approach to syncope ,diagnosis and management

pls see the slides in slideshare


APPROACH TO SYNCOPE ,DIAGNOSIS AND MANAGEMENT

  1. 1. Dr Asif Iqbal Approach with syncope
  2. 2. CLINICAL SCENARIO • Case #1 ,42 year old female, Chief complaint: passing out at work who Works in a pharmaceutical lab. Was sitting at her desk, felt nauseated and knew she was going to pass out.Per witnesses, was slump over chair and was unconscious for a few seconds. • Similar episodes 10 years ago.No family history of sudden cardiac death.No medications.No smoking. No alcohol. No drugs.
  3. 3. CLINICAL SCENARIO Case #2 ,82 year old male. Found unresponsive by his son Past medical history—HTN.Medications— HCTZ.Exam—BP -160/98. P-96, Now alert and oriented. Facial contusions. Otherwise normal exam. Q: How would you manage these 2 patients?
  4. 4. Syncope: Definition Transient loss of consciousness associated with absence of postural tone. Followed by rapid and complete recovery. Absence of prolonged confusion Result from global cerebral hypoperfusion Presyncope---prodromal symptom of fainting and typically has the same work up as syncope.
  5. 5. Syncope: Pathophysiology Decreased cerebral perfusion is common to all causes of syncope Cessation of cerebral perfusion for as little as 3-5 seconds can result in syncope Decreased cerebral perfusion may occur as a result of decreased cardiac output or decreased systemic vascular resistance.
  6. 6. Classification of syncope Noncardiac-typically involves prodromal symptoms that leads to loss of consciousness and muscle tone for <30 seconds and recovery within seconds. Orthostatic hypotension syncope-symptoms triggered by postural changes .common causes include dehydration and autonomic neuropathy(commonly seen in patients with diabetes) Neurally mediated (reflex) syncope –subclassified into carotid sinus syndrome,situational and vasovagal syncope(most common) Vasovagal syncope-sudden increase in vagal tone triggered by prolong standing ,emotional stress, painful stimuli. patient may experience prodromal symptoms of nausea, warmth ,diaphoresis prior to syncope .
  7. 7. Classification of syncope Cardiac-does not typically involved prodromal /postdromal symptoms, patient may have history of arrythmia ,valvular disease, structural heart disease .screen for the following potential etiologies -- • Left ventricular outflow tract obstruction (LVOTO)( eg.aortic stenosis, hypertropic obstructive cardiomyopathy),syncope with exertion or during exercise . • Arrythmia-history of CAD, MI,cardiomyopathy,wpw syndrome or reduced EF • Torsades de pointes-triggered by electrolyte abnormalities
  8. 8. Clues to the Etiology of Syncope . Cough, micturition, defecation, swallowing---situational syncope (reflex syncope) . Syncope with arm exercise---subclavian steal syndrome • Syncope with shaving---carotid sinus sydrome (reflex syncope) • Syncope with change of position---orthostatic syncope • Prodromal symptoms (nausea, diaphoresis)---neurally mediated reflex (vasovagal) • Syncope with exertion---AS, IHSS, arrhythmias-(cardiac syncope) • Abrupt onset---cardiac syncope • Blood pressure/pulse differential---Aortic dissection, subclavian steal syndrome • Post-syncopal disorientation; incontinence---seizure • dynamic systolic murmur that intensifies from squatting to standing or during Valsalva maneuver with f/h of scd -HOCM
  9. 9. Clues to the Etiology of Syncope • initiation or change in dosage -Alcohol, antianginal agents, antidepressants, antidiabetic agents, antihypertensives, antiparkinsonian agents, diuretics, insulin refers to Orthostatic hypotension syncope( Drug induced ) • h/o Acute blood loss (e.g., gastrointestinal bleeding, ectopic pregnancy), diarrhea, inadequate fluid intake, vomiting-Orthostatic hypotension syncope due to volume depletion present with hypotension,tachycardia,dehydration on exam • Young adults (predominantly female); associated with chronic fatigue syndrome and mitral valve prolapse with Severe orthostatic intolerance with marked tachycardia-Postural tachycardia syndrome(part of OHS)
  10. 10. Clues to the Etiology of Syncope Tongue biting,incontinence,prolonged confusion-seizure ,not syncope Use of Macrolides, antiemetics, antipsychotics, tricyclic antidepressants-think prolonged QT inteval Alcoholism, DM,MS,amyloidosis, Lewy body dementia, older age, spinal cord injury, uremia, Parkinson disease, renal replacement therapy think about Orthostatic hypotension syncope Elevated jugular venous pressure, hypotension, pulsus paradoxus, sinus tachycardia –think Cardiac tamponade
  11. 11. HISTORY Detailed history should take and decide-- (1)Is the loss of consciousness attributable to syncope? (2) Is there a history of cardiovascular disease (3) Are there clinical features to suggest a specific cause of syncope? Red flag symptoms—exertional onset ,chest pain ,dyspnoea,low back pain,palpitation,severe headache,focal neurological deficit ,diplopia,ataxia or dysarthia
  12. 12. Diagnosis of syncope The starting point of the diagnostic evaluation of TLOC of suspected syncopal nature is the initial syncope evaluation, which consists of: • Careful history taking concerning present and previous attacks, as well as eyewitness accounts, in person or through a telephone interview. • Detailed Physical examination, including supine and standing BP measurements and cardiac, nervous system examination . • Electrocardiogram (ECG).Serum glucose and electrolytes Based on these findings, additional examinations may be performed when needed: • Immediate ECG monitoring when there is a suspicion of arrhythmic syncope. • Echocardiogram when there is previous known heart disease, data suggestive of structural heart disease, or syncope secondary to cardiovascular cause.
  13. 13. Diagnosis of syncope • Carotid sinus massage (CSM) in patients aged >40 years.Diagnostic if ventricular pause is more than three seconds or if systolic blood pressure decreases by more than 50 mm Hg; contraindicated in patients with bruits or a history of transient ischemic attack/ cerebrovascular accident within the past three months • • Head-up tilt testing when there is suspicion of syncope due to OH or reflex syncope.Used in patients with negative initial findings, normal cardiac structure, and no evidence of ischemia; contraindicated in patients with ischemic heart disease, uncontrolled hypertension, left ventricular outflow tract obstruction, or aortic stenosis
  14. 14. Diagnosis of syncope • Blood tests when clinically indicated, e.g. haematocrit or haemoglobin when haemorrh age is suspected, oxygen saturation and blood gas analysis when hypoxia is suspected, troponin when cardiac ischaemia-related syncope is suspected, or D-dimer when pulmonary embolism is suspected, etc
  15. 15. treatment • NEURALLY MEDIATED SYNCOPE • Treatment of neurally mediated syncope includes reassurance, education, and physical therapy. In situational syncope, it is important to avoid potential triggers. Physical counterpressure maneuvers such as leg crossing, squatting, and tensing the lower extremities are effective at the onset of prodromal symptoms. One randomized trial showed that these maneuvers reduce syncope by 39%. Tilt training involves standing for prolonged periods, and compliance is generally poor. • Pharmacologic therapy with beta blockers, alpha agonists, and fludrocortisone has shown no effectiveness or conflicting results in reducing vasovagal syncope. • In one small randomized trial of patients with a history of recurrent vasovagal syncope, paroxetine prevented additional episodes in 82.4% compared with 47.1% in the placebo group over two years (P < .001), although guidelines recommend its use only in patients with concurrent psychiatric disease. • In patients with severe asystole from neurally mediated syncope, a double-blind, randomized, placebo-controlled trial showed that the use of permanent dual chamber pacing reduced the risk of recurrent syncope.
  16. 16. treatment • ORTHOSTATIC HYPOTENSION • Treatment of orthostatic hypotension includes education and lifestyle modifications, such as slowly transitioning from a supine or sitting position to standing and increasing fluid and sodium intake. • Contributing medications should be discontinued or decreased, if possible. • Other treatment modalities include elevating the head of the bed by 10 degrees, compression stockings/abdominal binders, and counterpressure maneuvers. • If these do not mitigate symptoms, midodrine and fludrocortisone are effective treatments
  17. 17. treatment CARDIAC SYNCOPE Management of cardiac syncope is directed at the underlying etiology. Options include antiarrhythmic drugs, cardiac pacing, catheter-directed ablation, and, rarely, implantable cardioverter-defibrillator placement.
  18. 18. CASE REVIEW Case #1 Continues Physical exam: Normal ,Orthostatics: Normal EKG: Normal,Labs: no anemia. Glucose normal.ECHO: Normal Tilt Table Test: after 7 minutes of 70 degrees upright-HR 36, BP 51/41, LOC. Regained consciousness with supine position. Conclusion DIAGNOSIS----Vasovagal Syncope OUTCOME---No reoccurence of symptoms when followed up at three months, 6 months, and 1 year later.
  19. 19. CASE REVIEW Case #2 Continues,Emergency Room workup— negative. Electrolytes, CBC normal. EKG showed NSR with occasional PVCs. Decision made to ADMIT. 2 hours later---Nonsustained Vtach.EP study— Inducible Vtach. Automated internal defibrillator placed.Cardiac cath---diffuse coronary artery disease.
  20. 20. ECG • Some e.c.g of syncope related condition................................................
  21. 21. reference American association of family physicians journals The European Society of Cardiology guidelines for the diagnosis and management of syncope 2018
  22. 22. Thanks for hearing

Comments

Popular posts from this blog

WHEN TO START INSULIN IN DIABETICS AND HOW TO ADJUST?