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![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
Soteriades ES, Evans JC, Larson MG, et al. Incidence and prognosis of syncope. N
Engl J Med. 2002;347(12):878-885. [Framingham Study Population]](https://image.slidesharecdn.com/syncope-141126102947-conversion-gate02/85/Syncope-9-320.jpg)
More Related Content
Syncope
- 1. Evaluation of Syncope Dr. Charles Nelson November 14, 2014
- 2. 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 UUnnddeerrllyyiinngg mmeecchhaanniissmm:: ttrraannssiieenntt gglloobbaall cceerreebbrraall hhyyppooppeerrffuussiioonn..
- 3. Syncope Mimics •Acute intoxication (e.g., alcohol) • Seizures • Sleep disorders • Somatization disorder (psychogenic pseudo-syncope) • Trauma/concussion • Hypoglycemia • Hyperventilation Brignole M, et al. Europace, 2004;6:467-537.
- 4. Syncope: Epidemiological Data • 40% population, presumed syncope at least once1 • 1-6% of hospital admissions2 • Approx 1% of ED visits per year3,4 • 10% of falls by elderly are believed due to syncope5 • Injuries: • 6% major morbidity (e.g., fractures, MVA)1 • Minor injury in 29%1 1Kenny RA, et al. eds. The Evaluation and Treatment of Syncope. Futura;2003:23-27. 2Kapoor W. Medicine. 1990;69:160-175. 3Brignole M, et al. Europace. 2003;5:293-298. 4 Blanc J-J, et al. Eur Heart J. 2002;23:815-820. 5Campbell A, et al. Age and Ageing. 1981;10:264-270.
- 5. Syncope & Collapse:Emergency Department US Data 2006 • Emergency Department visits • Primary Diagnosis ~1.13 million • Among all listed diagnoses >1.35 million • Hospital admission rate, ~36%
- 6. Impact of Syncopein USA: Annual Expenditures • Estimated hospital costs > $5400/hospitalization • Treating ‘falls’ in older adults1 >$7 billion 1. Benjamin C. Sun, MD, MPP, Jennifer A. Emond, MS, and Carlos A. Camargo, Jr., MD, DrPH “Direct medical costs of syncope-related hospitalizations in the USA Am J Cardiol 2005;95:668-671 2 Kenny RA, Kapoor WN. In: Benditt D, et al. eds. The Evaluation and Treatment of Syncope. Futura;2003:23-27.
- 7. Syncope & Collapse:Estimated Hospitalization Costs Conservative estimates of annual cost: • Syncope / Collapse - $2.4 billion • Asthma - $2.8 billion • HIV - $2.2 billion • COPD - $1.9 billion
- 8. Causes of TrueSyncope Orthostatic Cardiac Arrhythmia Structural Cardio- Pulmonary 1• VVS • CSS • Situational Cough Post-micturition 2• Drug-Induced • ANS Failure Primary Secondary 3• Bradycardia Sinus pause/arrest AV block •Tachycardia VT SVT • LongQT Synd 4 • Aortic Stenosis • HCM • Pulmonary Hypertension • Aortic Dissection Neurally- Mediated Reflex 6600%% 1155%% 1100%% 55%% Unexplained Causes = Approximately 10%
- 9. Impact of Syncopeon 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 Soteriades ES, Evans JC, Larson MG, et al. Incidence and prognosis of syncope. N Engl J Med. 2002;347(12):878-885. [Framingham Study Population]
- 10. Diagnostic Goal Establishcause of syncope with sufficient certainty to: • Assess prognosis confidently • Initiate effective preventive treatment
- 11. Neurological Tests: Tests: Rarely Rarely Diagnostic Diagnostic for Syncope for Syncope • EEG, Head CT, Head MRI carotid dopplers • May help diagnose seizure • Reasonable if syncope has resulted in closed head injury or if focal neuro findings Brignole M, et al. Europace. 2004;6:467-537.
- 12. Clinical Features SuggestingCause 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 CSS=carotid sinus syndrome
- 13. Neurally-Mediated Reflex Syncope(NMS) • Vasovagal Syncope (VVS) • Carotid Sinus Syndrome (CSS) • Situational Syncope – post-micturition – cough – swallow – defecation – blood drawing – etc.
- 14. NMS:Clinical Pathophysiology •Neurally-mediated physiologic reflex mechanism with two components: – Cardioinhibitory ( HR ) – Vasodepressor ( BP ) • Both components are usually present: – Vasodepressor may be masked in the presence of severe bradycardia – Pace or pre-treat with atropine in order to observe Vasodepressor component
- 15. Orthostatic Intolerance Syndromes Orthostatic Syncope PPOOTTSS Vasovagal Orthostatic Syncope Intolerance
- 16. Orthostatic Hypotension- Etiology • Drug-induced (very common) – Diuretics, Vasodilators • Primary autonomic failure – Multiple system atrophy, Parkinsonism • Secondary autonomic failure – Diabetes, Alcohol, Amyloid
- 17. Clinical/ECG Features ForCardiac Syncope • Presence of severe structural heart disease • Family history of sudden death • Syncope during exertion or while supine • Palpitations at time of syncope • Heart failure / LV Dysfunction • ECG / Monitor findings of: – Baseline Wide QRS Complex – Mobitz 1 second degree AVB – Sinus bradycardia <50 bpm – Documented Non Sustained or Sustained VT – Preexcitation, Long QT, t wave inversion – Bifasicular block Adapted from ESC Syncope Guidelines– Update 2004
- 18. Syncope Due toStructural CV Disease • Acute MI / Ischemia • Acquired coronary artery disease – Congenital coronary artery anomalies • Hypertrophic Cardiomyopathy (HCM) • Arrhythmogenic RV Dysplasia (ARVD) • Acute aortic dissection • Acute pulmonary embolus/pulmonary hypertension • Valvular abnormalities – Aortic stenosis – Mitral stenosis • Atrial myxoma • Intra-cardiac thrombus (ball-valve thrombus)
- 19. Syncope Due toCardiac Arrhythmias • Bradyarrhythmias – Sinus arrest, exit block – High grade or acute complete AV block • Tachyarrhythmias – Atrial fibrillation/flutter with rapid ventricular rate (e.g., WPW syndrome) – Paroxysmal SVT or VT – Torsades de pointes (e.g., long QT syndrome)
- 20. The Initial Evaluation:4 Key Questions • Did the patient suffer ‘true’ Transient Loss of Consciousness (TLOC)? • Was TLOC due to syncope or mimic? • Is heart disease present? • Does the medical history (including observations by witnesses) suggest a specific diagnosis?
- 21. Hospital Admission forDiagnosis or Treatment Occasionally may need to be admitted •No heart disease but sudden onset of palpitations shortly before syncope or high suspicion of cardiac syncope •Other sig condition associated with though not cause of syncope •Syncope in supine position, •Frequent recurrent episodes, injuries ESC Syncope Task Force 2004
- 22. Diagnostic Testing •Exertional syncope or exertional symptoms: stress test • Signs or symptoms CHF, murmurs: echo • Palpitations or tachycardia preceeding event: holter or event • Abnormal ekg (heart block, bifasicular block): holter or ILR • Suspected (but uncertain) NMS: tilt test • Pts that are orthostatic do not need tilt test
- 23. When do notneed refer to specialist • No need to refer when cause for syncope is certain, and no evidence of significant heart disease. • No need to refer if diagnosis is uncertain, but episode did not result in significant injury and is not recurrent.
- 24. When to referto specialist • When initial evaluation or testing indicates underlying significant heart disease (abnormal ekg or echo) • When need tilt testing to confirm cause of syncope • When syncope is recurrent in spite of treatment for suspected cause • When cause is uncertain and syncope is recurrent • Anytime you have a question that you cant answer or are not sure how to proceed in evaluating the patient.
- 25.
- 26. Treatment Strategies forOrthostatic Intolerance • Patient education, injury avoidance • Hydration – fluids, salt, diet – minimize caffeine/alcohol • Sleeping with head of bed elevated • Tilt Training, leg crossing, arm tensing • Support hose, abdominal binders • Drug therapies – fludrocortisone, midodrine, erythropoietin
Editor's Notes
- #2 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.
- #4 Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update 2004. Europace. 2004;6:467-537.
- #5 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.
- #6 National Hospital Discharge Survey (NHDS) 2003. National Ambulatory Medical Care Survey (NAMCS) 2002. Syncope is a growing problem. More patients are being seen in outpatient visits and are being admitted with this problem.
- #7 1Olshansky B. Syncope: Overview and approach to management. In: Grubb B and Olshansky B. eds. Syncope: Mechanisms and Management. Armonk, NY:Futura;1998:15-71. 2Kenny 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.
- #8 National Hospital Discharge Survey (NHDS) 2003. National Ambulatory Medical Care Survey (NAMCS) 2002. Syncope is a growing problem. More patients are being seen in outpatient visits and are being admitted with this problem.
- #9 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 Cardiomyopathy
- #12 most would put carotid dopplers in the same category, unless testing driven by symptoms or high vascular disease risk factors. Imaging may be justified are neurological findings or if there is concern that syncope may have resulted in a head injury Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update 2004. Europace. 2004;6:467-537.
- #13 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.
- #14 The neurally-mediated reflex causes of syncope are a group of related conditions in terms of symptomatic hypotension being caused by a variable combination of bradycardia and vasodilatation. Vasovagal syncope and carotid sinus syndrome are the most frequent conditions in this group. The others occur from time-to-time and are usually recognized only if a detailed medical history is obtained.
- #15 Syncope in vasovagal fainters, as in other forms of neurally-mediated reflex syncope, is due to systemic hypotension resulting in a transient period of inadequate cerebral blood flow. Hypotension is the result of 2 pathophysiologic components: 1. Marked bradycardia or inappropriately slow heart rate for the blood pressure (i.e., cardioinhibitory feature) 2. Vasodilatation The relative contribution of these 2 components varies among patients
- #16 Management Strategies for VVS Optimal management strategies for VVS are a source of debate. Patient education, reassurance, and instruction. When the patient has a relatively long prodrome, evasive action may prevent injury if not syncope. Control of fluids, salt, and diet may help reduce incidence. Support hose may limit blood pooling in the legs and feet. Drug therapy should be used as a second line option. Midodrine and beta-adrenergic blockers are the agents most thoroughly studied to date/ Pacing may benefit some patients Pacing today is generally considered a last resort unless the patient experiences prolonged asystole during episodes. Diagnosis of VVS with positive head-up tilt test and a cardioinhibitory or mixed reflex is a Class II indication for pacing. 2 large randomized controlled trials support the utility of pacing in very symptomatic VVS patients
- #17 Orthostatic hypotension is an important cause of syncope. The medical history is usually sufficient to establish the diagnosis. However, defining the specific cause requires careful consideration of a number of important conditions. The most important conditions predisposing to orthostatic syncope are listed here.
- #19 Pts with pul htn may be especially sensitive to diuretics or non selective vasodilators. MI—myocardial infarction HCM—hypertrophic cardiomyopathy
- #20 Both excessively slow as well as excessively rapid heart rates may result in sufficient drop in systemic pressure to cause syncope. In the case of tachycardias, the syncope tends to occur at the onset of the episode, before vascular constriction has an opportunity to occur. Syncope may also occur at termination of tachyarrhythmias, if a prolonged pause occurs prior to resumption of a stable rhythm. WPW—Wolff Parkinson White syndrome
- #21 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 Management Strategies for VVS Optimal management strategies for VVS are a source of debate. Patient education, reassurance, and instruction. When the patient has a relatively long prodrome, evasive action may prevent injury if not syncope. Control of fluids, salt, and diet may help reduce incidence. Support hose may limit blood pooling in the legs and feet. Drug therapy should be used as a second line option. Midodrine and beta-adrenergic blockers are the agents most thoroughly studied to date/ Pacing may benefit some patients Pacing today is generally considered a last resort unless the patient experiences prolonged asystole during episodes. Diagnosis of VVS with positive head-up tilt test and a cardioinhibitory or mixed reflex is a Class II indication for pacing. 2 large randomized controlled trials support the utility of pacing in very symptomatic VVS patients