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Definition and CausesTop
Syncope is a transient loss of consciousness caused by global cerebral hypoperfusion. It is characterized as a loss of postural tone with a rapid onset, short duration, and spontaneous recovery without neurologic deficits. Syncope can be classified into several broad categories (Table 1). In presyncope (a syncopal prodrome) the patient has a sensation of imminent loss of consciousness but true syncope does not occur.
Other causes of symptoms that can mimic syncope include sudden-onset conditions not associated with loss of consciousness, such as a fall or psychogenic pseudosyncope (appearance of a transient loss of consciousness in the absence of true loss of consciousness), or conditions associated with a partial or complete loss of consciousness not primarily related to cerebral hypoperfusion (metabolic disturbances [eg, hypoglycemia], hypoxia, hyperventilation with hypocapnia, seizure, drug or alcohol intoxication).
General Approach to SyncopeTop
1. Management of patients with loss of consciousness: see Loss of Consciousness.
2. Exclude other causes of transient loss of consciousness.
3. Identify clinical features suggestive of cardiac etiology.
4. Stratify patients into low risk and high risk (requiring prompt diagnostic testing).
5. Provide a provisional diagnosis and management plan.
6. Identify when driving privileges should be held (follow local laws and regulations).
Initial Evaluation of a Patient With Syncope
1. Detailed and comprehensive history:
1) Context at the onset of symptoms: After standing; with dehydration (decreased oral intake, bleeding, diarrhea, vomiting); with drug administration (suggestive of an orthostatic cause); related to strong emotions like fear, pain, or sight of blood (vasovagal); related to specific situations such as micturition, defecation, coughing, sneezing, or exercise (situational); on exertion; with head turning (carotid artery occlusion); or when supine.
2) Prodromal symptoms: Weakness, presyncope, visual blurring, diaphoresis, nausea, terminal warmth (vasovagal), palpitation, or lack of prodromal symptoms (cardiac).
3) Symptoms following the event: Rapid return of consciousness (cardiac) versus confusion, focal weakness, or delayed return to baseline (seizure).
4) Collateral history of the event: Appearance during the event, including the overall duration, presence of seizure symptoms, signs of pseudosyncope (slumping to the floor, lack of trauma, closed eyes, lack of diaphoresis).
5) Associated conditions: Primary autonomic failure (Parkinson disease, dementia with Lewy bodies, pure autonomic failure, multiple system atrophy) or secondary autonomic failure (diabetes mellitus, amyloidosis, spinal cord injuries, autoimmune autonomic neuropathy, paraneoplastic autonomic neuropathy, kidney failure); bradyarrhythmias such as sinus node dysfunction or heart block; tachyarrhythmias such as atrial fibrillation, long QT syndrome, Brugada syndrome, and other supraventricular tachyarrhythmias; structural heart disease like history of myocardial infarction and cardiomyopathy; valvular heart diseases like aortic stenosis; pulmonary embolism.
2. Physical examination:
1) Vital signs including orthostatic blood pressure and heart rate.
2) Neurologic examination: Screening examination for focal deficits. Examination of the lateral aspects of the tongue for signs of tongue biting indicating a seizure.
3) Cardiovascular examination: Jugular veins, enlarged/displaced apical beat, murmurs, bruits, signs of congestive heart failure.
4) Carotid sinus massage: Indicated in all patients aged >40 years with syncope of unknown origin compatible with a reflex mechanism. Carotid sinus hypersensitivity is defined as a ventricular pause lasting >3 seconds, a decrease in systolic blood pressure >50 mm Hg, or both. Check for carotid bruits before doing this maneuver. Do not perform carotid sinus massage if bruits are present.
5) Other: Signs of pulmonary embolism such as parasternal heave, unilateral leg swelling, tenderness, and erythema.
3. Investigations:
1) 12-lead electrocardiography (ECG) is performed in all patients to look for signs of conduction disturbances, ischemia, preexcitation syndromes (long QT, delta wave, or Brugada syndrome [right bundle branch block with ST-segment elevation in leads V1-V3]).
2) Echocardiography is performed in patients with signs of possible structural heart disease including aortic stenosis, hypertrophic cardiomyopathy, pulmonary embolism, pulmonary hypertension, and ischemia.
3) Other investigations are used to identify etiology of the syncopal event as dictated by the history, physical examination, and ECG. These include tilt table testing (orthostatic hypotension), extended ECG monitoring and electrophysiologic study (arrhythmia-related cardiac syncope), and in-hospital video recording (seizure).
Risk of Serious OutcomesTop
Patients with syncope who present to medical attention may have a significant risk of adverse outcomes during follow-up; however, the gravity of this risk varies widely depending on etiology (Table 2). The Calgary Syncope Symptom Score (CSSS) may be useful in the identification of patients with vasovagal syncope (Table 3).Evidence 1Weak recommendation (benefits likely outweigh downsides, but the balance is close or uncertain; an alternative course of action may be better for some patients). Low Quality of Evidence (low confidence that we know true effects of the intervention). Quality of Evidence lowered due to imprecision and indirectness to other subgroups. Expósito V, Guzmán JC, Orava M, Armaganijan L, Morillo CA. Usefulness of the Calgary Syncope Symptom Score for the diagnosis of vasovagal syncope in the elderly. Europace. 2013 Aug;15(8):1210-4. doi: 10.1093/europace/eut042. Epub 2013 Mar 10. PubMed PMID: 23478089. The Canadian Syncope Risk Score can be used to identify patients at high risk for serious adverse events after an emergency department visit for syncope. Other risk scores include the Osservatorio Epidemiologico sulla Sincope nel Lazio (OESIL) score and the San Francisco Syncope Rule (Table 4).Evidence 2Weak recommendation (benefits likely outweigh downsides, but the balance is close or uncertain; an alternative course of action may be better for some patients). Low Quality of Evidence (low confidence that we know true effects of the intervention). Quality of Evidence lowered due to imprecision and indirectness to patient-important outcomes. Serrano LA, Hess EP, Bellolio MF, et al. Accuracy and quality of clinical decision rules for syncope in the emergency department: a systematic review and meta-analysis. Ann Emerg Med. 2010 Oct;56(4):362-373.e1. doi: 10.1016/j.annemergmed.2010.05.013. Review. PubMed PMID: 20868906; PubMed Central PMCID: PMC2946941. Thiruganasambandamoorthy V, Kwong K, Wells GA, et al. Development of the Canadian Syncope Risk Score to predict serious adverse events after emergency department assessment of syncope. CMAJ. 2016 Sep 6;188(12):E289-98. PubMed PMID: 27378464; PubMed Central PMCID: PMC5008955. Quinn JV, Stiell IG, McDermott DA, Sellers KL, Kohn MA, Wells GA. Derivation of the San Francisco Syncope Rule to predict patients with short-term serious outcomes. Ann Emerg Med. 2004 Feb;43(2):224-32. PubMed PMID: 14747812. Colivicchi F, Ammirati F, Melina D, Guido V, Imperoli G, Santini M; OESIL (Osservatorio Epidemiologico sulla Sincope nel Lazio) Study Investigators. Development and prospective validation of a risk stratification system for patients with syncope in the emergency department: the OESIL risk score. Eur Heart J. 2003 May;24(9):811-9. PubMed PMID: 12727148. The Canadian Cardiology Society provides a list of major and minor risk factors predictive of short-term morbidity (Table 2). They recommend that higher-risk patients (>1 major risk factor) should be considered for further cardiac assessment (eg, echocardiography and cardiologist consultation within 2 weeks).Evidence 3Weak recommendation (benefits likely outweigh downsides, but the balance is close or uncertain; an alternative course of action may be better for some patients). Low Quality of Evidence (low confidence that we know true effects of the intervention). Quality of Evidence lowered due to a limited interstudy agreement on the specific factors listed. Major risk factors were arbitrarily defined as those independently identified in more than 1 publication and minor risk factors were identified in only 1 report. Sheldon RS, Morillo CA, Krahn AD, et al. Standardized approaches to the investigation of syncope: Canadian Cardiovascular Society position paper. Can J Cardiol. 2011 Mar-Apr;27(2):246-53. doi: 10.1016/j.cjca.2010.11.002. Review. PubMed PMID: 21459273. Brignole M, Moya A, de Lange FJ, et al. 2018 ESC Guidelines for the diagnosis and management of syncope. European heart journal. 2018 Mar 19;39(21):1883-948. doi: 10.1093/eurheartj/ehy037. PubMed PMID: 29562304. The subsequent management depends on the suspected cause of the syncope (Table 1).
Diagnostic Uncertainty and Recurrence Top
Recurrences of syncope are frequent. In patients with diagnostic uncertainty, further investigations can be considered. Tilt table testing, which provides a strong orthostatic stress to provoke vasovagal syncope, can be used in instances of undiagnosed recurrent syncope felt not to be of cardiac or cerebrovascular origin.
Standard 24- to 48-hour Holter monitoring can also be considered; however, unless the episodes are happening daily to weekly, there is little chance that a syncopal event will be recorded. A 1-month event recorder or an implantable loop recorder (ILR) could be used in selected patients soon after the initial encounter if there is diagnostic uncertainty with ongoing symptom reoccurrence.Evidence 4Strong recommendation (benefits clearly outweigh downsides; right action for all or almost all patients). Moderate Quality of Evidence (moderate confidence that we know true effects of the intervention). Quality of Evidence lowered due to the observational nature of the study but increased due to the large proportion of patients in whom the nature of syncope was explained. The findings apply to that specific population of patients. Edvardsson N, Frykman V, van Mechelen R, et al; PICTURE Study Investigators. Use of an implantable loop recorder to increase the diagnostic yield in unexplained syncope: results from the PICTURE registry. Europace. 2011 Feb;13(2):262-9. doi: 10.1093/europace/euq418. Epub 2010 Nov 19. PubMed PMID: 21097478; PubMed Central PMCID: PMC3024039. Furukawa T, Maggi R, Bertolone C, Fontana D, Brignole M. Additional diagnostic value of very prolonged observation by implantable loop recorder in patients with unexplained syncope. J Cardiovasc Electrophysiol. 2012 Jan;23(1):67-71. doi: 10.1111/j.1540-8167.2011.02133.x. Epub 2011 Jul 21. PubMed PMID: 21777327.
TablesTop
|
Etiology |
Causes |
Triggers |
Diagnosis |
Management |
|
VVS |
– Inappropriate reflex response leading to vasodilation or bradycardia – Most common type of syncope in all ages (46% of all events) – Usually benign and not requiring specific treatment; ensure adequate salt intake and hydration |
– Sudden, unexpected, or unpleasant stimulus (sight, sound, smell, pain)
– Following long periods of standing in crowded hot places
– After meals; concomitant nausea or vomiting |
– Typical history – Calgary Syncope Symptom Score (see table 1.3-4) – Tilt table testing can be considered in case of diagnostic uncertainty |
– Trigger avoidance – Advice on episodic management (sitting down, isometric exercises) – Orthostatic training (unproven benefit) – Dual-chamber pacemaker indicated in selected patients with episodes of prolonged asystole |
|
Carotid sinus syndrome |
– Hypersensitivity of afferent or efferent limbs of carotid sinus leading to bradycardia and/or vasodilation – Rarely in adults aged <50 years |
Syncope after head turning (eg, changing traffic lanes) |
– Carotid sinus massage – Asystole >3 s or fall in SBP >50 mm Hg |
– Dual-chamber pacemaker – Pharmacotherapy only in exceptional cases with specialist consultation (unproven benefit) |
|
Orthostatic hypotension |
Occurs when autonomic sympathetic vasomotor system fails to respond to challenges imposed by upright position, causing hypotension |
– Primary causes: Parkinson disease, MSA, pure autonomic failure – Secondary causes (more common): volume depletion due to alcohol or drugs (diuretics, beta and alpha blockade, vasodilators) |
– Sustained drop in BP (≥20 mm Hg drop in SBP, or SBP <90 mm Hg) within 3 min of standing – Consistent medical history |
– Discontinue offending drugs – Avoid circumstances that may trigger syncope – Increase intravascular volume with fluids or drugs: fludrocortisone 0.1-0.4 mg/d PO or midodrine 5-40 mg/d PO |
|
Cardiac syncope |
Can be structural or arrhythmogenic, leading to decreased cardiac output and drop in cerebral perfusion |
– Significant organic heart disease; syncope during physical exercise or in supine position, syncope preceded by palpitations, family history of SCD – Patients at high risk for VTE |
– ECG or telemetry changes of conduction delay, QT prolongation, IHD, hypertrophy
– Echocardiography |
– Referral to cardiologist for management of underlying cardiac disease – Interrogate pacemaker if in situ |
|
Cerebrovascular syncope |
Decreased cerebrovascular blood flow, can occur with: – Subclavian steal syndrome – TIA affecting vertebral and posterior arteries – Migraine variant |
– Subclavian steal syndrome: stenosis of subclavian artery proximal to vertebral artery causing reversal of flow during strenuous upper limb exercise – Ischemic risk factors (hypertension, dyslipidemia, prior CVA, smoker, DM) – Migraine triggers |
– Subclavian and/or carotid artery bruit, BP differential – Carotid US – Vertebral and subclavian angiography – MRA/MRI |
Referral to specialists for management of underlying disease depending on etiology (eg, neurologist for migraines, TIA; vascular surgeon for subclavian steal) |
|
BP, blood pressure; CVA, cerebrovascular accident; DM, diabetes mellitus; ECG, electrocardiography; IHD, ischemic heart disease; MRA, magnetic resonance angiography; MRI, magnetic resonance imaging; MSA, multiple system atrophy; PO, oral; SBP, systolic blood pressure; SCD, sudden cardiac death; TIA, transient ischemic attack; US, ultrasonography; VTE, venous thromboembolism; VVS, vasovagal syncope. | ||||
|
Risk factors |
Comments |
|
Major risk factors | |
|
Abnormal ECG |
Any bradyarrhythmia, tachyarrhythmia, conduction disorder, ischemia, or history of myocardial infarction |
|
History of cardiac disease |
Ischemic, arrhythmic, obstructive, valvular |
|
Hypotension |
SBP <90 mm Hg |
|
Minor risk factors | |
|
Cerebrovascular disease |
|
|
Family history of sudden cardiac death |
At age <50 years |
|
Specific situations |
Syncope while supine or during exercise, or no prodromal symptoms |
|
ECG, electrocardiography; SBP, systolic blood pressure. | |
|
Individual items of the Calgary Syncope Symptom Score |
Points if “YES” |
|
Is there a history of ≥1 of the following: bifascicular block, asystole, supraventricular tachycardia, diabetes mellitus? |
–5 |
|
At times, have bystanders noted you to be blue during your faint? |
–4 |
|
Did your syncope start when you were 35 years of age or older? |
–3 |
|
Do you remember anything about being unconscious? |
–2 |
|
Do you have lightheaded spells or faint with prolonged sitting or standing? |
1 |
|
Do you sweat or feel warm before a faint? |
2 |
|
Do you have lightheaded spells or faint with pain or medical settings? |
3 |
|
The diagnosis of vasovagal syncope is made if the score is ≥–2. | |
|
Source: Eur Heart J. 2006;27(3):344-50. | |
|
Canadian Syncope Risk Score |
San Francisco Syncope Rule |
OESIL risk score |
|
Risk factors | ||
|
– Predisposition to vasovagal symptoms (−1) – Heart disease history (+1) – SBP <90 or >180 mm Hg (+2) – Elevated troponin (+2) – Abnormal QRS axis (+1) – QRS duration >130 ms (+1) – Corrected QT interval >480 ms (+2) – Vasovagal syncope (−2) – Cardiac syncope (+2) |
– SBP <90 mm Hg – Shortness of breath – ECG: nonsinus rhythm or new changes – Hematocrit <30% |
– Age >65 years – History of CVD – Syncope without prodrome – Abnormal ECG findings |
|
Assessed endpoint | ||
|
30-day morbidity and mortality after presentation to ED: |
7-day morbidity and mortality after presentation to ED: |
1-year mortality: |
|
– Score −3 to 0: 0.4%-1.9% – Score 1-3: 3.1%-8.1% – Score 4-5: 12.9%-19.7% – Score 6-11: 28.9%-83.6% |
– No factors present: 0.3% – ≥1 factor present: 15.2% |
– 0-1 factor (low risk): 0.6% – 2-4 factors (high risk): 31% |
|
Score accuracy | ||
|
– Score ≥−2: sensitivity 99%, specificity 26% – Score ≥−1: sensitivity 98%, specificity 46% |
– Sensitivity 98% – Specificity 56% – LR+: 2.9 – LR−: 0.03 |
– Sensitivity 97% – Specificity 73% – LR+: 3.6 – LR−: −0.11 |
|
Adapted from CMAJ. 2016;188(12):E289-98, Ann Emerg Med. 2004;43(2):224-32, and Eur Heart J. 2003;24(9):811-9. | ||
|
CVD, cardiovascular disease; ECG, electrocardiography; ED, emergency department; LR+, positive likelihood ratio; LR–, negative likelihood ratio; OESIL, Osservatorio Epidemiologico sulla Sincope nel Lazio; SBP, systolic blood pressure. | ||
