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Syncope

  1. 1. Syncope Group 5 M.E. Gunasekara W.D.S.Tissera By: Medical Students Faculty of Health-Care Sciences Eastern University, Sri Lanka
  2. 2. DEFINITION Syncope is the sudden, transient loss of consciousness and postural tone with subsequent spontaneous recovery. Greek Syn with koptein, meaning to cut off
  3. 3.  Before syncope, the patient may experience a variety of prodromal symptoms, typically including the awareness of an impending faint.  The range of prognoses in syncope is wide, and the main task of the clinician, therefore, is to determine whether the patient has a benign or a life-threatening cause for syncope
  4. 4. PRINCIPAL CAUSES Neurally Mediated Syncope Orthostatic Syncope Cardiac Syncope Metabolic Disturbance Neurologic /Psychiatric Disorders Unexplained Aetiology
  5. 5. Neurally Mediated Syncope  Vasovagal, vasodepressor, or neurocardiogenic syncope also called the common faint, is often caused by a precipitating event such as prolonged standing, hypovolemia (commonly dehydration), fear, severe pain, the sight of blood, strong emotion, or instrumentation; however, it can also occur without obvious cause.
  6. 6. Contd…  Situational or reflex syncope is loss of consciousness during or immediately after coughing, micturition, swallowing, or defecation. Alcohol has been implicated in micturition-related syncope.  Carotid sinus syncope is induced by carotid sinus stimulation, resulting in hypotension, bradycardia, or both. In sensitive individuals, typically elderly men, carotid sinus syncope may develop with tight shirt collars or while shaving the neck.
  7. 7. Orthostatic Syncope  This type of syncope results from orthostatic hypotension, diagnosed by documentation of a 20 mm Hg or more decrease in systolic blood pressure during the initial 5 minutes after the patient is in upright position; the associated heart rate either remains unchanged or increases Common cause of syncope in the elderly and is exacerbated by medications  Autonomic insufficiency is a cause of orthostatic hypotension in diabetic patients, patients with Parkinson disease, and the elderly.
  8. 8. Cardiac Syncope  Syncope associated with cardiovascular disease portends a much higher risk of mortality than is the case in the absence of underlying structural heart disease. At highest risk of dying within 1 to 6 months  Arrhythmic syncope results from tachyarrhythmias (ventricular or supraventricular) and bradyarrhythmias ◦ Sinus arrest ◦ Atrial fibrillation(in WPW syndrome pt.) ◦ Sustained monomorphic VT ◦ Complete heart block ◦ LQTS ◦ Brugada syndrome ◦ Hypertrophic cardiomyopathy ◦ Pacemaker & ICD malfunction
  9. 9. Contd…  Structural syncope is caused by valvular stenosis (aortic, mitral, pulmonic), prosthetic valve dysfunction or thrombosis, hypertrophic cardiomyopathy, pulmonary embolism, pulmonary hypertension, cardiac tamponade, anomalous origin of the coronary arteries  Aortic dissection,subclavian steal, severe left ventricular dysfunction, and myocardial infarction  Left atrial myxomas or ballvalve thrombi that fall into the mitral valve during diastole can result in the obstruction of ventricular filling and in syncope.
  10. 10. Metabolic Disturbance  Syncope due to hypoglycemia is the loss of consciousness that accompanies a blood glucose level of less than 40 mg/dL and is preceded by tremors, confusion, salivation, hyperadrenergic state, and hunger.  Hypoglycemic syncope should be suspected in diabetic patients who take insulin or oral hypoglycemic agents.  the loss of consciousness caused by hypoglycemia is not associated with hypotension, persists even when the patient is in the supine position, and usually does not resolve until the blood glucose level is restored to normal.
  11. 11.  Hypoadrenalism, which can cause postural hypotension as a result of inadequate cortisol secretion  suspected when long-term steroid therapy is suddenly discontinued
  12. 12. Neurologic Disease  Neurologic conditions can mimic syncope by causing impairment or loss of consciousness; conditions include transient cerebral ischemia , migraines , temporal lobe epilepsy, atonic seizures, and unwitnessed grand mal seizures.  Disorders resembling syncope, but without loss of consciousness, include drop attacks (sudden loss of postural tone), cataplexy, and transient ischemic attacks of carotid origin
  13. 13. Psychiatric Conditions  Syncope or syncope-like syndromes associated with psychiatric conditions not associated with increased rates of mortality but have high 1-year recurrence rates (up to 50%)  Psychiatric conditions associated with syncope include generalized anxiety and panic disorders(hyperventilation leads to cerebral vasoconstriction and possible loss of consciousness), major depression,alcohol and substance abuse, and somatization disorders.  it is possible that recurrent syncope itself may secondarily give rise to psychiatric conditions such anxiety and panic attacks. A diagnosis of syncope resulting from psychiatric disorders is usually made
  14. 14. Unexplained Aetiology  Earlier studies reported that, in about half of the patients with syncope, no cause could be determined.
  15. 15. Hx / Ex / Ix
  16. 16. KEYS TO THE HISTORY  Rule out ◦ Structural heart disease(aortic stenosis, hypertrophic cardiomyopathy etc.) ◦ Life-threatening conditions(Acute MI, Upper GIT hemorrhage)
  17. 17.  Emphasis should be placed on, ◦ Circumstances surrounding syncopal event ◦ Nature of prodromal & associated symptoms ◦ Characterization of the recovery period ◦ Medications and drugs ◦ Presence of known cardiac disease ◦ Family history (e.g., Cardiomyopathy or LQTS) ◦ Psychiatric Hx ◦ Relation of syncopal events to posture, exertion & palpitations. ◦ Number & chronicity of prior syncopal and near-syncopal episodes
  18. 18. Circumstances Surrounding Onset  Sudden onset without a prodrome Arrhythmias  Autonomic symptoms (pallor, diaphoresis, nausea)+ precipitating factor(pain, extreme heat/emotion, viewing an unpleasant sight/prolonged standing) Vasovagal syncope  If immediately on standing Orthostatic syncope  Immediately after swallowing, coughing, defecation&micturition(Alcohol) Situational syncope
  19. 19. Contd…  With head rotation while the person is wearing tight collars Carotid syncope  Exertional syncope Structural heart disease(AS, Hypertrophic cardiomyopathy/Exercise-induced tachycardias)  Syn. in arm exercise Subclavian steal syndrome  Syn. in physical exertion (swimming), emotional stress,sudden, unexpected acoustic stimuli (sound of an alarm clock or telephone) LQTS
  20. 20. Posture at the Onset of Attack  Vasodepressor syncope in the upright position  Independent of posture Syn. resulting from arrhythmias and other causes(hypoglycemia /hyperventilation) that resemble Syn.  Pain/emotion-related vasovagal syncope- No any posture (needlestick/on the sight of blood/injury)  By definition, syncope caused by orthostatic hypotension occurs soon (within seconds to minutes) after the patient assumes an
  21. 21. Associated Symptoms  Not always present &depend on the cause of syncope.  Neurally Mediated Syncope ◦ Feel unsteady ◦ Be confused ◦ Ringing in the ears ◦ Visual disturbances(dimming/blurring/seeing spots) ◦ Warmth ◦ Nausea/Vomiting ◦ Facial pallor &diaphoresis
  22. 22. Contd…  Palpitations preceding cardiac syncope, especially an awareness of rapid heart beating, suggest an arrhythmic origin.  Neurologic syncope: brainstem findings (vertigo, dysarthria, ataxia, visual disturbances)  Postevent confusion is more likely to be caused by seizures  Loss of consciousness associated with headache indicates migraine or seizures  Throat / facial pain suggests glossopharyngeal or trigeminal neuralgia
  23. 23. Differentiating Syncope from Seizures  Clinically challenging  Both phenomena loss of consciousness  Myoclonic jerking may occur during the course of true syncope secondary to transient cerebral hypoxia  Patient>45years, disorientated after an episode, seizures are 5 times more likely. ◦ An exception!!! ◦ Arrhythmic syncope with a prolonged hypotensive episode ◦ Secondarily cause transient cerebral hypoxic injury and postevent disorientation
  24. 24. CLINICAL FEATURES SYNCOPE SEIZURES Loss of consciousness precipitated by micturition, exercise, pain,defecation, or stressful events + - Sweating and nausea before or during the event + - Aura - + Tongue biting - + Clonic or myoclonic jerks or rhythmic movements +/- ++ Disorientation after the event - + Slowness in returning to consciousness - + Unconscious >5 min - +
  25. 25. Age at Onset  Youth (<30 yr) ◦ Neurally mediated syncope ◦ Situational ◦ Undiagnosed seizures ◦ Cardiac syncope  Hypertrophic cardiomyopathy  Coronary artery anomalies  WPW syndrome, other SVT  LQTS and other inherited arrhythmic disorders  Middle-aged (30-65 yr) ◦ Neurally mediated syncope ◦ Cardiac (arrhythmic, mechanical/obstructive)
  26. 26. Contd…  Elderly (>65 yr) ◦ Neurally mediated syncope ◦ Cardiac (arrhythmic, mechanical/obstructive) ◦ Drugs: antihyperhypertensive medications, antidepressants, etc. ◦ Orthostatic hypotension
  27. 27. Drugs  Drugs can frequently cause syncope, particularly in the elderly.  Antihypertensive agents:doxazosin, clonidine, hydralazine,prazosin, angiotensin-converting enzyme inhibitors, and angiotensin II-receptor blockers.  Other drugs:morphine, nitroglycerin, phenothiazines, perioperative amiodarone, calcium channel blockers(nifedipine), citrated blood, aggressive diuretic therapy, interleukin-2, protamine, and quinidine.  After exposure to QT-prolonging drugs previously asymptomatic gene carriers may suddenly develop syncope/cardiac arrest caused by torsades de
  28. 28. Contd…  QT-prolonging drugs known to precipitate syncope by torsades de pointes include: ◦ Cardiac drugs:quinidine, procainamide, sotalol, disopyramide, amiodarone, and dofetilide ◦ Noncardiac drugs:macrolides, tricyclic antidepressants, phenothiazines, methadone, some antihistamines, and cisapride. ◦ Prone to induce torsades de pointes Women>Men
  29. 29. Pregnancy  Common in pregnancy  3rd trimester even in the supine position ◦ Compression of the Aorta and IVC by the enlarged uterus
  30. 30. HELPFUL SIGNS ON PHYSICAL EXAMINATION  Recording of HR ◦ Severe bradycardia:2nd / 3rd degree heart block ◦ Tachycardia: Ix of ventricular or supraventricular tachyarrhythmia.  Recording of supine&erect BP ◦ Orthostatic hypotension:20-mm Hg decrease in SBP or a 10-mm Hg decrease in DBP within 5 min after the patient stands upright  Aortic dissection:Assessment of pulse deficit & BP in the arms  Auscultation for ejection systolic murmur:AS & hypertrophic cardiomyopathy
  31. 31. Contd…  Respi. Examination: Respiratory rate & other chest findings to exclude; ◦ Pulmonary embolus ◦ Congestive heart failure ◦ COPD  Carotid sinus massage: Suspected carotid sinus syncope  Neurologic examination: Stroke or focal neurologic deficits suspected
  32. 32. DIAGNOSTIC TESTS  No diagnostic gold standards  Baseline laboratory tests: ◦ Blood glucose:Hypoglycemia ◦ Hematocrit:Blood loss ◦ Serum electrolytes:Hypokalemia & hypomagnesemia rule out in QT prolongation ◦ Pregnancy testing(S.βhCG):Women of childbearing age  12-lead ECG:Recorded in all patients with syncope ◦ Acute ischemia ◦ Heart blocks ◦ Bundle-branch blocks ◦ SVT/Nonsustained VT
  33. 33. Contd…  Exercise stress testing: myocardial ischemia, rate- dependent AV block, exercise-induced tachyarrhythmias  Echocardiogram: structural heart disease(AS, hypertrophic cardiomyopathy, left ventricular dysfunction, right ventricular dysplasia, pulmonary HTN  Head-up tilt-table testing: ◦ Neurally mediated syncope ◦ Tilted to 60-70 degrees for 20-45 min. ◦ Continuous monitoring of vital signs ◦ Provocative agent(isoproterenol), when results (- ) ◦ Not advisable for pregnant women and the
  34. 34. Contd…  Holter monitoring: ◦ For 24 to 48 hours ◦ To detect arrhythmogenic causes  Implantable loop recorders: ◦ Helpful in recurrent syncope ◦ Undiagnosed after Holter monitoring & electrophysiologic testing ◦ Subcutaneous implantable recorders, monitoring up to 18 months ◦ Single-lead ECG systems
  35. 35. Contd…  Electrophysiologic testing: ◦ Uncovering undocumented arrhythmic propensities ◦ Intracardiac electrical stimulation & monitoring of electrophysiologic parameters ◦ To detect bradyarrhythmias & tachyarrhythmias ◦ Parameters evaluated: sinus node function, AV conduction, inducibility of supraventricular & ventricular arrhythmias  Routine nonselective neurologic testing: ◦ In neurologic conditions ◦ Headcomputed tomography, electroencephalogram, & carotid Doppler studies  Psychiatric assessment: after excluding structural heart diseases
  36. 36. WHEN TO ADMIT,WHEN TO REFER, AND TO WHOM
  37. 37.  Threshold for admitting a patient, relatively low.  Emergency room to exclude life-threatening cardiopulmonary conditions (acute MI, pulmonary embolism), hypoglycemia, orthostatic hypotension & life-threatening arrhythmias (drug-induced torsades de pointes.)  Recurrent syncope,require hospitalization if, ◦ Not previously, evaluated/treated ◦ Suspected cardiopulmonary disease ◦ FHx of sudden death ◦ Possible secondary injury present ◦ Failure of treatment (especially of cardiac origin) ◦ Suspected pacemaker /ICD malfunction  Pt. with recurrent syncope, remains unexplained after initial medical evaluation/ known/ suspected cardiac origin, referred to a Cardiologist /Electrophysiologist
  38. 38. TAKE HOME MESSAGE…  Major challenge in the evaluation, ◦ Transient symptom, not a disease ◦ With causes ranging from benign to life- threatening ◦ No gold-standard test for establishing the diagnosis  But !!! ◦ With the appropriate use of HISTORY, PHYSICAL SIGNS, and DIAGNOSTIC TESTS patients with life-threatening syncope can be identified with a high degree of accuracy.

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