HYPOTENSION AND SYNCOPE CALISON FINAL. pptx

guidelines on hypotension and syncope

1. HYPOTENSION AND SYNCOPE LUIGI MARC O. CALISON, MD 1 ST YEAR ADULT CARDIOLOGY FELLOW Philippine Heart Center DEPARTMENT OF ADULT CARDIOLOGY DEPARTMENT OF ADULT CARDIOLOGY Gladys Ruth David, MD Electrophysiologist Moderator

2. Reference

3. OBJECTIVES 1. To Define Syncope and Transient Loss of consciousness. 2. To classify the Different types of Syncope thru clinical and diagn - ostic approaches 3. To discuss the diagnostic approach among patients with syncope

4. Question number 1 How do you define syncope? A. sudden falls, occurring without clear warning signs or symptoms and without an obvious external cause such as stumbling over an object. B abrupt, transient, complete loss of consciousness (LOC) associated with the inability to maintain postural tone, with rapid and spontaneous recovery C. L oss of vision that people may experience just before unconsciousness D. Burst of Uncontrolled Electrical Activity between Brain cells that causes temporary abnormalities in muscle tone or movements

5. Question number 1 How do you define syncope? A. sudden falls, occurring without clear warning signs or symptoms and without an obvious external cause such as stumbling over an object. B. Abrupt, transient, complete loss of consciousness (LOC) associated with the inability to maintain postural tone, with rapid and spontaneous recovery C. L oss of vision that people may experience just before unconsciousness D. Burst of Uncontrolled Electrical Activity between Brain cells that causes temporary abnormalities in muscle tone or movements

6. SYNCOPE DEFINITION

7. INCIDENCE

8. ASK: LOC : T ransient? R apid onset? S hort duration? F ollowed by spontaneous recovery?

9. TRANSIENT LOSS OF CONSCIOSUNESS T LOC  is defined as a state of real or apparent LOC with loss of awareness, characterized by amnesia for the period of unconsciousness, abnormal motor control, loss of responsiveness, and a short duration.

10. L ess common but potentially lethal causes of syncope long-QT syndrome A rrhythmogenic right ventricular dysplasia Brugada syndrome H ypertrophic cardiomyopathy I diopathic ventricular fibrillation (VF) catecholaminergic polymorphic ventricular tachycardia (VT) S hort-QT syndrome P ulmonary emboli

11. CLASSIFICATIONS OF SYNCOPE

12. PATHOPHYSIOLOGY

13. VASCULAR CAUSES OF SYNCOPE

14. ORTHOSTATIC HYPOTENSION AND OTHER SYNDROMES OF OTHROSTATIC INTOLERANCE I nadequate increase in peripheral resistance and heart rate (HR) upon standing.

15. Question number 2 This Orthostatis Intolerance syndrome presents with BP decrease on standing of >40 mmHg for systolic BP and/or >20 mmHg for diastolic BP within 15 seconds of standing? A. Classical OH B. Initial OH C. Delayed OH D. Postural Orthostatic Tachycardia syndrome

16. Question number 2 This Orthostatis Intolerance syndrome presents with BP decrease on standing of >40 mmHg for systolic BP and/or >20 mmHg for diastolic BP within 15 seconds of standing? A. Classical OH B. Initial OH C. Delayed OH D. Postural Orthostatic Tachycardia syndrome

17. ORTHOSTATIC INTOLERANCE SYNDROMES

18. OH SYNDROMES DEFINTITION REMARKS INITIAL OH BP decrease on standing of >40 mmHg for systolic BP and/or >20 mmHg for diastolic BP within 15 seconds of standing. BP then spontaneously and rapidly returns to normal( < 30 seconds) DELAYED OH OH occurring beyond 3 min of head-up tilt or active standing slow progressive decrease in BP. common in elderly persons POSTURAL ORTHOSTATIC TACHYCARDIA SYNDROME (POTS) Increase in heart rate of 30 beats/min or more on standing (or ≥40 beats/min in those 12 to 19 years of age) and absence of a more than 20-mm Hg reduction in systolic BP. associated with deconditioning, recent infections, chronic fatigue syndrome, joint hypermobility syndrome, and a spectrum of non-specific symptoms such as headache and chest pain.

19. In VVS the BP drop starts several minutes after standing up and the rate of BP drop accelerates until people faint, lie down, or do both In classical OH , the BP drop starts immediately on standing and the rate of drop decreases , so low BP may be sustained for many minutes FALL IN BLOOD PRESSURE

20. PRIMARY AUTAUTOONOMIC FAILURE

21. Question number 3 Which among the following situation best describe vasovagal syncope? A. a 20 year old women blacked out during phlebotomy for a routine blood test? B. a 65 years old women with lost of consciousness after arm exercises? C. a 35 years old man with sustained syncope during exercises and has a systolic murmur that intensifies on standing upright? D. a 74 years old man who experienced sudden syncope while shaving?

22. Question number 3 Which among the following situation best descrive vasovagal syncope? A. a 20 year old women blacked out during phlebotomy for a routine blood test? B. a 65 years old women with lost of consciousness after arm exercises? C. a 35 years old man with sustained syncope during exercises and has a systolic murmur that intensifies on standing upright? D. a 74 years old man who experienced sudden syncope while shaving?

23. REFLEX SYNCOPE

24. Neurally Mediated Hypotension or Syncope (Vasovagal Syncope)

25. Neurologic causes of TLOC Migraines, seizures, Arnold-Chiari malformations, and transient ischemic attacks, are u ncommon and account for less than 10% of all cases of syncope found to have had a seizure rather than true syncope.

26. Metabolic causes account for less than 5% of syncopal episodes

27. INITIAL EVALUATION

28. INITIAL QUESTIONS The initial evaluation should answer key questions: 

29. Was there a TLOC?

30. In case of TLOC.. Is it syncopal or non-syncopal? T he primary goal in the evaluation of a patient with syncope is to arrive at a presumptive determination of the cause of the syncope. The history and physical examination are by far the most important components of the evaluation of a patient with transient LOC and syncope and can be used to identify the cause in more than 25% of patients.

31. RISK STRATIFICATION >To recognize patients with a likely low -risk condition able to be discharged with adequate patient education. >To recognize patients with a likely high -risk cardiovascular condition requiring urgent investigation. High-risk patients : cardiac syncope. Low-risk patients : reflex syncope

32. Question number 4 Which Characteristic distinguishes seizure from syncope during Pallor > 5 seconds of premonitory symptoms Slow Pulse and Low BP Blue Face during the event

33. Question number 4 Which Characteristic distinguishes seizure from syncope during Pallor > 5 seconds of premonitory symptoms Slow Pulse and Low BP Blue Face during the event

34. PSYCHOGENIC SYNCOPE TYPES REMARKS PSYCHOGENIC PSEUDSYNCOPE ( PPS) Movements are absent BP, HR are normal or High EEG: normal PSYCOGENIC NON EPILEPTIC SEIZURE ( PNES) Impressive Limb Movements EEG: No Epileptiform Brain Activity during Attacks

35. Diagnosis of Psychogenic Syncope (1) The duration of PPS is as short as in syncope, but a much longer duration is a useful diagnostic finding: patients may lie immobile on the floor for 15–30 min. (2) The eyes are usually open in epileptic seizures and syncope but are usually closed in psychogenic TLOC. (3) The attack frequency is high, with several attacks occurring over a week or in a day (4) There is usually no recognisable trigger, and no sweating, pallor, or nausea beforehand.

36. Question Number 5 True of Carotid Sinus Hypersensitivity except? A. D iagnosed by the reproduction of clinical syncope during carotid sinus massage B. The Physiologic Response to carotid Hypersensitivity Syndrome cardioinhibitory, Vassodepressor or mixed. C. It is indicated in all patients with Syncope D. None of the above

37. Question Number 5 True of Carotid Sinus Hypersensitivity except? A. D iagnosed by the reproduction of clinical syncope during carotid sinus massage B. The Physiologic Response to carotid Hypersensitivity Syndrome cardioinhibitory, Vassodepressor or mixed. C. It is indicated in all patients with Syncope D. None of the above

38. DIAGNOSTIC TEST

39. Carotid Sinus Massage A pplying gentle pressure over the carotid pulsation, first one side and then the other, just below the angle of the jaw where the carotid bifurcation is located. Pressure should be applied for 5 to 10 seconds in both the supine and the upright position because an abnormal response to carotid sinus massage is present only in the upright position in up to one third of patients. A voided : previous transient ischemic attacks, strokes within the past 3 months, and carotid bruits, except if significant stenosis has been excluded by carotid Doppler studies. normal response to carotid sinus massage is a transient decrease in the sinus rate, prolongation of AV conduction, or both.

40. CAROTIS SINUS HYPERSENSITIVITY A ventricular pause lasting >3 s and/or a fall in systolic BP of >50 mmHg D iagnosed by the reproduction of clinical syncope during carotid sinus massage

41. ORTHOSTATIC CHALLENGE Currently, there are three methods for assessing the response to a change in posture from supine to erect.

42. ACTIVE STANDING

43. HUTT ( HEAD UP TILT TABLE TESTING) Valuable diagnostic test for evaluating patients with syncope, with a positive response indicating susceptibility to NMS. Useful for patients with suspected vasovagal syncope if the diagnosis is unclear after the initial evaluation The main indication for upright tilt testing is to confirm a diagnosis of NMS when the initial evaluation was insufficient to establish this diagnosis. Value in diagnosing psychogenic pseudosyncope . Not generally recommended in patients in whom the diagnosis can be established from the initial his- tory and physical examination. However, for some patients, confirmation of the diagnosis with a positive response to upright tilt testing is very reassuring.

44. TILT TABLE TESTING PROTOCOL Patients should be fasted for 2–4 h before the test. Ensure a supine pre-tilt phase of >5 min when there is no venous cannulation, and of>20min when there is venous cannulation. Tilt angle between 60o and 70o. Passive phase of tilt of >20 min duration and a maximum of 45 min. Use either sublingual nitroglycerin or intravenous isoproterenol for drug provocation if the passive phase is negative. The duration of the drug-challenge phase is 15–20 min: for nitroglycerin challenge, a fixed dose of 300–400 l g sublingually administered with the patient in the upright position; for isoproterenol challenge, an incremental infusion rate from 1 l g/min rising to 3 l g/min to increase average HR by about 20–25% over baseline. The test should be continued until complete LOC occurs or completion of the protocol.

45. TILT TESTING To confirm a diagnosis of reflex syncope in patients in whom this diagnosis was suspected but not confirmed by initial evaluation A ssessment of autonomic failure, especially for the reproduction of delayed OH (which could not . be detected by active standing because of its delayed onset) and postural orthostatic tachycardia syndrome (POTS).

46. PATTERNS OF TILT TABLE TESTING

47. 24 HOUR ABPM

48. ECHOCARDIOGRAPHY

49. STRESS TESTINGAND CORONARY ANGIOGRAPHY

50. ELECTROCARDIOGRAPHIC MONITORING

51. ELECTROPHYSIOLOGIC TESTING E stablish a diagnosis of sick sinus syndrome, carotid sinus hypersensitivity, heart block, SVT, and VT The 2017 ACC/AHA/ HRS syncope guidelines : > useful for evaluation of select patients with syncope of suspected arrhythmic etiology >EPS is not recommended for syncope evaluation in patients with a normal ECG and normal cardiac structure and function, unless an arrhythmic etiology is suspected Indications: abnormal findings on an ECG or structural heart disease, those whose clinical history suggests an arrhythmic cause of the syncope, and those with a family history of sudden death.

52. INIDCATION FINDINGS Asymptomatic sinus bradycardia (suspected sinus arrest causing syncope) > An abnormal response is defined as >1.6 or 2 s for SNRT, or >525 ms for corrected SNRT. >corrected SNRT >800 ms had an eight-fold higher risk of syncope than a SNRT below this value. B ifascicular BBB (impending high-degree AV block) > A prolonged HV interval >70 ms >Induction of second or third degree AV block by pacing or by pharmacological stress (ajmaline, procainamide, or disopyramide S uspected tachycardia. In patients with a previous myocardial infarction and preserved left . ventricular ejection fraction (LVEF): >sustained mono morphic VT is strongly predictive of the cause of syncope >induction of ventricular fibrillation (VF) is considered a . non-specific finding. ELECTROPHYSIOLOGIC STUDY INDICATIONS: 2018 ESC GUIDELINES

53. ELECTROPHYSIOLOGIC STUDY

54. SUMMARY: INTIAL EVALUATION

55. SUMMARY: DIAGNOSIS