Syncope

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Syncope

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1. Syncope The dizzy and woozy world

2. Syncope: Definition a syndrome in which loss of consciousness is: relatively sudden, temporary, self-terminating usually rapid recovery due to inadequate cerebral perfusion, most often triggered by a fall in systemic arterial pressure Transient Loss of Consciousness, or TLOC, is just that—as is illustrated here. It can be as simple as a benign ‘faint’ or a symptom of an underlying disease that may lead to sudden death. Or it may not be syncope at all. Transient Loss of Consciousness, or TLOC, is just that—as is illustrated here. It can be as simple as a benign ‘faint’ or a symptom of an underlying disease that may lead to sudden death. Or it may not be syncope at all.

3.

4. Transient Loss of Consciousness Concussion TLOC mimicks, without true loss of consciousness e.g., psychogenic “pseudo-syncope” ‘drop attacks’ cataplexy

5. Syncope: A Symptom, Not a Diagnosis Self-limited loss of consciousness and postural tone Relatively rapid onset Variable warning symptoms Spontaneous, complete, and usually prompt recovery without medical or surgical intervention

6. Section 2: Classification, Prevalence, Social & Economic Impact

7. Causes of True Syncope This slide provides a simple classification of the principal causes of syncope. This scheme lists the causes of syncope from the most commonly observed (Left) to the least common (Right). This ranking may be helpful in thinking about the strategy for evaluating syncope in individual patients. Within the boxes,the most common causes of syncope are indicated for each of the major diagnostic groups. VVS—Vasovagal Syncope CSS—Carotid Sinus Syndrome ANS—Autonomic Nervous System HCM—Hypertrophic CardiomyopathyThis slide provides a simple classification of the principal causes of syncope. This scheme lists the causes of syncope from the most commonly observed (Left) to the least common (Right). This ranking may be helpful in thinking about the strategy for evaluating syncope in individual patients. Within the boxes,the most common causes of syncope are indicated for each of the major diagnostic groups. VVS—Vasovagal Syncope CSS—Carotid Sinus Syndrome ANS—Autonomic Nervous System HCM—Hypertrophic Cardiomyopathy

8. Syncope Mimics: Real or Seemingly Real TLOC not due to Cerebral Hypoperfusion Acute Intoxication (e.g., alcohol) Seizures Sleep disorders Somatization disorder psychogenic pseudo-syncope Trauma/concussion Hypoglycemia Hyperventilation

9. Syncope: Epidemiological Data Major morbidity such as fractures and motor vehicle accidents are reported in 6% of patients. Minor injury such as laceration and bruises in 29%. 1Kenny RA, Kapoor WN. Epidemiology and social costs. In: Benditt D, Blanc J-J, et al. eds. The Evaluation and Treatment of Syncope. Elmsford, NY: Futura;2003:23-27. 2Kapoor W. Evaluation and outcome of patients with syncope. Medicine. 1990;69:160-175. 3Brignole M, Disertori M, Menozzi C, et al. Management of syncope referred urgently to general hospitals with and without syncope units. Europace. 2003;5:293-298. 4 Blanc J-J, L’ Her C, Touiza A, et al. Prospective evaluation and outcome of patients admitted for syncope over a 1 year period. Eur Heart J. 2002;23:815-820. 5Campbell A, Reinken J, Allan B, et al. Falls in old age: A study of frequency and related clinical factors. Age and Ageing. 1981;10:264-270. Major morbidity such as fractures and motor vehicle accidents are reported in 6% of patients. Minor injury such as laceration and bruises in 29%. 1Kenny RA, Kapoor WN. Epidemiology and social costs. In: Benditt D, Blanc J-J, et al. eds. The Evaluation and Treatment of Syncope. Elmsford, NY: Futura;2003:23-27. 2Kapoor W. Evaluation and outcome of patients with syncope. Medicine. 1990;69:160-175. 3Brignole M, Disertori M, Menozzi C, et al. Management of syncope referred urgently to general hospitals with and without syncope units. Europace. 2003;5:293-298. 4 Blanc J-J, L’ Her C, Touiza A, et al. Prospective evaluation and outcome of patients admitted for syncope over a 1 year period. Eur Heart J. 2002;23:815-820. 5Campbell A, Reinken J, Allan B, et al. Falls in old age: A study of frequency and related clinical factors. Age and Ageing. 1981;10:264-270.

10. Impact of Syncope on Mortality Risk Vasovagal Syncope has low mortality risk But recurrences are a concern Syncope of presumed cardiac cause is associated with high mortality risk Most evidence suggests that risk is similar to that of patients without syncope but with similar severity of heart disease

11. Syncope Electrical Problems Motor Problems Valve Stenosis Problems Fuel System Issues. Clots and such Supply and demand Issues Hemodynamic instability Homeostasis

12. Syncope Catecholamine Disorders Central Autonomic Disorders Orthostatic Intolerance Syndrome Paroxysmal Autonomic Syncope Peripheral Autonomic Disorders

13. Neurocardiogenic Syncope Orthostatic hypotension Orthostatic hypotension is defined as a drop of 20 mm Hg in systolic blood pressure and 10 mm Hg diastolic blood pressure on standing, associated with typical symptoms. 

14. Syncopal attacks in children 20% of children will have a syncopal episode before the age of 15 years. More than 70% are due to neurally-mediated reflex responses and vast majority are benign. Benign Vasovagal Syncope (simple faints) and Reflex Anoxic Seizures – aka- Reflex Asystolic Syncope. Both conditions are benign, upsetting for both the child and the parents. Careful history taking is the key to diagnosis.

15. Situational syncope A type of vasovagal syncope that occurs only during particular situations that cause unusual patterns of stimulation to certain nerves. The “stimulus” that triggers an exaggerated neurological reflex can be a wide range of different events. Dehydration, intense emotional stress, anxiety, fear, pain, hunger or use of alcohol or drugs.

16. Situational syncope Syncope may also occur immediately after peak exercise. This contrasts with collapses occurring during exercise, for example if the person has aortic stenosis. The cause is thought to be due to vasomotor center dysfunction.

17. Situational syncope Hyperventilation associated with panic or anxiety. Cough syncope. Carotid sinus hypersensitivity (turning the neck or wearing a tight collar). Micturition syncope.

18. Psychogenic syncope Sometimes syncope may be feigned. This is known as Psychogenic syncope.

19. Neurologic syncope: Loss of consciousness due to a neurological conditions. Seizure. Strokes, transient ischemic attacks. Migraines. Normal pressure hydrocephalus. Sleep disorders

20. Cardiac syncope: Loss of consciousness due to cardiovascular conditions that interferes with blood flow to the brain. Arrhythmia. Asystole. Conduction issues. Obstructed blood flow in the heart or blood vessels, valve disease, aortic stenosis, blood clot, or heart failure.

21. Syncope: Carotid Sinus Syndrome Carotid sinus hypersensitivity. Carotid sinus massage causes a three second, or longer, pause in the heart beat (cardio inhibition). Drop blood pressure by 50 mm Hg. or more (vasodepression).  56% of cases of unexplained syncope are found to have Carotid sinus hypersensitivity.

22. Postural syncope Postural hypotension: occurs when the blood pressure drops suddenly due to a quick change in position, such as from lying down to standing. Postural syncope can be related to certain medications or intravascular volume depletion due to bleeding, dehydration or vasomotor instability.

23. Vasovagal syncope When you stand up, gravity causes blood to settle in the lower part of your body, below the level of the diaphragm. In response, the heart and autonomic nervous system (ANS) react to maintain your blood pressure. These physiologic responses can be exaggerated or abnormally blunted.

24. Vasovagal syncope Vasovagal syncope may occur with orthostatic hypotension. The blood vessels do not constrict normally when the patient stands, causing blood to pool in the legs and the blood pressure to drop quickly.

25. Section 3: Diagnostic Strategy

26. The Initial Evaluation: 4 Key Questions Did the patient suffer ‘true’ Transient Loss of Consciousness (TLOC)? Was TLOC due to syncope or some other cause? Is heart disease present? Does the medical history (including observations by witnesses) suggest a specific diagnosis? The history must include detailed summary of events leading up to and following syncope events. Additionally, it is important to ascertain whether there is any evidence of underlying structural heart disease. The direction of subsequent evaluation differs in patients with and without heart disease.The history must include detailed summary of events leading up to and following syncope events. Additionally, it is important to ascertain whether there is any evidence of underlying structural heart disease. The direction of subsequent evaluation differs in patients with and without heart disease.

27. Diagnosis Careful review  of medical history and a physical exam. Detailed questions about symptoms and syncope episodes. Premonitory symptoms and the circumstances in which symptoms occur.

28. Diagnosis Medication history Bleeding disorders Seizure disorders Migraine Infections GI symptomtology

29. Diagnosis ECG Echocardiogram Holter monitor Long term event recorder Implantable loop recorder Electrophysiology study

30. Diagnosis Sick Sinus Syndrome AV Nodal disease Infra His Disease Tachyarrhythmia Blood sugar measurements Carotid Doppler and ultrasound EEG

31. Diagnostic Goal Establish cause of syncope with sufficient certainty to: Assess prognosis confidently Initiate effective preventive treatment

32. A Diagnostic Plan is Essential Initial Examination Detailed history & Physical exam (Supine/Standing BP) ECG, possibly Echocardiogram Risk Assessment In-hospital vs Out-of-hospital Diagnostic evaluation Presence of Structural Heart Disease (SHD) vs None Selected Testing Based on Initial Exam & Risk Ambulatory ECG Monitoring (Event-monitor, MCOT, ILR) Hospital-based Hemodynamics / Angio, StressTesting, EPS, Tilt-table

33. A Diagnostic Plan is Essential

34. Initial Examination: Essential Elements of the History Circumstances of recent event(s) Eyewitness account of event Symptoms at onset of event (warning symptoms) Sequelae Concomitant disease, especially cardiac Medication history Pertinent family history Cardiac disease, Sudden death Metabolic disorders Past medical history Neurological history Syncope The history must include detailed summary of events leading up to and following syncope events. Additionally, it is important to ascertain whether there is any evidence of underlying structural heart disease. The direction of subsequent evaluation differs in patients with and without heart disease.The history must include detailed summary of events leading up to and following syncope events. Additionally, it is important to ascertain whether there is any evidence of underlying structural heart disease. The direction of subsequent evaluation differs in patients with and without heart disease.

35. Clinical Features Suggesting Cause of Syncope ESC Syncope Task Force 2004 Neurally-mediated Reflex Syncope Absence of cardiac disease (except CSS) Long history of recurrences Associated with emotional event, pain, prolonged upright posture, hot environment, head rotation After strenuous exertion Orthostatic Syncope Associated with change to upright posture, prolonged standing, dehydration Recent addition of diuretic, vasodilator, etc History of neuropathy, diabetes, alcohol abuse Cardiac Syncope Definite structural heart disease, acute cardiac ischemia Family history of sudden death Occurred during exercise ECG evidence of prior MI, acute ischemia, AV block, long QT, preexcitation, etc The history must include detailed summary of events leading up to and following syncope events. Additionally, it is important to ascertain whether there is any evidence of underlying structural heart disease. The direction of subsequent evaluation differs in patients with and without heart disease.The history must include detailed summary of events leading up to and following syncope events. Additionally, it is important to ascertain whether there is any evidence of underlying structural heart disease. The direction of subsequent evaluation differs in patients with and without heart disease.

36. Syncope Risk Stratification: “Is in-hospital evaluation needed?”

37. Hospital Admission for Diagnosis or Treatment

38. Test to determine causes of syncope Head-up tilt test Blood volume determination: Hemodynamic testing: Autonomic reflex testing: Sleep study (Polysomnogram)

39. Initial Examination: Essential Elements of the Physical Examination Vital signs Heart rate, regularity Orthostatic blood pressure change CV Exam: Is heart disease present? ECG: Long QT, WPW, conduction system disease Echo: LV function, valve status, HCM Neurological exam Residual deficits? Carotid sinus massage Perform under clinically appropriate conditions preferably during tilt-table test. Monitor BP WPW—Wolff Parkinson White syndrome HCM—Hypertrophic CardiomyopathyWPW—Wolff Parkinson White syndrome HCM—Hypertrophic Cardiomyopathy

40. Carotid Sinus Massage (CSM) Method Massage, ~10 seconds, firm but do not occlude Supine and upright posture (on tilt-table) Suggests Carotid Sinus Syndrome (CSS) if: >3 sec asystole and/or >50 mmHg fall in systolic BP Or Reproduction of symptoms (usually only occurs with CSM during upright posture) Carotid sinus massage (CSM) is an often overlooked, yet highly cost effective test, especially in older syncope patients. CSM must be applied with care, and the method described here has proven both safe and effective. Note that an abnormal response to CSM (i.e., Carotid Sinus Hypersensitivity, CSH) is not diagnostic of Carotid Sinus Syndrome (CSS). Reproduction of symptoms is a crucial diagnostic element. To achieve symptom reproduction, it may be useful to conduct CSM with the patient in the upright posture. If the latter is to be done, the patient should be safely secured to a tilt-table in order to prevent injury from a fall. Note: May perform during tilt-table test. *Munro N, McIntosh S, Lawson J, et al. Incidence of complications after carotid sinus massage in older patients with syncope. J Am Geriatr Soc. 1994;42:1248-1251. Carotid sinus massage (CSM) is an often overlooked, yet highly cost effective test, especially in older syncope patients. CSM must be applied with care, and the method described here has proven both safe and effective. Note that an abnormal response to CSM (i.e., Carotid Sinus Hypersensitivity, CSH) is not diagnostic of Carotid Sinus Syndrome (CSS). Reproduction of symptoms is a crucial diagnostic element. To achieve symptom reproduction, it may be useful to conduct CSM with the patient in the upright posture. If the latter is to be done, the patient should be safely secured to a tilt-table in order to prevent injury from a fall. Note: May perform during tilt-table test. *Munro N, McIntosh S, Lawson J, et al. Incidence of complications after carotid sinus massage in older patients with syncope. J Am Geriatr Soc. 1994;42:1248-1251.

41. Carotid Sinus Massage (CSM) Relative contraindications Carotid bruit Pre-existing clinically significant carotid arterial disease CVA within previous 3 months Acute MI within previous 3 months Complications Transient neurological symptoms Less than 0.2% Carotid sinus massage (CSM) is an often overlooked, yet highly cost effective test, especially in older syncope patients. CSM must be applied with care, and the method described here has proven both safe and effective. AMI might cause false positive CSM. Note that an abnormal response to CSM (i.e., Carotid Sinus Hypersensitivity, CSH) is not diagnostic of Carotid Sinus Syndrome (CSS). Reproduction of symptoms is a crucial diagnostic element. To achieve symptom reproduction, it may be useful to conduct CSM with the patient in the upright posture. If the latter is to be done, the patient should be safely secured to a tilt-table in order to prevent injury from a fall. Note: May perform during tilt-table test. *Munro N, McIntosh S, Lawson J, et al. Incidence of complications after carotid sinus massage in older patients with syncope. J Am Geriatr Soc. 1994;42:1248-1251. Carotid sinus massage (CSM) is an often overlooked, yet highly cost effective test, especially in older syncope patients. CSM must be applied with care, and the method described here has proven both safe and effective. AMI might cause false positive CSM. Note that an abnormal response to CSM (i.e., Carotid Sinus Hypersensitivity, CSH) is not diagnostic of Carotid Sinus Syndrome (CSS). Reproduction of symptoms is a crucial diagnostic element. To achieve symptom reproduction, it may be useful to conduct CSM with the patient in the upright posture. If the latter is to be done, the patient should be safely secured to a tilt-table in order to prevent injury from a fall. Note: May perform during tilt-table test. *Munro N, McIntosh S, Lawson J, et al. Incidence of complications after carotid sinus massage in older patients with syncope. J Am Geriatr Soc. 1994;42:1248-1251.

42. Additional Diagnostic Tests - 1: Selected Use Based on Initial Examination and Risk Stratification Ambulatory ECG Holter Monitoring Typical Event Recorder External MCOT Loop Recorder Records & transmits ECG data with / without patient activation Insertable Loop Recorder ** Permits remote ‘downloading’ Wireless transmission in certain devices

43. Additional Diagnostic Tests - 2: Selected Use Based on Initial Examination and Risk Stratification Head-Up Tilt Test (usually combined with CSM) Electrophysiology Study (EPS) Non-invasive Risk Stratification for Life-threatening ventricular tachyarrhythmias† SAECG HRV HR turbulence Microvolt Twave alternans

44. Heart Monitoring Options Syncope Occurs Infrequently, Long-term Monitoring is Likely to be Most Effective

45. External Mobile Cardiac Outpatient Telemetry (MCOT) ECG Recorder

46. Insertable Loop Recorder (ILR) An ECG monitoring system that is implanted subcutaneously Capable of recording, storing, and if necessary remotely transmitting ECG signals Patient-activated and/or automatically-activated Longevity of current ILRs up to 36 months Indicated for Patients with unexplained syncope / TLOC Patients who experience transient symptoms that may suggest a cardiac arrhythmia Patients at increased risk of cardiac arrhythmias

47. Symptom-Rhythm Correlation: ILR Permits both Patient-triggered and Automatic Activation The gold standard for determining if a syncope episode is due to an arrhythmia is to record the rhythm during symptoms (symptom rhythm correlation). The ILR may help rule-in or rule-out arrhythmogenic causes. This slide depicts findings from an ILR interrogation as they appear on the programmer screen. In order to view stored event data, one taps the screen with the touch pen on the area of the summary graph that one wishes to view in more detail. This takes the viewer to the first zoom level of the event ECG waveform data and centers the area of the event you tapped. To view the event in greater detail, one taps the screen over the ECG of interest. On-screen calipers are available at every zoom level to measure cycle length. Intervals can be measured in milliseconds or beats per minute. Note: A - represents auto activated event P - indicates time patient activated the event The gold standard for determining if a syncope episode is due to an arrhythmia is to record the rhythm during symptoms (symptom rhythm correlation). The ILR may help rule-in or rule-out arrhythmogenic causes. This slide depicts findings from an ILR interrogation as they appear on the programmer screen. In order to view stored event data, one taps the screen with the touch pen on the area of the summary graph that one wishes to view in more detail. This takes the viewer to the first zoom level of the event ECG waveform data and centers the area of the event you tapped. To view the event in greater detail, one taps the screen over the ECG of interest. On-screen calipers are available at every zoom level to measure cycle length. Intervals can be measured in milliseconds or beats per minute. Note: A - represents auto activated event P - indicates time patient activated the event

48. ILR Symptom-Rhythm Correlation: Case Examples These are examples of ECG recordings obtained by the Reveal® ILR system in 2 symptomatic patients. The gold standard for determining if a syncope episode is due to an arrhythmia is to record the rhythm during symptoms, ie, symptom-rhythm correlation. The ILR may help rule-in or rule-out arrhythmogenic causes. These strips depict findings from an ILR interrogation as they appear on the programmer screen. In order to view the event in greater detail, one taps the screen over the ECG of interest. On-screen calipers are available at every zoom level to measure cycle length in milliseconds or beats per minute. Note that the ‘A’ represents an auto-activated event; the P indicates when the patient activated the device. Upper strip: Infra-Hisian AV block: dual chamber pacemaker. Lower strip: VT and VF: ICD, meds. These are examples of ECG recordings obtained by the Reveal® ILR system in 2 symptomatic patients. The gold standard for determining if a syncope episode is due to an arrhythmia is to record the rhythm during symptoms, ie, symptom-rhythm correlation. The ILR may help rule-in or rule-out arrhythmogenic causes. These strips depict findings from an ILR interrogation as they appear on the programmer screen. In order to view the event in greater detail, one taps the screen over the ECG of interest. On-screen calipers are available at every zoom level to measure cycle length in milliseconds or beats per minute. Note that the ‘A’ represents an auto-activated event; the P indicates when the patient activated the device. Upper strip: Infra-Hisian AV block: dual chamber pacemaker. Lower strip: VT and VF: ICD, meds.

49. Head-Up Tilt Test (HUT) Protocols vary Performed with or without provocative drugs Goals: Unmask VVS susceptibility Reproduce symptoms Patient learns VVS warning symptoms Patient more confident of diagnosis Not useful for predicting treatment benefit The rationale for undertaking head-up tilt (HUT) testing in patients suspected of having vasovagal (VVS) syncope is summarized here. In essence, the test may not only provide useful diagnostic information, but it also provides an opportunity for patients to become more familiar with the condition and its possible warning signs. The latter may prove to be of considerable diagnostic utility in many individuals. Provocative drugs: isoproterenol vs. sublingual nitroglycerin—discuss pros and consThe rationale for undertaking head-up tilt (HUT) testing in patients suspected of having vasovagal (VVS) syncope is summarized here. In essence, the test may not only provide useful diagnostic information, but it also provides an opportunity for patients to become more familiar with the condition and its possible warning signs. The latter may prove to be of considerable diagnostic utility in many individuals. Provocative drugs: isoproterenol vs. sublingual nitroglycerin—discuss pros and cons

50. VVS: Typical HUT Protocols - 1 Basic Preparation 4 hour fast Continuous ECG monitor Continous BP monitor Finapress or equivalent preferred Arterial line, if placed >1 hour before Sphygmomanometer discouraged Diagnosing VVS VVS is most effectively diagnosed if the detailed medical history is ‘classic’. However, this is not often the case, and supporting evidence is needed, Such supportive evidence may include: Patient history, physical examination, ECG, and other tests provide no diagnosis for patient complaints of syncope. Patient experiences syncope during head-up tilt-table testing. Test completion without syncope is a negative result. The following HUT protocol is based on the ACC Consensus Document on tilt-table testing (Benditt 1996). Other accepted HUT protocols do exist. Overnight fast, morning test ECG (at least 3 leads) Continuous blood pressure monitoring Patient remains supine on the table for 15-30 minutes. Tilt to 60-80 degrees for 20-45 minutes. Lower to horizontal and administer isoproterenol at 1-5 ?g/min until heart rate increases 25%. Re-tilt for 10 minutes REFERENCE: Benditt DG, Ferguson DW, Grubb BP, et al. Tilt table testing for syncope. ACC Expert Consensus Document. JACC. 1996;28(1):263-275. Diagnosing VVS VVS is most effectively diagnosed if the detailed medical history is ‘classic’. However, this is not often the case, and supporting evidence is needed, Such supportive evidence may include: Patient history, physical examination, ECG, and other tests provide no diagnosis for patient complaints of syncope. Patient experiences syncope during head-up tilt-table testing. Test completion without syncope is a negative result. The following HUT protocol is based on the ACC Consensus Document on tilt-table testing (Benditt 1996). Other accepted HUT protocols do exist. Overnight fast, morning test ECG (at least 3 leads) Continuous blood pressure monitoring Patient remains supine on the table for 15-30 minutes. Tilt to 60-80 degrees for 20-45 minutes. Lower to horizontal and administer isoproterenol at 1-5 ?g/min until heart rate increases 25%. Re-tilt for 10 minutes REFERENCE: Benditt DG, Ferguson DW, Grubb BP, et al. Tilt table testing for syncope. ACC Expert Consensus Document. JACC. 1996;28(1):263-275.

51. VVS: Typical HUT Protocols - 2 Tilt Procedure Tilt to 60°- 70°, 20 min Positive end-point: Syncope If negative, then drug provocation Nitroglycerine 0.4mg SL, or Isoproterenol 1-5 mcg/min, to increase Heart Rate to 125% baseline Repeat tilt, duration 10 minutes Diagnosing VVS VVS is most effectively diagnosed if the detailed medical history is ‘classic’. However, this is not often the case, and supporting evidence is needed, Such supportive evidence may include: Patient history, physical examination, ECG, and other tests provide no diagnosis for patient complaints of syncope. Patient experiences syncope during head-up tilt-table testing. Test completion without syncope is a negative result. The following HUT protocol is based on the ACC Consensus Document on tilt-table testing (Benditt 1996). Other accepted HUT protocols do exist. Overnight fast, morning test ECG (at least 3 leads) Continuous blood pressure monitoring Patient remains supine on the table for 15-30 minutes. Tilt to 60-80 degrees for 20-45 minutes. Lower to horizontal and administer isoproterenol at 1-5 ?g/min until heart rate increases 25%. Re-tilt for 10 minutes REFERENCE: Benditt DG, Ferguson DW, Grubb BP, et al. Tilt table testing for syncope. ACC Expert Consensus Document. JACC. 1996;28(1):263-275. Diagnosing VVS VVS is most effectively diagnosed if the detailed medical history is ‘classic’. However, this is not often the case, and supporting evidence is needed, Such supportive evidence may include: Patient history, physical examination, ECG, and other tests provide no diagnosis for patient complaints of syncope. Patient experiences syncope during head-up tilt-table testing. Test completion without syncope is a negative result. The following HUT protocol is based on the ACC Consensus Document on tilt-table testing (Benditt 1996). Other accepted HUT protocols do exist. Overnight fast, morning test ECG (at least 3 leads) Continuous blood pressure monitoring Patient remains supine on the table for 15-30 minutes. Tilt to 60-80 degrees for 20-45 minutes. Lower to horizontal and administer isoproterenol at 1-5 ?g/min until heart rate increases 25%. Re-tilt for 10 minutes REFERENCE: Benditt DG, Ferguson DW, Grubb BP, et al. Tilt table testing for syncope. ACC Expert Consensus Document. JACC. 1996;28(1):263-275.

52. Induction of VVS by Upright Posture Cardioinhibitory & Vasodepressor Components Heart Rate monitor and Finapres® pressure tracing illustrating posture-induced vasovagal syncope. Note that blood pressure tended to fall in advance of the bradycardia component. Heart Rate monitor and Finapres® pressure tracing illustrating posture-induced vasovagal syncope. Note that blood pressure tended to fall in advance of the bradycardia component.

53. Neurological Tests for TLOC: EEG, Head CT / MRI Not useful for syncope evaluation Imaging may be warranted if there is concern about head injury from ‘fall’ May be useful in non-syncope TLOC patients but neurological consultation is advised prior to tests

54. Neurological Tests for TLOC: EEG, Head CT, Head MRI 1Kapoor W. Evaluation and outcome of patients with syncope. Medicine. 1990;69:160-175. 2Linzer M, Yang E, Estes M, et al. Diagnosing syncope Part 2: Unexplained Syncope. Ann Intern Med. 1997;127:76-86. 1Kapoor W. Evaluation and outcome of patients with syncope. Medicine. 1990;69:160-175. 2Linzer M, Yang E, Estes M, et al. Diagnosing syncope Part 2: Unexplained Syncope. Ann Intern Med. 1997;127:76-86.

55. Treatment Treatment is aimed at preventing a syncope recurrence Taking new medications or making changes to your current medications Wearing support garments or compression stockings to improve circulation

56. Treatment Making certain dietary changes such as eating small, more frequent meals; increasing salt, fluid and potassium; and avoiding caffeine and alcohol Taking certain precautions when changing positions from sitting to standing Proamitine, Florinef, Sudafed,Nadolol

57. Treatment Elevating the head of your bed while sleeping. Avoiding or changing the situations or "triggers" that cause a syncope episode Biofeedback training to control a rapid heartbeat.

58. Treatment Pacemaker implantation to regulate the heart rate -- only as needed for certain medical conditions Implantable cardiac defibrillator (ICD), which constantly monitors your heart rate and rhythm and corrects a fast, abnormal rhythm -- only as needed for certain medical conditions

59. Treatment About 30 percent of people with one episode of syncope will have a recurrence. The underlying cause of syncope and the patient's age, gender and presence of other medical conditions will affect the prognosis or outlook.

60. Central Autonomic Disorders Multiple System Atrophy - Shy Drager Syndrome Parkinson's Disease

61. Orthostatic Intolerance Syndrome Postural Tachycardia Syndrome (POTS) Mitral Valve Prolapse Idiopathic Hypovolumia Paroxysmal Autonomic Syncope Neurocardiogenic Syncope

62. Peripheral Autonomic Disorders Acute Idiopathic Polyneuropathy - Guillain Barré Syndrome Chagas' Disease Diabetic Autonomic Failure Familial Dysautonomia Pure Autonomic Failure

63. Catecholamine Disorders Baroreflex Failure Dopamine -ß- Hydroxylase Deficiency Pheochromocytoma Neuroblastoma Chemodectoma Familial Paraganglioma Syndrome

64. Catecholamine Disorders Tetrahydrobiopterin Deficiency Aromatic L-Amino Acid Decarboxylase Deficiency Menkes Disease Monoamine Oxidase Deficiency States Disorders of Dopamine Metabolism

66. Autonomic reflex testing QUANTITATIVE PSUDOMOTOR AXON REFLEX TESTING (QSART) QSART offers quantitative measurement of axon reflex-mediated sudomotor (sweat) responses and the evaluation of postganglionic sympathetic small nerve fibers. Measurements are taken at four skin sites on the upper and lower extremities.

67. RESTING SWEAT TESTING This test measures the amount of sweat produced while the body is at rest as another index of activity of small nerve fibers. During testing, the patient lies quietly and is usually very comfortable. VASOMOTOR TESTING Skin temperatures at various sites on the arms and legs is recorded using a highly sensitive thermometer.

68. EVALUATION OF CARDIAC-VAGAL AND ADRENERGIC FUNCTIONS DEEP BREATHING: This is one of the most reliable cardiovascular heart rate tests for evaluating autonomic function and measures heart rate responses to deep slow breathing.

69. VALSALVA MANEUVER This test mimics everyday activities which require heavy lifting or straining, that may result in lightheadedness or even loss of consciousness. During the Valsalva maneuver, the patient is asked to exhale steadily into a bugle for 15 seconds at 40 mmHg while in the supine position.

70. TILT TABLE TEST Current standardized tilt protocols possess the sensitivity and specificity to identify individuals with pre-syncope, syncope, and orthostatic hypotension. Tilt table testing evaluates beat-to-beat heart rate and blood pressure, respiration and carbon dioxide responses to passive standing.

71. QUANTITATIVE SENSORY TESTING Quantitative sensory testing evaluates sensation of vibration, cold, warm, heat, and pain. It can be used for the patients with chronic pain.

72. Neurology testing ELECTROENCEPHALOGRAPHIC MONITORING (EEG) TRANSCRANIAL DOPPLER MONITORING (TCD) TCD enables noninvasive monitoring of cerebral blood flow from intracranial vessels for evaluation of vasospasm, stroke and migraine headache.

73. 24-HOUR ABP MONITORING Enables noninvasive ambulatory monitoring of blood pressure over the period of 24 hours

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