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Bradyarrhythmias and pacemaker choice
The document discusses bradyarrhythmias and pacemaker selection. It provides an overview of conduction systems, mechanisms of sinus node dysfunction and AV block. It reviews evaluations for bradyarrhythmias including ECG, tests, and etiologies. Guidelines for pacemaker indications are presented for various conditions like sinus node dysfunction, AV block, bifascicular/trifascicular block, and neurocardiogenic syncope. Complications and special considerations like EMI and device settings are also mentioned.
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Bradyarrhythmias and pacemaker choice
- 1. 台大醫院內科心臟電生理教學演講系列 (2010)時間：每週二，下午 17:30-18:30 地點： 14C 教室 ( 錫琴講堂 ) Bradyarrhythmias and pacemaker choice 游治節 Chih-Chieh Yu Aug. 03, 10’
- 2. Consultation on TEL(1) 68 y/o man ECG: Junctional bradycardia What’s on your mind?
- 3. Junctional bradycardia? Possiblemechanism~ Sinus arrest/bradycardia with junctional escape rhythm CAVB with junctional escape rhythm Sinus rhythm AFib JUNCTIONAL BRADYCARDIA (<30bpm)
- 4. Bradyarrhythmias Outlines Identifymechanism Identify etiology Identify treatment
- 5. Conduction system SAnode Atrium AV node His bundle Purkinji system
- 6. Conduction system SAnode Atrium P-HisA P-dCS AV node: Escape rate: 30~55bpm His bundle Escape rate: 30~50bpm Mobitz II second degree/2:1 Autonomic intervention may not change conduction Infra-His Escape rate: 15~40bpm
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- 10. AV Block ECGof 1degreeAVB
- 11. 2nd degree AVblock
- 12. 2nd degree AVblock
- 13. Complete AV blockSupraHis & InfraHis Block
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- 16. Identify Etiology Reversiblecause? Treatment?
- 17. Bradyarrhythmias Outlines Identifymechanism Identify etiology Identify treatment
- 18. Causes of sinusnode and AV node dysfunction Medication: BB, nDHP-CCB Digoxin, Amiodarone, Sotalol Ischemia Metabolic effect Electrolyte acidosis Hypothermia Hypothyroidism/ adrenal insufficiency Secondary Inflammatory disease Autoimmune, viral Infiltrative disease Neuromuscular disease Previous cardiac surgery Degenerative change Congenital Autonomic effect
- 19. Evaluation History /Physical examination ECG Endocrine function / electrolyte UCG Holter ECG / Loop event recorder Treadmill testing Head-up Tilting EP study
- 20. SA nodeanatomy
- 21.
- 22. Head-Up Tilt TableTesting Protocol Fast > 2 hours continuous ECG and blood pressure mornitering Tilt to 60~80° 20~45 minutes
- 23. Head-Up Tilt Test(HUT)
- 24. In the EPlab Sinus node response Atropine (0.04mg/kg): 20~50% increase Isoproterenol (1~3ug/min): 25% increase Esmolol: Propranolol (0.1mg/kg): 12.5~22.5% decrease Intrinsic heart rate (117.2-0.57xage) Total autonomic blockade: atropine + esmolol (propranolol)
- 25. EP test SAconduction time: (A2-A3)-(BCL)/2=45~125ms Set A1-A2 between earliest third of zone II or 100ms less than BCL Impact factor: Sinus arrhythmia SA entrance block or delay Pacemaker shift Limitation: wide range of normal value
- 26.
- 27. EP test Sinusnode recovery time test cSNRT= (SNRT – baseline HR) <550ms Represents overall function- including automaticity and conduction function. Good predictor of bradytachyarrhythmic syndrome (pace up to 200 bpm) Some phenomenon: Greatest suppression occur at slow rate: entrance block Secondary pauses: impaired sinus node conduction
- 28. EP test forAV block AV node: Influenced by autonomic tone pronouncedly (consider chemically denervation) AH time 60~125ms Wenchebach phenomenon Rapid atrial pacing: HV block > 400ms AEST: AVERP > 450 ms
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- 31. EP test forAV block Infra-His: HV 35~55ms Mostly common with type II second-degree Alternating bundle branch block HV dissociation Adams-Stokes attacks Precipitates Torsades de Pointes
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- 33. Consultation on TEL(3)Medical Hx: Rheumatic heart disease s/p mitral mechanical replacement Drug History: digoxin/Dilatrend/Herbesser Acute renal failure with Metabolic acidosis and Hyperkalemia ARB What to do now?
- 34. Management Key pointslife-threatening or not symptomatic or not Acute management stabilized vital signs increase in ventricular rate Long term management Remove the reversible cause define treatment Holter ER ICU
- 35. Consultation on TEL(4) admitted to ICU with a TPM via her right internal jugular vein Improved renal function ECG: Atrial fibrillation with rapid ventricular response
- 36. Consultation on TEL(5) Dilatrend 3,125mg+Herbesser 30mg in the evening AFib with SVR at midnight (TPM pacing 60bpm) PPM considered
- 37. Pacemaker nomenclature Chamberpaced (O/A/V/D) Chamber sensed (O/A/V/D) Response(O/I/T/D) Rate modulate(O/R) Multisite pacing (O/A/V/D)
- 38. Pacing mode selectionDDD/AAI (atrial based pacing) vs. VVI lower mortality lower Af incidence AV search Search AV/Managed ventricular pacing (MVP TM ) AV search hysteresis ventricular intrinsic preference (VIP TM )
- 39. Pacing In SinusNode Dysfunction
- 40. Class I Indications: Pacing in Sinus Node Dysfunction SN dysfunction with documented symptomatic bradycardia , including frequent sinus pauses that produce symptoms. May be a consequence of essential long-term drug therapy for which there is no alternative. Symptomatic chronotropic incompetence .
- 41. Chronotropic Incompetence MaxRest Heart Rate Time Start Activity Stop Activity Quick Unstable Slow
- 42. Class IIa Indications: Pacing in Sinus Node Dysfunction SN dysfunction with HR <40 bpm , developing either spontaneously or as a result of necessary drug therapy, when a clear association between significant symptoms consistent with bradycardia and the actual presence of bradycardia has not been documented. Syncope of unexplained origin when major abnormalities of sinus node function are discovered or provoked in EP studies .
- 43. Class IIb Indications: Pacing in Sinus Node Dysfunction In minimally symptomatic patients, chronic heart rates <40 bpm, while awake.
- 44. Class III Indications: Pacing in Sinus Node Dysfunction SN dysfunction in asymptomatic patients including those in whom substantial bradycardia (HR <40 bpm) is a result of long-term drug treatment . SN dysfunction in patients in whom symptoms suggestive of bradycardia are clearly documented not to be associated with a slow HR. SN dysfunction with symptomatic bradycardia due to nonessential drug therapy .
- 45. Pacing In AcquiredAV Block
- 46. Class I Indications: Pacing for Acquired AV Block Third-degree and advanced second degree AV block at any anatomic level with: Bradycardia and symptoms (including heart failure) presumed due to AV block, Arrhythmias and other medical conditions requiring drugs that result in symptomatic bradycardia, Documented asystole 3.0 sec. or escape rate <40 bpm in awake, symptom-free patients. Post AV junction ablation, Postoperative AV block not expected to resolve after cardiac surgery, Neuromuscular diseases with AV block, with or without symptoms.
- 47. Class I Indications:Pacing for Acquired AV Block Second-degree AV block regardless of type or site of block, with associated symptomatic bradycardia.
- 48. Class IIa Indications: Pacing for Acquired AV Block Asymptomatic third-degree AV block at any anatomic site with average, awake ventricular rate 40 bpm , especially if cardiomegaly or LV dysfunction is present. Asymptomatic type II second-degree AV block with a narrow QRS. Asymptomatic type I second-degree AV block at intra- or infra-His levels found at EP study. First or second degree AV block with symptoms similar to "pacemaker syndrome“.
- 49. Class IIb Indications: Pacing for Acquired AV Block Marked first-degree AV block (>0.30 sec.) in patients with LV dysfunction and CHF in whom a shorter AV interval results in hemodynamic improvement, presumably by left atrial filling pressure. Neuromuscular diseases with any degree of AV block (including first degree AV block), with or without symptoms.
- 50. Class III Indications: Pacing for Acquired AV Block Asymptomatic first-degree AV block. Asymptomatic type I second-degree AV block at the supra-His level. AV block expected to resolve and unlikely to recur (e.g., drug toxicity, Lyme disease, etc), or during hypoxia in sleep apnea syndrome in absence of symptoms.
- 51. Pacing In congenitalAV block Symptomatic Wide QRS HR<50 bpm EP test: Infra-Hisian block
- 52. Pacing for Chronic Bifascicular and Trifascicular Block
- 53. A 90 yearold lady with syncope
- 54. Class I Indications: Pacing in Chronic Bifasicular and Trifasicular Block Intermittent third-degree AV block. Type II second-degree AV block. Alternating bundle-branch block.
- 55. Class IIa Indications: Pacing in Chronic Bifasicular and Trifasicular Block Syncope not demonstrated to be due to AV block when other likely causes have been excluded, specifically ventricular tachycardia. Incidental finding at EP study of markedly prolonged HV interval ( > 100 ms) in asymptomatic patients. Incidental finding at EP study of pacing-induced infra-His block that is not physiological.
- 56. Class IIb Indications: Pacing in Chronic Bifasicular and Trifasicular Block Neuromuscular diseases…with any degree of fascicular block with or without symptoms, because there may be unpredictable progression of AV conduction disease.
- 57. Class III Indications: Pacing in Chronic Bifasicular and Trifasicular Block Fascicular block without AV block or symptoms. Fascicular block with first-degree AV block without symptoms.
- 58.
- 59. Chronic high degreeAV block: Narrow QRS escape rhythm (may have wide QRS complexes if BBB) H potential preceded QRS complex (retrograde if slower and no response to atropine) Rapid ventricular pacing to check the stability of His bundle escape rhythm Exercise to check chronotropic insufficiency
- 60. Pacing in NeurocardiogenicSyncope
- 61. Class I Indications: Pacing in Neurocardiogenic Syncope Recurrent syncope caused by carotid sinus stimulation; minimal carotid sinus pressure induces ventricular asystole >3 sec duration in absence of any medication that depresses the SN or AV conduction.
- 62. Class IIa Indications:Pacing in Neurocardiogenic Syncope Recurrent syncope without clear, provocative events and with a hypersensitive cardioinhibitory response. Significantly symptomatic and recurrent neurocardiogenic syncope associated with bradycardia documented spontaneously or at the time of tilt-table testing .
- 63. Class IIb andIII Indications: Pacing in Neurocardiogenic Syncope Class IIb: None Class III: Hyperactive cardioinhibitory response to CS stimulation in absence of symptoms or in the presence of vague symptoms such as dizziness, lightheadedness, or both. Recurrent syncope, lightheadedness or dizziness in absence of hyperactive cardioinhibitory response. Situational vasovagal syncope in which avoidance behavior is effective.
- 64. EMI (electromagneticinterference) Industrial strength welding, degaussing equip, induction oven, cellular phones, antitheft Hospital: electrocautery, cardioversion, MRI, lithotripsy, RFCA, diathermy->Reassess device Effect: reprogram, generator damage, PM inhibit, reverse to fall-back mode, noise reversion mode, electrical reset, myocardial thermal damage MRI: relative contraindication, rapid hemodynamic unstable Ventricular rhythm, theoretical possible thermal damage Operation: routine interrogation, cardioversion/defibrillate (AP paddle position,4-inch from PM) ICD deactivation, VOO/DOO by magnet,
- 65. EMI (electromagneticinterference) (EMI) 2.5 mV Should have paced 80 80
- 66. ERI (elective replacementindicator) Medtronic: VVI 65 St.Jude: PR+100ms Biotronic: PR-11% VDD/SSI EOL (End of Life)
- 67. Magnet response asynchronouspacing Medtronic: 85bpm St. Jude: 98.6~86.3bpm Biotronik: PR ICD: off defibrillation function
- 68. Complication of PPMFailure to output Failure to capture Failure to sense Pacemaker -mediated tachycardia Runaway pacemaker Pacemaker syndrome Twiddler's syndrome Cardiac monitor pseudomalfunction Pacemaker pseudomalfunction
Editor's Notes
- #11 Student Notes Instructor Notes Transition/Auto-animated slide
- #13 Type I: narrow QRS, progressive prolongation of PR, progressive shortening of RR, pause less than two PP intervals. However, 50% atypical
- #14 Rate, QRS width
- #20 Generally speaking, it’s easy to deal with if the diagnosis has been coded with pathological bradycardia. However, in most of the situations, we could not relate pt’s symptoms into this diagnosis. That’s why we need varieties of tools to help us differentiate.
- #21 55~60 from RCA 40~45 from LCX
- #22 If, ICaL Ik 共同決定 diastolic depolarization 的速率 Rate 受 sympathetic and parasympathetic 調控 Cells within the sinoatrial (SA) node are the primary pacemaker site within the heart. These cells are characterized as having no true resting potential , but instead generate regular, spontaneous action potentials. Unlike non-pacemaker action potentials in the heart, and most other cells that elicit action potentials (e.g., nerve cells, muscle cells), the depolarizing current is carried primarily by relatively slow, inward Ca++ currents instead of by fast Na+ currents. There are, in fact, no fast Na+ channels and currents operating in SA nodal cells. This results in a slower action potentials in terms of how rapid they depolarize. Therefore, these pacemaker action potentials are sometimes referred to as &quot;slow response&quot; action potentials. SA nodal action potentials are divided into three phases. Phase 4 is the spontaneous depolarization (pacemaker potential) that triggers the action potential once the membrane potential reaches threshold between -40 and -30 mV). Phase 0 is the depolarization phase of the action potential. This is followed by phase 3 repolarization. Once the cell is completely repolarized at about -60 mV, the cycle is spontaneously repeated. The changes in membrane potential during the different phases are brought about by changes in the movement of ions (principally Ca++ and K+, and to a lesser extent Na+) across the membrane through ion channels that open and close at different times during the action potential. When a channel is opened, there is increased electrical conductance (g) of specific ions through that ion channel. Closure of ion channels causes ion conductance to decrease. As ions flow through open channels, they generate electrical currents (i or I) that change the membrane potential. In the SA node, three ions are particularly important in generating the pacemaker action potential. The role of these ions in the different action potential phases are illustrated in the figure and described below: At the end of repolarization, when the membrane potential is very negative (about -60 mV), ion channels open that conduct slow, inward (depolarizing) Na+ currents. These currents are called &quot;funny&quot; currents and abbreviated as &quot; If &quot;. These depolarizing currents cause the membrane potential to begin to spontaneously depolarize, thereby initiating Phase 4 . As the membrane potential reaches about -50 mV, another type of channel opens. This channel is called transient or T-type Ca++ channel . As Ca++ enters the cell through these channels down its electrochemical gradient, the inward directed Ca++ currents further depolarize the cell. As the membrane continues to depolarize to about -40 mV, a second Ca++ channel opens. These are the so-called long-lasting, or L-type Ca++ channels . Opening of these channels causes more Ca++ to enter the cell and to further depolarize the cell until an action potential threshold is reached (usually between -40 and -30 mV). During Phase 4 there is also a slow decline in the outward movement of K+ as the K+ channels responsible for Phase 3 continue to close. This fall in K+ conductance (gK+) contributes to the pacemaker potential. Phase 0 depolarization is primarily caused by increased Ca++ conductance (gCa++) through the L-type Ca++ channels that began to open toward the end of Phase 4. The &quot;funny&quot; currents, and Ca++ currents through the T-type Ca++ channels, decline during this phase as their respective channels close. Because the movement of Ca++ through these channels into the cell is not rapid, the rate of depolarization (slope of Phase 0) is much slower than found in other cardiac cells (e.g., Purkinje cells ). Repolarization occurs ( Phase 3 ) as K+ channels open (increased gK+) thereby increasing the outward directed, hyperpolarizing K+ currents. At the same time, the L-type Ca++ channels close, gCa++ decreases, and the inward depolarizing Ca++ currents diminish. During depolarization, the membrane potential (Em) moves toward the equilibrium potential for Ca++, which is about +134 mV. During repolarization, g’Ca++ (relative Ca++ conductance) decreases and g’K+ (relative K+ conductance) increases, which brings Em closer toward the equilibrium potential for K+, which is about -96 mV). Therefore, the action potential in SA nodal cells is primarily dependent upon changes in Ca++ and K+ conductances as summarized below: Em = g'K+ (-96 mV) + g'Ca++ (+134 mV) Although pacemaker activity is spontaneously generated by SA nodal cells, the rate of this activity can be modified significantly by external factors such as by autonomic nerves, hormones, drugs, ions, and ischemia/hypoxia . It is important to note that action potentials described for SA nodal cells are very similar to those found in the atrioventrcular (AV) node . Therefore, action potentials in the AV node, like the SA node, are determined primarily by changes in slow inward Ca++ and K+ currents, and do not involve fast Na+ currents. AV node action potentials also have intrinsic pacemaker activity produced by the same ion currents as described above for SA nodal cells.
- #24 ECG leads and intra-arterial pressure tracing illustrating the final moments of a head-up tilt test just prior to induced syncope. Note that blood pressure tended to fall in advance of the bradycardia component. Later, even though the patient is returned to supine posture,and the heart rate returns to normal, it may take some time for the arterial pressure to fully recover. The latter is due to persistent vasodilatation which may disappear slowly.
- #26 Using drugs to eliminate the effect of autonomic system. However, some limitation is not avoidable.
- #28 Using drugs to eliminate the effect of autonomic system. However, some limitation is not avoidable.
- #39 Included is a summary of some studies depicting long-term results of AV synchronous (atrial based) and non-synchronous (VVI/R) pacing In addition to heart rate and stroke volume, the propensity for development of atrial fibrillation with the associated risks of thromboembolic events, stroke, and reduced survival is an important issue. Studies have shown that atrial-based pacing modes (modes that can sense and respond to P waves) have a much lower incidence of developing atrial fibrillation than modes that only pace and sense in the ventricle. For this reason, as well as the increase in cardiac output due to AV synchrony, it is advantageous to use atrial-based pacing modes whenever possible. Note : Exceptions include instances when it is not possible to sense the atrium or conditions in which it would not be beneficial to sense the atrium, such as chronic atrial fibrillation or flutter, inability to achieve adequate pacing/sensing thresholds, or an inexcitable atrium. Higano, et al. Hemodynamic importance of atrioventricular synchrony during low levels of exercise. PACE, 1990; 13:509 Abstact. Gallik DM, et al. Comparison of ventricular function in atrial rate adaptive versus dual chamber rate adaptive pacing during exercise. PACE , 1994; 17(2):179-185 Santini, et al. New Perspectives in Cardiac Pacing. Mount Kisco, NY: Futura Publishing, 1991. Rosenquist M, et al. Relative importance of activation sequence compared to atrioventricular synchrony during low levels of exercise. AM J Cardiology, 1991;67:148-156. SulkeN, et al. “Sbuclinical pacemaker syndrome: A randomized study of symptom free patients with ventricular demand (VVI) pacemakers upgraded to dual chamber devices. Brit Heart J , 1992; 67(1):57-64. In addition to heart rate and stroke volume, the propensity for development of atrial fibrillation with the associated risks of thromboembolic events, stroke, and reduced survival is an important issue. Studies have shown that atrial-based pacing modes (modes that can sense and respond to P waves) have a much lower incidence of developing atrial fibrillation than modes that only pace and sense in the ventricle. For this reason, as well as the increase in cardiac output due to AV synchrony, it is advantageous to use atrial-based pacing modes whenever possible. Note : Exceptions include instances when it is not possible to sense the atrium or conditions in which it would not be beneficial to sense the atrium, such as chronic atrial fibrillation or flutter, inability to achieve adequate pacing/sensing thresholds, or an inexcitable atrium. Rosenquist M, et al. Long-term pacing in sinus node disease: Effects of stimulation mode on cardiovascular morbidity and mortality. AM Heart J . 1988; 116(1 pt.1): 16-22. Santini M., et al. Relation of prognosis in sick sinus syndrome to age, conduction defects, and modes of permanent cardiac pacing. AM J Cardiol . 1990; 65(11):729-735. Stangl K, et al. Differences between atrial single chamber pacing (AAI) and ventricular single chamber acing (VVI) with respect to prognosis and antiarrhythmic effect in patients with SSS. PACE , 1990; 13(12):863-868. Zanini R, et al. Morbidity and mortality of patients with sinus node disease: comparative effects of atrial and ventricular pacing. PACE , 1990; 13(12): 2076-2079.
- #41 Sinus node dysfunction may express itself as chronotropic incompetence in which there is inadequate sinus response to exercise or stress. Rate-responsive pacemakers have clinically benefited patients by restoring physiological heart rate during activity.
- #42 It is important to be able to able to increase heart rate with activity (chronotropic competence). The pacemaker and mode selected should provide the ability to increase rate with activity either by “tracking” the sinus node or, if the sinus node is not chronotropically competent, by providing the rate response via a sensor.
- #43 In the patient with syncope without clinical correlation with a bradyarrhythmia, eletrophysiologic testing may be appropriate. If major abnormalities of sinus node function are found during electrophysiologic testing, even if no correlation exists, pacing would be a Class I Ia indication based on the EP findings.
- #44 The heart rate value was previously <35 bpm. The previous values were not determined from clinical trial data, but rather, physician judgment and patient symptoms. The change reflects growing evidence that the site of origin of the escape rhythm and degree of patient symptoms are as important or more important than the escape rate.
- #47 Non-randomized studies suggest that pacing does improve survival in patients with third-degree AV block, especially when the block is associated with syncope. New changes introduce the importance of the site of the block and introduce “advanced second-degree AV block” as a class I indication. Advanced second degree AV block refers to the block of two or more consecutive P-waves but with some conducted beats, indicating some preservation of AV conduction. This change demonstrates that advanced second-degree AV block can be as clinically serious as 3 rd degree AV block. In recommendation 1a, heart failure is specifically introduced as a major symptom that merits consideration when dealing with AV block-induced bradycardia.
- #48 In recommendation 1e, “cardiac surgery” was added to specifically define the situation(s) in which this recommendation applies. Recommendation 1f has been expanded to indicate that pacing therapy is recommended in patients with neuromuscular diseases and AV block whether or not they are symptomatic, in view of the unpredictable progression of AV conduction in this group of diseases.
- #49 Type I second-degree AV block is usually due to delay in the AV node, irrespective of QRS width . Progression to advanced AV block is uncommon. Type II second-degree AV block is usually infranodal (either intra- or infra-His) especially when the QRS is wide. Symptoms are frequent and progression to advanced AV block is common. When type II second-degree AV block occurs with a wide QRS, pacing becomes a Class I recommendation. The “narrow QRS” addition in #2 will now enable physicians to indicate patients for pacing that present with type-II second-degree AV block on evaluation (Holter or ECG)—whether or not they are symptomatic.
- #50 A long PR interval may identify a group of patients with LV dysfunction some of whom may benefit from dual chamber pacing with a shorter AV delay. Some small, nonrandomized trials have suggested that there may be some symptomatic and functional improvement by pacing patients with shorter AV intervals. Pacing therapy is recommended in patients with neuromuscular diseases and AV block whether or not they are symptomatic, in view of the unpredictable progression of AV conduction in this group of diseases.
- #51 Addition of hypoxia occurring during periods of sleep apnea as a cause of transient AV block that is unlikely to recur once sleep apnea syndrome has been treated. However, if symptoms are present, pacing is indicated as in other conditions.
- #55 Bifascicular block refers to ECG evidence of impaired conduction below the AV node in two fascicles of the right and left bundles. Alternating BBB (aka bilateral bundle-branch block) refers to situations in which clear ECG evidence for block in all 3 fascicles is seen on successive ECGs. Patients with such ECG abnormalities and symptomatic, advanced AV block have a high mortality rate and significant incidence of sudden death. Type II second-degree AV block and a wide QRS indicate diffuse conduction system disease and constitute an indication for pacing even in the absence of symptoms.
- #56 If the cause of syncope in the presence of bifascicular or trifasicuclar block cannot be determined with certainty or if treatments used may exacerbate AV block, prophylactic pacing is indicated, especially if syncope may have been due to transient third-degree AV block. Of the many laboratory variables, the PR and HV intervals have been identified as possible predictors of third-degree AV block and sudden death. PR interval prolongation is common in patients with bifascicular block, but the delay is often at the level of the AV node . Some investigators have suggested that asymptomatic patients with bifascicular block and a prolonged HV interval should be considered for permanent pacing if the HV interval exceeds 100 msec.
- #57 New Class IIb recommendation for pacing therapy in patients with neuromuscular diseases and fascicular block. Clinical experience suggests that progression of AV conduction disturbance is unpredictable, and high-grade AV block can develop in asymptomatic patients with these diseases.
- #62 CSS is defined as syncope or presyncope resulting from an extreme reflex response to CS stimulation. There are two main components of the reflex: Cardioinhibitory: resulting from increased parasympathetic tone and manifested by slowing of the sinus rate or prolongation of the PR interval and advanced AV block, alone or in combination. Vasodepressor: secondary to reduction in sympathetic activity resulting in loss of vascular tone and hypotension. This effect is independent of heart rate changes. Evidence has emerged that suggests that elderly patients who have sustained otherwise unexplained falls may have carotid sinus hypersensitivity. In a study of 175 elderly patients who had fallen without loss of consciousness and had pauses >3 sec during CS massage, were randomized to pacing or nonpacing therapy. The paced group had a significantly lower likelihood of subsequent falling episodes during follow up.
- #63 Neurocardiogenic syncope (NCS) accounts for 10% to 40% of syncope episodes. Approximately 25% of patients have a predominant vasodepressor reaction without significant bradycardia. An additional large percentage of patients will have a mixed vasodepressor/vasoinhibitory component of their symptoms. Dual-chamber pacing, carefully prescribed on the basis of tilt-table testing, may be effective in reducing symptoms if the patient has a significant cardioinhibitory component to the cause of their symptoms. Results from two randomized trials in highly symptomatic patients with bradycardia demonstrated that permanent pacing increased the time to first syncopal event. In one of these trials the actuarial rate of recurrent syncope at 1 year was 18.5% for pacemaker patients and 59.7% for control patients. One study demonstrated that DDD pacing with rate-drop response function was more effective than beta-blockade in preventing recurrent syncope in highly symptomatic patients with vasovagal syncope and relative bradycardia during tilt-table testing. The evaluation of patients with syncope of undetermined origin should take into account clinical status and not overlook other, more serious causes of syncope such as VT.