What is the management of syncope?

Management of Syncope

The management of syncope requires a structured, mechanism-based approach prioritizing risk stratification through detailed history and ECG, followed by targeted interventions addressing the specific underlying cause—whether cardiac arrhythmia requiring device therapy, orthostatic hypotension requiring volume expansion and vasopressors, or reflex syncope requiring education and physical counterpressure maneuvers. 1

Initial Risk Stratification and Evaluation

High-risk features requiring immediate attention and potential hospitalization include: 1, 2

• Older age (>60 years), male sex, and known structural heart disease 1, 2
• Syncope during exertion or in supine position 1, 2
• Brief or absent prodrome suggesting arrhythmic cause 1, 2
• Abnormal ECG findings (bifascicular block, significant conduction defects, QT prolongation, signs of ischemia) 1
• Family history of sudden cardiac death or inheritable cardiac conditions 1, 2
• Abnormal cardiac examination revealing murmurs, gallops, or signs of heart failure 1, 2

Low-risk features suggesting neurally mediated syncope and outpatient management: 2, 3

• Younger age without cardiac disease 2, 3
• Syncope only when standing with clear positional triggers 2, 3
• Recognizable prodromal symptoms (lightheadedness, nausea, diaphoresis) 2, 3
• Specific situational triggers (emotional stress, prolonged standing, hot environments) 2, 3

Diagnostic Workup Based on Clinical Presentation

Core Initial Assessment Components

All patients require: 1, 2, 3

• Detailed history focusing on position during event, activity at onset, prodromal symptoms, witness accounts, and recovery phase 2, 3
• Orthostatic blood pressure measurements in lying, sitting, and standing positions 2, 3
• 12-lead ECG to identify arrhythmias, conduction abnormalities, or structural disease 1, 2, 3
• Cardiovascular examination assessing for murmurs, gallops, rubs, and signs of structural heart disease 2, 3

Targeted laboratory testing only when clinically indicated: 2, 3

• Hematocrit if blood loss or anemia suspected 3
• Electrolytes and renal function if dehydration or metabolic cause suspected 3
• Cardiac biomarkers (BNP, troponin) only when cardiac cause suspected, not routinely 3

Advanced Testing for Suspected Cardiac Syncope

When structural heart disease or arrhythmia suspected: 1, 2

• Echocardiography for evaluation of structural abnormalities, valvular disease, or reduced ejection fraction 1, 2
• Prolonged ECG monitoring (Holter, event recorder, or implantable loop recorder) based on symptom frequency 1, 2
• Exercise stress testing for syncope during or after exertion 1, 2
• Electrophysiological studies in selected cases with suspected arrhythmic syncope 1, 2

Testing for Reflex and Orthostatic Syncope

When neurally mediated or orthostatic syncope suspected: 1, 2

• Tilt table testing for recurrent unexplained syncope in young patients without heart disease 1, 2
• Carotid sinus massage in patients over 40 years with recurrent syncope 1, 2
• Autonomic function testing when autonomic failure suspected 1

Important caveat: Brain imaging (CT/MRI), EEG, and carotid ultrasound are NOT recommended routinely for syncope evaluation without focal neurological findings, as diagnostic yield is extremely low (0.24-1%) 2, 3

Treatment Strategies by Mechanism

Reflex (Neurally Mediated) Syncope

First-line non-pharmacological interventions are most effective: 1, 4

• Patient education regarding benign prognosis, trigger avoidance, and recognition of prodromal symptoms 1, 4
• Physical counterpressure maneuvers (leg crossing, hand grip, arm tensing) reduce syncope recurrence by 39% when prodrome present 1, 4
• Increased fluid intake (2-2.5 liters daily) and salt supplementation to maintain intravascular volume 1, 4
• Avoidance of triggers (hot crowded environments, prolonged standing, emotional stress) 1, 4
• Compression garments (at least thigh-high) to reduce venous pooling 4

Pharmacological options for refractory cases: 1, 4, 5

• Midodrine (alpha-agonist) provides dose-dependent improvement in standing blood pressure, though supine hypertension must be monitored 4, 6
• Fludrocortisone (0.1-0.2 mg daily) increases plasma volume, though evidence is limited 1, 4, 7
• Beta-blockers are NOT recommended as evidence fails to support efficacy and may worsen cardioinhibitory responses 1

Cardiac pacing considerations: 1

• Reserved for cardioinhibitory or mixed carotid sinus syndrome 1
• May be considered for cardioinhibitory vasovagal syncope with >5 attacks per year, severe injury risk, and age >40 years 1
• Not indicated for purely vasodepressor syncope 1

Orthostatic Hypotension

Non-pharmacological management is cornerstone: 1, 4, 8

• Discontinuation or reduction of hypotensive medications (diuretics, vasodilators, alpha-blockers) 1, 4
• Increased fluid (2-2.5 liters daily) and salt intake 1, 4
• Head-up tilt sleeping (>10 degrees) to reduce nocturnal pressure natriuresis 1
• Abdominal binders and compression stockings to reduce gravitational pooling 1, 4
• Small frequent meals with reduced carbohydrate content to prevent postprandial hypotension 1, 5
• Physical counterpressure maneuvers and gradual position changes 1, 4

Pharmacological therapy for neurogenic orthostatic hypotension: 4, 6, 7

• Midodrine (starting 2.5-10 mg three times daily) is first-line vasopressor, with last dose 3-4 hours before bedtime to minimize supine hypertension 4, 6
• Droxidopa improves symptoms in Parkinson disease, pure autonomic failure, and multiple system atrophy 4
• Fludrocortisone (0.1-0.2 mg daily) increases plasma volume but requires monitoring for supine hypertension and hypokalemia 4, 7, 5
• Acute water ingestion (240-480 mL) provides temporary relief with peak effect at 30 minutes 4

Critical monitoring requirements: 6, 7

• Blood pressure monitoring for supine hypertension, especially with midodrine (avoid if supine BP persistently elevated) 6
• Serum potassium monitoring with fludrocortisone due to enhanced hypokalemia risk 7
• Renal function assessment before initiating midodrine, with starting dose of 2.5 mg in renal impairment 6

Cardiac Syncope

Treatment must address specific underlying cause: 1

• Arrhythmias require antiarrhythmic drugs, catheter ablation, pacemaker, or ICD implantation as appropriate 1
• Structural heart disease requires correction when possible (valve replacement, revascularization) 1
• Patients with cardiac syncope warrant urgent cardiology consultation and preferential access to interventions 1

Specialized Syncope Unit Approach

Structured care pathways improve outcomes and reduce hospitalizations: 1

• Cohesive multidisciplinary team with expertise in cardiology, neurology, emergency medicine, and geriatrics 1
• Core equipment includes ECG, phasic blood pressure monitoring, tilt table, loop recorders (external and implantable), 24-hour ambulatory monitoring, and autonomic function testing 1
• Preferential access to echocardiography, electrophysiology studies, stress testing, and cardiac interventions 1
• Majority of syncope patients should be evaluated as outpatients or day cases unless high-risk features present 1

Common Pitfalls to Avoid

• Do not order comprehensive laboratory panels, brain imaging, EEG, or carotid ultrasound without specific clinical indications 2, 3
• Do not prescribe beta-blockers for reflex syncope as evidence does not support efficacy 1
• Do not overlook medication-induced orthostatic hypotension as a reversible cause 1, 3
• Do not miss cardiac syncope in patients with structural heart disease or abnormal ECG—these require urgent evaluation 1, 2, 3
• Do not allow patients on midodrine to take doses before prolonged supine periods or within 3-4 hours of bedtime 4, 6
• Do not fail to monitor for supine hypertension and hypokalemia when using vasopressors and mineralocorticoids 6, 7

Driving Restrictions

Cardiac arrhythmias causing syncope: 1

• Private drivers: disqualified until successful treatment established 1
• Vocational drivers: disqualified until arrhythmia controlled, LVEF >0.40, and no ventricular tachycardia on monitoring 1

After pacemaker implantation: 1

• Private drivers: one week restriction until appropriate function established 1
• Vocational drivers: longer restriction until appropriate function confirmed 1