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Syncope Nabeel Kouka, MD, DO, MBA www.brain101.info
Syncope <ul><li>Definition </li></ul><ul><li>Epidemiology </li></ul><ul><li>Etiology </li></ul><ul><li>Diagnosis & Evaluat...
Syncope - Definitions <ul><li>ACP 1997 - Transient loss of consciousness (LOC) with loss of postural tone, from which reco...
Syncope:   A   Symptom…Not a Diagnosis   <ul><li>Self-limited loss of consciousness and postural tone </li></ul><ul><li>Re...
The Significance of Syncope <ul><li>The only difference between  </li></ul><ul><li>syncope and sudden death  </li></ul><ul...
The Significance of Syncope 1  National Disease and Therapeutic Index on Syncope and Collapse, ICD-9-CM 780.2, IMS America...
<ul><li>Individuals <18 yrs </li></ul><ul><li>Military Population 17- 46 yrs </li></ul><ul><li>Individuals 40-59 yrs*  </l...
The Significance of Syncope <ul><li>500,000 new syncope patients each year  5 </li></ul><ul><li>170,000 have recurrent syn...
<ul><li>Some causes of syncope are potentially fatal </li></ul><ul><li>Cardiac causes of syncope have the highest mortalit...
Impact of Syncope 1 Linzer,  J Clin Epidemiol , 1991. 2 Linzer,  J Gen Int Med , 1994. Anxiety/ Depression Alter Daily Act...
Syncope - Mechanism <ul><li>Global cerebral hypoperfusion </li></ul><ul><li>Interruption of sympathetic outflow </li></ul>...
Syncope - Etiology <ul><li>Reflex mediated - 40% </li></ul><ul><li>Unexplained - 25% </li></ul><ul><li>Cardiac - 15% </li>...
Syncope - Etiology Orthostatic Cardiac Arrhythmia Structural Cardio- Pulmonary *  <ul><li>1 </li></ul><ul><li>Vasovagal (c...
Causes of Syncope 1 1 Kapoor W. In Grubb B, Olshansky B (eds)  Syncope: Mechanisms and Management .  Armonk NY; Futura Pub...
Causes of Syncope-like States <ul><li>Migraine* </li></ul><ul><li>Acute hypoxemia* </li></ul><ul><li>Hyperventilation* </l...
Syncope  Diagnostic Objectives <ul><li>Distinguish ‘True’ Syncope from other ‘Loss of Consciousness’ spells: </li></ul><ul...
Initial Evaluation (Clinic/Emergency Dept.) <ul><li>Detailed history </li></ul><ul><li>Physical examination </li></ul><ul>...
Syncope  Basic Diagnostic Steps <ul><li>Detailed History & Physical </li></ul><ul><ul><li>Document details of events </li>...
Syncope   Evaluation and Differential Diagnosis <ul><li>Complete Description </li></ul><ul><ul><li>From patient and observ...
12-Lead ECG <ul><li>Normal or Abnormal? </li></ul><ul><ul><li>Acute MI </li></ul></ul><ul><ul><li>Severe Sinus Bradycardia...
Carotid Sinus Massage <ul><li>Site:  </li></ul><ul><ul><li>Carotid arterial pulse just below thyroid cartilage </li></ul><...
Carotid Sinus Massage <ul><li>Outcome:   </li></ul><ul><ul><li>3 sec asystole and/or 50 mmHg fall in systolic blood pressu...
Head-up Tilt Test (HUT) <ul><li>Unmasks VVS susceptibility </li></ul><ul><li>Reproduces symptoms </li></ul><ul><li>Patient...
Electroencephalogram <ul><li>Not a first line of testing </li></ul><ul><li>Syncope from Seizures </li></ul><ul><ul><li>Abn...
Ambulatory ECG Initiated Wireless (internet) Event Monitoring <ul><li>Useful for infrequent events </li></ul><ul><li>Impla...
Reveal ®  Plus  Insertable Loop Recorder Patient Activator Reveal ®  Plus ILR 9790 Programmer
Conventional EP Testing in Syncope <ul><li>Limited utility in syncope evaluation </li></ul><ul><li>Most useful in patients...
Diagnostic Limitations <ul><li>Difficult to correlate spontaneous events and laboratory findings </li></ul><ul><li>Often m...
Challenges of Syncope <ul><li>Cost </li></ul><ul><ul><li>Cost/year </li></ul></ul><ul><ul><li>Cost/diagnosis </li></ul></u...
Unexplained Syncope Diagnosis History and Physical Exam  Surface ECG <ul><li>Neurological Testing   </li></ul><ul><li>Head...
Typical Cardiovascular Diagnostic Pathway History and Physical, ECG Syncope Known SHD   No SHD   Echo EPS + Treat > 30 day...
Specific Conditions
Neurally-Mediated Reflex Syncope  (NMS) <ul><li>Vasovagal syncope (VVS) </li></ul><ul><li>Carotid sinus syndrome (CSS) </l...
NM Reflex Syncope: Pathophysiology <ul><li>Multiple triggers </li></ul><ul><li>Variable contribution of vasodilatation and...
NMS – Basic Pathophysiology Benditt DG, Lurie KG, Adler SW, et al. Pathophysiology of vasovagal syncope. In:  Neurally med...
<ul><li>Neurally Mediated Physiologic Reflex Mechanism with two Components: </li></ul><ul><ul><li>Cardioinhibitory  (  HR ...
Diagnosing VVS <ul><li>Patient history and physical exam </li></ul><ul><li>Positive tilt table test </li></ul><ul><ul><li>...
Management Strategies for VVS <ul><li>Optimal management strategies for VVS are a source of debate </li></ul><ul><ul><li>P...
VVS: Treatment Overview <ul><li>Education  </li></ul><ul><ul><li>symptom recognition  </li></ul></ul><ul><ul><li>reassuran...
VVS: Tilt-Training <ul><li>Objectives </li></ul><ul><ul><li>Enhance Orthostatic Tolerance </li></ul></ul><ul><ul><li>Dimin...
VVS: Pharmacologic Rx <ul><li>Salt /Volume </li></ul><ul><ul><li>Salt tablets, ‘sport’ drinks, fludrocortisone </li></ul><...
Pacing in VVS <ul><li>Recent clinical studies demonstrated benefits of pacing in select VVS patients: </li></ul><ul><ul><l...
VVS Pacing Trials Conclusions <ul><li>DDD pacing reduces the risk of syncope  </li></ul><ul><li>in patients with recurrent...
Carotid Sinus Syndrome (CSS) <ul><li>Syncope clearly associated with carotid sinus stimulation is rare (≤1% of syncope)  <...
Etiology of CSS <ul><li>Sensory nerve endings in the carotid sinus walls respond to deformation </li></ul><ul><li>“ Deaffe...
Carotid Sinus Hypersensitivity(CSH) <ul><li>Abnormal response to CSM </li></ul><ul><li>Absence of symptoms attributable to...
CSS and Falls in the Elderly <ul><li>30% of people >65 yrs of age fall each year 1 </li></ul><ul><ul><li>Total is 9,000,00...
Role of Pacing in CSS -- Syncope Recurrence Rate Brignole et. Al. Diagnosis, natural history and treatment. Eur JCPE. 1992...
Principal Causes of  Orthostatic Syncope <ul><li>Drug-induced  (very common) </li></ul><ul><ul><li>diuretics </li></ul></u...
Syncope Due to Arrhythmia or Structural CV Disease: General Rules   <ul><li>Often life-threatening and/or exposes patient ...
Principal Causes of Syncope due to Structural Cardiovascular Disease <ul><li>Acute MI / Ischemia </li></ul><ul><ul><li>Acq...
Syncope Due to Cardiac Arrhythmias <ul><li>Bradyarrhythmias </li></ul><ul><ul><li>Sinus arrest, exit block </li></ul></ul>...
Rhythms During Recurrent Syncope Krahn A, et al.  Circulation.  1999; 99: 406-410 Normal Sinus Rhythm 58% Normal Sinus Rhy...
Treatment of Syncope Due to Bradyarrhythmia <ul><li>Class I indication for pacing using dual- chamber system wherever adeq...
Treatment of Syncope Due to Tachyarrhythmia <ul><li>Atrial Tachyarrhythmias; </li></ul><ul><ul><li>AVRT due to accessory p...
Conclusion <ul><li>Syncope is a common symptom,  </li></ul><ul><li>often with dramatic consequences, </li></ul><ul><li>whi...
Conclusion <ul><li>Syncope is a common symptom,  </li></ul><ul><li>often with dramatic consequences, </li></ul><ul><li>whi...
 
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  • Syncope 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.
  • 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. 1,2 The 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: 815-820. 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;69:160-175.
  • 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: 1256-1306.
  • Studies 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;69:160-175. 2.Silverstein M, et al. Patients with syncope admitted to medical intensive care units. JAMA 1982;248:1185-1189. 3.Martin G, et al. Prospective evaluation of syncope. Ann Emerg Med 1984;13:499-504. 4.Kapoor W, et al. A prospective evaluation and follow-up of patients with syncope. N Eng J Med 1983;309:197-204. 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;83:700-708.
  • 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%. 1-4 This 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;69:160-175. 3.Silverstein M, Singer D, Mulley A. Patients with syncope admitted to medical intensive care units. JAMA. 1982;248:1185-1189. 4.Martin G, Adams S, Martin H. Prospective evaluation of syncope. Ann Emerg Med. 1984;13:499-504.
  • Impact of Syncope 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;44:1037-1043. 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;9:181-186.
  • 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. 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.
  • These 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.
  • Syncope 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.
  • 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.
  • 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.
  • A 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.
  • 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.
  • 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.
  • 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.
  • The 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.
  • Neurologic 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.
  • The 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.
  • 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%. 1,2 The 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. 1. 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;82:117-119. 2. Krahn A, Klein GJ, Yee R, Skanes AC. Randomized assessment of syncope trial. Conventional diagnostic testing versus a prolonged monitoring strategy. Circulation 2001;104:46-51
  • Conventional 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: 1256-1306.
  • Determining 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.
  • Syncope 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.
  • Searching 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: Electrocardiogram EEG: Electroencephalogram MRI: Magnetic Resonance Imaging Echo: Echocardiogram EP Study: Electrophysiology Study MI: Myocardial Infarction SHD: Structural Heart Disease ENT: ears-nose-throat
  • This flow chart shows a typical sequence of testing, patients may undergo in search of a diagnosis. SHD (Structural Heart Disease)
  • The 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.
  • 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.
  • Neurally-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.
  • Physiology of Fainting The 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.
  • 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
  • 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.
  • Management Strategies for VV S 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
  • The 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.
  • Head-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.
  • 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.
  • Role of Pacing in Treating VVS The 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.
  • Carotid 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 slides REFERENCE Brignole M, Alboni P, Benditt DG, et al. Guidelines on management (diagnosis and treatment) of syncope. Eur Heart Journal 2001; 22: 1256-1306.
  • Etiology of CSS The 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, pp. 25-29. Kenny RA, McIntosh SJ. Carotid sinus syndrome. In: Syncope in the older patient . Kenny RA (ed). London: Chapman &amp; Hall Medical, 1996, pp. 107-108 .
  • Underlying 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; 62:697-703. Katritsis D, Ward DE, Camm AJ. Can we treat carotid sinus syndrome? PACE. 1991;14(9):1367-74. 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.
  • CSS and Falls in the Elderly Falls 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):820-23.
  • Role of Pacing in Treatment of CSS CSS is a Class I indication for pacing (AHA and BPEG). Pacing therapy may be effective for CSS that is either Cardioinhibitory or Mixed cardioinhibitory/vasodepressor AV 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;4:247-254.
  • 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.
  • Syncope 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.
  • A 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.
  • 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.
  • The 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.
  • This 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.
  • Transcript of "Syncope"

    1. 1. Syncope Nabeel Kouka, MD, DO, MBA www.brain101.info
    2. 2. Syncope <ul><li>Definition </li></ul><ul><li>Epidemiology </li></ul><ul><li>Etiology </li></ul><ul><li>Diagnosis & Evaluation Options </li></ul><ul><li>Specific Conditions </li></ul>
    3. 3. Syncope - Definitions <ul><li>ACP 1997 - Transient loss of consciousness (LOC) with loss of postural tone, from which recovery is spontaneous. </li></ul><ul><li>ACEP 2001 - Sudden, transient LOC with inability to maintain tone & is distinct from seizures, coma, vertigo, hypoglycemia and other states of altered consciousness. </li></ul><ul><li>ESC 2001 - Transient, self limited LOC with a relatively rapid onset and usually leading to fainting; the subsequent recovery is spontaneous, complete, and usually prompt. </li></ul><ul><li>AFP 2005 - Transient loss of consciousness, usually accompanied by falling, and with spontaneous recovery. </li></ul>
    4. 4. Syncope: A Symptom…Not a Diagnosis <ul><li>Self-limited loss of consciousness and postural tone </li></ul><ul><li>Relatively rapid onset </li></ul><ul><li>Variable warning symptoms </li></ul><ul><li>Spontaneous complete recovery </li></ul>
    5. 5. The Significance of Syncope <ul><li>The only difference between </li></ul><ul><li>syncope and sudden death </li></ul><ul><li>is that in one you wake up. 1 </li></ul>1 Engel GL. Psychologic stress, vasodepressor syncope, and sudden death. Ann Intern Med 1978; 89: 403-412.
    6. 6. The Significance of Syncope 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. Eur Heart J, 2002; 23: 815-820. 3 Day SC, et al, AM J of Med 1982 4 Kapoor W. Evaluation and outcome of patients with syncope. Medicine 1990;69:160-175
    7. 7. <ul><li>Individuals <18 yrs </li></ul><ul><li>Military Population 17- 46 yrs </li></ul><ul><li>Individuals 40-59 yrs* </li></ul><ul><li>Individuals >70 yrs* </li></ul><ul><li>15% </li></ul><ul><li>20-25% </li></ul><ul><li>16-19% </li></ul><ul><li>23% </li></ul>Syncope Reported Frequency *during a 10-year period Brignole M, Alboni P, Benditt DG, et al. Eur Heart J, 2001; 22: 1256-1306.
    8. 8. The Significance of Syncope <ul><li>500,000 new syncope patients each year 5 </li></ul><ul><li>170,000 have recurrent syncope 6 </li></ul><ul><li>70,000 have recurrent, infrequent, unexplained syncope 1-4 </li></ul>1 Kapoor W, Med . 1990;69:160-175. 2 Silverstein M, et al. JAMA . 1982;248:1185-1189. 3 Martin G, et al. Ann Emerg. Med . 1984;12:499-504. 4 Kapoor W, et al. N Eng J Med . 1983;309:197-204. 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;83:700-708. explained: 53% to 62% infrequent, unexplained: 38% to 47% 1-4
    9. 9. <ul><li>Some causes of syncope are potentially fatal </li></ul><ul><li>Cardiac causes of syncope have the highest mortality rates (5 year mortality - 50 %, 1 year mortality - 30 %) </li></ul>The Significance of Syncope 1 Day SC, et al. Am J of Med 1982;73:15-23. 2 Kapoor W. Medicine 1990;69:160-175. 3 Silverstein M, Sager D, Mulley A. JAMA . 1982;248:1185-1189. 4 Martin G, Adams S, Martin H. Ann Emerg Med. 1984;13:499-504.
    10. 10. Impact of Syncope 1 Linzer, J Clin Epidemiol , 1991. 2 Linzer, J Gen Int Med , 1994. Anxiety/ Depression Alter Daily Activities Restricted Driving Change Employment 73% 1 71% 2 60% 2 37% 2 Proportion of Patients
    11. 11. Syncope - Mechanism <ul><li>Global cerebral hypoperfusion </li></ul><ul><li>Interruption of sympathetic outflow </li></ul><ul><li>Increased vagal tone </li></ul><ul><li>Other mechanisms - edema, cerebral autoregulation, central serotonin pathways. </li></ul><ul><li>The trigger for the switch in autonomic response remains one of the unresolved mysteries in cardiovascular physiology* </li></ul><ul><li>Hainsworth. Syncope: what is the trigger? Heart 2003; 89: 123-124 </li></ul>
    12. 12. Syncope - Etiology <ul><li>Reflex mediated - 40% </li></ul><ul><li>Unexplained - 25% </li></ul><ul><li>Cardiac - 15% </li></ul><ul><li>Others - 20% </li></ul><ul><ul><li>Orthostatic Hypotention </li></ul></ul><ul><ul><li>Cerebrovascular / Neurologic </li></ul></ul><ul><ul><li>Psychiatric </li></ul></ul><ul><ul><li>Hypoglycemia </li></ul></ul><ul><ul><li>Medications </li></ul></ul>
    13. 13. Syncope - Etiology Orthostatic Cardiac Arrhythmia Structural Cardio- Pulmonary * <ul><li>1 </li></ul><ul><li>Vasovagal (common faint) </li></ul><ul><li>Carotid Sinus </li></ul><ul><li>Neuralgia </li></ul><ul><li>• Situational </li></ul><ul><ul><li>Cough </li></ul></ul><ul><ul><li>Post- </li></ul></ul><ul><ul><li>micturition </li></ul></ul><ul><li>2 </li></ul><ul><li>Drug </li></ul><ul><li>Induced </li></ul><ul><li>• ANS </li></ul><ul><li>Failure </li></ul><ul><ul><li>Primary </li></ul></ul><ul><ul><li>Secondary </li></ul></ul><ul><li>3 </li></ul><ul><li>Brady </li></ul><ul><ul><li>Sick sinus </li></ul></ul><ul><ul><li>AV block </li></ul></ul><ul><li>• Tachy </li></ul><ul><ul><li>VT </li></ul></ul><ul><ul><li>SVT </li></ul></ul><ul><li>Long QT Syndrome </li></ul><ul><li>4 </li></ul><ul><li>Aortic Stenosis </li></ul><ul><li>HOCM </li></ul><ul><li>• Pulmonary </li></ul><ul><li>Hypertension </li></ul><ul><li>5 </li></ul><ul><li>Psychogenic </li></ul><ul><li>• Metabolic </li></ul><ul><li>e.g. hyper- </li></ul><ul><li>ventilation </li></ul><ul><li>Neurological </li></ul>Non- Cardio- vascular Reflex (Neurally) Mediated Unknown Cause = 34% 24% 11% 14% 4% 12% DG Benditt, UM Cardiac Arrhythmia Center
    14. 14. Causes of Syncope 1 1 Kapoor W. In Grubb B, Olshansky B (eds) Syncope: Mechanisms and Management . Armonk NY; Futura Publishing Co, Inc: 1998; 1-13. 13-41 34 Unknown 4-38 14 Cardiac Arrhythmias 1-8 4 Organic Heart Disease 3-32 10 Neurological 1-7 2 Psychiatric 1-7 3 Medications 4-10 8 Orthostatic hypotension 0-4 1 Carotid Sinus 1-8 5 <ul><li>Situational </li></ul>8-37 18 <ul><li>Vasovagal </li></ul>Reflex-mediated: Prevalence (Range) % Prevalence (Mean) % Cause
    15. 15. Causes of Syncope-like States <ul><li>Migraine* </li></ul><ul><li>Acute hypoxemia* </li></ul><ul><li>Hyperventilation* </li></ul><ul><li>Somatization disorder (psychogenic syncope) </li></ul><ul><li>Acute Intoxication (e.g., alcohol) </li></ul><ul><li>Seizures </li></ul><ul><li>Hypoglycemia </li></ul><ul><li>Sleep disorders </li></ul>* may cause ‘true’ syncope
    16. 16. Syncope Diagnostic Objectives <ul><li>Distinguish ‘True’ Syncope from other ‘Loss of Consciousness’ spells: </li></ul><ul><ul><li>Seizures </li></ul></ul><ul><ul><li>Psychiatric disturbances </li></ul></ul><ul><li>Establish the cause of syncope with sufficient certainty to: </li></ul><ul><ul><li>Assess prognosis confidently </li></ul></ul><ul><ul><li>Initiate effective preventive treatment </li></ul></ul>
    17. 17. Initial Evaluation (Clinic/Emergency Dept.) <ul><li>Detailed history </li></ul><ul><li>Physical examination </li></ul><ul><li>12-lead ECG </li></ul><ul><li>Echocardiogram (as available) </li></ul>
    18. 18. Syncope Basic Diagnostic Steps <ul><li>Detailed History & Physical </li></ul><ul><ul><li>Document details of events </li></ul></ul><ul><ul><li>Assess frequency, severity </li></ul></ul><ul><ul><li>Obtain careful family history </li></ul></ul><ul><li>Heart disease present? </li></ul><ul><ul><li>Physical exam </li></ul></ul><ul><ul><li>ECG: long QT, WPW, conduction system disease </li></ul></ul><ul><ul><li>Echo: LV function, valve status, HOCM </li></ul></ul><ul><li>Follow a diagnostic plan... </li></ul>
    19. 19. Syncope Evaluation and Differential Diagnosis <ul><li>Complete Description </li></ul><ul><ul><li>From patient and observers </li></ul></ul><ul><li>Type of Onset </li></ul><ul><li>Duration of Attacks </li></ul><ul><li>Posture </li></ul><ul><li>Associated Symptoms </li></ul><ul><li>Sequelae </li></ul>History – What to Look for
    20. 20. 12-Lead ECG <ul><li>Normal or Abnormal? </li></ul><ul><ul><li>Acute MI </li></ul></ul><ul><ul><li>Severe Sinus Bradycardia/pause </li></ul></ul><ul><ul><li>AV Block </li></ul></ul><ul><ul><li>Tachyarrhythmia (SVT, VT) </li></ul></ul><ul><ul><li>Preexcitation (WPW), Long QT, Brugada </li></ul></ul><ul><li>Short sampling window (approx. 12 sec) </li></ul>
    21. 21. Carotid Sinus Massage <ul><li>Site: </li></ul><ul><ul><li>Carotid arterial pulse just below thyroid cartilage </li></ul></ul><ul><li>Method: </li></ul><ul><ul><li>Right followed by left, pause between </li></ul></ul><ul><ul><li>Massage, NOT occlusion </li></ul></ul><ul><ul><li>Duration: 5-10 sec </li></ul></ul><ul><ul><li>Posture – supine & erect </li></ul></ul>
    22. 22. Carotid Sinus Massage <ul><li>Outcome: </li></ul><ul><ul><li>3 sec asystole and/or 50 mmHg fall in systolic blood pressure with reproduction of symptoms = </li></ul></ul><ul><li>Carotid Sinus Syndrome (CSS) </li></ul><ul><li>Contraindications </li></ul><ul><ul><li>Carotid bruit, known significant carotid arterial disease, previous CVA, MI last 3 months </li></ul></ul><ul><li>Risks </li></ul><ul><ul><li>1 in 5000 massages complicated by TIA </li></ul></ul>
    23. 23. Head-up Tilt Test (HUT) <ul><li>Unmasks VVS susceptibility </li></ul><ul><li>Reproduces symptoms </li></ul><ul><li>Patient learns VVS warning symptoms </li></ul><ul><li>Physician is better able to give prognostic / treatment advice </li></ul>
    24. 24. Electroencephalogram <ul><li>Not a first line of testing </li></ul><ul><li>Syncope from Seizures </li></ul><ul><ul><li>Abnormal in the interval between two attacks – Epilepsy </li></ul></ul><ul><ul><li>Normal – Syncope </li></ul></ul>
    25. 25. Ambulatory ECG Initiated Wireless (internet) Event Monitoring <ul><li>Useful for infrequent events </li></ul><ul><li>Implantable type more convenient (ILR) </li></ul>Loop Recorder <ul><li>Useful for infrequent events </li></ul><ul><li>Limited value in sudden LOC </li></ul>Event Recorder Useful for infrequent events Holter (24-48 hours) Comments Method
    26. 26. Reveal ® Plus Insertable Loop Recorder Patient Activator Reveal ® Plus ILR 9790 Programmer
    27. 27. Conventional EP Testing in Syncope <ul><li>Limited utility in syncope evaluation </li></ul><ul><li>Most useful in patients with structural heart disease </li></ul><ul><ul><li>Heart disease……..50-80% </li></ul></ul><ul><ul><li>No Heart disease…18-50% </li></ul></ul><ul><li>Relatively ineffective for assessing bradyarrhythmias </li></ul>Brignole M, Alboni P, Benditt DG, et al. Eur Heart Journal 2001; 22: 1256-1306.
    28. 28. Diagnostic Limitations <ul><li>Difficult to correlate spontaneous events and laboratory findings </li></ul><ul><li>Often must settle for an attributable cause </li></ul><ul><li>Unknowns remain 20-30% 1 </li></ul>1 Kapoor W. In Grubb B, Olshansky B (eds) Syncope: Mechanisms and Management . Armonk NY; Futura Publishing Co, Inc: 1998; 1-13.
    29. 29. Challenges of Syncope <ul><li>Cost </li></ul><ul><ul><li>Cost/year </li></ul></ul><ul><ul><li>Cost/diagnosis </li></ul></ul><ul><li>Quality of Life Implications </li></ul><ul><ul><li>Work/financial </li></ul></ul><ul><ul><li>Mobility (automobiles) </li></ul></ul><ul><ul><li>Psychological </li></ul></ul><ul><li>Diagnosis & Treatment </li></ul><ul><ul><li>Diagnostic yield and repeatability of tests </li></ul></ul><ul><ul><li>Frequency and clustering of events </li></ul></ul><ul><ul><li>Difficulty in managing/treating/controlling future events </li></ul></ul><ul><ul><li>Appropriate risk stratification </li></ul></ul><ul><ul><li>Complex Etiology </li></ul></ul>
    30. 30. Unexplained Syncope Diagnosis History and Physical Exam Surface ECG <ul><li>Neurological Testing </li></ul><ul><li>Head CT Scan </li></ul><ul><li>Carotid Doppler </li></ul><ul><li>MRI </li></ul><ul><li>Skull Films </li></ul><ul><li>Brain Scan </li></ul><ul><li>EEG </li></ul><ul><li>CV Syncope Workup </li></ul><ul><li>Holter </li></ul><ul><li>ELR or ILR </li></ul><ul><li>Tilt Table </li></ul><ul><li>Echo </li></ul><ul><li>EPS </li></ul><ul><li>Other CV Testing </li></ul><ul><li>Angiogram </li></ul><ul><li>Exercise Test </li></ul><ul><li>SAECG </li></ul>Psychological Evaluation ENT Evaluation Endocrine Evaluation Adapted from: W.Kapoor.An overview of the evaluation and management of syncope. From Grubb B, Olshansky B (eds) Syncope: Mechanisms and Management. Armonk, NY: Futura Publishing Co., Inc.1998.
    31. 31. Typical Cardiovascular Diagnostic Pathway History and Physical, ECG Syncope Known SHD No SHD Echo EPS + Treat > 30 days; > 2 Events Tilt/ILR < 30 days - Adapted from: Linzer M, et al. Annals of Int Med, 1997. 127:76-86. Syncope: Mechanisms and Management . Grubb B, Olshansky B (eds) Futura Publishing 1999 Zimetbaum P, Josephson M. Annals of Int Med , 1999. 130:848-856. Krahn A et al. ACC Current Journal Review ,1999. Jan/Feb:80-84. Tilt ILR Tilt Holter/ ELR ILR
    32. 32. Specific Conditions
    33. 33. Neurally-Mediated Reflex Syncope (NMS) <ul><li>Vasovagal syncope (VVS) </li></ul><ul><li>Carotid sinus syndrome (CSS) </li></ul><ul><li>Situational syncope </li></ul><ul><ul><li>post-micturition </li></ul></ul><ul><ul><li>cough </li></ul></ul><ul><ul><li>swallow </li></ul></ul><ul><ul><li>defecation </li></ul></ul><ul><ul><li>blood drawing </li></ul></ul><ul><ul><li>etc. </li></ul></ul>
    34. 34. NM Reflex Syncope: Pathophysiology <ul><li>Multiple triggers </li></ul><ul><li>Variable contribution of vasodilatation and bradycardia </li></ul>
    35. 35. NMS – Basic Pathophysiology 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 Cerebral Cortex Vascular Bed Bradycardia/ Hypotension Baro- receptors Heart Feedback via Carotid Baroreceptors Other Mechanoreceptors Parasympathetic (+) sympathetic (+) ¯ Heart Rate ¯ AV Conduction _ Vasodilatation
    36. 36. <ul><li>Neurally Mediated Physiologic Reflex Mechanism with two Components: </li></ul><ul><ul><li>Cardioinhibitory ( HR ) </li></ul></ul><ul><ul><li>Vasodepressor ( BP ) </li></ul></ul><ul><li>Both components are usually present </li></ul>Vasovagal Syncope (VVS): Clinical Pathophysiology
    37. 37. Diagnosing VVS <ul><li>Patient history and physical exam </li></ul><ul><li>Positive tilt table test </li></ul><ul><ul><li>Overnight fast </li></ul></ul><ul><ul><li>ECG </li></ul></ul><ul><ul><li>Blood pressure </li></ul></ul><ul><ul><li>Supine and upright </li></ul></ul><ul><ul><li>Tilt to 60-80 degrees </li></ul></ul><ul><ul><li>Isoproterenol </li></ul></ul><ul><ul><li>Re-tilt </li></ul></ul>DG Benditt, Tilt Table Testing, 1996. 60° - 80°
    38. 38. Management Strategies for VVS <ul><li>Optimal management strategies for VVS are a source of debate </li></ul><ul><ul><li>Patient education, reassurance, instruction </li></ul></ul><ul><ul><li>Fluids, salt, diet </li></ul></ul><ul><ul><li>Tilt Training </li></ul></ul><ul><ul><li>Support hose </li></ul></ul><ul><li>Drug therapies </li></ul><ul><li>Pacing </li></ul><ul><ul><li>Class II indication for VVS patients with positive HUT and cardioinhibitory or mixed reflex </li></ul></ul>
    39. 39. VVS: Treatment Overview <ul><li>Education </li></ul><ul><ul><li>symptom recognition </li></ul></ul><ul><ul><li>reassurance </li></ul></ul><ul><ul><li>situation avoidance </li></ul></ul><ul><li>Tilt-Training </li></ul><ul><ul><li>prescribed upright posture </li></ul></ul><ul><li>Pharmacologic Agents </li></ul><ul><ul><li>salt/volume management </li></ul></ul><ul><ul><li>beta-adrenergic blockers </li></ul></ul><ul><ul><li>SSRIs </li></ul></ul><ul><ul><li>vasoconstrictors (e.g., midodrine) </li></ul></ul><ul><li>Cardiac Pacemakers </li></ul>
    40. 40. VVS: Tilt-Training <ul><li>Objectives </li></ul><ul><ul><li>Enhance Orthostatic Tolerance </li></ul></ul><ul><ul><li>Diminish Excessive Autonomic Reflex Activity </li></ul></ul><ul><ul><li>Reduce Syncope Susceptibility / Recurrences </li></ul></ul><ul><li>Technique </li></ul><ul><ul><li>Prescribed Periods of Upright Posture </li></ul></ul><ul><ul><li>Progressive Increased Duration </li></ul></ul>
    41. 41. VVS: Pharmacologic Rx <ul><li>Salt /Volume </li></ul><ul><ul><li>Salt tablets, ‘sport’ drinks, fludrocortisone </li></ul></ul><ul><li>Beta-adrenergic blockers </li></ul><ul><ul><li>1 positive controlled trial (atenolol), </li></ul></ul><ul><ul><li>1 on-going RCT (POST) </li></ul></ul><ul><li>Disopyramide </li></ul><ul><li>SSRIs </li></ul><ul><ul><li>1 controlled trial </li></ul></ul><ul><li>Vasoconstrictors (e.g., midodrine) </li></ul><ul><ul><li>1 negative controlled trial (etilephrine) </li></ul></ul>
    42. 42. Pacing in VVS <ul><li>Recent clinical studies demonstrated benefits of pacing in select VVS patients: </li></ul><ul><ul><li>VPS I </li></ul></ul><ul><ul><li>VASIS </li></ul></ul><ul><ul><li>SYDIT </li></ul></ul><ul><ul><li>VPS II –Phase I </li></ul></ul><ul><ul><li>ROME VVS Trial </li></ul></ul>
    43. 43. VVS Pacing Trials Conclusions <ul><li>DDD pacing reduces the risk of syncope </li></ul><ul><li>in patients with recurrent, refractory, </li></ul><ul><li>highly-symptomatic, cardioinhibitory </li></ul><ul><li>vasovagal syncope. </li></ul>
    44. 44. Carotid Sinus Syndrome (CSS) <ul><li>Syncope clearly associated with carotid sinus stimulation is rare (≤1% of syncope) </li></ul><ul><li>CSS may be an important cause of unexplained syncope / falls in older individuals </li></ul>
    45. 45. Etiology of CSS <ul><li>Sensory nerve endings in the carotid sinus walls respond to deformation </li></ul><ul><li>“ Deafferentation” of neck muscles may contribute </li></ul><ul><li>Increased afferent signals to brain stem </li></ul><ul><li>Reflex increase in efferent vagal activity and diminution of sympathetic tone results in bradycardia and vasodilation </li></ul>Carotid Sinus
    46. 46. Carotid Sinus Hypersensitivity(CSH) <ul><li>Abnormal response to CSM </li></ul><ul><li>Absence of symptoms attributable to CSS </li></ul><ul><li>CSH reported frequent in ‘fallers’ (Kenny) </li></ul><ul><li>CSH  CSS </li></ul>
    47. 47. CSS and Falls in the Elderly <ul><li>30% of people >65 yrs of age fall each year 1 </li></ul><ul><ul><li>Total is 9,000,000 people in USA </li></ul></ul><ul><ul><li>Approximately 10% of falls in elderly persons are due to syncope 2 </li></ul></ul><ul><li>50% of fallers have documented recurrence 3 </li></ul><ul><li>Prevalence of CSS among frequent and unexplained fallers unknown but… </li></ul><ul><ul><li>CSH present in 23% of >50 yrs fallers presenting at ER 3 </li></ul></ul>1 Falling in the Elderly: U.S. Prevalence Data. Journal of the American Geriatric Society, 1995. 2 Campbell et al: Age and Aging 1981;10:264-270. 3 Richardson 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. 48. Role of Pacing in CSS -- Syncope Recurrence Rate Brignole et. Al. Diagnosis, natural history and treatment. Eur JCPE. 1992; 4:247-254 57% %6 % Recurrence <ul><li>Class I indication for pacing (AHA and BPEG) </li></ul><ul><li>Limit pacing to CSS that is: </li></ul><ul><ul><li>Cardioinhibitory </li></ul></ul><ul><ul><li>Mixed </li></ul></ul><ul><li>DDD/DDI superior to VVI </li></ul>(Mean follow-up = 6 months)
    49. 49. Principal Causes of Orthostatic Syncope <ul><li>Drug-induced (very common) </li></ul><ul><ul><li>diuretics </li></ul></ul><ul><ul><li>vasodilators </li></ul></ul><ul><li>Primary autonomic failure </li></ul><ul><ul><li>multiple system atrophy </li></ul></ul><ul><ul><li>Parkinsonism </li></ul></ul><ul><li>Secondary autonomic failure </li></ul><ul><ul><li>diabetes </li></ul></ul><ul><ul><li>alcohol </li></ul></ul><ul><ul><li>amyloid </li></ul></ul><ul><li>Alcohol </li></ul><ul><ul><li>orthostatic intolerance apart from neuropathy </li></ul></ul>
    50. 50. Syncope Due to Arrhythmia or Structural CV Disease: General Rules <ul><li>Often life-threatening and/or exposes patient to high risk of injury </li></ul><ul><li>May be warning of critical CV disease </li></ul><ul><ul><li>Aortic stenosis, Myocardial ischemia, Pulmonary hypertension </li></ul></ul><ul><li>Assess culprit arrhythmia / structural abnormality aggressively </li></ul><ul><li>Initiate treatment promptly </li></ul>
    51. 51. Principal Causes of Syncope due to Structural Cardiovascular Disease <ul><li>Acute MI / Ischemia </li></ul><ul><ul><li>Acquired coronary artery disease </li></ul></ul><ul><ul><li>Congenital coronary artery anomalies </li></ul></ul><ul><li>HOCM </li></ul><ul><li>Acute aortic dissection </li></ul><ul><li>Pericardial disease / tamponade </li></ul><ul><li>Pulmonary embolus / pulmonary hypertension </li></ul><ul><li>Valvular abnormalities </li></ul><ul><ul><li>Aortic stenosis, Atrial myxoma </li></ul></ul>
    52. 52. Syncope Due to Cardiac Arrhythmias <ul><li>Bradyarrhythmias </li></ul><ul><ul><li>Sinus arrest, exit block </li></ul></ul><ul><ul><li>High grade or acute complete AV block </li></ul></ul><ul><li>Tachyarrhythmias </li></ul><ul><ul><li>Atrial fibrillation / flutter with rapid ventricular rate (e.g. WPW syndrome) </li></ul></ul><ul><ul><li>Paroxysmal SVT or VT </li></ul></ul><ul><ul><li>Torsades de pointes </li></ul></ul>
    53. 53. Rhythms During Recurrent Syncope Krahn A, et al. Circulation. 1999; 99: 406-410 Normal Sinus Rhythm 58% Normal Sinus Rhythm 58% Bradycardia 36% Tachyarrhythmia 6%
    54. 54. Treatment of Syncope Due to Bradyarrhythmia <ul><li>Class I indication for pacing using dual- chamber system wherever adequate atrial rhythm is available </li></ul><ul><li>Ventricular pacing in atrial fibrillation with slow ventricular response </li></ul>
    55. 55. Treatment of Syncope Due to Tachyarrhythmia <ul><li>Atrial Tachyarrhythmias; </li></ul><ul><ul><li>AVRT due to accessory pathway – ablate pathway </li></ul></ul><ul><ul><li>AVNRT – ablate AV nodal slow pathway </li></ul></ul><ul><ul><li>Atrial fib  – Pacing, linear / focal ablation, ICD selected pts </li></ul></ul><ul><ul><li>Atrial flutter – Ablation of reentrant circuit </li></ul></ul><ul><li>Ventricular Tachyarrhythmias; </li></ul><ul><ul><li>Ventricular tachycardia – ICD or ablation where appropriate </li></ul></ul><ul><ul><li>Torsades de Pointes – withdraw offending Rx or ICD (long-QT/Brugada) </li></ul></ul><ul><li>Drug therapy may be an alternative in many cases </li></ul>
    56. 56. Conclusion <ul><li>Syncope is a common symptom, </li></ul><ul><li>often with dramatic consequences, </li></ul><ul><li>which deserves thorough investigation </li></ul><ul><li>and appropriate treatment of its cause. </li></ul>
    57. 57. Conclusion <ul><li>Syncope is a common symptom, </li></ul><ul><li>often with dramatic consequences, </li></ul><ul><li>which deserves thorough investigation </li></ul><ul><li>and appropriate treatment of its cause. </li></ul>
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