EM guidemap - Syncope

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Introduction and general principles

History of present illness

Risk factors for syncope

Examination

Diagnostic testing

Medical decision-making Appendix
Introduction and general principles

- syncope is defined as a transient loss of consciousness associated with a loss of postural tone, and most diseases causing syncope produce a transient LOC by temporarily decreasing cerebral blood flow

An emergency physician, when faced with a syncope-patient in an ED setting, should first seek to exclude life-threatening causes of syncope, which require immediate diagnostic evaluation/treatment + hospital admission

If there are no overt life-threatening causes of syncope, then an emergency physician should attempt to identify patients with situational syncope, vasovagal syncope and benign orthostatic (postural) syncope - who are candidates for home discharge after any necessary stabilization treatment in the ED

- young patients (< 45 years), who have a history of a short-lived syncopal episode with no other associated ongoing symptoms, rarely have serious causes of syncope if the syncope did not occur during exertion, and hospital admission and/or an extensive workup is rarely necessary

- emergency physicians are often faced with the dilemma that the cause of the syncope is not immediately apparent after a brief clinical examination, and a decision has to be made whether it is necessary to admit the patient to hospital

If the cause of the syncope is not readily apparent after initial clinical evaluation in the ED, then an emergency physician should attempt to decide whether certain categories of syncope-patients require admission to hospital

- examples of syncope patients warranting hospitalization include:-

(* see the medical decision-making section for further details)

- there is no universally accepted approach to the further inpatient/outpatient workup of patients, whose cause of syncope is not readily apparent => a suggested algorithm is included in the appendix section as a general guide

History of the present illness

- critical historical elements include the mode of onset and progression of event, body position at onset of event, the depth of altered consciousness, the duration of the syncopal episode and the rate of recovery of consciousness

(* by paying close attention to the details, an emergency physician should be able to differentiate syncope from seizures, non-specific near-syncopal events, non-specific ligheadedness and dysequilibrium syndromes)

- sudden unheralded syncope at rest, particularly in a non-erect posture, is ominous - especially if significant injury results => suggests a cardiac arrhythmia

- associated palpitations or an irregular heart beat suggests cardiac syncope secondary to a cardiac arrhythmia

- certain antecedent symptoms lasting > 10 seconds (darkening vision or tunnel vision or graying vision, lightheadedness, swaying sensation, nausea, sweating, feeling "hot", face and distal limb numbness), especially if preceded by a provocative emotional event and occurring in an upright position suggest vaso-vagal syncope (also called vasodepressor or reflex or neurocardiogenic syncope)

(* vasovagal syncope is also more likely to happen in overcrowded social settings where prolonged mandatory standing is a requirement eg. church, military parades in hot weather)

- antecedent/accompanying chest pain (AMI or PE) or abdominal pain (ectopic pregnancy) or back pain (ruptured abdominal aortic aneurysm or dissecting aortic aneurysm) or headache (SAH) suggests serious pathology

- prominent antecedent/accompanying dyspnea suggests hyperventilation syndrome, pulmonary embolism or pulmonary hypertension

- accompanying brainstem symptoms (diplopia or blurred vision, dysarthria, dysphagia, deafness, vertigo, ataxia, limb weakness or hypoesthesia, face pain or hypoesthesia) suggest vertebro-basilar artery insufficiency or basilar artery migraine

- the patient’s posture at the time of syncope is very important – sudden syncope in a non-erect position signifies serious pathology , while lightheadedness for 30 - 60 seconds after suddenly standing/walking and immediately preceding the syncopal episode suggests underlying orthostatic hypotensive syndromes (autonomic neuropathy and/or volume depletion and/or drug-induced vasodilatation)

- sudden syncope related to turning or hyperextending the head (eg. when shaving or while wearing tight constricting neckwear) suggests carotid sinus syncope

- sudden syncope during strenuous physical activity (exertional syncope ) suggests potentially serious pathology (HOCM or aortic stenosis, or atrial myxoma or anomalous coronary artery; or a malignant arrhythmia  eg. torsade des pointes and VT)

- pscyhological triggering events (painful stimuli, sudden bad news) suggest vasovagal syncope

(* however sudden stress/excitement in patients with long QT syndrome can trigger torsades des pointes)

- evidence of volume loss may precede syncope (vomiting, diarrhea) or accompany syncope (hematemesis or melena)

- syncope related to strenuous unilateral upper arm activity suggests subclavian steal syndrome

- situational syncope is self-diagnostic - cough syncope, micturition syncope, defecation syncope, hair-grooming syncope, adolescent stretch syncope, deglutition (swallow) syncope, glossopharyngeal syncope and "weight-lifter blackouts"

- antecedent "glue-sniffing" or "huffing" suggests a ventricular arrhythmia and/or hypoxia as the cause of the syncope; sympathomimetic drug abuse (cocaine or amphetamines) suggest a tachyarhythmia

- recurrent bouts of progressive gradual loss of consciousness over several minutes while walking or standing + NO sweating + NO pallor + fixed heart rate suggest chronic dysautonomic syncope

(* patients often also have a history of hypohidrosis, impotence, blurred vision, urinary difficulties, constipation, nocturnal polyuria and " coat-hanger" pain [neck and shoulders ache - present only when standing])

- recent meal ingestion in an elderly patient may suggest post-prandial hypotensive syncope

- short-lived myoclonic seizures or twitching are compatible with convulsive syncope, and do not imply a true seizure

(* a true seizure is more likely if an aura and/or convulsions precede the fall, tongue biting and/or urinary incontinence occurs, convulsions are generalized and last longer than 30 seconds, prolonged post-ictal confusion-lethargy occurs => see the table in the appendix section for further details)
 

Clinical clue table
Clinical clue Suggests
Sudden syncope at rest when non-erect Cardiac arrhythmia, atrial myxoma
Sudden syncope on exertion Aortic stenosis, HOCM, atrial myxoma, malignant cardiac arrhythmia
Preceding "lightheadness" prodrome when erect Vasovagal syncope, orthostatic hypotension
Preceding palpitations Cardiac arrhythmia
Preceding or accompanying dyspnea Pulmonary embolism, tension pneumothorax, cardiac tamponade, air embolism
Preceding or accompanying chest pain AMI, PE, cardiac tamponade, dissecting aneurysm, tension pneumothorax, mitral valve prolapse
Preceding or accompanying back pain Dissecting aortic aneurysm, leaking AAA
Preceding or accompanying abdominal pain Leaking AAA, ectopic pregnancy
Occurring when turning head to side, or looking up Carotid sinus syncope
Occurring when exercising upper arm Subclavian steal syndrome
Occurring during (or immediately after) coughing, laughing, vomiting, swallowing, urination, defecation, combing hair, stretching Situational syncope
Occurring after prolonged standing Vasovagal syncope
Occurring after emotional upset Vasovagal syncope, prolonged QT interval and torsade
Recent illicit drug use Cardiac arrhythmia, air or foreign body embolism
Recent sudden headache SAH
Recent neurological symptoms Brain stem stroke, vertebro-basilar artery insufficiency, basilar migraine, carotid or vertebral artery dissection, dissecting aortic aneurysm
Recent vaginal insufflation Air embolism
Recent black stools GI bleed
Recent fluid loss (diarrhea, vomiting, sweating) Orthostatic hypotension, Addisonian crisis
Recent meal  Postprandial hypotensive syncope
Polypharmacy, recent sialdenafil  use Orthostatic syncope
History of fever or myalgia or arthalgia or rash Atrial myxoma, cardiac tamponade
History of known cardiac ischemia or structural heart disease Cardiac arrhythmia, pro-arrhythmia drug effect, valve dysfunction
History of mechanical heart valve Thrombosis of valve
Recent history of cancer, prolonged immobilization, leg injury or surgery Pulmonary embolism
History of autonomic dysfunction (impotence, anhydrosis, sphincter dysfunction) Orthostatic hypotension secondary to autonomic neuropathy
History of recurrent syncope Cardiac arrhythmia, carotid sinus syncope, atrial myxoma, aortic stenosis, subclavian steal syndrome, prolonged QT interval - torsade
Family history of syncope or sudden death HOCM, prolonged QT syndrome
Pacemaker Pacemaker failure

Risk factors for syncope

Underlying causes of orthostatic hypotension

- volume depletion (vomiting, diarrhea, excessive perspiration, diuretic use)

- blood loss

- adrenal insufficiency

- primary or secondary dysautonomias (multiple sclerosis, Guillane-Barre syndrome, spinal cord injury, tabes dorsalis, Parkinsonism, Shy-Drager syndrome, diabetic autonomic neuropathy)

- peripheral neuropathy (chronic alcoholism, diabetes)

- polypharmacy in elderly patients with impaired baroreceptor reflexes

- prolonged recumbency and secondary "cardiac-deconditioning"

Drugs predisposing to syncope

- vasodilators (alpha blockers, beta blockers, ACEI’s, calcium channel blockers, nitrates, phenothiazines)

- cardio-inhibitor drugs (beta blockers, digoxin)

- psycho-active drugs (anti-convulsants, CNS sedative-depressants, anti-histamines, anti-depressants, anti-psychotics)

Conditions predisposing to a prolonged QT interval and torsade des pointes
 
Acquired causes Enviromental and endocrinological causes Medicinal and 
toxicological causes		 Congenital causes  Neurological causes
Ischemic coronary artery disease Hypothermia  Class 1A antidysrhythmics - quinidine, procainamide, disopyramide Jervell-Lange-Nielsen          syndrome Subarachnoid hemorrhage
Congestive heart failure Bulemia, stringent dieting Class 1C antidysrhythmics - flecainide, encainide Romano-Ward sydrome Cerebrovascular occlusive disease
Rheumatic heart disease  Hypothyroidism Phenothiazine overdose  Refsum syndrome Traumatic brain injury
Myocarditis Hypokalemia Butyrophenone overdose Mitral valve prolapse Encephalitis
  Hypocalcemia Tetracyclic/tricyclic antidepressant overdose    
  Hypomagnesemia Organophosphate overdose    
    Macrolide antibiotics + terfenadine or astemizole or cisapride    
    Azole antigungals + terfenadine or astemizole or cisapride    

Examination

- a selective examination can offer clinical clues as to the etiology of the syncope

Blood pressure

- difference in blood pressure between left and right upper limbs > 20mmHg is abnormal (suggests dissecting aortic aneurysm or subclavian steal syndrome)

- difference in blood pressure between upper and lower limbs > 20mmHg when recumbent is abnormal (suggests a dissecting aortic aneurysm)

Pulse volume

- decreased and delayed upstoke (aortic stenosis/hypertrophic obstructive cardiomyopathy)

- positive pulsus paradoxus (cardiac tamponade, massive pulmonary embolism)

- absent pulses (dissection of the aorta, cardiac emboli)

Neck bruits

- suggests great artery stenosis eg. subclavian steal syndrome or carotid artery dissection

Jugular venous pressure

- increased in heart failure or pulmonary embolism or cardiac tamponade (positive Kussmaul’s sign)

- 'cannon' a waves suggests AV conduction block

Apex beat

- displaced and forceful (LVH), forceful (RVH)

Heart sounds

- decreased (pericardial tamponade)

- 3rd/4th heart sounds (ventricular failure or LV overload)

- loud second heart sound (pulmonary embolism or pulmonary hypertension)

- ejection systolic murmurs (aortic stenosis or hypertrophic cardiomyopathy - increased murmur when standing, decreased when squatting)

- machinary murmur (air embolism)

- "tumor plop" or diastolic murmur (atrial myxoma)

- varying heart sounds/murmurs (thrombotic occlusion of a prosthetic valve)

Abdomen

- pulsatile masses (abdominal aneurysm)

- rectal exam for melena or heme-occult positive stools (gastro-intestinal bleeding)

- absent/decreased femoral pulses (dissection of the aorta)

Neuro exam

- signs of vertebro-basilar artery TIA/CVA or neuropathy or myelopathy
Diagnostic testing

Cardiac monitoring

- immediate and continuous monitoring during the ED evaluation period is highly recommended

- arrhythmias may be etiologically significant

(* no study has determined the ideal duration of ED cardiac monitoring

ECG

- an abnormal ECG may be etiologically significant, although the 'definitive' diagnostic yield is low (< 5%)

- ECG abnormalities include:-

Pulse oximetry

- a low reading may suggest a possible etiology (cyanotic congenital heart disease, pulmonary embolism, pulmonary hypertension

Blood testing

- not generally useful

- Hb/Hct helpful in establishing baseline in bleeding patients

- glucose and electrolytes have no/little utility

(* hyponatremia + hyperkalemia may rarely suggest Addison's disease; hypoglycemnia rarely produces syncope without ongoing symptoms of hypoglycemia)

- serum HCG rarely helpful in reproductive age female patients

(* very rare patient with an ectopic pregnancy presenting as syncope without any abdominal pain/vaginal bleeding)

Carotid sinus massage

- may be useful in diagnosing carotid sinus syncope in elderly patients

- first performed on the right side for a minimum of 5 seconds (preferably 15 seconds) => measure pulse rate and blood pressure => wait 120 seconds => repeat test on the left side

- positive response = longer than 3 seconds of asystole, and/or systolic blood pressure drop of > 50 mmHg when supine

- borderline positive response = slowing of heart rate > 30 - 40% and/or systolic blood pressure drop of > 30mmHg when supine

- 90% of positive-test patients have the cardio-inhibitory or combined response, while only 10% have the vaso-depressor response

- up to 10% of elderly patients have carotid sinus hypersensitivity to some degree, however only < 5 - 20% of these patients have carotid sinus syndrome (carotid sinus syncope etiologically related to carotid artery hypersensitivity)

- carotid sinus syncope can only be definitively diagnosed when syncope or near-syncope occurs during carotid massage

(* carotid sinus massage is contra-indicated in patients with a history of a CVA, a recent AMI or when a neck bruit is present

Orthostatic vital signs

- the patient should be recumbent for at least 5 minutes prior to performing the test and the patient should stand for at least 2 minutes

- a positive test is defined as a systolic blood pressure decrease of > 20 - 30mmHg, a diastolic decrease of >10 - 15mmHg and/or heart rate increase of greater than 30 bpm when standing

- the test is non-dependable, often inconsistent and has a low specificity

- a significant drop in blood pressure + fixed heart rate suggests dysautonomia

- a significant drop in blood pressure + increased heart rate suggests volume depletion and/or excessive vasodilatation

- an insignificant drop in blood pressure + marked increase in heart rate suggests postural tachycardia syndrome, which is a heterogenous entity (history of frequent fainting, symptoms of autonomic overactivity - palpitations, diaphoresis, tremulousness, visual blurring, non-anginal chest pain, "spaced-out" feelings, inability to concentrate, inability to breathe, sensations of impending doom)

Echocardiography

- diagnostic yield low in the absence of historical or physical signs of organic heart disease

- only definitely indicated in patients with exertion-related syncope, in all patients who have a prosthetic heart valve, or when the clinical suspicion of organic heart disease is high (eg. strong clinical suspicion of obstructive cardiac lesions - HOCM, AS or atrial myxoma)

-some conservative physicians believe that organic heart disease cannot be fully excluded prior to performing echocardiography (unsuspected findings are found in 5 - 10% of unselected patients) and that echocardiograph should routinely be performed in all patients, or definitely in patients > 50 years

Exercise-stress testing

- indicated for patients with exertion-related syncope or suspected CAD

- should always be preceded by echocardiography to first rule-out cardiac obstructive pathology eg. HOCM, aortic stenosis, atrial myxoma

Signal-averaged electrocardiography

- not usually helpful with many false-positives

- may be useful in selecting patients for electrophysiological studies when CAD is present and secondary VT suspected

Intracardiac electrophysiologic studies

- expensive, invasive and with low yield

- not indicated in patients with clinically normal hearts and a normal ECG

- most useful in patients with known organic heart disease (patients with a history of a MI or CHF - especially if the ejection fraction < 40%) and/or an abnormal ECG

- usefulness is mainly based on the ability of EPS testing to induce malignant arrhythmias eg. sustained monomorphic ventricular tachycardia

- induction of non-sustained VT, polymorphic VT and VF during testing is of no/uncertain clinical usefulness

- less useful for detecting bradyarrhythmias

- sinus node recovery time > 3 seconds may reflect sinus node disease requiring a pacemaker

- an HV interval exceeding 100 msec or infranodal block induced by pacing suggest AV nodal disease and a bradycarrhythmic cause of the syncope

Neurological testing - EEG, CT scan, transcranial/carotid Dopplers

- not indicated unless there is substantial reason to suspect a seizure or other significant neuropathology
Medical decision-making

An overriding concern and uncertainty about what may happen to the patient in the near future may cause an emergency physician to unnecessarily admit too many patients

Patients who can clearly be discharged include those with a classical presentation of vasovagal syncope (irrespective of age), those with situational syncope, those with mild, reversible orthostatic syncope (including polypharmacy syndrome in the elderly patient) and patients with hysterical conversion syncope

Indications for admission of patients presenting with syncope include:

ACEP task force recommendations for admission include:

Admit patients with syncope and any of the following:

1. A history of congestive heart failure or ventricular arrhythmias
2. Associated chest pain or other symptoms compatible with acute coronary syndrome
3. Evidence of significant congestive heart failure or valvular heart disease on physical
    examination
4. ECG findings of ischemia, arrhythmia, prolonged QT interval, or bundle branch block

Consider admission for patients with syncope and any of the following:

1. Age older than 60 years
2. History of coronary artery disease or congenital heart disease
3. Family history of unexpected sudden death
4. Exertional syncope in younger patients without an obvious benign etiology for the
    syncope

24-hour Holter (continuous ambulatory electrocardiographic) monitoring

- traditional approach to syncope of unknown etiology with low yield

- 4% true positives (symptoms correlate with arrhythmia) and 15% false positives (symptoms without any arrhythmia); 14% of patients have an asymptomatic arrhythmia which may suggest a cause for the syncope (sinus pauses, non-sustained VT, Mobitz type II block)

- extending the continuous ambulatory electrocardiograhic monitoring to 72 hours results in a slightly higher yield

- if no symptoms/arrhythmias are detected, arrhythmogenic syncope cannot be excluded => further testing is required for patients with recurrent syncope, or if there is a strong clinical suspicion of malignant cardiac arrythmias eg. known severe structural heart disease +/- history of recurrent palpitations

Long-term event and memory loop recorders

- provide continuous ambulatory electrocardiographic recordings for prolonged periods (weeks)

- useful for patients who have recurrent syncope (> 1x/4 weeks)

Implantable loop recoders

- latest development based on a loop-based memory system capable of providing continuous ambulatory electrocardiographic recording for up to 18 months

- indicated for patients with recurrent syncope with no definite organic heart disease

Tilt table testing

- used to confirm neurocardiogenic syncope in a patient, who does not have a classical history of vaso-vagal (vasodepressor) syncope; has also been useful in diagnosing neurally-mediated syncope, which manifests as post-exertional syncope

- used to investigate recurrent syncope in elderly patients with probable autonomic neuropathy

- some cardiologists reserve tilt testing for patients with unexplained, recurrent syncope in whom cardiac causes of syncope, including arrhythmias, have been excluded by echocardiography and Holter monitoring and EPS
testing

- can also be used to differentiate convulsive syncope from true seizures

Psychiatric evaluation

- may be indicated in young patients who faint frequently for no apparent reason, especially when symptoms are suggestive of postural tachycardia syndrome
Appendix


Causes of syncope
 Vasomotor/vascular

 Hypovolemia 

  • dehydration
  • fluid loss
  • "third" spacing
  • osmotic/iatrogenic diuresis
 Hemorrhage 
  • ruptured abdominal aortic aneurysm
  • ectopic pregnancy
  • GIT bleeding
  • trauma-induced
 Vasomotor insufficiency 

 Postural orthostasis 

 Vasodepressor (vaso-vagal) syncope 

 Glossopharyngeal neuralgia 

 Trigeminal neuralgia 

 Autonomic/peripheral neuropathy 

 Subclavian steal syndrome 

 Anaphylactic shock 

 Cardiac

 Dysrhythmias 

  • tachyarrhythmias
  • bradyarrhythmias
 Carotid sinus hypersensitivity 

 Pacemaker malfunction 

 Myocardial ischemia 

 Dissection of the aorta 

 Mechanical outflow obstruction or 
 venous return impedance 

  • aortic stenosis
  • hypertrophic obstructive cardiomyopathy
  • pulmonary stenosis
  • pulmonary embolus
  • primary pulmonary hypertension
  • atrial myxoma
  • prosthetic valve malfunction/thrombosis
  • pericardial tamponade
  • tricuspid stenosis
  • mitral stenosis
  • retrictive cardiomyopathy
  • tension pneumothorax
 Congenital heart disease 
  • anomalous origin of the left coronary artery
  • Eisenmenger's syndrome
  • Tetralogy of Fallot
  Situational
  • cough (post-tussive) 
  • micturition 
  • defecation 
  • swallowing 
  • postprandial 
  • weight-lifters 
  • adolescent stretch 
  • hair grooming
  • trumpet player's
 Metabolic
  • "hypoglycemia"
  • addisonian crises
  • pheochromocytoma
  • hypothyroidism
 Central nervous system
  • subarachnoid hemorrhage
  • "seizures"
  • basilar migraine
  • posterior circulation TIA's
  • vertebral artery dissection
  • carotid artery dissection
 Miscellaneous
  • air embolism
  • amniotic fluid embolism
  • foreign body embolism
  • asphyxia/hypoxia
  • carbon monoxide poisoning
  • breath-holding attacks
  • hyperventilation syndrome
  • conversion disorder
  • pro-arrhythmic drugs
  • polypharmacy
  • "glue sniffing or huffing"
  • postural tachycardia syndrome

Differentiating syncope from seizure
Feature Syncope Seizure
Aura Absent Rarely present
Antecedent "dizziness-prodrome" prior to event Sometimes present Absent
Color at onset of event Sometimes pale Sometimes florid/purple
Jerking movements Infrequent and short-lived (seconds) Common and longer-lasting (minutes)
Pattern of convulsions Uncoordinated myoclonic jerks and twitches - after LOC Generalized tonic and/or clonic movements - coincident with LOC
Upturning of eyes Common Uncommon
Forced conjugate deviation of eyes Absent Common
Tongue biting - lateral Absent Common
Urinary incontinence Rare Common
Duration of event Seconds Minutes
Prolonged disorientation or sleepiness after event Absent-rare Present-common
Increase in CK enzyme or lactate Absent Present

Suggested algorithm for workup of syncope

Disclaimer : My EM guidemaps reflect my personal approach to problem-solving/managing clinical cases in an ED setting and they should not be regarded as the standard of care. They merely represent the personal opinions of the author and they should only be used in clinical practice if the reader-user has substantial reason to believe that the clinical advice contained in the guidemaps is valid and accurate. The guidemaps are not meant to be "authoritative" and the reader-user should consult standard medical textbooks and expert opinion articles/guidelines for more authoritative advice. The reader-user should particularly confirm all drug doses, their indications and contra-indications, prior to their use.