CONTENTS

• Definitions
• Common causes & mimics
  • [1] Cardiac syncope
  • [2] Orthostatic hypotension
  • [3] Neurally mediated reflex 
  • [4] Syncope mimics
• Syncope evaluation:
  • [1] History
    • General syncope history
    • High-risk features
  • [2] Bedside syncope evaluation
    • Physical examination
    • POCUS
    • ECG
  • [3] Advanced testing
• Management of common syncope syndromes
• Pathophysiology

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definitions

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• Definitions of syncope:
  • Clinical definition: Transient, non-traumatic loss of consciousness with loss of postural tone, followed by spontaneous complete recovery.
  • Pathophysiologic definition: Transient loss of consciousness due to globally reduced cerebral perfusion.
• Presyncope is lightheadedness due to reduced cerebral perfusion (without loss of consciousness).
• Transient loss of consciousness (TLCO) – a broader category of events that includes non-syncope etiologies (e.g., seizure).

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common causes & mimics of syncope

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[1/4] cardiac syncope (~5-10%; primary concern)

bradyarrhythmia

• AV block (2nd or 3rd degree block).
• Sick sinus syndrome.
• Pacemaker malfunction (e.g., lead malfunction, R-on-T due to failure to sense, battery depletion). (Gaggin 2021)
• Negative chronotropic medication.

tachyarrhythmia

• Ventricular tachycardia/fibrillation, e.g.:
  • Torsade de pointes.
  • Prior myocardial infarction.
  • Myocarditis.
  • Various cardiomyopathies.
• Supraventricular tachycardia (e.g., atrial fibrillation or AV node reentry tachycardia). To cause syncope, there usually must be another underlying cardiac disorder.
• Wolff Parkinson White syndrome (may cause syncope without an additional cardiovascular disorder).

flow-limiting lesions (often cause exertional syncope)

• Pulmonary hypertension:
  • Acute PE.
  • Chronic pulmonary hypertension.
• Aortic stenosis (syncope may reflect aortic stenosis itself, reflex vasodilation, or primary cardiac arrhythmia). (Griffin 2022)
• Mitral stenosis.
• Myxoma.
• Prosthetic valve thrombosis/dysfunction.
• Hypertrophic cardiomyopathy.

shock of any etiology (no physiologic reserve; any hemodynamic perturbation may precipitate syncope)

• Gastrointestinal hemorrhage.
• Hypovolemic shock.
• Pericardial tamponade.
• Tension pneumothorax.

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[2/4] orthostatic hypotension

underlying autonomic dysfunction

• Primary autonomic dysfunction:
  • Primary autonomic dysfunction (Bradbury-Eggleston syndrome).
  • Multiple system atrophy (Shy-Drager syndrome).
  • Familial dysautonomia (Riley-Day syndrome).
  • POTS (paroxysmal orthostatic tachycardia syndrome; exam shows severe orthostasis with marked tachycardia). (37983697)
• Secondary autonomic dysfunction:
  • Parkinson disease, Lewy body dementia.
  • Diabetes.
  • Amyloidosis.
  • Multiple sclerosis.
  • Spinal tumors, spinal cord injury.
  • Chronic kidney disease.
  • Paraneoplastic autonomic neuropathy.
  • Advanced age.

exacerbating factors

• Hypovolemia (e.g., diuretics).
• Anemia.
• Medications:
  • Vasodilators: nitrates, alpha-blockers.
  • Sympatholytics (e.g., clonidine).
  • Other antihypertensives. (Sadhu 2023)
• Negative inotropes.
• Alcohol.
• Anticholinergic medications (e.g., tricyclic antidepressants).

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[3/4] neurogenic (reflex) syncope

vasovagal syncope (aka neurocardiogenic syncope)

• Triggers:
  • Prolonged standing (especially in warm environments).
  • Emotional stressors (e.g., sight of blood, fear).
  • Pain.

situational syncope

• Stimulation of the esophagus, lung, rectum, or bladder, e.g.:
  • Micturition.
  • Defecation.
  • Cough.
  • Swallowing.
  • Nausea/vomiting.
  • Insertion of a rectal tube, foley catheter, etc.
• Valsalva maneuver (e.g., weightlifting).

carotid sinus syncope

• Triggered by stimulation of the carotid sinus, e.g.:
  • Shaving, tight collar.
  • Sudden head turn.
• Risk factors:
  • It usually occurs in patients >40 years old.
  • History of neck surgery or radiation. (37983697)
• Evaluate with a carotid sinus massage (discussed further below: ⚡️).

neuralgia

• Trigeminal neuralgia.
• Glossopharyngeal neuralgia.

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[4/4] syncope mimics 

seizure vs. syncope

• Preceding symptoms?
  • Aura suggests seizure (e.g., smell, taste, or rising sensation).
  • Lightheadedness, palpitations, or other features of syncope suggest syncope.
• Features of the event?
  • Eye deviation can be present in either:
    • Seizure: lateral conjugate deviation is common.
    • Syncope: upward gaze is common.
  • Skin color:
    • Pallor is consistent with syncope.
    • Cyanosis is common in seizures.
  • Duration of movements:
    • Syncope: often brief, a few seconds, and fewer movements (<10 jerks). Syncope often causes brief tonic posturing and a few myoclonic jerks.
    • Seizure: may be prolonged over minutes.
  • Duration of LOC:
    • Syncope: often brief, seconds.
    • Seizure: may be longer, up to minutes.
  • Timing:
    • Syncope: LOC first, movements after LOC.
    • Seizure: Jerking precedes or coincides with LOC.
• Evaluation afterward:
  • Tongue biting:
    • Syncope: tongue biting is rare; it may involve the tip of the tongue.
    • Seizure: tongue biting is common; it may involve the lateral side of the tongue (likelihood ratio of +8). (38892942)
  • Recovery:
    • Syncope: rapid recovery without neurologic sequelae.
    • Seizure: slow recovery, may take hours. Focal neurologic deficits can persist (Todd paralysis). (37983697, 38892942)

other neurologic mimics

• Subclavian steal syndrome.
• Migraine.
• Vertebrobasilar transient ischemic attack (should have additional features such as vertigo, diplopia, visual field disturbance, hemifacial numbness, dysarthria, and ataxia).

hyperventilation syncope

• Hyperventilation causes reduced CO2 levels and cerebral vasoconstriction.
• Suggested by: young age (20-40 years old), frequent spells, additional symptoms related to hypocarbia (e.g., vertigo, numbness, reproducible syncope may occur due to hyperventilation).

other syncope mimics

• Cataplexy (loss of muscular tone associated with emotion/laughter).
• Functional syncope.
• Malingering.

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syncope history

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general syncope history

[1/7] preceding events & situation

• General context:
  • ? Ongoing symptoms (e.g., dyspnea).
  • ? New medication initiation.
  • ? Acute illness, dehydration.
  • ? Bleeding.
  • ? Trauma.
• ? Vasovagal stimuli (e.g., pain, anxiety, prolonged standing).
• ? Situational stimuli (e.g., cough, micturition, defecation, gastrointestinal/urinary procedure).
• ? Head turning, shaving, neck massage (carotid sinus syndrome).
• ? Arm exercise and/or elevation (subclavian steal).
• ? Exertional (suggest cardiac etiology, especially flow-limiting lesions, catecholamine-induced arrhythmia, left main coronary artery stenosis).
• ? Syncope in a lying position excludes orthostatic hypotension and suggests cardiac etiology.
• ? Syncope after standing up suggests orthostatic hypotension or cardiac etiology.

[2/7] prodromal symptoms

• ? Neurologic:
  • Headache, smells, aura, confusion – suggest seizure.
  • Vertigo, dysarthria, diplopia – suggest transient ischemic attack.
• ? Vasovagal (nausea, lightheadedness, sweating, flushing, pallor, blurry vision). (Griffin 2022)
• ? Orthostatic (prodromal symptoms may include dizziness, palpitations, sweating, and hearing or vision disturbance). (Griffin 2022)
• ? Presyncope (lightheadedness, dimming of vision, tunnel vision, and tinnitus may occur) indicates cardiovascular etiology rather than neurologic.
• ? Cardiovascular symptoms (palpitations, chest pain, dyspnea).
• ? Throat or facial pain (glossopharyngeal or trigeminal neuralgia).
• ? Absolutely none (suggests seizure or arrhythmia).

[3/7] description of the event by bystanders

• ? Pallor (cardiovascular).
• ? Seizure-like activity (tongue-biting, incontinence, head-turning, motor activity >30 seconds).
  • Syncope can often be associated with seizure-like activity. This differentiation is discussed above.
• ? Trauma:
  • Trauma may require additional trauma evaluation (e.g., CT head).
  • Significant trauma suggests cardiac etiology (e.g., malignant arrhythmia).

[4/7] symptoms following event

• ? Immediately well (suggests orthostatic hypotension).
• ? Vasovagal (immediately regain normal consciousness, but have ongoing malaise, nausea, and lightheadedness).
• ? Seizure (confusion >5 minutes, may have focal neurologic signs).
• ? Persistent palpitations, feeling unwell (may reflect ongoing arrhythmia).

[5/7] syncope pattern

• Repeated syncopal events may occur with benign or malignant etiologies.
• >4 years of syncopal episodes suggests a lower risk. (37983697)

[6/7] past medical history, especially:

• ? Prior episodes of syncope.
  • Frequent episodes over several years may be somewhat reassuring (suggestive of vasovagal, orthostatic, or situational syncope).
• ? Cardiac disease.
• ? Neurologic disease.
• ? Medications (especially recently initiated).
• ? Illicit substance use.

[7/7] family history, especially:

• ? Sudden death, cardiomyopathy, or arrhythmia syndrome (e.g., Long QT syndrome, Wolff Parkinson White syndrome).
• ? Other heart disease.

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high-risk features of syncope (including some non-history elements) 

High-risk features are indicators of cardiac syncope. This is included here because most of these relate to the syncope history and they are essential elements to evaluate: 

• Age >40-60 years old.
• Family history of sudden cardiac death.
• Known structural heart disease (e.g., coronary artery disease, cardiomyopathy, valvular disease).
• History of serious arrhythmia (including patients with a permanent pacemaker or ICD).
• Syncopy history is consistent with cardiovascular etiology:
  • Lack of prodrome.
  • Syncope while exertional, supine, or driving. (Sadhu 2023)
    • Exertional syncope should be evaluated with an exercise stress test if other investigations are unrevealing (e.g., CBC and echocardiography). (37983697)
  • Resultant trauma.
  • Palpitations at the time of syncope.
  • Complaint of chest pain and/or dyspnea.
• Abnormal vital signs and/or physical examination.
• ECG suggests conduction abnormality, arrhythmia, or ischemia.

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bedside syncope evaluation

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physical examination

vital signs & challenges

• Shock index (HR/SBP) > ~0.8 suggests shock of any etiology.
• A blood pressure differential between arms may suggest subclavian stenosis or aortic dissection. (Gaggin 2021)
• Orthostatic vital signs: after 1 minute and after 3 minutes of standing:
  • Orthostatic hypotension is suggested by a >20 mm fall in systolic Bp with standing or >10 mm fall in diastolic blood pressure, especially if accompanied by symptoms of lightheadedness.
  • ⚠️ Orthostatic hypotension is common, with rates up to ~30% in patients >70 years old. Detecting orthostatic hypotension doesn't necessarily prove that the patient had orthostatic syncope, nor does it exclude cardiogenic syncope. (38892942)
  • POTS (postural orthostatic tachycardia syndrome) may be suggested if the heart rate increases by >30 b/m or the standing heart rate is >120 b/m without an alternative explanation.
• Carotid sinus massage?
  • ESC guidelines recommend carotid sinus massage for patients >40 years old with syncope of unknown origin compatible with a reflex mechanism. However, the net benefit of this diagnostic maneuver remains debatable. (38892942) 
  • If there is no history of stroke/TIA or carotid bruit, gently massage the right carotid artery carotid artery for 10 seconds at the anterior margin of the sternocleidomastoid muscle at the level of the cricoid cartilage. If this doesn't induce sinus pause >3 seconds or hypotension (fall in SBP by >50 mm), repeat on the other side. (Gaggin 2021) 

other findings of note 

• Cardiac auscultation for valvular lesions.
• Neurological examination (evaluation for signs of vertebrobasilar insufficiency such as diplopia, visual field disturbance, hemifacial numbness, and ataxia).
• Tongue laceration may support seizure.

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POCUS

• Right ventricular dilation: PE or pulmonary hypertension.
• Left ventricular dysfunction: Increased likelihood of malignant arrhythmias.
• Evaluate for volume status.
• Evaluate for aortic or mitral valve disease.
• Evaluate for pericardial effusion.

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syncope ECG

ECG is a fundamental diagnostic tool for the evaluation of syncope. Sometimes, ECG may identify an immediate diagnosis (e.g., bradyarrhythmia). In other instances, ECG may provide evidence of structural heart disease that assists with risk stratification.

* Indicates findings that have been associated with increased risk. Of course, this doesn't include all high-risk features (many of which may be too rare to statistically correlate with poor outcomes in clinical trials).

rhythm

• Non-sinus rhythm (e.g., atrial fibrillation).*
• Marked sinus bradycardia (<40 b/m) while awake.
• Sinus pause >3 seconds.
• Mobitz II or third-degree heart block.*
• Multiple PVCs.*
• Evidence of pacemaker malfunction.

intervals

• QT prolongation.*
• QRS prolongation:
  • LBBB.*
  • Bifascicular block.*
  • Alternating left and right bundle branch blocks.
  • Intraventricular conduction delay.*
• Short PR interval: Accessory pathway (Wolff Parkinson White syndrome).*

axis

• Left axis deviation.*

chambers

• Left ventricular hypertrophy.*

morphology

• Brugada pattern.
• Arrhythmogenic right ventricular cardiomyopathy (Epsilon wave, TWI in V1-V3, and ventricular late potentials).
• New ischemic changes.*
• Prior myocardial infarction.
• Evidence of PE or pulmonary hypertension (e.g., S-wave in lead I, TWI in right precordial leads). (Gaggin 2021)
• (Early repolarization doesn't seem to correlate with increased risk.) (34064050)

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advanced testing

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Advanced testing is not required for all patients with syncope. Instead, this should be obtained selectively (based on the history and bedside evaluation as described above).

laboratory studies

• Electrolytes, including magnesium (may increase the risk of arrhythmia).
• Complete blood count with differential:
  • Evaluate for anemia.
  • Elevated neutrophil/lymphocyte ratio may suggest an underlying illness causing physiologic stress.
• Therapeutic drug levels (e.g., digoxin).
• Pregnancy test as applicable.
• Troponin (only if EKG and/or clinical features suggest ischemia).
• D-dimer (only if history and examination suggest pulmonary embolism – see evaluation of PE here 📖).

pacemaker interrogation

• The device should be interrogated if the patient has a pacemaker or AICD.

formal echocardiogram

• Subtle wall motion abnormalities may function as a focus of malignant arrhythmia.
• A structurally normal heart is reassuring but doesn't exclude arrhythmia.

head CT scan

• This may be indicated for focal neurologic findings or a headstrike.

CT angiography to evaluate for PE

• All comers with syncope do not need a CT angiogram. This should be obtained only if features of the history and examination suggest PE.
• (Discussion of the appropriate approach to PE diagnosis: 📖)

ongoing observation of cardiac rhythm, which may include:

• Telemetry (in ED +/- hospital admission).
• Ambulatory Holter monitor:
  • Continuous 24-48 hours of monitoring.
  • It is more useful if there are frequent events (≧1 event/week).
• External patch monitor or external loop monitor.
  • More useful for infrequent events.

cardiac MRI

• Generally, CMRI has limited utility in the evaluation of syncope.
• Potential indications:
  • Evaluation for ARVC (arrhythmogenic right ventricular cardiomyopathy).
  • Evaluation for myocarditis.

exercise testing

• Indications:
  • It may be helpful in syncope during or after exertion.
  • Should be performed after echocardiography to exclude a flow-limiting lesion (e.g., aortic stenosis, hypertrophic cardiomyopathy, pulmonary hypertension).
• Potential findings could include:
  • Mobitz II or third-degree AV block during exercise.
  • Hypotension with exercise (may indicate left main coronary stenosis).
  • Catecholaminergic polymorphic ventricular tachycardia. (Gaggin 2021)

invasive electrophysiological (EP) study

• Indications:
  • Features of cardiac syncope in a patient with underlying cardiac disease or a concerning ECG (especially in the context of prior myocardial infarction).
  • EP testing is contraindicated for patients with a normal ECG and no heart disease or palpitations associated with syncope.
• Predictors of positive results from EP study:
  • Ejection fraction <40%.
  • ECG suggests conduction system disease (e.g., bundle branch block).
  • History of myocardial infarction.
  • History of nonsustained VT. (Griffin 2022)
• Positive results may include:
  • HV interval >100 ms (delay in conduction from the his bundle to the ventricle).
  • Inducible 2nd- or 3rd-degree AV block with atrial pacing.
  • Inducible sustained ventricular tachycardia >150 b/m
  • Inducible sustained supraventricular tachycardia >180 b/m. (Gaggin 2021)

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management of common syncope syndromes

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Management depends on the underlying etiology of syncope. Some basic management strategies for common syncope syndromes are below: 

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neurogenic (reflex) syncope 

• Maintain adequate volume status (e.g., possible benefit from fludrocortisone).
• Education:
  • Avoid triggers if possible.
  • Sit down immediately if feeling prodromal symptoms.
• Beta-blockers: Metoprolol may be helpful in patients >40 years old with frequent vasovagal syncope (beta-blockade may block the progression that begins with sympathetic overactivity, followed by vasodilation and syncope). (Griffin 2022)
• Pacemaker:
  • Vasovagal syncope: A pacemaker may be considered for patients with documented episodes of asystole (>3s during syncope or >6s without symptoms).
  • Carotid sinus syncope: pacemaker insertion may be reasonable for patients with documented asystole in response to carotid sinus stimulation.

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orthostatic syncope

• Advise patients to stand up gradually.
• Support stockings are safe and potentially beneficial.
• Discontinue medications that may exacerbate orthostatic syncope (e.g., diuretics, antihypertensives).
• Midodrine may be helpful.
• Maintain an adequate volume status (e.g., possible benefit from fludrocortisone and/or high-sodium diet).

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pathophysiology

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• Cessation of blood flow for 6-8 seconds causes loss of consciousness. (Griffin 2022)
• Syncope may be caused by a similar range of pathophysiologies as are responsible for shock.  These include:
  • Bradyarrhythmia.
  • Tachyarrhythmia (especially ventricular tachycardia).
  • Vasodilation with reduced systemic vascular resistance.
  • Fixed cardiac output that cannot increase during exercise (e.g., aortic stenosis, pulmonary hypertension).

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questions & discussion

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To keep this page small and fast, questions & discussion about this post can be found on another page here.

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