressants, QT-prolonging drugs, CNS depressants (eg, opioids, sedatives), others (vincristine, digoxin, insulin, marijuana, alcohol, cocaine)
Did the patient actually experience a sudden, transient LOC? Was there spontaneous recovery without resuscitation?
Certain historical features may point toward a nonsyncopal event (Table 99-1). History should delineate if there was actual loss of consciousness. A mechanical fall or confusion (altered consciousness) would not be termed syncope or even LOC.
If the patient did actually lose consciousness, consideration of nonsyncopal etiologies of transient LOC including intoxications, hypoglycemia, hypoxia, or severe anemia may be appropriate even though these rarely lead to LOC. These patients may have more gradual development of symptoms prior to a syncopal episode and/or delayed recovery (many minutes to hours) compared with true syncope.
When LOC was witnessed, description of tonic-clonic activity obviously points toward seizure as a nonsyncopal etiology of transient LOC; however, lay person witnesses of seizure activity may not be reliable in description. When a seizure is not witnessed, historical features that may point toward seizure as an etiology include lateral tongue biting or laceration (reasonably specific for seizure), pre-LOC aura, and bowel or bladder incontinence (the latter, a nonspecific finding that may occur in syncope as well). Prolonged recovery (more than one or a few minutes) to normal mentation is another hallmark of seizure, and differs significantly compared to true syncope.
Importantly, many patients with syncope are misdiagnosed as seizure due to misperception of witnesses or misinterpretation of body movement descriptions from bystanders. Any syncopal episode can lead to brief myoclonic activity (occurs in up to 10% of patients with vasovagal syncope and other types of syncope), and up to 1% of syncope patients can have benign brief (lasting one or a few seconds) “full body stiffening” prior to awakening. Many may misinterpret this as seizure activity (which alternately should last minutes or longer rather than seconds).
Extended duration of actual LOC is referred to as coma rather than syncope (which is transient). LOC that required resuscitation or defibrillation to return a pulse and consciousness is referred to as sudden cardiac death and not syncope.
Cardiac Syncope (Inadequate Cardiac Output, Arrhythmias)
Historical features suggesting cardiac etiologies of syncope include chest pain prior to syncope, syncope during exertion, and syncope while supine. In ventricular tachycardia, patients may present with syncope that has no prodrome. Often those patients recall no specific symptoms prior to the syncopal episode, only recall awakening, and are often injured from a fall.
Is this patient having an acute MI?
Up to 10% of patients with acute myocardial infarction (MI) present with syncope. Similarly, up to 7% of patients who present with syncope and no chest pain may have ischemia as the cause of their syncopal event. Please refer to Chapter 124 on acute coronary syndromes (ACS) for relevant aspects of history and examination presentation of patients with acute MI or unstable angina. Any patient who presents with syncope who also had chest pain either before or after the syncopal episode needs to be evaluated for possible ACS with cardiac enzymes, telemetry monitoring, serial ECGs, and stress testing if indicated. In patients who have syncopebut no chest pain, four factors are predictive of ACS as the etiology of the syncope: (1) arm, neck, shoulder, and throat pain, (2) history of stable angina (provoked by exercise), (3) the presence of rales on physical examination, and (4) electrocardiographic ischemic abnormalities.
Patients without ischemic abnormalities on ECG are not at risk for an acute ischemic event compared to those with ischemic abnormalities on ECG.
Is there obstruction to flow resulting in inadequate cardiac output?
Patients may have valvular, subvalvular, or vascular obstruction leading to reduced or transiently blocked cardiac output and a syncopal event. Valvular causes include aortic stenosis (AS), mitral stenosis, pulmonic stenosis (PS), or prosthetic valve malfunction. Historical features may include exertional syncope.
Subvalvular cardiac causes include hypertrophic obstructive cardiomyopathy (HOCM) and atrial myxoma. Classic symptoms in HOCM include postexertional syncope. Vascular obstruction can occur due to pulmonary embolus (PE) or significant pulmonary hypertension. Of all patients admitted to the hospital with syncope, less than 1% are due to PE. However, despite occurring uncommonly clinicians should consider the diagnosis in patients with pleuritic chest pain, shortness of breath or symptoms to suggest lower-extremity venous thromboembolism.
Are ventricular arrhythmias suspected as the cause of syncope?
Risk factors include CAD, valvular AS, cardiomyopathy, congenital heart disease, prolonged QT interval on ECG, use of antiarrhythmic drugs especially in patients with reduced LV function, hypo- or hyperkalemia, and hypomagnesemia. History may include palpitations, chest pain, or syncope in association with exercise. However, classically patients with ventricular arrhythmia causing syncope present with no symptoms at all prior to the syncopal event, and injury can occur commonly. Syncope while supine is also concerning for possible ventricular arrhythmia. Finally, a variety of drugs may prolong the QT interval (www.qtdrugs.org), and place patients at risk for torsades de pointe.
Are supraventricular arrhythmias or bradyarrhythmias suspected as a cause of syncope?
While syncope occurs uncommonly in supraventricular tachyarrhythmias, risk factors may include prior history or risk of atrial fibrillation, atrial flutter, multifocal atrial tachycardia, and AV node reentrant tachycardia. Malignant bradyarrhythmias can lead to syncopal events, and may be due to conduction system disease, especially with AV nodal blocking agents, pacemaker malfunction, bundle branch blocks (BBB), or bifascicular block.
Is the patient having a benign vasovagal episode?
Reflex syncope, also known as vasodepressor syncope, vasovagal syncope, neurocardiogenic syncope, or the “common faint,” is the most common cause of syncope. Reflex syncope is mediated by inappropriate vasodepressor (ie, loss of vasoconstriction during standing) or cardioinhibitory (ie, reflex reaction characterized by bradycardia and/or asystole) responses to orthostatic challenge or emotional stress. It may also be precipitated by Valsalva (eg, micturition, defecation, swallowing) or mobilization after prolonged bed rest.
Diagnosis is clinical by eliciting classic symptoms. The classic prodrome, exhibited by a sympathetic response—diaphoresis, palpitations/tachycardia, piloerection, anxiety, pallor—followed by a parasympathetic response—nausea and/or vomiting, warmth/venodilation, low heart rate—can help correctly diagnose the condition. Obviously, individual patients may exhibit only a portion of the classic symptoms.
In reflex syncope related to carotid sinus hypersensitivity, classically there is no mechanical trigger leading to syncope, and it should be diagnosed by provocation through carotid sinus massage. Occasionally, these patients may describe syncope after rapid head or neck movements.
Sometimes, reflex syncope can occur in response to serious vascular events, particularly subarachnoid hemorrhage or aortic dissection. In these cases, the syncope itself may be a benign reflex event, but the underlying precipitant is life threatening and must be identified through additional historical clues such as severe headache or intense chest and back pain.
Is orthostasis causing the patient's syncope?
Syncope due to orthostatic hypotension (OH) can occur with (1) inadequate venous return (low cardiac output), (2) structural damage to the autonomic nervous system (ANS), or (3) transient impairment of normal autonomic nervous system function. The latter may occur with medications that block the normal autonomic responses of the heart (eg, beta-blockers or nonselective calcium channel blockers [CCBs]), or with medications that block the normal autonomic responses of the vasculature (eg, peripherally-acting CCBs or alpha-blockers).
Inadequate venous return may be caused by volume depletion due to inadequate intake or excess losses through the gastrointestinal track, kidneys, or insensible losses (skin, lungs). Low venous return due to venous pooling can occur within the splanchnic system following a meal or in the peripheral venous system (eg, venous insufficiency).
Low peripheral resistance can result from primary or secondary autonomic nervous system (ANS) failure (Figure 99-2). With an intact ANS, drug-induced ANS failure or inappropriate vasodepression during a reflex response can cause syncope. These etiologies can be categorized as syncope due to orthostatic intolerance or orthostatic hypotension (OH). Vasovagal syncope occurs when the initial adaptation reflex is appropriate with orthostatic challenge, but eventually venous return falls and there is an inappropriate cardioinhibitory response, leading to bradycardia (and low cardiac output) while blood pressure (peripheral vascular resistance) is already low.
Finally, postural orthostatic tachycardia syndrome (POTS) is a poorly understood entity believed to occur due to autonomic dysfunction that can be exacerbated by deconditioning. It is manifested by a pathologic excess of venous pooling, early palpitations (in which HR increases by 30 bpm, or up to 120 bpm with standing) and BP instability in response to the venous pooling. It may be associated with chronic fatigue syndrome.
In the elderly, in addition to drug-induced OH, there are two predominant forms of OH: classical OH and delayed OH. In classical OH, chronic ANS failure impairs sympathetic vasoconstriction leading to low systemic vascular resistance in an orthostatic challenge. systemic vascular resistance (SVR) in an orthostatic challenge. In delayed OH, a decline in venous return is coupled with inappropriately low CO and impaired vasoconstriction, leading to syncope.
Initial physical examination should focus on vital signs, including orthostatic assessment and thorough cardiac and neurologic evaluations. At least two retrospective studies (including more than 2700 patients) have shown that orthostatic evaluation is documented in less than 40% of patients admitted to the hospital with syncope. The orthostatic evaluation is a critical piece of information (irrespective of having received intravenous fluids in the emergency department), and should always include heart rate in addition to pulse. Supine parameters should be obtained after the patient has been resting quietly for a few minutes, followed by having the patient stand upright if possible. Obtain and record blood pressure immediately upon standing, then repeat the process in the next two to three minutes, with a pulse rate obtained at the end of the standing period. Cardiac examination should include inspection, evaluation of arterial and venous pulsations and bruits (especially carotid auscultation), and cardiac palpation and auscultation. Evaluation for rales, jugular venous distention, any displacement of the apical impulse, and S3 can aid in the diagnosis. A neurologic examination should include level of consciousness and orientation, cranial nerves, motor, sensory, cerebellar, and gait evaluations.