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Syncope ppt

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definition, classification, evaluation and clinical differentiation of syncope

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Syncope ppt

  1. 1. Approach to a Patient with Syncope -Dr. Sachin Adukia
  2. 2.  Syncope is a transient, self-limited loss of consciousness due to acute global impairment of cerebral blood flow.  The onset is rapid, duration brief, and recovery spontaneous and complete.  A syncopal prodrome (presyncope) is common, although LOC may occur without warning.  Typical presyncopal symptoms  include dizziness, lightheadedness or faintness, weakness, fatigue, and visual, auditory disturbances.
  3. 3. Pathophysiological basis  Gradual failure of cerebral perfusion, with a reduction in cerebral oxygen availability.  Cerebral perfusion/oxygenation cut off for 8–10 s,  then loss of consciousness and postural tone,  pallor and sweating,  brief (lasting seconds) extensor stiffening or spasms,  few irregular myoclonic jerks of limbs  The whole episode is brief, usually <10 s.
  4. 4. Syncope and age groups  Neurally mediated syncope – MC cause of syncope.  slightly higher in females than males.  In young subjects- family history in first-degree relatives.  Cardiovascular - in emergency room settings and in older patients.  Syncope due to basilar migraine - more common in young females.  Orthostatic hypotension –  increases in prevalence with age because of reduced baroreflex responsiveness,  decreased cardiac compliance,  attenuation of the vestibulosympathetic reflex  explained by the greater prevalence of  predisposing neurologic disorders,  physiologic impairment,  and vasoactive medication use among institutionalized patients.
  5. 5. 3 General Categories  Neurally mediated (also called reflex or vasovagal syncope)  transient change in the reflexes responsible for maintaining cardiovascular homeostasis.  Episodic vasodilation (or loss of vasoconstrictor tone) and bradycardia occur in varying combinations, resulting in temporary failure of blood pressure control.  Orthostatic hypotension due to autonomic failure:  cardiovascular homeostatic reflexes are chronically impaired.  Cardiac syncope: arrhythmias or structural cardiac diseases
  6. 6. Vasovagal syncope  most common form of neurally mediated syncope,  Results from  excessive vagal tone,  Abnormal catecholamine response to stress,  venous pooling during an upright stance  and impaired cardiac filling.  The frequency of vasovagal syncopes varies considerably from one to two during a lifetime to as common as more than once a day.
  7. 7. C/F of Vasovagal syncope  Symptoms of orthostatic intolerance  dizziness, lightheadedness, and fatigue,  premonitory features of autonomic activation  diaphoresis, pallor, palpitations, nausea, hyperventilation, and yawning.  During the syncopal event, proximal and distal myoclonus (typically arrhythmic and multifocal) may occur, raising the possibility of epilepsy.  The eyes typically remain open and usually deviate upward. Pupils are usually dilated. Roving eye movements may occur.  Grunting, moaning, snorting, and stertorous breathing may be present.  Urinary incontinence may occur. Fecal incontinence is very rare.  Postictal confusion is also rare  Although visual and auditory hallucinations and  near death and out-of-body experiences are sometimes reported.
  8. 8. ORTHOSTATIC HYPOTENSION  Defined As: systolic drop at least 20 mmHg or diastolic drop at least 10 mmHg within 3 min of standing or head-up tilt on a tilt table,  Is a manifestation of sympathetic vasoconstrictor (autonomic) failure  In most cases, there is no compensatory increase in HR despite hypotension;  with partial autonomic failure, HR may increase but insufficient to maintain CO  “delayed” orthostatic hypotension, occurs beyond 3 min of standing; reflects mild or early sympathetic adrenergic dysfunction.  “initial” orthostatic hypotension occurs within 15 s of standing: reflects a transient mismatch between CO and PVR, and does not represent autonomic failure.
  9. 9.  Upright posture- pooling of 500–1000 mL blood in LL and splanchnic circulation.  decrease in venous return and reduced ventricular filling – diminished CO and BP.  compensatory reflex response, initiated by baroreceptors in carotid sinus, aortic arch:  resulting in increased sympathetic outflow  decreased vagal nerve activity  This increases peripheral resistance, venous return, and CO and limits the fall in BP.  If this response fails, as in orthostatic hypotension and transiently in neurally mediated syncope, cerebral hypoperfusion occurs.  Cessation of blood flow for 6–8 s will result in LOC,  impairment of consciousness -if blood flow < 25 mL/min per 100 g brain tissue.  Clinically fall in systemic SBP to ~50 mmHg or lower will result in syncope.
  10. 10. Characteristic symptoms of Orthostatic hypotension  lightheadedness, dizziness, and presyncope  nonspecific, such as generalized weakness, fatigue, cognitive slowing, leg buckling, or headache.  Visual blurring - due to retinal or occipital lobe ischemia.  Neck pain, suboccipital, posterior cervical, and shoulder region (the “coat- hanger headache”), - neck muscle ischemia  Orthostatic Dyspnea – VQ mismatch due to inadequate perfusion of ventilated lung apices)  Angina - impaired myocardial perfusion  Symptoms exacerbated by exertion, prolonged standing, increased ambient temperature, or meals.
  11. 11. Iatrogenic cause of Ortho. HypoTN  Drugs may lower peripheral resistance  Alpha-adrenoreceptor antagonists  antihypertensive agents of several classes  nitrates and other vasodilators;  Tricyclic agents  phenothiazines  Iatrogenic volume depletion due to diuresis  Volume depletion due to medical causes  hemorrhage,  vomiting,  diarrhea,  decreased fluid intake
  12. 12. Rare causes  Patients with postural tachycardia syndrome (POTS) frequently experience orthostatic symptoms without orthostatic hypotension, but syncope can occur occasionally.  Rarely, SACD, syringomyelia etc damage the descending sympathetic pathways, producing orthostatic hypotension
  13. 13. San Francisco Syncope rule  CHESS  C - CHF  H – Hematocrit <30%  E – ECG Abnormal  S – Shortness of breath  S – SBP in triage area <90  should only be applied to patients whom no cause of syncope is identified
  14. 14. Other causes of Syncope
  15. 15. Syncope in Special situations Syncope induced by Valsalva manoeuvre  increased intrathoracic pressure limits the venous return to the heart  increases vagal tone,  resulting in decreased cardiac outflow and syncope.
  16. 16. Micturition syncope  usually in men while standing for nighttime micturition.  Several mechanisms :  postural – standing on leaving a warm bed causing hypotension  straining – Valsalva manoeuvre increasing an already high nocturnal vagal tone, causing bradycardia  emptying bladder – abrupt decrease in stimulus to bladder stretch receptors causing reflex vasodilatation and hypotension.
  17. 17. Carotid sinus syncope  Common cause of unexplained falls in elderly>50 years, increses with age  Activation of one or both carotid sinuses causes peripheral vasodilation, hypotension and syncope in carotid sinus hypersensitivity.  Clinical attacks of are attributed to carotid sinus pressure by head turning or tight collars.  Diagnostic carotid sinus massage may be positive in asymptomatic elderly patients but carries a risk of  prolonged asystole,  transient or permanent neurological deficit,  stroke and sudden death.
  18. 18. Cough (tussive) syncope  LOC occurs after a paroxysm of severe coughing, most likely in obese men (smokers or chronic bronchitis)  Before losing consciousness, the patient may feel lightheaded.  face becomes flushed secondary to congestion, then pale.  Diaphoresis  loss of muscle tone  Several factors  blockage of venous return by raised intrathoracic pressure.  weight-lifting syncope - similar mechanism
  19. 19.  Hypoglycemic syncope  Hypoadrenalism - syncope orthostatic hypotension.  Disturbances of Ca, Mg, K metabolism: rare causes  Anoxic syncope- occurs d/t lack of oxygen or production of vasodepressor
  20. 20. EEG changes in syncopal subjects (2 patterns)  “Slow-flat-slow” pattern  normal background activity is replaced with high-amplitude slow delta. This is followed by sudden flattening of the EEG—a cessation or attenuation of cortical activity—followed by the return of slow waves, and then normal activity.  “Slow pattern,”  is characterized by increasing and decreasing slow wave activity only  EEG flattening in the slow-flat-slow pattern denotes severe cerebral hypoperfusion.  Despite the presence of myoclonic movements and other motor activity during some syncopal events, EEG seizure discharges are not detected.  Convulsive syncope is a term used for any type of syncope manifesting with convulsive movements.
  21. 21. Seizure types that must be distinguished from syncope  Orbitofrontal  complex partial seizures, associated with autonomic changes  Temporal lobe syncope  complex partial seizures with sudden falls and altered awareness, followed by confusion and gradual recovery
  22. 22. Syncopal attacks provoking epileptic seizures  Anoxic epileptic seizures  Occasionally, true epileptic seizures are triggered by nonepileptic syncopes in children and adults.  This combination of syncope and epileptic seizure is called an anoxic epileptic seizure
  23. 23. Epileptic seizures imitating syncope  Epileptic seizures may manifest with syncopal like attacks – “ictal syncope” in Panayiotopoulos syndrome  ‘Ictal syncope’ is used to describe this state, because ‘unresponsiveness with loss of postural tone’ is the defining clinical symptom of syncope.  She complained of ‘dizziness’ and then her eyes deviated to the left, she fell on the floor and she became totally flaccid and unresponsive for 5 minutes
  24. 24. Differential diagnosis of Blackouts • Syncope • Epilepsy • Psychogenic non-epileptic seizures •Cataplexy  Drop attack • Transient CSF obstruction • Transient ischaemic attack - anterior and posterior circulation • Panic attack, • Falls / trauma • Hypoglycaemia • Basilar migraine  Malingeering  Intoxication
  25. 25. APPROACH Careful history  Full a description as possible of the first faint  Precipitating factors,  posture,  type of onset of the faint (abrupt or gradual),  position of head and neck,  the presence and duration of preceding and associated symptoms,  duration of loss of consciousness,  rate of recovery,  and sequelae.  question an observer about  clonic movements,  color changes,  diaphoresis,  pulse,  respiration,  urinary incontinence,  nature of recovery.
  26. 26. Clinical examination  Valsalva maneuver  Orthostatic drop  Assess BP in both arms when suspecting cerebrovascular disease, subclavian steal, or Takayasu arteritis.  Pulse: rate and rhythm  Extra Cardiac Ascultation: carotid, ophthalmic, and supraclavicular bruits  Carotid sinus massage in older patients suspected of having carotid sinus syncope  The response to carotid massage is vasodepressor, cardioinhibitory, or mixed
  27. 27. Investigations  Doppler flow of cerebral vessels  MRA  EEG has a low diagnostic yield  To do only when a seizure disorder is suspected  Tilt-table testing in unexplained syncope in high-risk settings or with recurrent faints in the absence of heart disease  False positives - 10% of healthy persons may faint,  specificity -90%  ECG  Prolonged Holter monitoring  Implantable loop recordings  Radionuclide cardiac scanning,  Echocardiography
  28. 28. Treatment of Vasovagal syncope  Reassurance, avoidance of provocative stimuli, and plasma volume expansion with fluid  Isometric counterpressure maneuvers of the limbs (leg crossing or handgrip and arm tensing) to maintain pressure in the autoregulatory zone,  Fludrocortisone, vasoconstricting agents, and beta- adrenoreceptor antagonists  no consistent evidence from RCT any pharmacotherapy
  29. 29. Treatment of Orthostatic hypotension  REMOVE REVERSIBLE CAUSES—----------------usually vasoactive medications  NONPHARMACOLOGIC INTERVENTIONS  education : staged moves from supine to upright;  Warnings about the hypotensive effects of large meals;  isometric counterpressure maneuvers that increase intravascular pressure  raising the head of the bed to reduce supine hypertension.  Intravascular volume expansion : fluid and salt.  PHARMACOLOGIC INTERVENTION  fludrocortisone acetate vasoconstricting agents -midodrine, l-dihydroxyphenylserine, pseudoephedrine  INTRACTABLE SYMPTOMS  pyridostigmine,  yohimbine,  desmopressin  erythropoietin
  30. 30. Treatment of cardiac syncope-  Treatment of underlying disorder.  cardiac pacing for sinus node disease and AV block,  ablation,  antiarrhythmic drugs, and  cardioverter-defibrillators
  31. 31. References  Bradley 7th edtn  Harrison 19th edtn  Panayiotopoulos 2nd edtn  Essential Neurology 4th edtn THANK YOU

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