Syncope Clinical Guide

Introduction

Syncope is defined as a transient loss of consciousness due to global cerebral hypoperfusion characterized by rapid onset, short duration, and spontaneous recovery. It accounts for up to 3% of emergency department visits and 1–6% of hospital admissions, with substantial morbidity and healthcare costs. Differentiating benign neurally mediated episodes from life-threatening cardiac causes is essential for optimal triage and management.

Epidemiology and Risk Stratification

• Incidence: Lifetime prevalence of syncope is 35–40%, peaking in adolescence and after age 70.
• High-Risk Groups: Older adults with structural heart disease, sinus node dysfunction, or electrolyte disturbances carry increased risk of adverse events.
• Prognostic Indicators: Underlying cardiac etiology, abnormal ECG findings, chest pain or palpitations preceding syncope, and absence of prodrome signal higher risk of mortality and recurrence.

Classification

1. Reflex (Neurally Mediated) Syncope: Most common (30–50%) and often benign.
2. Vasovagal (Neurocardiogenic): Triggered by emotional distress, pain, or prolonged standing; characterized by prodromes (nausea, diaphoresis).
3. Carotid Sinus Hypersensitivity: Exaggerated baroreceptor response to neck manipulation; consider in older adults with falls or unexplained syncope.
4. Situational: Occurs during specific activities (micturition, defecation, cough, swallowing).
5. Orthostatic Hypotension: Defined by ≥20 mm Hg drop in systolic or ≥10 mm Hg drop in diastolic blood pressure within three minutes of standing.
6. Volume Depletion: Dehydration, hemorrhage, or diuretics.
7. Autonomic Failure: Parkinson’s disease, diabetic neuropathy, amyloidosis.
8. Drug-Induced: Antihypertensives, vasodilators, antidepressants.
9. Cardiac Syncope: Accounts for 5–10% but carries highest mortality risk.
10. Arrhythmogenic: Bradyarrhythmias (sick sinus syndrome, AV block), tachyarrhythmias (ventricular tachycardia).
11. Structural Heart Disease: Aortic stenosis, hypertrophic cardiomyopathy, pulmonary embolism, myocardial infarction.
12. Cerebrovascular and Other Causes: Rare; carotid artery stenosis, subclavian steal syndrome, or subarachnoid hemorrhage presenting with transient ischemic attacks.

Pathophysiology

Syncope results from a transient mismatch between cerebral metabolic demand and perfusion. In reflex syncope, aberrant autonomic reflexes produce vasodilation and/or bradycardia. Orthostatic hypotension stems from inadequate autonomic compensation and venous pooling. Cardiac syncope arises when arrhythmias or mechanical obstruction abruptly impede cardiac output.

Clinical Evaluation

History

• Event Circumstances: Posture, triggers (emotional stress, exertion), and situational factors.
• Prodromal Symptoms: Lightheadedness, diaphoresis, visual changes, nausea—suggest reflex syncope.
• Associated Features: Palpitations, chest pain, dyspnea before or after event raise concern for cardiac etiology.
• Recurrence and Injuries: Frequency and injuries sustained help gauge risk.

Physical Examination

• Vital Signs: Orthostatic blood pressure and heart rate measurements supine and standing.
• Cardiac Exam: Murmurs (aortic stenosis), irregular rhythm (atrial fibrillation).
• Neurologic Assessment: Focal deficits or postictal confusion—suggest seizure.
• Carotid Sinus Massage: Performed under monitoring when hypersensitivity suspected and no contraindications (e.g., carotid bruit, stroke history).

Differential Diagnosis

• Seizure Disorders: Prodromes of aura, tonic–clonic movements, tongue biting, postictal confusion.
• Hypoglycemia: Check finger-stick glucose.
• Psychogenic Pseudosyncope: Occurs in context of psychiatric disorders; normal hemodynamics during episodes.

Diagnostic Workup

1. Electrocardiogram: First-line; assesses arrhythmias, conduction delays, ischemia.
2. Laboratory Tests: CBC, electrolytes, glucose, cardiac biomarkers if myocardial injury suspected.
3. Imaging:
4. Echocardiography: Structural heart disease evaluation.
5. Carotid Doppler: When cerebrovascular cause suspected.
6. Ambulatory Monitoring: Holter or event recorders for intermittent arrhythmias.
7. Autonomic Testing:
8. Tilt-Table Test: Diagnoses vasovagal and orthostatic hypotension with reproducible symptoms.
9. Tilt-Table with Isoproterenol: Enhances diagnostic yield in suspected neurocardiogenic syncope.

Management Strategies

Reflex Syncope

• Education and Lifestyle: Avoid triggers, maintain hydration, regular salt intake.
• Physical Counterpressure Maneuvers: Leg crossing, handgrip, and tensing buttock muscles during prodrome.
• Pharmacotherapy: Midodrine or fludrocortisone for recurrent, refractory cases.

Orthostatic Hypotension

• Volume Repletion: Increase fluids and salt; discontinue offending medications.
• Compression Garments: Abdominal binders and thigh-high stockings.
• Pharmacologic Agents: Midodrine or droxidopa in autonomic failure.

Cardiac Syncope

• Arrhythmia Management: Pacemaker placement for bradyarrhythmias; antiarrhythmic drugs or catheter ablation for tachyarrhythmias.
• Structural Lesions: Valve replacement for severe aortic stenosis; pulmonary embolectomy for massive pulmonary embolism.

Disposition and Follow-Up

• Risk Stratification Tools: San Francisco Syncope Rule, Canadian Syncope Risk Score to guide admission vs. outpatient evaluation.
• Safety Netting: Instruct patients on warning signs (chest pain, palpitations, syncope without prodrome) and ensure timely follow-up.

Conclusion

Effective syncope management hinges on a structured approach: thorough history, focused examination, targeted diagnostics, and tailored therapy based on etiology and risk. Interdisciplinary collaboration between emergency medicine, cardiology, neurology, and primary care optimizes patient outcomes and reduces unneeded hospitalizations.