3 Syncope - DefinitionsACP Transient loss of consciousness (LOC) with loss of postural tone, from which recovery is spontaneous.ACEP Sudden, transient LOC with inability to maintain tone & is distinct from seizures, coma, vertigo, hypoglycemia and other states of altered consciousness.ESC Transient, self limited LOC with a relatively rapid onset and usually leading to fainting; the subsequent recovery is spontaneous, complete, and usually prompt.AFP Transient loss of consciousness, usually accompanied by falling, and with spontaneous recovery.
4 Syncope: A Symptom…Not a Diagnosis Self-limited loss of consciousness and postural toneRelatively rapid onsetVariable warning symptomsSpontaneous complete recoverySyncope should be considered as a symptom not as a diagnosis. The basis of syncopal symptoms should be sought through careful evaluation. Only after a cause is established can an effective treatment regimen be developed.
5 The Significance of Syncope The only difference betweensyncope and sudden deathis that in one you wake up.11 Engel GL. Psychologic stress, vasodepressor syncope, and sudden death. Ann Intern Med 1978; 89:
6 The Significance of Syncope Syncope is a relatively common problem that affects over 1 million people in the U.S. each year. Syncope accounts for 1 to 6% of hospital admissions and 3% of emergency room visits each year.1,2The incidence of syncope is greater than 500,000 new patients per year.1.National Disease and Therapeutic Index on Syncope and Collapse, ICD-9-CM 780.2, IMS America, 1997.2. 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; 23:3.Day SC, et al. Evaluation and outcome of emergency room patients with transient loss of consciousness. Am J Med 1982;73:15-23.4.Kapoor W. Evaluation and outcome of patients with syncope. Medicine 1990;69:1 National Disease and Therapeutic Index on Syncope and Collapse, ICD-9-CM 780.2, IMS America, 19972 Blanc J-J, L’her C, Touiza A, et al. Eur Heart J, 2002; 23:3 Day SC, et al, AM J of Med 19824 Kapoor W. Evaluation and outcome of patients with syncope. Medicine 1990;69:
7 Syncope Reported Frequency Individuals <18 yrsMilitary Population yrsIndividuals yrs*Individuals >70 yrs*15%20-25%16-19%23%Multiple reports have examined the frequency with which syncope occurs in various populations. This slide provides an overview of such findings. In essence the frequency with which syncope is reported to have occurred in various study groups is approximately 20%. The basis for syncope would be expected to differ substantially among these groups. Younger patients will have a greater proportion of vasovagal syncope, whereas older individuals may reasonably be expected to have a higher likelihood of underlying structural heart disease, and hence a greater predilection to more worrisome etiologies.Brignole M, Alboni P, Benditt DG, et al. “Guidelines on Management (Diagnosis and Treatment) of Syncope. Eur Heart J 2001; 22:*during a 10-year periodBrignole M, Alboni P, Benditt DG, et al. Eur Heart J, 2001; 22:
8 The Significance of Syncope explained: 53% to 62%infrequent, unexplained: 38% to 47% 1-4Studies have shown that the cause of syncope remains undiagnosed in as many as 47% of the patients who present with this symptom.There are approximately 170,000 recurrent syncope patients in the U.S. today, meaning that up to 70,000 patients with recurrent, infrequent syncope may be going undiagnosed and therefore, improperly treated.Of these patients, 20,000 may have undergone extensive testing with no diagnosis.1.Kapoor W. Evaluation and outcome of patients with syncope. Medicine 1990;69:2.Silverstein M, et al. Patients with syncope admitted to medical intensive care units. JAMA 1982;248:3.Martin G, et al. Prospective evaluation of syncope. Ann Emerg Med 1984;13:4.Kapoor W, et al. A prospective evaluation and follow-up of patients with syncope. N Eng J Med 1983;309:5.National Disease and Therapeutic Index, IMS America, Syncope and Collapse #780.2; Jan 1997-Dec 1997.6.Kapoor W, et al. Diagnostic and prognostic implications of recurrences in patients with syncope. Am J Med 1987;83:500,000 new syncope patients each year 5170,000 have recurrent syncope 670,000 have recurrent, infrequent, unexplained syncope 1-41 Kapoor W, Med. 1990;69:2 Silverstein M, et al. JAMA. 1982;248:3 Martin G, et al. Ann Emerg. Med. 1984;12:4 Kapoor W, et al. N Eng J Med. 1983;309:5 National Disease and Therapeutic Index, IMS America, Syncope and Collapse #780.2; Jan 1997-Dec 1997.6 Kapoor W, et al. Am J Med. 1987;83:
9 The Significance of Syncope Some causes of syncope are potentially fatalCardiac causes of syncope have the highest mortality rates (5 year mortality - 50 %, 1 year mortality - 30 %)Cardiac causes include both arrhythmias and structural heart problems, both of which contribute to high mortality rates. One of the goals, therefore, is to attempt to either rule out or rule in arrhythmic disorders.Syncope is a serious clinical problem with a reported mortality and major morbidity rate of over 7%.1 Among patients with an underlying cardiac cause of syncope, the reported 1-year mortality rate ranges from 18 to 33%.1-4This means that within 5 years, most of the patients whose syncope has a cardiac cause will have died.1.Day SC, et al. Evaluation and outcome of emergency room patients with transient loss of consciousness. Am J Med. 1982;73:15-23.2.Kapoor W. Evaluation and outcome of patients with syncope. Medicine 1990;69:3.Silverstein M, Singer D, Mulley A. Patients with syncope admitted to medical intensive care units. JAMA. 1982;248:4.Martin G, Adams S, Martin H. Prospective evaluation of syncope. Ann Emerg Med. 1984;13:1 Day SC, et al. Am J of Med 1982;73:15-23.2 Kapoor W. Medicine 1990;69:3 Silverstein M, Sager D, Mulley A. JAMA ;248:4 Martin G, Adams S, Martin H. Ann Emerg Med. 1984;13:
10 Impact of Syncope 73% 1 71% 2 60% 2 Proportion of Patients 37% 2 Syncope result in substantial cost to patients and to society. For example, syncope patients live with lifestyle altering restrictions that affect daily activities, mobility, and employment. In addition, syncope and falling in the elderly commonly cause injury, institutionalization and premature death. Falls directly or indirectly cause 12% of deaths in geriatric population. (Baraff 1997).____________________Linzer M, Pontinen M, Gold DT, et al. Impairment of physical and psychological function in recurrent syncope. J Clin Epidemiol. 1991;44:Linzer M, Gold DT, Pontinen M, et al. Recurrent syncope as a chronic disease: Preliminary validation of a disease-specific measure of functional impairment. J Gen Int Med. 1994;9:Anxiety/ DepressionAlter Daily ActivitiesRestricted DrivingChange Employment1Linzer, J Clin Epidemiol, 1991.2Linzer, J Gen Int Med, 1994.
11 Syncope - Mechanism Global cerebral hypoperfusion Interruption of sympathetic outflowIncreased vagal toneOther mechanisms - edema, cerebral autoregulation, central serotonin pathways.The trigger for the switch in autonomic response remains one of the unresolved mysteries in cardiovascular physiology*Hainsworth. Syncope: what is the trigger? Heart 2003; 89:
13 Syncope - Etiology Reflex (Neurally) Mediated Orthostatic Cardiac ArrhythmiaStructuralCardio-PulmonaryNon-Cardio-vascular1Vasovagal (common faint)Carotid SinusNeuralgia• SituationalCoughPost-micturition2DrugInduced• ANSFailurePrimarySecondary3BradySick sinusAV block• TachyVTSVTLong QT Syndrome*4Aortic StenosisHOCM• PulmonaryHypertension5Psychogenic• Metabolice.g. hyper-ventilationNeurologicalThis 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. The numbers at the bottom of each column provide an approximate value for the average frequency (Kapoor 1998) with which that category appears in published reports summarizing diagnostic findings. It should be noted that orthostatic causes are not often referred to specialists and consequently tend to be under represented in the literature.24%11%14%4%12%Unknown Cause = 34%DG Benditt, UM Cardiac Arrhythmia Center
14 Causes of Syncope1 Cause Prevalence (Mean) % Prevalence (Range) % Reflex-mediated:Vasovagal188-37Situational51-8Carotid Sinus10-4Orthostatic hypotension84-10Medications31-7Psychiatric2Neurological103-32Organic Heart Disease4Cardiac Arrhythmias144-38Unknown3413-41These frequencies cited were based on the general experience reported in the literature at the time (circa 1998). Subsequently, diagnostic criteria and techniques have improved. Consequently, the numbers should be relied on only for “ballpark” estimates.1Kapoor W. In Grubb B, Olshansky B (eds) Syncope: Mechanisms and Management. Armonk NY; Futura Publishing Co, Inc: 1998; 1-13.
15 Causes of Syncope-like States Migraine*Acute hypoxemia*Hyperventilation*Somatization disorder (psychogenic syncope)Acute Intoxication (e.g., alcohol)SeizuresHypoglycemiaSleep disorders* may cause ‘true’ syncope
16 Syncope Diagnostic Objectives Distinguish ‘True’ Syncope from other ‘Loss of Consciousness’ spells:SeizuresPsychiatric disturbancesEstablish the cause of syncope with sufficient certainty to:Assess prognosis confidentlyInitiate effective preventive treatmentSyncope is often confused with other apparent loss of consciousness diagnoses. It is crucial to consider this distinction first, prior to embarking on a diagnostic evaluation.
17 Initial Evaluation (Clinic/Emergency Dept.) Detailed historyPhysical examination12-lead ECGEchocardiogram (as available)The first steps in the evaluation of the patient with syncope can be carried out in the clinic (The Initial Evaluation). A detailed medical history (especially focusing on syncope events) and careful physical examination often provide important clues. A 12-lead ECG and if necessary an echocardiogram are reasonably included at this stage. A careful Initial Evaluation may often provide a satisfactory diagnosis. In other cases, this Evaluation will permit more development of a cost-effective diagnostic strategy.
18 Syncope Basic Diagnostic Steps Detailed History & PhysicalDocument details of eventsAssess frequency, severityObtain careful family historyHeart disease present?Physical examECG: long QT, WPW, conduction system diseaseEcho: LV function, valve status, HOCMFollow a diagnostic plan...General rules for initiating the diagnostic evaluation of the syncope patient. 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.
19 Syncope Evaluation and Differential Diagnosis History – What to Look forComplete DescriptionFrom patient and observersType of OnsetDuration of AttacksPostureAssociated SymptomsSequelaeA comprehensive Medical History is key to the cost-effective diagnostic assessment of syncope patients. Critical historical features that need to be sought are listed here.
20 12-Lead ECG Normal or Abnormal? Short sampling window (approx. 12 sec) Acute MISevere Sinus Bradycardia/pauseAV BlockTachyarrhythmia (SVT, VT)Preexcitation (WPW), Long QT, BrugadaShort sampling window (approx. 12 sec)The 12-lead ECG samples only a brief period of the cardiac rhythm (about 12 s). Consequently, absence of an abnormal rhythm is not a useful observation.The 12-lead ECG may, however, offer some useful clues for the syncope evaluation. If present, the findings noted on this slide may help lead to the choice of appropriate additional tests.
21 Carotid Sinus Massage Site: Method: Carotid arterial pulse just below thyroid cartilageMethod:Right followed by left, pause betweenMassage, NOT occlusionDuration: 5-10 secPosture – supine & erectCarotid 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.
22 Carotid Sinus Syndrome (CSS) Carotid Sinus MassageOutcome:3 sec asystole and/or 50 mmHg fall in systolic blood pressure with reproduction of symptoms =Carotid Sinus Syndrome (CSS)ContraindicationsCarotid bruit, known significant carotid arterial disease, previous CVA, MI last 3 monthsRisks1 in 5000 massages complicated by TIACarotid 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.
23 Head-up Tilt Test (HUT) Unmasks VVS susceptibilityReproduces symptomsPatient learns VVS warning symptomsPhysician is better able to give prognostic / treatment adviceThe rationale for undertaking head-up tilt (HUT) testing in patients suspected of having vasovagal 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.
24 Electroencephalogram Not a first line of testingSyncope from SeizuresAbnormal in the interval between two attacks – EpilepsyNormal – SyncopeNeurologic studies (Head CT/MRI, EEG) are rarely useful in the diagnostic evaluation of the basis for syncope. Imaging may be justified if there is concern that syncope may have resulted in a head injury. Otherwise, absent apparent abnormal neurologic signs, such testing should be relegated to low priority.
25 Ambulatory ECG Method Comments Holter (24-48 hours) Useful for infrequent eventsEvent RecorderLimited value in sudden LOCLoop RecorderImplantable type more convenient (ILR)Wireless (internet) Event MonitoringInitiatedThe various forms of Ambulatory ECG recording techniques currently available are listed in this slide. ILRs are currently available. Internet monitoring is just being initiated, and although very promising, its utility is as yet uncertain.
26 Reveal® Plus Insertable Loop Recorder The Reveal® Plus Insertable Loop Recorder system offers long-term, continuous, subcutaneous ECG monitoring and event-specific recording. This implantable device is designed to improve patient compliance with long-term AECG monitoring.The system includes an implanted loop recorder, a hand-held patient Activator, and a programmer with telemetry head that communicates noninvasively with the implanted device.When a patient experiences an episode, the device stores an ECG using the Activator or through the use of a auto-activating feature.The Reveal® Plus ILR can monitor continuously for up to 14 months. The probability of capturing an event is high—approximately 65-88%.1,2The ECG captured during the episode may “reveal” the ECG during the patient’s episode or may allow the clinician to rule in or rule out arrhythmic causes.The stored ECG data is retrieved, viewed, and printed or saved to a disk, using a Medtronic 9790 programmer with a 9766 A or AL programmer head.The Reveal ILR can then be re-started for continued monitoring.Krahn A, et al. Final results from a pilot study with an insertable loop recorder to determine the etiology of syncope in patients with negative noninvasive and invasive testing. Am J Cardiol, 1998;82:2. Krahn A, Klein GJ, Yee R, Skanes AC. Randomized assessment of syncope trial. Conventional diagnostic testing versus a prolonged monitoring strategy. Circulation 2001;104:46-51Patient ActivatorReveal® Plus ILR9790 Programmer
27 Conventional EP Testing in Syncope Limited utility in syncope evaluationMost useful in patients with structural heart diseaseHeart disease…… %No Heart disease…18-50%Relatively ineffective for assessing bradyarrhythmiasConventional EP testing (I.e.,EPS, electrical stimulation without autonomic studies such as HUT) has not been highly effective in substantiating a basis for syncope. In this regard, EPS has been more effective in patients with structural cardiovascular disease than in those with normal cardiovascular status. Further, EPS has been more effective in patients with tachyarrhythmias than in those with bradyarrhythmias.Brignole M, Alboni P, Benditt DG, et al. “Guidelines on Management (Diagnosis and Treatment) of Syncope. Eur Heart Journal 2001; 22:Brignole M, Alboni P, Benditt DG, et al. Eur Heart Journal 2001; 22:
28 Diagnostic Limitations Difficult to correlate spontaneous events and laboratory findingsOften must settle for an attributable causeUnknowns remain 20-30% 1Determining a definitive basis for syncope can often be frustrating. Patience is a necessity. However, not infrequently one must settle for the most reasonable ‘attributable’ cause.1Kapoor W. In Grubb B, Olshansky B (eds) Syncope: Mechanisms and Management. Armonk NY; Futura Publishing Co, Inc: 1998; 1-13.
29 Challenges of Syncope Cost Quality of Life Implications Cost/yearCost/diagnosisQuality of Life ImplicationsWork/financialMobility (automobiles)PsychologicalDiagnosis & TreatmentDiagnostic yield and repeatability of testsFrequency and clustering of eventsDifficulty in managing/treating/controlling future eventsAppropriate risk stratificationComplex EtiologySyncope impacts patient quality of life, and health care costs in important ways.Establishing a precise diagnosis is often challenging due to the unpredictability of events and the limited positive predictive value of most available tests. The ‘gold standard’ remains the recording of the cardiac rhythm (and if possible the arterial pressure) during a spontaneous faint.
30 Unexplained Syncope Diagnosis History and Physical ExamSurface ECGENT EvaluationEndocrine EvaluationCV Syncope WorkupHolterELR or ILRTilt TableEchoEPSNeurological TestingHead CT ScanCarotid DopplerMRISkull FilmsBrain ScanEEGOther CV TestingAngiogramExercise TestSAECGSearching for a Diagnosis:Patients can enter the diagnostic process at various points based on their presenting symptoms and/or syncope-related injuries. Also, the process of deriving a diagnosis for syncope can vary from institution to institution. As noted earlier, the diagnosis of syncope begins with a patient history and physical, and a surface electrocardiogram recording.If this initial evaluation suggests a cardiovascular cause such as myocardial infarction or structural heart disease, an echocardiogram and electrophysiologic study (EPS) may be performed. If no diagnosis is reached with these tests, the physician may move to any of the following tests, in any order: tilt table testing, Holter monitor, external loop recorder (ELR), or Reveal® Plus Insertable Loop Recorder(IRL). If none of those tests yield a diagnosis, some tests may be performed repeatedly and/or other specialists might be consulted for further testing including: endocrinology, neurology, psychiatry, ENT, etc.If no structural cardiovascular problems are suspected, the physician may choose diagnostic testing based on suspected vasovagal etiology and frequency and severity of symptoms.New diagnostic tools, such as ILRs, will cause significant discussions about when to use them, given their high diagnostic yields and high patient compliance.NOTES:ECG: ElectrocardiogramEEG: ElectroencephalogramMRI: Magnetic Resonance ImagingEcho: EchocardiogramEP Study: Electrophysiology StudyMI: Myocardial InfarctionSHD: Structural Heart DiseaseENT: ears-nose-throatPsychological EvaluationAdapted from: W.Kapoor.An overview of the evaluationand management of syncope. From Grubb B, Olshansky B (eds)Syncope: Mechanisms and Management.Armonk, NY: Futura Publishing Co., Inc.1998.
31 Typical Cardiovascular Diagnostic Pathway SyncopeHistory and Physical, ECGKnown SHDNo SHD> 30 days; > 2 Events< 30 daysEchoThis flow chart shows a typical sequence of testing, patients may undergo in search of a diagnosis.SHD (Structural Heart Disease)EPSTilt Holter/ ELR ILRTilt ILR-+Tilt/ILRTreatAdapted from:Linzer M, et al. Annals of Int Med, :76-86.Syncope: Mechanisms and Management. Grubb B, Olshansky B (eds) Futura Publishing 1999Zimetbaum P, Josephson M. Annals of Int Med, :Krahn A et al. ACC Current Journal Review,1999. Jan/Feb:80-84.
32 Specific ConditionsThe next session of this set deals with some of the more important causes of syncope. Specific conditions are dealt with approximately in the order of the frequency with which they may be expected to occur in clinical practice.
33 Neurally-Mediated Reflex Syncope (NMS) Vasovagal syncope (VVS)Carotid sinus syndrome (CSS)Situational syncopepost-micturitioncoughswallowdefecationblood drawingetc.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.
34 NM Reflex Syncope: Pathophysiology Multiple triggersVariable contribution of vasodilatation and bradycardiaNeurally-mediated reflex syncope can be triggered by a wide variety of situations (thus the commonly used term ‘situational’ syncope). Extended periods of upright posture, and medical procedures, are among the more common situations associated with vasovagal faints.
35 NMS – Basic Pathophysiology Cerebral CortexVascular BedBradycardia/ HypotensionBaro-receptorsHeartFeedback via Carotid Baroreceptors Other MechanoreceptorsParasympathetic (+)sympathetic (+)¯ Heart Rate ¯ AV Conduction_VasodilatationPhysiology of FaintingThe physiology of the common faint is depicted graphically in this slide (based on Figure 1 in Benditt 1996). The afferent trigger signals (e.g., pain, emotional upset, dehydration) are not depicted. The efferent loop of the neural reflex comprises:Parasympathetic signals from the cerebral cortex drive heart rate down and slow (or even block) AV conduction.Sympathetic signals increase dilation of the vascular bed.Bradycardia and/or hypotension result.Carotid baroreceptors and other mechanoreceptors sense effects driven by parasympathetic and sympathetic systems and provide paradoxical feedback to the central nervous system.The result may be a downward spiral in heart rate and blood pressure leading to syncope.__________________Benditt DG, Lurie KG, Adler SW, et al. Pathophysiology of vasovagal syncope. In: Neurally mediated syncope: Pathophysiology, investigations and treatment. Blanc JJ, Benditt D, Sutton R. Bakken Research Center Series, v. 10. Armonk, NY: Futura, 1996.Benditt DG, Lurie KG, Adler SW, et al. Pathophysiology of vasovagal syncope. In: Neurally mediated syncope: Pathophysiology, investigations and treatment. Blanc JJ, Benditt D, Sutton R. Bakken Research Center Series, v. 10. Armonk, NY: Futura, 1996
36 Vasovagal Syncope (VVS): Clinical Pathophysiology Neurally Mediated Physiologic Reflex Mechanism with two Components:Cardioinhibitory ( HR )Vasodepressor ( BP )Both components are usually presentSyncope 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. VasodilatationThe relative contribution of these 2 components varies among patients
37 Diagnosing VVS Patient history and physical exam Positive tilt table testOvernight fastECGBlood pressureSupine and uprightTilt to degreesIsoproterenolRe-tilt60° - 80°Diagnosing VVSVVS 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 testECG (at least 3 leads)Continuous blood pressure monitoringPatient remains supine on the table for minutes.Tilt to degrees for minutes.Lower to horizontal and administer isoproterenol at 1-5 g/min until heart rate increases 25%.Re-tilt for 10 minutesREFERENCE:Benditt DG, Ferguson DW, Grubb BP, et al. Tilt table testing for syncope. ACC Expert Consensus Document. JACC. 1996;28(1):DG Benditt, Tilt Table Testing, 1996.
38 Management Strategies for VVS Optimal management strategies for VVS are a source of debatePatient education, reassurance, instructionFluids, salt, dietTilt TrainingSupport hoseDrug therapiesPacingClass II indication for VVS patients with positive HUT and cardioinhibitory or mixed reflexManagement Strategies for VVSOptimal 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 patientsPacing 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
39 VVS: Treatment Overview Educationsymptom recognitionreassurancesituation avoidanceTilt-Trainingprescribed upright posturePharmacologic Agentssalt/volume managementbeta-adrenergic blockersSSRIsvasoconstrictors (e.g., midodrine)Cardiac PacemakersThe treatment of recurrent VVS should focus primarily on education and salt/volume maintenance. Thereafter, physical maneuvers such as tilt-training are recommended. Pharmacologic and pacing treatment options remain for patients who continue to be symptomatic.
40 VVS: Tilt-Training Objectives Technique Enhance Orthostatic Tolerance Diminish Excessive Autonomic Reflex ActivityReduce Syncope Susceptibility / RecurrencesTechniquePrescribed Periods of Upright PostureProgressive Increased DurationHead-up tilt testing (HUT) has proved to be of considerable clinical value in establishing susceptibility to VVS in syncope patients. As with any test, the observations during HUT must be considered in the light of all clinical data in a given patient.
41 VVS: Pharmacologic Rx Salt /Volume Beta-adrenergic blockers Salt tablets, ‘sport’ drinks, fludrocortisoneBeta-adrenergic blockers1 positive controlled trial (atenolol),1 on-going RCT (POST)DisopyramideSSRIs1 controlled trialVasoconstrictors (e.g., midodrine)1 negative controlled trial (etilephrine)This slide summarizes the key pharmacologic treatment options in VVS patients. Salt/volume education in conjunction with reassurance and/or tilt-training are the primary treatment avenues. Drug therapy should be reserved as a second-line option.
42 Role of Pacing in Treating VVS Pacing in VVSRecent clinical studies demonstrated benefits of pacing in select VVS patients:VPS IVASISSYDITVPS II –Phase IROME VVS TrialRole of Pacing in Treating VVSThe perception of pacing as therapy for selected VVS patients has been changing with increased understanding of the syndrome, improved diagnostic techniques (especially tilt testing), and the development of improved therapies.VVS with a positive head-up tilt test and a predominately cardioinhibitory response may be considered a Class II indication for pacing.DDD/DDI with rate hysteresis sometimes has been successful, although it suffers from limitations.In recent years, new rate drop therapies specifically designed for treatment of neurocardiogenic syncope have been introduced.
43 VVS Pacing Trials Conclusions DDD pacing reduces the risk of syncopein patients with recurrent, refractory,highly-symptomatic, cardioinhibitoryvasovagal syncope.
44 Carotid Sinus Syndrome (CSS) Syncope clearly associated with carotid sinus stimulation is rare (≤1% of syncope)CSS may be an important cause of unexplained syncope / falls in older individualsCarotid sinus syndrome (CSS) is an important and often overlooked cause of syncope, and in addition is believed to be a frequent cause of unexplained falls in older individuals.The method of carotid sinus massage, and the findings diagnostic of CSS were presented on previous slidesREFERENCEBrignole M, Alboni P, Benditt DG, et al. Guidelines on management (diagnosis and treatment) of syncope. Eur Heart Journal 2001; 22:
45 Etiology of CSSSensory nerve endings in the carotid sinus walls respond to deformation“Deafferentation” of neck muscles may contributeIncreased afferent signals to brain stemReflex increase in efferent vagal activity and diminution of sympathetic tone results in bradycardia and vasodilationEtiology of CSSThe etiology of CSS rests in part from afferent signals arising in the carotid baroreceptors, and inappropriate concomitant signals from nearby neck muscles:Sensory nerve endings in the carotid sinus walls respond to deformation.An increase in afferent traffic results in cardioinhibition and vasodilatation.Differentiation of nearby neck muscles may contribute. The CNS is not informed of neck movement and consequently the carotid baroreceptor afferents are interpreted as indicating a rise in central arterial pressure.____________________Blanc JJ, L’Heveder J, Mansourati J, et al. Pathophysiology of carotid sinus syndrome. In: Neurally mediated syncope: Pathophysiology, investigation and treatment. Blanc JJ, Benditt D, Sutton R (eds). Armonk, NY: Futura, 1996, ppKenny RA, McIntosh SJ. Carotid sinus syndrome. In: Syncope in the older patient. Kenny RA (ed). London: Chapman & Hall Medical, 1996, ppCarotid Sinus
46 Carotid Sinus Hypersensitivity(CSH) Abnormal response to CSMAbsence of symptoms attributable to CSSCSH reported frequent in ‘fallers’ (Kenny)CSH CSSUnderlying Cause: Carotid Sinus Hypersensitivity (CSH)The underlying cause of CSS is considered to be a hypersensitive carotid sinus. Carotid Sinus Hypersensitivity (CSH) is diagnosed by using Carotid Sinus Massage (CSM).CSH is considered present when a 5-second massage results in either more than 3 seconds of asystole or more than a 50 mm/Hg fall in systolic blood pressure.CSH is a necessary but not a sufficient condition for diagnosing CSS. The latter refers to symptoms such as bradycardia, dizziness, pre-syncope, syncope, and falling resulting from a hypersensitive carotid sinus reflex (Katritsis 1991).Many subjects who exhibit CSH are free of symptoms and require no treatment. In one study, 38% of patients being catheterized for angiography responded positively to CSM (Brown 1980)._________________Brown KA, Maloney JD, Smith HC, et al. Carotid sinus reflex in patients undergoing coronary angiography: Relationship of degree and location of coronary artery disease to response to carotid sinus massage. Circulation. 1980; 62:Katritsis D, Ward DE, Camm AJ. Can we treat carotid sinus syndrome? PACE. 1991;14(9):Sutton R. Carotid sinus syndrome: clinical presentation, epidemiology, and natural history. In: Neurally mediated syncope: Pathophysiology, investigation and treatment. Blanc JJ, Benditt D, Sutton R (eds). Armonk, NY: Futura, 1996, p. 138.
47 CSS and Falls in the Elderly 30% of people >65 yrs of age fall each year1Total is 9,000,000 people in USAApproximately 10% of falls in elderly persons are due to syncope250% of fallers have documented recurrence3Prevalence of CSS among frequent and unexplained fallers unknown but…CSH present in 23% of >50 yrs fallers presenting at ER 3CSS and Falls in the ElderlyFalls are the leading cause of injury among the elderly. According to “Falling in the Elderly” (1995):30% of the population older than 65 years of age falls each year.In the U.S., that amounts to about 9,000,000 people.50% of these fallers have documented recurrence.8% of the population greater than 70 years of age visit an ER for a fall.40% of these visits result in hospitalization.What is the contribution of cardioinhibitory CSS to these falls? This is an area of active research, but already-published results are suggestive: In one study, 279 fallers 50 years or older presenting to an emergency room with frequent or unexplained falls (at least 3 in previous 12 months) underwent carotid sinus massage, and 65 (23%) exhibited cardioinhibitory carotid sinus hypersensitivity (Richardson 1997).____________________Falling in the Elderly: U.S. Prevalence Data. Journal of the American Geriatric Society, December, 1995.Richardson DA, Bexton RS, Shaw FE, Kenny RA. Prevalence of cardioinhibitory carotid sinus hypersensitivity in patients 50 years or over presenting to the Accident and Emergency Department with “unexplained” or “recurrent” falls. PACE March 1997 (Part II):1Falling in the Elderly: U.S. Prevalence Data. Journal of the American Geriatric Society,2 Campbell et al: Age and Aging 1981;10:3Richardson DA, Bexton RS, et al. Prevalence of cardioinhibitory carotid sinus hypersensitivity in patients 50 years or over presenting to the Accident and Emergency Department with “unexplained” or “recurrent” falls. PACE 1997
48 Role of Pacing in CSS -- Syncope Recurrence Rate Class I indication for pacing (AHA and BPEG)Limit pacing to CSS that is:CardioinhibitoryMixedDDD/DDI superior to VVI57%% RecurrenceRole of Pacing in Treatment of CSSCSS is a Class I indication for pacing (AHA and BPEG).Pacing therapy may be effective for CSS that is eitherCardioinhibitoryorMixed cardioinhibitory/vasodepressorAV sequential pacing (DDD/DDI) is clearly preferable to ventricular demand (VVI) pacing.____________________Wagshal AB, Wang SKS. Carotid sinus hypersensitivity. In: Syncope: Mechanisms and management. Grubb BP, Olshansky B (eds). Armonk, NY: Futura, 1998.Brignole M, Menozzi C. Carotid sinus syndrome: Diagnosis, natural history and treatment. Eur J C P E. 1992;4:%6(Mean follow-up = 6 months)Brignole et. Al. Diagnosis, natural history and treatment. Eur JCPE. 1992; 4:
49 Principal Causes of Orthostatic Syncope Drug-induced (very common)diureticsvasodilatorsPrimary autonomic failuremultiple system atrophyParkinsonismSecondary autonomic failurediabetesalcoholamyloidAlcoholorthostatic intolerance apart from neuropathyOrthostatic 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.
50 Syncope Due to Arrhythmia or Structural CV Disease: General Rules Often life-threatening and/or exposes patient to high risk of injuryMay be warning of critical CV diseaseAortic stenosis, Myocardial ischemia, Pulmonary hypertensionAssess culprit arrhythmia / structural abnormality aggressivelyInitiate treatment promptlySyncope occurring as a result of cardiac arrhythmias or in association with underlying structural heart disease requires careful and aggressive evaluation. Whereas syncope in patients with normal hearts is often relatively benign, syncope in the presence of cardiac disease is often indicative of a potentially life-threatening problem.
51 Principal Causes of Syncope due to Structural Cardiovascular Disease Acute MI / IschemiaAcquired coronary artery diseaseCongenital coronary artery anomaliesHOCMAcute aortic dissectionPericardial disease / tamponadePulmonary embolus / pulmonary hypertensionValvular abnormalitiesAortic stenosis, Atrial myxomaA list of important structural cardiovascular abnormalities to be considered during the diagnostic evaluation of syncope is provided. The list is not intended to be exhaustive of the possibilities, but provides some of the more commonly found conditions.
52 Syncope Due to Cardiac Arrhythmias BradyarrhythmiasSinus arrest, exit blockHigh grade or acute complete AV blockTachyarrhythmiasAtrial fibrillation / flutter with rapid ventricular rate (e.g. WPW syndrome)Paroxysmal SVT or VTTorsades de pointesBoth 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.
53 Rhythms During Recurrent Syncope Bradycardia36%Normal Sinus Rhythm58%Normal Sinus Rhythm58%Tachyarrhythmia6%Krahn A, et al. Circulation. 1999; 99:
54 Treatment of Syncope Due to Bradyarrhythmia Class I indication for pacing using dual- chamber system wherever adequate atrial rhythm is availableVentricular pacing in atrial fibrillation with slow ventricular responseThe treatment of bradyarrhythmias associated with intrinsic conduction system disease resulting in syncope is usually cardiac pacing. On occasion, removal of an offending drug may be sufficient. The problem of neurally-mediated reflex bradyarrhythmias are dealt with separately.
55 Treatment of Syncope Due to Tachyarrhythmia Atrial Tachyarrhythmias;AVRT due to accessory pathway – ablate pathwayAVNRT – ablate AV nodal slow pathwayAtrial fib– Pacing, linear / focal ablation, ICD selected ptsAtrial flutter – Ablation of reentrant circuitVentricular Tachyarrhythmias;Ventricular tachycardia – ICD or ablation where appropriateTorsades de Pointes – withdraw offending Rx or ICD (long-QT/Brugada)Drug therapy may be an alternative in many casesThis slide provides an overview of the multiple tachyarrhythmias that may cause syncope. EPS has proven more valuable in assessing tachyarrhythmia causes of syncope than those due to bradycardia.
56 Conclusion Syncope is a common symptom, often with dramatic consequences,which deserves thorough investigationand appropriate treatment of its cause.
57 Conclusion Syncope is a common symptom, often with dramatic consequences,which deserves thorough investigationand appropriate treatment of its cause.
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