Approach to a patient with Syncope

Definition Of Syncope: Symptom of sudden transient loss of consciousness due to global cerebral hypoperfusion.

Causes Of Syncope: 

• Neurocardiogenic (a.k.a. vasovagal, ~20%; ): ↑ sympathetic tone → vigorous contraction of LV →
mechanoreceptors in LV trigger ↑ vagal tone  → ↓ HR (cardioinhibitory) and/or
↓ BP (vasodepressor) cough, deglutition, defecation, & micturition → ↑ vagal tone and thus can be precipitants related disorder:
carotid sinus hypersensitivity (exagg vagal resp to carotid massage)

• Orthostatic hypotension (10%)
hypovolemia/diuretics, deconditioning; vasodilat. (esp. if combined w/ chronotropes)
autonomic neuropathy [primary = Parkinson’s, Shy-Drager, Lewy body dementia, POTS (dysautonomia in the young); secondary =DM, EtOH, amyloidosis, CKD]

• Cardiovascular
Arrhythmia (15%)
Bradyarrhythmias: Sick sinus syndrome, high-grade AV block, chronotropes, PPM malfunction
Tachyarrhythmias: VT, SVT (syncope rare unless structural heart disease or WPW)
Mechanical (5%)
Endocardial/Valvular: AS, MS, PS, prosthetic valve thrombosis, myxoma
Myocardial: pump dysfxn from MI or outflow obstruction from HCMP (but usually VT)
Pericardial: tamponade
Vascular: PE, PHT, aortic dissection, ruptured AAA, subclavian steal


• Neurologic (10%): seizure (technically not syncope), TIA/CVA, vertebrobasilar insufficiency, dissection of cerebral arteries, migraine, narcolepsy

• Miscellaneous . causes of loss of consciousness (but not syncope):
hypoglycemia,
hypoxia,
anemia,
psychogenic

Workup (etiology cannot be determined in ~40% of cases)

• History (from Patient and witnesses if available)

• activity and posture before the incident
• precipitating factors: exertion (Aortic Stenosis, Hyoertrophic cardiomyopathy), 
• positional (orthostatic hypotension), 
• stressors such as sight of blood, pain, emotional distress, fatigue, prolonged standing, warm environment, 
• any association with cough/micturition/defecation/swallowing (neurocardiogenic), head turning or shaving (carotid sinus hypersens.); arm exercise (subclavian steal)
• prodrome (eg, diaphoresis, nausea, blurry vision): cardiac <~5 sec, vasovagal >~5 sec
• associated symptoms: chest pain, palp., neurologic, postictal, bowel or bladder incontinence 

• Past Medical History: prior syncope, previous cardiac or neurologic diseases.

Medications that may act as precipitants

• vasodilators: alpha-blockers, nitrates, ACEI/ARB, Calcium channel blockers, hydralazine, phenothiazines,diuretics; 
• proarrhythmic or QT prolonging: class IA, IC or III antiarrhythmics 
• psychoactive drugs: antipsychotics, Tricyclic antidepressants, barbiturates, benzodiazepines

• Family history: h/o sudden cardiac death in family or syncope (vasovagal may have genetic component)

• Physical exam

• Vital signs including orthostatics ( if supine → standing results in >20 mmHg ↓ SBP, >10 mmHg ↓ DBP, or >10–20 bpm ↑ HR), BP in both arms
• Perform a complete cardiovascualr examination. 
• Neurologic exam: pay attention to focal findings, evidence of tongue biting;

• ECG (abnormal in ~50%, but only definitively identifies cause of syncope in ~10%)

Other diagnostic studies are decided on the basis of history and examination. 

• ECG suggesting tachy or brady-induced syncope; Pt w/ PPM/ICD

Treatment

• Arrhythmia, cardiac mechanical or neurologic syncope: treat the underlying disorder

• Vasovagal syncope: no proven benefit for midodrine, fludrocortisone, disopyramide

• Orthostatic syncope: volume replete ; 

if chronic → rise from supine to standing slowly, compressive stockings, midodrine, fludrocortisone, high Na diet