SYNCOPE.pdf
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This document provides an overview of syncope (transient loss of consciousness). It discusses the main causes as neurally-mediated syncope, orthostatic hypotension, and cardiac syncope. Neurally-mediated syncope is due to a transient change in reflexes controlling cardiovascular homeostasis, leading to vasodilation and bradycardia. Orthostatic hypotension results from autonomic failure impairing homeostasis reflexes. Cardiac syncope is caused by arrhythmias or structural heart issues decreasing cardiac output. The document also reviews epidemiology, pathophysiology, evaluation, and treatment of syncope.
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SYNCOPE.pdf
- 1. SYNCOPE Ch.Gnana bhaskar Post graduate 1st year General medicine
- 2. INTRODUCTION *Syncope is a transient,self limited loss of consciousness due to acute global impairment of cerebral blood flow. *Onset is rapid,duration brief and recovery spontaneous and complete. *Other differentials for transient loss of consciousness are:seizures,vertebrobasilar ischemia,hypoxemia and hypoglycemia. *A syncopal prodrome includes dizzines,lightheadedness,faintness,weakness,fatigue,visual and auditory disturbances. *sometimes loss of conciousness occur without any warning symptoms.
- 3. Causes of syncope: 1.Neurally mediated syncope(reflex or vasovagal syncope) 2.Orthostatic hypotension 3.Cardiac syncope *Neurally mediated syncope includes hetrogenous group of functional disorders that are characterised by transient change in reflexes responsible for maintaining cardiovascular homeostasis.-Episodic vasodilation and bradycardia occur in varying combinations,resulting in temporary failure of blood pressure control.
- 4. *Orthostatic hypotension is due to autonomic failure,these cardiovascular homeostatic reflexes are chronically impaired. *Cardiacsyncope is due to arrythmias,structural cardiac diseases that causes decrease in cardiac output.
- 5. EPIDEMIOLOGY *3% of all emergency department visits. *1% of hospital admissions. *Lifetime cumulative incidence of upto 35% in general population. *Peak incidence in young between 10-30 years. *Most common is neurally mediated syncope ;women>men. *>70 years incidence of syncope is high. * 2nd most common is d/t structural heart disease/arrhythmia.
- 6. *Orthostatic hypotension-prevalence increases with increasing age d/t: 1.decreased baroreceptor responsiveness. 2.decreased cardiac compliance. 3.alteration of vestibulosympathetic reflex associated with aging. *Syncope of non cardiogenic and unexplained origin has excellent prognosis. *Syncope of cardiac cause has high risk of sudden cardiac death.
- 7. PATHOPHYSIOLOGY *Upright posture imposes a unique physiological stress in humans. *Most of syncopal episodes occur from a standing position. *Standing causes,500-1000ml pooling of blood in lower extremities,buttocks&splanchnic circulation. *This pooling causes ——> decreased venous return to heart—->decreased cardiac output——->decreased blood pressure. *This changes provoke compensatory response by baroreceptors in carotid sinus and aortic arch ——>which causes increase in peripheral vascular resistance & increased venous return to heart.
- 8. *If this response fails chronically, causes orthostatic hypotension.transiently causes neurally mediated syncope. *Hypotension and cerbral hypoperfusion occurs. *Syncope is consequense of global cerebral hypoperfusion and failure of cerebral blood flow autoregulatory mechanism. *Latency of autoregulatory response —5-10 sec. *Typically cerbral blood flow —50-60 ml/min per 100 gram of brain tissue and remains relatively constant over perfusion pressure ranging from 50-150 mm hg.
- 9. *Cessation of blood flow —->6-8 sec causes loss of consciousness. *Impairment of consciousness —>when blood flow <25ml/min per 100 gm brain tissue. *Clinically—> SBP<50 mm hg causes syncope. *Determinants of blood pressure—>cardiac output &systemic vascular resistance. *Low Cardiac output—> low blood volume,increased thoracic pressure,massive pulmonary embolism,cardiac causes like—>brady&tachy arrhytmias,valvular heart diseases,myocardial injury.
- 10. *Systemic vascular resistance is decreased by central and peripheral autonomic nervous system diseases ,sympatholytic medications and transiently during neurally mediated syncope. *Increased cerebral vascular resistance,most frequently due to hypocarbia induced by hyperventilation,may also contribute to pathophysiology of syncope.
- 11. EEG changes in syncopal subjects *2 patterns 1)Slow -flat-slow—>normal background is replaced with high amplitude slow delta waves followed by sudden flayyening of eeg—a cessation or attenuation of cortical activity—followed by return of slow waves and then normal activity. 2)Slow pattern—->increasing and decreasing slow wave activity. *EEG flattening that occurs in slow—flat—slow pattern is a marker of more cerebral hypoperfusion. *Despite the presence of myoclonic movements and other motor activity during some syncopal events,eeg seizure discharges are not detected.
- 13. High risk features indicating hospitalization or intensive evaluation of syncope *chest pain suggesting coronary ischemia. *features of congestive heart failure. *moderate or severe valvular disease / severe structural cardiac disease. *ecg features of ischemia. *history of ventricular arrhytmia. *prolonged QT interval (>500ms) *Repetitive sinoatrial block or sinus pauses
- 14. *persistent bradycardia *Bi- or trifascicular or intraventricular conduction delay with QRS duration >120 ms *Atrial fibrillation *Nonsustained ventricular tachycardia *Family history of sudden death *Brugada pattern on ECG *Palpitations at time of syncope
- 15. NEURALLY MEDIATED SYNCOPE ● Sudden transient change in autonomic efferent activity with increased parasympathetic outflow and sympathetic inhibition which results in bradycardia ,vasodilation and decreased vasoconstrictor tone ● This results in decreased cerebral blood flow to below compensatory limits of autoregulation ● Types: ● 1)vasovagal- provoked by intense emotion,pain and stress ● 2)situational reflex syncope -have specific localised stimuli that provoke reflex vasodilation and bradycardia leads to syncope ● The afferent trigger may be in pulmonary ,git ,urogenital,heart,carotid artery
- 16. ● Hyperventilation causes hypocarbia and cerebral vasoconstriction ● Increased intrathoracic pressure impairs venous return to heart ● The above two play major role in many situational reflex syncope ● The afferent is different but efferent response via vagus and sympathetic pathways is similar
- 17. MECHANISM ● Decr. Arterial pressure unloads baroreceptor -terminals of affternsts of 9th and 10th cranial nerve in carotid sinus and aortic arch ● Decr.affrent impulses that are related from these mechanical receptors through 9th and 10th to NTS in dorsomedial medulla ● Decr. 10th nerve input to sinus node is mediated via NTS to NA ● Increased sympathetic activity (efferent) mediated by NTS projection to CVLM(excitatory),RVLM(Inhibitory) ● The activation of RVLM presympathetic neurons in response to hypotension is due to disinhibition ●
- 18. ● In response to sustained fall in Bp ,vasopressin release is mediated by projections from A1 noradrenergic cell group in ventrolateral medulla ● This activates vasopressin synthesis neurons in magnocellular portion of paraventricular nucleus and supraoptic nucleus of hypothalamus
- 20. NEURALLY MEDIATED SYNCOPE CAUSES ● Vasovagal syncope -provoked fear,anxiety,intense emotion,sight of blood, unpleasant sights and odors,orthostatic stress. ● Pulmonary -cough syncope,weightlifters syncope,sneeze syncope,airway instrumentation. ● Urogenital-post micturition syncope, urogenital tract instrumentation,prostatic massage. ● Gastrointestinal -swallow syncope,glossopharyngeal neuralgia,git instrumentation,rectal examination, defecation syncope. ● Cardiac -Bezold jarisch reflex,cardiac outflow obstruction ● Carotid sinus-carotid sinus massage ● Occular-occular pressure,occular surgery
- 21. ● Clinical features of NEURALLY MEDIATED SYNCOPE ● Dizziness,lightheadedness,fatigue,diaphoresis , pallor, palpitations, nausea, hyperventilation, yawning ● During syncipal episode -proximal and distal myoclonus may occur raising the possibility of seizures ● Eyes remain open and usually deviated upwards ● Pupils dilated ● Grunting, moaning,snorting,strenuous breathing ● Urinary incontinence may occur ● Feacal incontinence is very rare ● Postictal confusion is rare
- 22. ● Predisposing factors and provocative stimuli are: ● Motionless upright position ● Warm ambient temperature ● Intravascular volume depletion ● Alcohol ingestion ● Hypoxemia ,anemia,pain ● Sight of blood ● Venipuncture
- 23. ● Treatment : ● Fludricortisone ● Vasoconstriction agents ● Beta adrenegic antagonists
- 24. ORTHOSTATIC HYPOTENSION ● Defined as reduction of SBP>20 mm hg or DBP>10 mm hg within 3 mins of standing ● It is manifestation of sympathetic vasoconstrictor (autonomic)failure ● In most of cases there is no compensatory increase in heart rate despite hypotension ● In some cases with partial autonomic failure heart rate increased to some degree but insufficient to increase cardiac output ● Delayed orthostatic hypotension:decrease in BP over >3 mins of standing ● Initial orthostatic hypotension:decrease in BP<15 Sec of standing it is a mismatch between Cardiac output and peripheral vascular resistance,it doesn't represent autonomic failure
- 25. ● Clinical features: ● Lightheadedness, dizziness,presyncope(nearfaintness)in response to sudden postural change ● Nonspecific: generalized weakness,fatigue,headache ● Coat hanger headache-neckpain typically in suboccipital and post.cervical and shoulder region ● Pt. may have orthostatic dyspnea -due to ventilation-perfusion mismatch due to inadequate perfusion of lung apices ● Angina (inadequate myocardial perfusion -even with normal coronary arteries)
- 26. ● Supine hypertension is common in patients with orthostatic hypotension due to automatic failure. ● CAUSES OF ORTHOSTATIC HYPOTENSION : ● Primary autonomic failure due to idiopathic central and peripheral neurodegenerative diseases -the synucleinopathies Lewy body diseases Parkinson's disease Lewy body dementia Pure autonomic failure ● Multiple system atrophy ● Secondary automatic failure due to automatic peripheral neuropathies
- 27. Diabetes Hereditary amyloidosis Primary amyloidosis Idiopathic immune mediated autonomic neuropathy Sjogrens syndrome HIV neuropathy ● Postprandial hypotension ● Iatrogenic (drug induced ) ● Volume depletion
- 28. ● Drug induced: ● Alpha adrenegic antagonists used to treat hypertension and prostatic hypertrophy ● Antihypertensive medications ● Nitrates and vasodilators ● Tricyclic agents and phenothiazines
- 30. ● Treatment: ● No pharmacologic intervention -staged movement from supine to standing position, warning of hypotensive episode after large meals, elevation of head end of bed to decrease supine hypertension, intravascular volume should me expanded by increased dietary fluids and salt ● Pharmacologic intervention - midodrine and pseudoephedrine ● Pateint with intractable symptoms -pyrodostigmine,atomoxetine,yohimbine,desmopressin acetate, erythropoietin
- 31. CARDIAC SYNCOPE ● Caused by arrhythmias and structural heart diseases ● Bradyarrhythmias:severe sinus node dysfunction (SA block ,sinus arrest) AV block(Mobitz type 2 , Complete AV block) ● Tachycardia-bradycardia syndrome-prolonged pause after following termination of tachycardia episode is frequent cause of syncope in this patients ● Syncope due to bradycardia or asystole is refered to as stokes Adam attack ● Ventricular tachyarrhytmia frequently causes syncope Syncopal episode likelihood in ventricular tachyarrhytmia is dependent on ventricular rate.rates <200 beats /min are less likely to cause syncope
- 32. ● Several disorders associate with cardiac electrophysiologic instability and arrhytmogencity are due to mutations in ion channel subunits : ● Long QT syndrome
- 33. ● Prolonged cardiac repolarization and therefore predisposition to ventricular arrhythmias ● Syncope and sudden cardia death in pt with long QT syndrome result from polymorphic ventricular tachycardia called Torsedes de pointes that degenrates into ventricular fibrillation ● Brugada syndrome: It is a sodium channelopathy SCN5A, idiopathic ventricular fibrillation in association with right ventricular ECG abnormalities without structural heart disease. ● Catecholaminergic polymorphic tachycardia is inherited, genetically heterogeneous disorder associated with excercise or stress induced ventricular arrhytmia,syncope or sudden death
- 34. ● Structural heart disease: ● Valvular heart disease,MI,hypertrophic and other cardiomyopathies,cardiac masses like atrial myxoma and pericardial effusion these may compromise cardiac output and leads to syncope
- 35. THANK YOU