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Approach to syncope
Syncope is a transient loss of consciousness due to transient global cerebral hypoperfusion. It is characterized by rapid onset, short duration, and spontaneous recovery. The most common causes are reflex-mediated syncope and orthostatic hypotension, which account for one-third of syncopal episodes. Evaluation involves detailed history taking and physical examination, including orthostatic vital signs and carotid sinus massage. Tilt table testing can be used to confirm neurogenic causes when initial evaluation is insufficient.
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Approach to syncope
- 1. Approach to syncope Dr.Gagan V SR – Cardiology
- 2. • Syncope (Greek:synkope)literally means a “cessation”, “cutting short” or “pause” • Syncope is a transient loss of consciousness due to transient global cerebral hypoperfusion characterized by rapid onset, short duration, and spontaneous recovery. • Cessation of blood flow leads to loss of conciousness within 10 minutes
- 3. • Important clinicalproblem • Disabling, may cause injuries • Upto 25% of victims of sudden cardiac death in age 15 to 35 years presented initially with syncope/presyncope • first episode of syncope between 10 and 30 years with a peak at 15 years of age • Second peak ≥ 65
- 4. • Prognosis ofsyncope – Structural heart disease/arrhythmias – increased risk of sudden cardiac death – Orthostatic hypotension – twofold increased risk of mortality because of associated comorbidities – Neurally mediated syncope – excellent prognosis
- 5. Causes of real/apparentloss of conciousness • Syncope • Neurologic – Epilepsy – Vertebrobasilar TIA • Metabolic syndromes/Coma – Hyperventilation with hypocapnia – Hypoglycemia – Hypoxemia – Drug/alcohol intoxication – Coma • Psychogenic syncope – Anxiety/panic disorders – Somatization disorders
- 6. • Syncope ischaracterized by – Loss of conciousness – Transient – Rapid – Short duration – And rapid recovery
- 7. Causes of Syncope •Vascular • Cardiac • Syncope of Unknown origin
- 8. Vascular • Anatomic – Vascularsteal syndrome (subclavian artery steal syndrome) • Orthostatic – Autonomic insufficiency – Idiopathic – Volume depletion – Drug and alcohol induced • Reflex induced – Carotid sinus hypersensitivity – Neurally mediated syncope (common faint,vasodepressor,neuroc ardiogenic,vasovagal) – Glossopharyngeal syncope – Situational (acute hemorrhage, cough, defecation, laugh, micturition, sneeze, laugh, swallow, postprandial)
- 9. Cardiac • Anatomic – Obstructivecardiac valve disease – Aortic dissection – Atrial myxoma – Pericardial disease, tamponade – Hypertrophic obstructive cardiomyopathy – Myocardial ischemia, infarction – Pulmonary embolism – Pulmonary hypertension • Arrhythmias • Bradyarrhythmias – AV block, – Sinus node dysfunction, bradycardia • Tachyarrhythmias – Supraventricular tachycardia • Atrial fibrillation • Paroxysmal supraventricular tachycardia (AVNRT, WPW) • Other – Ventricular tachycardia • Structural heart disease • Inherited syndromes (ARVD, HCM, Brugada syndrome, long-QT syndrome) • Drug-induced proarrhythmia – Implanted pacemaker or ICD malfunction
- 10. Vascular causes • Reflexmediated and orthostatic hypotension • Most common • One third of all syncopal episodes
- 11. Vascular Orthostatic hypotension • Standingcauses 500 – 800 ml blood to displace into abdomen and lower extremities • Decrease in cardiac output • Stimulation of aortic, carotid and cardiopulmonary baroreceptors • Reflex increase in sympathetic outflow • Increase in heart rate, cardiac contractility and systemic resistance • Any abnormality in this mechanism causes orthostatic intolerance
- 12. • Syncope, presyncope,tremulousness, palpitation, fatigue, diaphoresis, blurred/tunnel vision • Orthostatic hypotension defined as drop of 20/10 mm Hg within 3 minutes of standing • Asymptomatic/symptomatic • Usually worse in morning, after food, after exercise • After food occurs due to redistribution in gut esp in elderly • Upto 20 mm Hg drop in SBP after food can be seen in elderly upto one third
- 13. • Initial orthostatichypotension – Decrease of > 40 mm Hg immediately after standing with rapid return to normal (<30 sec) • Delayed progressive orthostatic hypotension – Slow progressive decrease in SBP on standing
- 14. • Drugs mostcommon cause of orthostatic hypotension, either by volume depletion or vasodilation • Elderly are susceptible – Reduced baroreceptor sensitivity – Decreased cerebral blood flow – Renal sodium wasting – Impaired thirst mechanism
- 16. Orthostatic hypotension neurogenic causes •Primary and secondary autonomic failure • Primary autonomic failure – Pure autonomic failure (Bradbury Eggleston syndrome) – Multiple System Atrophy (Shy Drager syndrome) – Parkinson diseases with autonomic failure • Postural orthostatic tachycardia syndrome (POTS) – Milder form of chronic autonomic failure – Orthostatic intolerance char by symptoms – Increase of heart rate 28 beats/min – Absence of change in blood pressure within 5 minutes of standing or upright tilt
- 17. Reflex mediated syncope •Cardiovascular responses become inappropriate in response to a trigger that results in vasodilation with/without bradycardia and drop in BP and global cerebral hypoperfusion • Trigger – afferent limb • Response – efferent limb • Efferent common – increased vagal tone and withdrawal of peripheral sympathetic tone • Bradycardia, vasodilatation, hypotension, presyncope/syncope
- 18. • Vasodepressor typeresponse – Hypotension due to peripheral vasodilation predominates • Cardioinhibitory response – Bradycardia/asystole predominates • Mixed – Both vasodilation and bradycardia
- 19. • Micturition syncope –Mechanoreceptors in bladder – Elderly at night – Vasodilation following bladder emptying – Drugs – α adrenergic blockers for BOO • Defecation syncope – Gut wall tension receptos • Swallowing syncope – Afferents from upper GIT
- 21. Evaluation of syncope •History and physical examination most important components of evaluation • Cause can be identified in >25% of patients • Confirmation of syncope – Complete loss of conciousness? – Rapid onset, short duration and transient? – Recovery spontaneous, complete and without sequelae? – Loss of postural tone?
- 22. • Past historyof cardiac disease, diabetes • Family history of cardiac disease, syncope or sudden cardiac death • Medications that can cause syncope • Quantify the number and chronicity of prior syncopal and presyncopal episodes • Identify precipitating factors body position and activity prior to syncope • Type and duration of prodromal and recovery symptoms • Witness accounts also important
- 24. Physical examination • Identifystructural heart disease • Level of hydration • Neurological disease – dysautonomia or cerebrovascular accident • Orthostatic vital signs – BP and heart rate to be measured in supine and standing position after 3 mins – Early orthostatic hypotension – 20/10 mm Hg drop in BP within 3 minutes of standing – POTS – increase in 28 beats/min or more within 5 mins of standing with symptoms of orthostatic hypotension
- 25. • Carotid sinusmassage – To identify carotid sinus hypersensitivity in patients more than 40 years of age – To avoid in patients with history of TIA, CVA within 3 months, carotid bruit unless significant stenosis ruled out by doppler – Apply gentle pressure over carotid bifurcation ie just below angle of jaw – Pressure applied for 5 to 10 sec in both supine and upright position – Carotid sinus hypersensitivity defined as sinus pause more than 3 seconds in duration or fall in SBP of 50 mm Hg or more – Response can be cardioinhibitory (asystole) or vasodepressive (fall in SBP) – Complications are neurologic
- 26. Tests Tilt-Table testing • 20min horizontal pre tilt stabilization phase • Upright tilt testing at angle between 60 to 80 degrees for 30 to 45 minutes • Sensitivity can be increased with decreased specificity by – Longer tilt duration – Steeper tilt angles – Provocative agents like isoprenaline and Nitroglycerine – Isoprenaline – 1 – 3 μg/min to increase heart rate 25% – Nitroglycerine 300 to 400 μg spray sublingually after 20 min unmedicated phase in upright position
- 27. • Positive responseimplies susceptibility to neurally mediated syncope • Indication – confirmation of neurogenic syncope when initial evaluation is insufficient to confirm same • Not recommended when diagnosis can be confirmed otherwise • Reflex hypotension or bradycardia without syncope is less specific for neurally mediated syncope • In patients with structural heart disease other causes to be ruled out before confirming neurally mediated syncope • Psychogenic pseudosyncope - loss of conciousness with no change in vital signs • No value in assessing treatment of neurally mediated syncope