Syncope Ppt Powerpoint Presentation slides Ryan Ferrell Medical Slideshow HPV Vaccine and Syncope . Reports of syncope received by the VAERS has been

Syncope

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Tarik on Aug 26, 2009 Says :

thank you very much for this share.

Patti on Apr 24, 2009 Says :

This is a great PowerPoint. I would love to be able to download or print this for use. I am studying as a Nurse Practitioner and would find this helpf

anil on Apr 16, 2009 Says :

how much dangerous syncope is?

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Notes

Show Notes

Slide 1 :

SyncopeA Diagnostic and Treatment Strategy Ryan S. Ferrell, M.D. EP Conference 8/18/06 KUMC

Slide 2 :

Syncope: Transient Loss of Consciousness (TLOC)

Slide 3 :

Syncope Sudden transient loss of consciousness with associated loss of postural tone. Recovery is spontaneous without neurologic deficit and without requiring electrical or chemical cardioversion. Generally a fall in systolic blood pressure below 70 mmHg or a mean arterial pressure of 40 mmHg results in loss of consciousness. Cerebral blood flow usually decreases with aging, making the elderly at higher risk for syncope.

Slide 4 :

Syncope Syncope as a symptoms can be caused by a variety of medical diseases that produce a transient interruption of cerebral blood flow. A genuine effort should be made to determine a specific cause of syncope as identifying a specific cause can help in the selection of therapy, prevent recurrences, minimize expensive evaluations, and decrease morbidity. Patients with cardiac syncope have higher rates of mortality and sudden death at follow up. Identifying and treating cardiac syncope can improve outcome.

Slide 5 :

Classification of Transient Loss of Consciousness (TLOC) Syncope Neurally-mediated reflex syndromes Orthostatic hypotension Cardiac arrhythmias Structural cardiovascular disease Disorders Mimicking Syncope With loss of consciousness, i.e., seizure disorders, concussion Without loss of consciousness, i.e., psychogenic “pseudo-syncope” Real or Apparent TLOC Brignole M, et al. Europace, 2004;6:467-537.

Slide 6 :

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 Underlying mechanism is transient global cerebral hypoperfusion. Brignole M, et al. Europace, 2004;6:467-537.

Slide 7 :

Presentation Overview I. Etiology, Prevalence, Impact II. Diagnosis III. Specific Conditions and Treatment IV. Special Issues

Slide 8 :

Section I:Etiology, Prevalence, Impact

Slide 9 :

Causes of True Syncope Orthostatic Cardiac Arrhythmia Structural Cardio- Pulmonary 1 VVS CSS • Situational Cough Post- Micturition 2 Drug-Induced • ANS Failure Primary Secondary 3 Brady SN Dysfunction AV Block • Tachy VT SVT Long QT Syndrome 4 Acute Myocardial Ischemia Aortic Stenosis HCM Pulmonary Hypertension Aortic Dissection Neurally- Mediated Unexplained Causes = Approximately 1/3 DG Benditt, MD. U of M Cardiac Arrhythmia Center

Slide 10 :

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.

Slide 11 :

Impact of Syncope 1Kenny RA, Kapoor WN. In: Benditt D, 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. 40% will experience syncope at least once in a lifetime1 1-6% of hospital admissions2 1% of emergency room visits per year3,4 10% of falls by elderly are due to syncope5 Major morbidity reported in 6%1eg, fractures, motor vehicle accidents Minor injury in 29%1eg, lacerations, bruises

Slide 12 :

Impact of Syncope: US Trends *All patients discharged with syncope and collapse (ICD-9 Code:780.2) listed among diagnoses. NHDS 2003. NAMCS 2002. Inpatient Trend* Physician Office Visits** **Syncope and collapse (ICD-9 Code: 780.2) listed as primary reason for visit. (000s) (000s)

Slide 13 :

Impact of Syncope: US Trends EmergencyDepartment Visits* HospitalOutpatient Visits* (000s) + Not available NHAMCS 2002. + *Syncope and collapse (ICD-9 Code:780.2) listed as primary reason for visit. (000s)

Slide 14 :

Impact of Syncope: NHS Hospitals, England, 2002-2003* 74,813 hospital consults for syncope and collapse 80% required hospital admission Average length of stay: 6.1 days 327,201 hospital bed days, second only to senility *Hospital Episode Statistics, Dept. of Health, Eng. 2002-2003.

Slide 15 :

Impact of Syncope: Costs Estimated hospital costs exceeded $10 billion US1 Estimated physician office expenses exceeded $470 million2 £104,285 spent on 1,334 patients with syncopal codes (UK) (EaSyAS)3 Hospital admission: 67% of investigational costs Over $7 billion is spent annually in the US to treat falls in older adults4 1Kenny RA, Kapoor WN. In: Benditt D, et al. eds. The Evaluation and Treatment of Syncope. Futura;2003:23-27. 2OutPatientView v. 6.0. Solucient LLC, Evanston IL. 3Farwell D, et al. J Cardiovasc Electrophysiol. 2002;13(Supp):S9-S13. 4Olshansky B. In: Grubb B and Olshansky B. eds. Syncope: Mechanisms and Management. Futura. 1998:15-71.

Slide 16 :

Impact of Syncope: Quality of Life 1Linzer M. J Clin Epidemiol. 1991;44:1037. 2Linzer M. J Gen Int Med. 1994;9:181. Anxiety/Depression Alter DailyActivities RestrictedDriving ChangeEmployment 73%1 71%2 60%2 37%2 Percent of Patients

Slide 17 :

Syncope Mortality Low mortality vs. high mortality Neurally-mediated syncope vs. syncope with a cardiac cause 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]

Slide 18 :

Implications of Syncope for Driving a Vehicle Those who drive and have recurrent syncope risk their lives and the lives of others Places considerable burden on the physician Essential to know local laws and physician responsibilities Some states – Invasion of privacy to notify motor vehicle department* Other states – Reporting is mandatory* Olshansky B, Grubb B. In: Syncope: Mechanisms and Management. Futura. Armonk, NY. 1998. *Medtronic, Inc. Follow-up Forum. 1995/96;1(3):8-10.

Slide 19 :

Challenges of Syncope Diagnosis Complex Quality of life implications Work Mobility (automobiles) Psychological Cost Cost/year Cost/diagnosis

Slide 20 :

Section II:Diagnosis

Slide 21 :

Diagnostic Objectives Distinguish true syncope from syncope mimics Syncope vs. dizziness, presyncope, drop attacks, vertigo, & seizures. Remember syncope can result in seizure-like activity. Determine presence of heart disease Search for the presence of structural heart disease such as valvular stenosis, cardiomyopathy, or myocardial infarction. This may suggest more malignant causes such as ventricular tachycardia. Critical as most important factor in prognosis and risk stratification. Establish the cause of syncope with sufficient certainty to: Assess prognosis confidently Initiate effective preventive treatment

Slide 22 :

A Diagnostic Plan is Essential Initial Examination Meticulous patient history Physical exam ECG Supine and upright blood pressure Review patient’s Medication list Monitoring Holter Event Recorder Insertable Loop Recorder (ILR) Cardiac Imaging Echocardiogram Special Investigations Head-up tilt test Hemodynamics Electrophysiology study (EPS) Brignole M, et al. Europace, 2004;6:467-537.

Slide 23 :

Diagnostic Flow Diagram for TLOC Brignole M, et al. Europace, 2004;6:467-537.

Slide 24 :

Initial Exam: Detailed Patient History Circumstances of recent event Eyewitness account of event Prodrome Symptoms at onset of event Sequelae Medications (proarrhythmic and QT prolonging agents) Circumstances of more remote events Concomitant disease, especially cardiac Pertinent family history Ask patient specifically about a positive family history of unexpected sudden cardiac death Cardiac disease Metabolic disorders Past medical history Neurological history Syncope Brignole M, et al. Europace, 2004;6:467-537.

Slide 25 :

Initial Exam: Thorough Physical Vital signs Heart rate Orthostatic blood pressure change Cardiovascular exam: Is heart disease present? ECG: Long QT, pre-excitation, conduction system disease Echo: LV function, valve status (AS), HOCM Neurological exam Abnormalities of cognition & speech, visual fields, motor strength, sensation, tremor, and gait disturbance. Carotid sinus massage Perform under clinically appropriate conditions preferably during head-up tilt test Monitor both ECG and BP Brignole M, et al. Europace, 2004;6:467-537.

Slide 26 :

Carotid Sinus Massage (CSM) Method1 Massage, 5-10 seconds Don’t occlude Supine and upright posture (on tilt table) Outcome Positive carotid test is defined by cardiac asystole for 3 seconds or longer, or 50 mmHg fall in systolic BP, or 30 mmHg drop in SBP with reproduction of symptoms. Reproduction of symptoms is necessary for Carotid Sinus Syndrome. Absolute contraindications2 Carotid bruit, known significant carotid arterial disease, previous TIA/CVA last 3 months (unless recent carotid duplex study). Complications Primarily neurological Less than 0.2%3 Usually transient 1Kenny RA. Heart. 2000;83:564.2Linzer M. Ann Intern Med. 1997;126:989. 3Munro N, et al. J Am Geriatr Soc. 1994;42:1248-1251.

Slide 27 :

Other Diagnostic Tests Ambulatory ECG Holter monitoring (48 hour study preferred) Event recorder Intermittent vs. Loop Insertable Loop Recorder (ILR) Head-Up Tilt (HUT) Includes drug provocation (NTG, isoproterenol) Carotid Sinus Massage (CSM) Adenosine Triphosphate Test (ATP) Electrophysiology Study (EPS) Brignole M, et al. Europace, 2004;6:467-537.

Slide 28 :

Diagnostic Assessment: Yields (N=3411 to 4332) References Available

Slide 29 :

Neurological Tests: Rarely Diagnostic for Syncope EEG, Head CT, Head MRI May help diagnose seizure Brignole M, et al. Europace. 2004;6:467-537.

Slide 30 :

Head-Up Tilt Test (HUT) Protocols vary Useful as diagnostic adjunct in atypical syncope cases Useful in teaching patients to recognize prodromal symptoms Not useful in assessing treatment Brignole M, et al. Europace. 2004;6:467-537.

Slide 31 :

Head-Up Tilt Test:ECG Leads and Intra-Arterial Pressure Tracing DG Benditt, MD. U of M Cardiac Arrhythmia Center 2 1

Slide 32 :

Adenosine Triphosphate (ATP) Test Ongoing investigation in the US Provokes a short and potent cardioinhibitory vasovagal response Advantages Simple Inexpensive Correlation with pacing benefit Seems to identify a unique mechanism of syncope found in patients with: Advanced age More hypertension More ECG abnormalities Brignole M. Heart. 2000;83:24-28. Donateo P. J Am Coll Cardiol. 2003;41:93-98. Flammang D. Circ. 1999;99:2427-2433.

Slide 33 :

Insertable Loop Recorder (ILR) The ILR is an implantable patient – and automatically – activated monitoring system that records subcutaneous ECG and is indicated for: Patients with clinical syndromes or situations at increased risk of cardiac arrhythmias Patients who experience transient symptoms that may suggest a cardiac arrhythmia

Slide 34 :

Conventional EP Testing in Syncope Greater diagnostic value in older patients or those with SHD Less diagnostic value in healthy patients without SHD Useful diagnostic observations: Inducible monomorphic VT SNRT > 3000 ms or CSNRT > 600 ms Inducible SVT with hypotension HV interval = 100 ms (especially in absence of inducible VT) Pacing induced infra-nodal block Benditt D. In: Topol E, ed. Textbook of Cardiovascular Medicine. Lippencott;2002:1529-1542. Lu F, et al. In: Benditt D, et al. The Evaluation and Treatment of Syncope. Futura. 2003;80-95. Brignole M, et al. Europace. 2004;6:467-537.

Slide 35 :

Diagnostic Limitations of EPS Difficult to correlate spontaneous events and laboratory findings Positive findings1 Without SHD: 6-17% With SHD: 25-71% Less effective in assessing bradyarrhythmias than tachyarrhythmias2 EPS findings must be consistent with clinical history Beware of false positive 1Linzer M, et al. Ann Int Med. 1997;127:76-86. 2Lu F, et al. In: Benditt D, et al. The Evaluation and Treatment of Syncope. Futura. 2003;80-95.

Slide 36 :

ISSUEInternational Study of Syncope of Uncertain Etiology Multicenter, international, prospective study Analyzed the diagnostic contribution of an ILR in three predefined groups of patients with syncope of uncertain origin: Isolated syncope: No SHD, Normal ECG1 Negative tilt Positive tilt Patients with heart disease and negative EP test2 Patients with bundle branch block and negative EP test3 1Moya A. Circulation. 2001; 104:1261-1267. 2Menozzi C, et al. Circulation. 2002;105:2741-2745. 3Brignole M, et al. Circulation. 2001;104:2045-2050.

Slide 37 :

ISSUEPatients with Isolated Syncope and Tilt-Positive Syncope Moya A. Circulation. 2001;104:1261-1267.

Slide 38 :

ISSUEIsolated Syncope vs. Tilt-Positive Syncope Conclusions Results similar in the two arms, including syncope recurrence and ECG correlation Tilt-negative patients had as many bradycardias (18%) astilt-positive patients (21%) Most frequent finding was asystole secondary to progressive sinus bradycardia, suggesting a neuro-mediated origin Homogeneous findings from tilt-negative and tilt-positive infer low sensitivity of tilt-testing Moya A. Circulation. 2001;104:1261-1267.

Slide 39 :

ISSUE Patients with Heart Disease and a Negative EP Test Menozzi C, et al. Circulation. 2002;105:2741-2745. AV block + asystole: 1 A.Fib + asystole: 1 Sinus arrest: 1 Sinus tachycardia: 1 Rapid A.Fib: 2 Sustained VT: 1 Parox. A.Fib/AT: 1 Post tachycardia pause: 1 No rhythm variations: 4 Sinus tachycardia: 1

Slide 40 :

ISSUEPatients with Heart Disease and a Negative EP Test Conclusions Patients with unexplained syncope, overt heart disease, and negative EP study had a favorable medium-term outcome Mechanism of syncope was heterogeneous Ventricular tachyarrhythmia was unlikely “ILR-guided strategy seems reasonable, with specific therapy safely delayed until a definite diagnosis is made.” Menozzi C, et al. Circulation. 2002;105:2741-2745.

Slide 41 :

ISSUEPatients with Bundle Branch Block and Negative EP Test Brignole M., ET AL.,Circulation. 2001;104:2045-2050. * 5 of these also had =1 presyncope ** Drop-out before primary-end point ILR-Detected: 19 AVB: 12 (63%) SA: 4 (21%) Asystole-undefined: 1 (5%) NSR: 1 (5%) Sinus tachy: 1 (5%) Not Detected: 3 ILR-DetectedPre-Syncope:2 Pts (4%)** AVB: 2 (4%)

Slide 42 :

ISSUEPatients with Bundle Branch Block and Negative EP Test Conclusion: In patients with BBB and negative EP study, most syncopal recurrences have a homogeneous mechanism that is characterized by prolonged asystolic pauses mainly attributable to sudden-onset paroxysmal AV block. Brignole M. Circulation. 2001;104:2045-2050.

Slide 43 :

Section III:Specific Conditions and Treatment

Slide 44 :

Specific Conditions Cardiac arrhythmia Brady/Tachy Long QT syndrome Torsade de pointes Brugada Drug-induced Structural cardio-pulmonary Neural-mediated Vasovagal Syncope (VVS) Carotid Sinus Syndrome (CSS) Orthostatic

Slide 45 :

Cardiac Syncope Includes cardiac arrhythmias and SHD One of the goals, therefore, is to attempt to either rule out or rule in arrhythmic disorders. Often life-threatening May be warning of critical CV disease Tachy and brady arrhythmias Myocardial ischemia, aortic stenosis, pulmonary hypertension, aortic dissection Assess culprit arrhythmia or structural abnormality aggressively Initiate treatment promptly Brignole M, et al. Europace. 2004;6:467-537.

Slide 46 :

“…cardiac syncope can be a harbinger of sudden death.” Survival with and without syncope 6-month mortality rate of greater than 10% Cardiac syncope doubled the risk of death Includes cardiac arrhythmias and SHD Soteriades ES, et al. N Engl J Med. 2002;347:878.

Slide 47 :

Syncope Due to Structural Cardiovascular Disease: Principle Mechanisms Acute MI/Ischemia 2° neural reflex bradycardia – Vasodilatation, arrhythmias, low output (rare) Hypertrophic cardiomyopathy Limited output during exertion (increased obstruction, greater demand), arrhythmias, neural reflex Acute aortic dissection Neural reflex mechanism, pericardial tamponade Pulmonary embolus/pulmonary hypertension Neural reflex, inadequate flow with exertion Valvular abnormalities Aortic stenosis – Limited output, neural reflex dilation in periphery Mitral stenosis, atrial myxoma – Obstruction to adequate flow Brignole M, et al. Europace. 2004;6:467-537.

Slide 48 :

Syncope Due to Cardiac Arrhythmias Bradyarrhythmias Sinus arrest, exit block High grade or acute complete AV block Can be accompanied by vasodilatation (VVS, CSS) Tachyarrhythmias Atrial fibrillation/flutter with rapid ventricular rate (eg, pre-excitation syndrome) Paroxysmal SVT or VT Torsade de pointes Brignole M, et al. Europace. 2004;6:467-537.

Slide 49 :

ILR Recordings CASE: 28 year-old man presents to ER multiple times after falls resulting in trauma. VT: Ablated and medicated. CASE: 83 year-old woman with syncope due to bradycardia: Pacemaker implanted. Reveal ® ILR recordings; Medtronic data on file.

Slide 50 :

Long QT Syndromes Mechanism Abnormalities of sodium and/or potassium channels (LQTC1&2=K+, LQTC3=Na+) Susceptibility to polymorphic VT (Torsade de pointes) Prevalence Drug-induced forms – Common Genetic forms – Relatively rare, but increasingly being recognized “Concealed” forms: May be common Provide basis for drug-induced torsade Schwartz P, Priori S. In: Zipes D and Jalife J, eds. Cardiac Electrophysiology. Saunders;2004:651-659.

Slide 51 :

Syncope: Torsade de Pointes From the files of DG Benditt, MD. U of M Cardiac Arrhythmia Center

Slide 52 :

Drug-Induced QT Prolongation(List is continuously being updated) Antiarrhythmics Class IA ...Quinidine, Procainamide, Disopyramide Class III…Sotalol, Ibutilide, Dofetilide, Amiodarone, NAPA* Antianginal Agents Bepridil* Psychoactive Agents Phenothiazines, Amitriptyline, Imipramine, Ziprasidone Antibiotics Erythromycin, Pentamidine, Fluconazole, Ciprofloxacin and its relatives Nonsedating antihistamines Terfenadine*, Astemizole Others Cisapride*, Droperidol, Haloperidol *Removed from U.S. Market Brignole M, et al. Europace, 2004;6:467-537. www.arizonacert.org

Slide 53 :

Treatment of Long QT Suspicion and recognition are critical Emergency treatment Intravenous magnesium Pacing to overcome bradycardia or pauses Isoproterenol to increase heart rate and shorten repolarization ICD if prior SCA or strong family history If drug induced: Reverse bradycardia Withdraw drug Avoid ALL long-QT provoking agents If genetic: Avoid ALL long-QT provoking agents For more information visit www.longqt.org Schwartz P, Priori S. In: Zipes D and Jalife J, eds. Cardiac Electrophysiology. Saunders;2004:651-659.

Slide 54 :

Treatment of Syncope Due to Bradyarrhythmia Class I indication for pacing using dual chamber system wherever possible Ventricular pacing in atrial fibrillation with slow ventricular response ACC/AHA/NASPE 2002 Guideline Update. Circ. 2002;106:2145-2161.

Slide 55 :

Treatment of Syncope Due to Tachyarrhythmia Atrial tachyarrhythmias AVRT due to accessory pathway – Ablate pathway AVNRT – Ablate AV nodal slow pathway Atrial fib – Pacing, linear/focal ablation for paroxysmal AF Atrial flutter – Ablate the IVC-TV isthmus of the re-entrant circuit for ‘typical’ flutter Ventricular tachyarrhythmias Ventricular tachycardia – ICD or ablation where appropriate Torsade de pointes – Withdraw offending drug or implant ICD (long QT/Brugada/short QT) Drug therapy may be an alternative in many cases Brignole M, et al. Europace. 2004;6:467-537.

Slide 56 :

Neurally-Mediated Reflex Syncope Vasovagal Syncope (VVS) Carotid Sinus Syndrome (CSS) Situational syncope Micturition Defecation Cough Deglutition Sneezing Blood drawing Trumpet playing Brignole M, et al. Europace, 2004;6:467-537.

Slide 57 :

VVSClinical Pathophysiology Neurally-mediated physiologic reflex mechanism with two components: 1. Cardioinhibitory (? HR) 2. Vasodepressor (? BP) despite heart beats, no significant BP generated Both components are usually present Wieling W, et al. In: Benditt D, et al. The Evaluation and Treatment of Syncope. Futura. 2003;11-22. 1 2

Slide 58 :

VVSIncidence Most common form of syncope 8% to 37% (mean 18%) of syncope cases Depends on population sampled Young without SHD, ? incidence Older with SHD, ? incidence Linzer M, et al. Ann Intern Med. 1997;126:989.

Slide 59 :

VVS vs. CSS In general: VVS patients younger than CSS patients Ages range from adolescence to older adults (median 43 years) History: Episodes of neurocardiogenic syncope are typically associated with post-episode fatigue or weakness. Linzer M, et al. Ann Intern Med. 1997;126:989.

Slide 60 :

From the files of DG Benditt, MD. U of M Cardiac Arrhythmia Center VVS Spontaneous 16 year-old male, healthy, athletic, monitored for fainting.

Slide 61 :

VVSDiagnosis History and physical exam, ECG and BP Head-Up Tilt (HUT) – Protocol: Fast > 2 hours ECG and continuous blood pressure, supine, and upright Tilt to 70°, 20 minutes Isoproterenol/Nitroglycerin if necessary End point – Loss of consciousness 60° - 80° Benditt D, et al. JACC. 1996;28:263-275. Brignole M, et al. Europace, 2004;6:467-537.

Slide 62 :

VVS General Treatment Measures Optimal treatment strategies for VVS are a source of debate Treatment goals Acute intervention Physical maneuvers, eg, crossing legs or tugging arms Lowering head Lying down Long-term prevention Tilt training Education Diet, fluids, salt Support hose Drug therapy Pacing Brignole M, et al. Europace, 2004;6:467-537.

Slide 63 :

VVS Tilt Training Protocol Objectives Enhance orthostatic tolerance Diminish excessive autonomic reflex activity Reduce syncope susceptibility/recurrences Technique Prescribed periods of upright posture against a wall Start with 3-5 min BID Increase by 5 min each week until a duration of 30 min is achieved Reybrouck T, et al. PACE. 2000;23(4 Pt. 1):493-498.

Slide 64 :

VVS Tilt Training: Clinical Outcomes Treatment of recurrent VVS Reybrouck, et al.*: Long-term study 38 patients performed home tilt training After a period of regular tilt training, 82% remained free of syncope during the follow-up period However, at the 43-month follow-up, 29 patients had abandoned the therapy Conclusion: The abnormal autonomic reflex activity of VVS can be remedied. Compliance may be an issue. *Reybrouck T, et al. PACE. 2000;23:493-498.

Slide 65 :

VVS Tilt Training: Clinical Outcomes Foglia-Manzillo, et al.*: Short-term study 68 patients 35 tilt training 33 no treatment (control) Tilt table test conducted after 3 weeks 19 (59%) of tilt trained and 18 (60%) of controls had a positive test Tilt training was not effective in reducing tilt testing positivity rate Poor compliance in the majority of patients with recurrent VVS *Foglio-Manzillo G, et al. Europace. 2004;6:199-204.

Slide 66 :

VVS Pharmacologic Treatment Fludrocortisone Beta-adrenergic blockers Preponderance of clinical evidence suggests minimal benefit1 SSRI (Selective Serotonin Re-Uptake Inhibitor) 1 small controlled trial2 Vasoconstrictors 1 negative controlled trial (etilefrine)3 2 positive controlled trials (midodrine)4,5 1Brignole M, et al. Europace, 2004;6:467-537. 2Di Girolamo E, et al. JACC. 1999;33:1227-1230. 3Raviele A, et al. Circ. 1999;99:1452-1457. 4Ward C, et al. Heart. 1998;79:45-49. 5Perez-Lugones A, et al. J Cardiovasc Electrophysiol. 2001;12(8):935-938.

Slide 67 :

Midodrine for VVS Perez-Lugones A, Schweikert R, Pavia S, et al. J Cardiovasc Electrophysiol. 2001;12(8):935-938. Months p < 0.001 Symptom-Free Interval 0 Fluid Midodrine

Slide 68 :

The Role of Pacing as Therapy for Syncope VVS with +HUT and cardioinhibitory response:Class IIb indication for pacing Three randomized, prospective trials reported benefits of pacing in select VVS patients: VPS I1 VASIS2 SYDIT3 Subsequent study results less clear VPS II4 Synpace5 INVASY6 1Connolly SJ. J Am Coll Cardiol. 1999;33:16-20. 2Sutton R. Circulation. 2000;102:294-299. 3Ammirati F. Circ. 2001;104:52-57. 4Connolly S. JAMA. 2003;289:2224-2229. 5Giada F. PACE . 2003;26:1016 (abstract). 6Occhetta E, et al. Europace. 2004;6:538-547.

Slide 69 :

VPS I (North American Vasovagal Pacemaker Study) Objective: To evaluate pacemaker therapy for severe recurrent vasovagal syncope Randomized, prospective, single center N=54 patients 27: DDD pacemaker with rate drop response 27: No pacemaker Inclusion: Vasodepressor response Primary outcome: First recurrence of syncope Connolly SJ. J Am Coll Cardiol. 1999;33:16-20.

Slide 70 :

100 90 80 70 60 50 40 30 20 10 0 0 3 6 9 12 15 Time in Months No Pacemaker (PM) 2P=0.000022 Pacemaker Cumulative Risk (%) Connolly SJ. J Am Coll Cardiol. 1999;33:16-20. Results: 6 (22%) with PM had recurrence vs. 19 (70%) without PM 84% RRR (2p=0.000022) VPS I (North American Vasovagal Pacemaker Study)

Slide 71 :

VASIS (VAsovagal Syncope International Study) Objective: To evaluate pacemaker therapy for severe cardioinhibitory tilt-positive neurally mediated syncope Randomized, prospective, multi-center N=42 patients 19: DDI pacemaker (80 bpm) with rate hysteresis (45 bpm) 23: No pacemaker Inclusion: Positive cardioinhibitory response Primary outcome: First recurrence of syncope Sutton R. Circulation. 2000;102:294-299.

Slide 72 :

Sutton R. Circulation. 2000;102:294-299. Pacemaker (PM) No Pacemaker p=0.0004 Years % Syncope-Free 100 80 60 40 20 0 2 3 4 5 6 Results: 1 (5%) with PM had recurrence vs. 14 (61%) without PM VASIS (VAsovagal Syncope International Study)

Slide 73 :

SYDIT (SYncope DIagnosis and Treatment) Objective: To compare the effects of cardiac pacing with pharmacological therapy in patients with recurrent vasovagal syncope Randomized, prospective, multi-center N=93 patients 46: DDD pacemaker with rate drop response 47: Atenolol 100 mg/d Inclusion: Positive HUT with relative bradycardia Primary outcome: First recurrence of syncope Ammirati F. Circulation. 2001;104:52-57.

Slide 74 :

SYDIT (SYncope DIagnosis and Treatment) Ammirati F. Circulation. 2001;104:52-57. 0.6 0.7 0.8 0.9 1.0 0 100 200 300 400 500 600 700 800 900 1000 Drug Pacemaker (PM) Time (Days) % Syncope-Free p=0.0032 Results: 2 (4%) with PM had syncope recurrence vs. 12 (26%) without PM

Slide 75 :

VPS II (Vasovagal Pacemaker Study II) Objective: To determine if pacing therapy reduces the risk of syncope in patients with vasovagal syncope Randomized, double-blind, prospective, multi-center N=100 patients 52: Only sensing without pacing 48: DDD pacemaker with rate drop response Inclusion: Positive HUT with (HRxBP) < 6000/min x mm Hg Primary outcome: First recurrence of syncope Connolly S. JAMA. 2003;289:2224-2229.

Slide 76 :

Dual Chamber Pacing (DDD) Only Sensing Without Pacing (ODO) 1.0 0.8 0.6 0.4 0.2 0 Months Since Randomization Cumulative Risk 6 5 4 3 2 1 0 Connolly S. JAMA. 2003;289:2224–2229. Results: 33% with pacing had recurrence vs. 42% with only sensing(not statistically significant) VPS II (Vasovagal Pacemaker Study II)

Slide 77 :

SYNPACE(Vasovagal SYNcope and PACing) Objective: To determine if pacing therapy will reduce syncope relapses in patients with recurrent vasovagal syncope, compared to those with a pacemaker programmed to OFF Randomized, double-blind, prospective, multi-center, placebo-controlled N=29 patients 16: DDD PM with rate drop response programmed ON 13: PM programmed OFF (OOO mode) Inclusion: Recurrent VVS and +HUT with asystolic or mixed response Primary outcome: First recurrence of syncope Raviele A.. Europace. 2001;3:336–341. Raviele A, et al. Eur Heart J. 2004;25:1741-1748.

Slide 78 :

SYNPACE(Vasovagal SYNcope and PACing) Raviele A, et al. Eur Heart J. 2004;25:1741-1748. Results: 50% with pacing ON had recurrence vs. 38% with pacing OFF(not statistically significant) 0.6 0.7 0.8 0.9 1.0 0 200 400 600 800 1000 Pacemaker OFF % Syncope-Free p=0.58 0.5 0.4 0.3 0.2 0.1 0.0 Pacemaker ON Days Since Randomization

Slide 79 :

INVASY(INotropy Controlled Pacing in VAsovagal Syncope) Objective: To evaluate Closed Loop Stimulation (CLS), a form of rate-adaptive pacing using RV impedance, in preventing recurrence of VVS Randomized, prospective, single-blind, multi-center N=50 patients 41: CLS therapy 9: Control (pacemaker programmed in DDI) Inclusion: Recurrent VVS and +HUT with cardioinhibition Primary outcome: Recurrence of two VVSs during a minimum of 1 year of follow-up Occhetta E, et al. Europace. 2004;6:538-547.

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Slide 81 :

Role of Pacing as Therapy for Syncope: Summary Three earlier studies single blind – Bias? Pacemaker implantation may modulate reflex syncope and autonomic responses1 Study results may differ based on pre-implant selection criteria and tilt-testing techniques Pacing therapy is effective in some but not all (cardioinhibition vs. vasodepression) In five pacing studies, syncope recurred in 33/156 (21%) of paced patients, 72/162 (44%) in non-paced patients (p<0.000)2 1Kapoor W. JAMA. 2003;289:2272-2275.2Brignole M, et al.. Europace. 2004;6:467-537.

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CSSCarotid Sinus Syndrome Syncope clearly associated with carotid sinus stimulation is rare (=1% of syncope) CSS may be an important cause of unexplained syncope/falls in older individuals Prevalence higher than previously believed Carotid Sinus Hypersensitivity (CSH) No symptoms No treatment Kenny RA, et al. J Am Coll Cardiol. 2001;38:1491-1496. Brignole M, et al. Europace. 2004;6:467-537. Sutton R. In: Neurally Mediated Syncope: Pathophysiology, Investigation and Treatment. Blanc JJ, et al. eds. Armonk, NY: Futura;1996:138.

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CSSEtiology Sensory nerve endings in the carotid sinus walls respond to deformation “Deafferentation” of neck muscles may contribute Increased afferent signals tobrain stem Reflex increase in efferent vagal activity and diminution of sympathetic tone results in bradycardia and vasodilatation Carotid Sinus

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Falls:Incidence, Recurrence, CSH* 1 J Am Geriatr Soc. 1995. 2 Richardson D, et al. PACE. 1997;20:820. Incidence> Age 65 Recurrence CSH* Presentin Fallers > Age 50Presenting at ER 30% 1 50% 1 23% 2 % of Population *Carotid Sinus Hypersensitivity

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57% %6 % Recurrence CSS Role of Pacing – Syncope Recurrence Rate Class I indication for pacing (AHA and BPEG) Limit pacing to CSS that is: Cardioinhibitory Mixed DDD/DDI superior to VVI Mean follow-up = 6 months Brignole M, et al. Eur JCPE. 1992;4:247-254.

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SAFE PACESyncope And Falls in the Elderly – Pacing And Carotid Sinus Evaluation Objective Determine whether cardiac pacing reduces falls in older adults with carotid sinus hypersensitivity Randomized controlled trial (N=175) Adults > 50 years, non-accidental fall, positive CSM Pacing (n=87) vs. No Pacing (n=88) Results More than 1/3 of adults over 50 years presented to the Emergency Department because of a fall With pacing, falls ? 70% Syncopal events ? 53% Injurious events ? 70% Kenny RA. J Am Coll Cardiol. 2001;38:1491-1496.

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SAFE PACE Conclusions Strong association between non-accidental falls and cardioinhibitory CSH These patients usually not referred for cardiac assessment Cardiac pacing significantly reduced subsequent falls CSH should be considered in all older adults who have non-accidental falls Kenny RA, J Am Coll Cardiol. 2001; 38:1491-1496.

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Orthostatic Hypotension Etiology Drug-induced (very common) Diuretics Vasodilators Primary autonomic failure Multiple system atrophy Parkinson’s Disease Postural Orthostatic Tachycardia Syndrome (POTS) Secondary autonomic failure Diabetes Alcohol Amyloid Brignole M, et al. Europace, 2004;6:467-537.

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Treatment Strategies for Orthostatic Intolerance Patient education, injury avoidance Hydration Fluids, salt, diet Minimize caffeine/alcohol Sleeping with head of bed elevated Tilt training, leg crossing, arm pull Support hose Drug therapies Fludrocortisone, midodrine, erythropoietin Tachy-Pacing (probably not useful) Brignole M, et al. Europace, 2004;6:467-537.

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Section IV: Special Issues

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Syncope: Diagnostic Testing in Hospital Strongly Recommended Suspected/known ‘significant’ heart disease ECG abnormalities suggesting potential life-threatening arrhythmic cause Syncope during exercise Severe injury or accident Family history of premature sudden death Brignole M, et al. Europace. 2004;6:467-537.

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SEEDS: Syncope Evaluation in the Emergency Department Study Survival Free from Death Shen W, et al. Circ. 2004;110(24):3636-3645. Survival Free from Recurrence Long-Term Clinical Outcomes 100% 90% 80% 70% Years 2 1 0 P=0.30 Syncope Unit Group Standard Care Group 100% 90% 80% 70% Years 2 1 0 P=0.72 Syncope Unit Group Standard Care Group Results: Syncope unit improved diagnostic yield in the ED and reducedhospital admission and length of stay

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The Integrated Syncope Unit To optimize the effectiveness of the evaluation and treatment of syncope patients at a given center Best accomplished by: Cohesive, structured care pathway Multidisciplinary approach Core equipment available Preferential access to other tests or therapy Majority of syncope evaluations – Out-patient or day cases 1Kenny RA, Brignole M. In: Benditt D, et al. eds. The Evaluation and Treatment of Syncope. Futura;2003:55-60. 2Brignole M, et al. Europace, 2004;6:467-537.

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Conclusion Syncope is a common symptom with many causes Deserves thorough investigation and appropriate treatment A disciplined approach is essential AHA/ACCF and ESC guidelines offer current best practices Brignole M, et al. Europace, 2004;6:467-537.

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Challenges of Syncope Cost Quality of life implications Diagnosis and treatment Diagnostic yield and repeatability of tests Frequency and clustering of events Difficulty in managing/treating/controlling future events Appropriate risk stratification Complex etiology Olshansky B. In: Grubb B and Olshansky B. eds. Syncope: Mechanisms and Management. Futura. 1998:15-71. Brignole M, et al. Europace, 2004;6:467-537.

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