Syncope resident survival guide

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Karol Gema Hernandez, M.D. [2]; Alejandro Lemor, M.D. [3]

Syncope Resident Survival Guide Microchapters
Overview
Causes
Classification
Diagnosis
Treatment
Do's
Don'ts

Overview

Syncope is the transient loss of consciousness (LOC) due to cerebral hypoperfusion and it is characterized by a rapid onset, a short duration and a spontaneous complete recovery. It is important to identify the cause of the syncope and recognize high risk patients (those with structural heart disease or abnormal EKG). The initial management depends on the etiology of the syncope (reflex, orthostatic hypotension or cardiovascular).

Causes

Life Threatening Causes

Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated.

• Hemorrhage
• Hypotension
• Hypoxia
• Ruptured abdominal aortic aneurysm
• Ventricular arrhythmia

Common Causes

• Aortic stenosis
• Arrhythmia
• Medications (vasodilators, diuretics, antiarrhythmics, antipsychotics)
• Orthostatic hypotension
• Vagal stimulation
• Vertebrobasilar insufficiency

Classification

Syncope is classified based on the pathophysiology of the etiology.

Cardiovascular syncope

❑ Arrhythmias (bradycardia or tachycardia)
❑ Structural heart disease
❑ Drug-induced arrhythmyas

Orthostatic hypotension

❑ Primary autonomic failure (pure autonomic failure, Parkinson's disease)
❑ Secondary autonomic failure (diabetes, uremia)
❑ Drug-induced (alcohol, vasodilators, diuretics)
❑ Hypovolemia (hemorrhage, diarrhea)

Reflex syncope

❑ Vasovagal
❑ Situational (cough, sneeze, postprandial, post-exercise)
❑ Carotid sinus hypersensitivity

Diagnosis

Diagnostic Algorithm in Patients with Suspected Syncope

Shown below is an algorithm summarizing the diagnostic approach to syncope based on the 2009 ESC Guidelines for the Diagnosis and Management of Syncope.

Abbreviations: TIA: Transient ischemic attack; EEG: Electroencephalography; HF: Heart failure; AF: Atrial fibrillation; SVT: Supraventricular tachycardia; VT: Ventricular tachycardia; MI: Myocardial infarction; BBB: Bundle branch block; SCD: Sudden cardiac death; CAD: Coronary artery disease; ARVC: Arrhythmogenic right ventricular cardiomyopathy.

Characterize symptoms ❑ Loss of consciousness (LOC) ❑ Rapid or slow onset ❑ Short or long duration ❑ Spontaneous complete recovery or incomplete recovery ❑ Prodrome: ❑ Diaphoresis ❑ Nausea ❑ Lightheadedness ❑ Pallor ❑ Warmth ❑ Blurry vision ❑ Chest pain (suggestive of cardiovascular syncope) ❑ Palpitations ❑ Position prior to LOC: ❑ Supine (suggestive of cardiovascular syncope) ❑ Supine to erect posture (suggestive of orthostatic hypotension or reflex syncope) ❑ Prolonged standing (suggestive of reflex syncope) ❑ Activity prior to LOC: ❑ Driving ❑ Machine operation ❑ Flying ❑ Competitive athletics (suggestive of cardiovascular or reflex syncope) ❑ Bowel or bladder incontinence (suggestive of reflex syncope)

Inquire about medications intake: ❑ Nitrates ❑ Diuretics ❑ Antiarrhythmic ❑ Alpha blocker ❑ Beta blocker ❑ ACE inhibitors or ARB ❑ Hydralazine ❑ Ethanol ❑ Benzodiazepines ❑ Antipsychotics ❑ Tricyclic antidepressants ❑ Barbiturates

Obtain a detailed past medical history: ❑ Previously healthy ❑ Previous syncope episodes ❑ Time since previous episode ❑ Number of previous episodes ❑ Cardiovascular disease: ❑ Arrhythmia ❑ Heart block (LBBB, RBBB) ❑ Valvular heart disease ❑ Heart failure ❑ Hypertrophic cardiomyopathy ❑ Cardiac tumor ❑ Neurological diseases: ❑ Parkinson's disease ❑ Diabetic neuropathy ❑ Metabolic disorders (diabetes) ❑ Recent trauma

Identify possible triggers: Suggestive of reflex syncope ❑ Emotional stress ❑ Crowded places (agoraphobia) ❑ Warm weather ❑ Prolonged standing ❑ Cough ❑ Micturition ❑ Defecation ❑ Swallowing ❑ Head motion ❑ Arm motion ❑ Shaving Suggestive of cardiovascular or orthostatic hypotension ❑ Trauma ❑ Change in position ❑ Fatigue ❑ Exertion

Examine the patient Vitals ❑ Heart rate ❑ Irregular rhythm (suggestive of AF) ❑ Tachycardia (suggestive of orthostatic hypotension, cardiovascular or reflex syncope) ❑ Bradycardia (suggestive of cardiovascular syncope) ❑ Blood pressure: ❑ Measure in both arms, while standing and supine ❑ Orthostatic hypotension (Fall in systolic BP ≥ 20 mmHg and/or in diastolic BP of at least≥ 10 mmHg between the supine and sitting BP reading) ❑ Hypertension (suggestive of cardiovascular syncope) ❑ Respiratory rate ❑ Tachypnea (suggestive of reflex syncope) Respiratory ❑ Rales (suggestive of HF) Cardiovascular ❑ Palpitations (suggestive of arrhythmia) ❑ Carotid bruits (suggestive of cardiovascular syncope) ❑ Murmurs: ❑ Aortic stenosis: crescendo-decrecendo systolic ejection murmur best heard at the upper right sternal border ❑ Pulmonary stenosis: systolic ejection murmur best heard at the left second intercostal space ❑ Heart sounds ❑ Loud P2 (suggestive of pulmonary hypertension) Neurologic ❑ Focal abnormalities (suggestive of stroke or cerebral mass) ❑ Hemiparesis ❑ Vision loss ❑ Aphasia ❑ Hypertonia ❑ Glasgow coma scale ❑ Signs suggestive of Parkinson's disease: ❑ Tremor ❑ Rigidity ❑ Bradykinesia/Akinesia ❑ Postural instability ❑ Shuffling gait

Order labs and tests ❑ EKG (most important initial test) ❑ Myocardial infarction ❑ Tachyarrhythmia ❑ Heart block ❑ Bradyarrhythmia ❑ Long or short QT ❑ Bradyarrhythmia ❑ Electrolytes ❑ Hyponatremia ❑ Hypernatremia ❑ Hypokalemia ❑ Glucose (rule out hypoglycemia) ❑ ABG ❑ Hypoxia ❑ Hypocapnea (suggestive of tachypnea, rule out psychiatric disease)

Order imaging studies ❑ Echocardiography in case of: ❑ Structural heart disease ❑ Myocardial infarction ❑ Cardiac valve disease ❑ Head CT in case of: ❑ Head trauma ❑ TIA

Confirm diagnosis of syncope Must have this 3 characteristics: ❑ Short duration ❑ Rapid onset ❑ Complete spontaneous recovery

Syncope

Non-syncopal LOC

Known etiology

Unknown etiology

Consider additional tests ❑ Stool guaiac test (rule out GI bleeding) ❑ Blood and urine toxicology tests (rule out intoxication)

Diagnostic criteria ❑ Cardiovascular ❑ Arrhythmia and cardiac ischemia-related syncope is diagnosed by EKG specific findings (Class I; Level of Evidence: C) ❑ Cardiovascular syncope is diagnosed when syncope presents with structural heart disease (Class I; Level of Evidence: C) ❑ Orthostatic hypotension (OH) ❑ Diagnosed when syncope occurs after standing up and there is documentation of OH. (Class I; Level of Evidence: C) ❑ Reflex ❑ Vasovagal syncope: if is precipitated by emotional distress and is associated with typical prodome. (Class I; Level of Evidence: C) ❑ Situational syncope: if occurs during or after specific triggers. (Class I; Level of Evidence: C)

Risk stratification Determine if there are any high risk criteria: ❑ Severe structural heart disease ❑ CAD ❑ 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 ❑ Conduction abnormalities with QRS >120 ms ❑ Sinus bradycardia ❑ Pre-excited QRS complex ❑ Long or short QT ❑ Brugada pattern ❑ ARVC ❑ Important comorbidities: ❑ Severe anemia ❑ Electrolyte disturbance

Rule out other possible diagnoses: ❑ With loss of consciousness: ❑ Coma (Glasgow coma scale < 8, profound state of unconsciousness) ❑ Sudden cardiac arrest (absence of pulse) ❑ Epilepsy (inquire past medical history) ❑ Findings: aura, prolonged confusion, muscle ache, ❑ Perform neurological evaluation (Class I; Level of Evidence: C) ❑ Perform tilt testing (Class IIb; Level of Evidence: C) , preferably with concurrent EEG and video monitoring if doubt of mimicking epilepsy ❑ Intoxication ❑ Vertebrobasilar TIA ❑ Without loss of consciousness: ❑ Cataplexy ❑ Drop attacks ❑ Functional /psychogenic pseudosyncope ❑ Perform a psychiatric evaluation (Class I; Level of Evidence: C). ❑ TIA of carotid origin

High risk

Low risk

❑ Immediate in-hospital monitoring (in bed or telemetry) to look for abnormalities suggestive of arrhythmic syncope (Class I; Level of Evidence: B).

Recurrent syncopes Cardiac or neurally mediated tests as appropriate: ❑ Holter if > 1 episode/week (Class I; Level of Evidence: B). ❑ External loop recorder (ELR) if interval between episodes < 4 weeks (Class IIa; Level of Evidence: B).

Single syncope

If suspicion of structural heart disease: ❑ Order an echocardiography (Class I; Level of Evidence: B).

Was it in high risk setting? ❑ Potential risk of physical injury ❑ Occupational implications

If yes: Treat as according

No structural heart disease

Yes

No: No further evaluation

Do a tilt test (Class I; Level of Evidence: B).

Diagnostic criteria ❑ Induction of reflex hypotension or bradycardia with reproduction of syncope is diagnostic for reflex syncope (Class I; Level of Evidence: B). ❑ Induction of progressive orthostatic hypotension with or without symptoms is diagnostic for orthostatic hypotension (Class I; Level of Evidence: B).

Treatment

Therapeutic Algorithm in Patients with Confirmed Syncope

Shown below is an algorithm summarizing the therapeutic approach to syncope based on the 2009 ESC Guidelines for the Diagnosis and Management of Syncope.

Abbreviations: AF: Atrial fibrillation; SVT: Supraventricular tachycardia; VT: Ventricular tachycardia; MI: Myocardial infarction; BBB: Bundle branch block.

Determine the etiology

Cardiovascular syncope ❑ Presence of definitive structural hearth disease ❑ Aortic stenosis ❑ Acute myocardial infarction ❑ Hypertrophic cardiomyopathy ❑ Pericardial disease ❑ Cardiac tumors ❑ Family history of unexplained sudden death ❑ Occurred during exertion or supine ❑ Abnormal EKG ❑ Sudden onset of palpitations before syncope Abnormal EKG findings ❑ Mobitz I second degree AV block ❑ Non-sustained VT ❑ Premature QRS complexes ❑ Wide QRS(≥ 0.12 s) ❑ Long or short QT intervals ❑ Early repolarization ❑ Q waves (myocardial infarction) ❑ Bifascicular block

Orthostatic hypotension ❑ After standing up or prolonged standing ❑ Start of new antihypertensive drug or dosage change ❑ Presence of autonomic neuropathy ❑ Prolonged standing ❑ Associated with crowd or hot spaces

Reflex Syncope ❑ Absence of heart disease ❑ History of recurrent syncope ❑ After unpleasant sight, smell, sound or pain ❑ Associated to nausea or vomit ❑ Prolonged standing ❑ Associated with crowd or hot spaces ❑ Head rotation or pressure to carotid sinus ❑ After exertion ❑ Postprandial

Depends on the cause of the arrhythmia: ❑ Schedule for cardiac pacing surgery in patients with: ❑ Sinus node disease (Class I; Level of Evidence: C) ❑ Mobitz II AV block or complete AV block (Class I; Level of Evidence: B) ❑ BBB with positive electrophysiological study (Class I; Level of Evidence: B) ❑ Schedule for catheter ablation in patients with: ❑ SVT (Class I; Level of Evidence: C) ❑ VT (Class I; Level of Evidence: C) In absence of structural hearth disease ❑ Administer antiarrhythmic drug therapy in patients with: ❑ AF (Class IIa; Level of Evidence: C) ❑ Failed catheter ablation (Class I; Level of Evidence: C) ❑ Schedule for implantable cardioverter defibrillator surgery in patients with: ❑ VT with heart disease (Class I; Level of Evidence: B) ❑ Electrophysiological study induced VT with previous MI (Class I; Level of Evidence: B) ❑ VT with inherited cardiomyopathy or channelopathy (Class IIa; Level of Evidence: B)

❑ Adequate hydration and salt intake (Class I; Level of Evidence: C) ❑ Adjunctive therapy if needed: ❑ Administer midodrine 10 mg PO q8hr (Class IIa; Level of Evidence: B) Contraindicated in severe heart disease, acute renal failure, pheochromocytoma, severe hypertension or thyrotoxicosis ❑ or fludrocortisone 0.1 mg/day PO (Class IIa; Level of Evidence: C) ❑ Isometric physical counterpressure maneuvers (PCM) may be indicated (Class IIb; Level of Evidence: C) ❑ Head-up tilt sleeping (>10 °) to increase fluid volume may be indicated (Class IIb; Level of Evidence: C)

❑ Explain diagnosis and provide reassurance (Class I; Level of Evidence: C) ❑ Explain risk of recurrence and avoidance of triggers (Class I; Level of Evidence: C) ❑ Isometric physical counterpressure maneuvers (PCM) in patients with prodrome(Class I; Level of Evidence: B): ❑ Hand grip and arm tensing ❑ Leg crossing ❑ Cardiac pacing should be considered in: ❑ Dominant cardioinhibitory carotid sinus syndrome (Class IIa; Level of Evidence: B) ❑ Recurrent reflex syncope, age >40 years and spontaneous cardioinhibitory response during monitoring (Class IIa; Level of Evidence: B)

Do's

• Tilt testing should be considered to discriminate between reflex syncope and OH (Class IIa; Level of Evidence: C).
• Perform tilt testing if the cause of syncope is a psychiatric disease (Class IIb; Level of Evidence: C).
• Tilt testing may be considered for differentiating syncope with jerking movements from epilepsy (Class IIb; Level of Evidence: C).
• If syncope happened after standing up position, there should be documentation with active standing or tilt testing in order to diagnose orthostatic hypotension.
• Perform carotid sinus massage if patient >40 years with syncope of unknown etiology after initial evaluation (Class I; Level of Evidence: B)..
• If multiple unexplained falls; perform tilt testing.
• Consider implantable loop recorder before embarking on cardiac pacing in patients with suspected or confirmed reflex syncope presenting with frequent or traumatic syncopal episodes.
• Evaluate neurologically if syncope is due to autonomic failure, to evaluate underlying disease.

Don'ts

• Don't perform carotid sinus massage in patients with previous TIA or stroke within the past 3 months and in patients with carotid sinus bruits (except if carotid sinus Doppler studies excluded significant stenosis).
• Don't use tilt testing for assessment of treatment.
• Don't perform isoproterenol tilt test in patients with ischemic heart disease.
• Don't use adenosine stress test as a diagnostic test to select patients for cardiac pacing, owing to lack of correlation with spontaneous syncope.
• Don't perform electrophysiologic study if there is already indication for implantable cardioverter defibrillator in patients with ischemic heart with suspected arrhythmic cause.
• Don't perform electrophysiologic study in patients with normal EKG, no heart disease, and no palpitations.

References

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