Cardiacc Rhythm Management Devices in Anesthesiology

Dr. William Kostis - Associate Professor of Medicine Division of Cardiovascular Disease and Hypertension

Transcript

1. Rutgers, The State University of New Jersey Cardiac Rhythm Management Devices in Anesthesiology William J. Kostis, PhD, MD Associate Professor of Medicine Division of Cardiovascular Disease and Hypertension October 14, 2020
2. CRM Devices in Anesthesiology Disclosures •  No relevant disclosures
3. CRM Devices in Anesthesiology Cardiac Rhythm Management Devices •  Cardiac Rhythm Management Devices •  Many types of devices •  Many indications for devices •  Many device functions •  Many ways to implant these devices •  Many ways to program these devices •  Many acronyms to describe device types and functions •  Many months and years spent becoming proficient with all of the above •  What are the most important questions for those in Anesthesiology?
4. CRM Devices in Anesthesiology Some Basic Questions •  Some Basic Questions •  What types of devices are there? •  How do they manage rhythm disorders? •  What information can they provide? •  Who needs them? •  (and what that may imply about a patient?) •  What might I need to do to help manage them?
5. CRM Devices in Anesthesiology Primary Functions of CRM Devices •  Prevent bradyarrhythmias •  Due to problems with impulse generation or impulse propagation •  PPM, ICD*, TVP •  Prevent sudden cardiac death (SCD) •  Cardioversion of VT / Defibrillation of VF •  Antitachycardia Pacing (ATP) for pace-termination of VT •  ICD •  Provide heart rhythm monitoring •  Ambulatory monitor, ILR, PPM, ICD •  Improve cardiac function •  Cardiac Resynchronization Therapy (CRT) •  CRT-D, CRT-P
6. CRM Devices in Anesthesiology Bradycardia •  Bradycardia results from disorders of either: •  Impulse generation •  Impulse propagation / conduction
7. CRM Devices in Anesthesiology Bradycardia •  Impaired impulse generation in sinoatrial node •  Leads to sinus bradycardia •  Subsidiary pacemaker may take over •  Ectopic atrial rhythm •  Junctional escape rhythm •  Ventricular escape rhythm •  Sinus node dysfunction (SND) •  First described as sick sinus syndrome by Ferrer in 1968 •  abnormalities of the sinus node and surrounding atrial tissue •  sinus arrest, inappropriate sinus bradycardia, and chronotropic incompetence •  Tachy-brady syndrome (SND + increasing presence of subsidiary pacemakers) •  Atrial arrhythmias •  Conversion pauses
8. CRM Devices in Anesthesiology Bradycardia •  Sinus bradycardia (due to impulse generation disorder) •  Sinus node dysfunction •  Hypervagotonia •  Conditioned athletes •  Apnea (e.g. OSA) •  Pain, cough, Valsalva, micturition, etc. •  Negative chronotropic drugs •  BB, non-dihydropyridine CCB, amiodarone, digoxin, ivabradine •  Acetylcholinesterase inhibitors, opioids, benzodiazepines, clonidine •  Hypothyroidism •  Hyperkalemia •  Ischemia (SA nodal artery; RCA:LCx [60:40]) •  Cushing reflex (increased ICP) •  with hypertension and respiratory depression) •  Congenital / channelopathies
9. CRM Devices in Anesthesiology Bradycardia •  Sinus bradycardia (due to impulse propagation disorder) •  Sinoatrial nodal exit block •  First-degree (cannot be detected on surface EKG) •  Second-degree (Type I) •  Progressive prolongation of conduction block within the sinus node until complete exit block occurs (progressive shortening of P-P intervals before block on surface EKG) •  Second-degree (Type II) •  Spontaneous block of sinus impulse (leading to a sinus pause which is an exact multiple of the preceding P-P interval on surface EKG) •  Third-degree •  Sinus arrest (evidence of a subsidiary pacemaker [ectopic atrial, junctional, ventricular] may be present on surface EKG)
10. CRM Devices in Anesthesiology •  Bradycardia due to impulse propagation disorder in AVN or HPS •  Due to atrioventricular (AV) block •  First-degree AV block (typically nodal, unless evidence of infranodal dz) •  Second-degree (Type I) AV block •  Progressive prolongation of PR interval prior to non-conducted P-wave (typically nodal) •  Second-degree (Type II) AV block •  Spontaneous non-conduction of P-wave without change in PR interval (typically infranodal) •  2:1 AV block •  Non-conduction of every other P-wave (nodal or infranodal) •  Vagal / sympathetic maneuvers or presence of infranodal disease may help to infer whether nodal or infranodal •  High-grade AV block •  Non-conduction of multiple P-waves with occasional conduction without change in PR interval (typically infranodal) •  Third-degree / Complete AV block •  No anterograde conduction from A to V •  May be subsidiary pacemaker for escape rhythm (junctional or ventricular) or may lead to asystole Bradycardia
11. CRM Devices in Anesthesiology •  First-degree AV block •  May be physiologic (hypervagotonia) •  Idiopathic fibrosclerosis of the conduction system (i.e., Lev’s disease [old], Lenegre’s disease [young] •  Negative dromotropic agents •  BB, non-dihydropyridine CCB, amiodarone, digoxin •  Inflammation •  Myocarditis, Lyme •  Infiltration •  Sarcoid, amlyoid •  Thyroid disease •  Hypo- and hyper- •  Hyperkalemia •  Ischemia (AV nodal artery; RCA:LCx [80:20]) •  Iatrogenic (surgical, catheter, etc.) •  Neuromuscular disease •  Congenital Bradycardia
12. CRM Devices in Anesthesiology Intraventricular Block •  Intraventricular block •  RBBB •  LBBB •  LAFB / LPFP •  Bifascicular block •  Trifascicular block •  Evidence of disease in all 3 fascicles •  Typically presents with alternating BBB, or RBBB with alternating LAFB and LPFB •  Term should NOT be used to describe bifascicular block + first-degree AV block (as the long PR is often nodal rather than infranodal) •  Intraventricular block etiologies •  Ischemia / Infarction •  Myocarditis / Fibrosis •  Infiltrative CM, hypertensive heart disease (LBBB) •  PHTN, PE (RBBB) •  Iatrogenic (surgical, catheter, etc.) •  Neuromuscular disease
13. CRM Devices in Anesthesiology Sinus Bradycardia •  Resting sinus bradycardia and/or chronotropic incompetence
14. CRM Devices in Anesthesiology Sinus Node Dysfunction •  SND / Tachy-Brady Syndrome (AF with long conversion pause)
15. CRM Devices in Anesthesiology SA Nodal Exit Block (Type I) •  SA Exit Block (Type I)
16. CRM Devices in Anesthesiology SA Nodal Exit Block (Type II) •  SA Exit Block (Type II)
17. CRM Devices in Anesthesiology Second-Degree AV Block (Mobitz II) •  Second-Degree AV Block (Mobitz I)
18. CRM Devices in Anesthesiology Second-Degree AV Block (Mobitz II) •  Second-Degree AV Block (Mobitz II)
19. CRM Devices in Anesthesiology 2:1 AV Block •  2:1 AV Block (nodal or infranodal?)
20. CRM Devices in Anesthesiology •  2:1 AV Block (nodal or infranodal?; same patient) 2:1 AV Block
21. CRM Devices in Anesthesiology CHB
22. CRM Devices in Anesthesiology A Helpful Identity •  The product of cycle length in ms and heart rate in bpm is always 60,000 •  Examples •  at 60 bpm, the CL is 1000 ms (1 second) •  at 120 bpm, the CL is 500 ms •  a tachycardia with CL 200 ms has a rate of 300 bpm •  a tachycardia with CL 240 ms has a rate of 250 bpm CL [ms] Ÿ HR [bpm] = 60,000
23. CRM Devices in Anesthesiology Basics of Single-Chamber Pacing •  Demand Pacing (e.g. VVI pacing mode) •  A timer of a certain cycle length is established based on the lower rate limit (e.g. 60 bpm -> 1000 ms) •  The device will pace after the timer elapses, unless it is inhibited by a sensed event, which will then reset the timer.
24. CRM Devices in Anesthesiology VVI 60
25. CRM Devices in Anesthesiology •  Temporary Transvenous Pacemakers (TVPs) –  Prevent bradycardia via pacing –  Typically programmed in VVI mode –  Typically inserted via R IJ venous access –  May also be inserted via other routes (e.g. femoral vein) –  Fluoroscopic guidance is preferred (and may be essential; e.g. femoral access) –  Balloon-tipped bipolar pacing wire is placed in the RV –  Pacing is accomplished with external programmable pulse generator –  RA TVPs are also possible, but not typical –  Temporary permanent pacemakers (standard pacing lead with externalized PPM) are occasionally used Temporary Transvenous Pacemakers (TVPs)
26. CRM Devices in Anesthesiology Temporary Transvenous Pacing •  Temporary Transvenous Pacing Wire (TVP) Indications •  Bradycardia leading to hemodynamic compromise •  Complete or high-grade AV block with unstable escape (ventricular) •  Complete or high-grade AV block with very slow JER (<40) •  Sinus node dysfunction with significant sinus pauses (>5 seconds) •  Need for overdrive pacing (e.g. to prevent TdP) •  Alternative / Temporizing measures •  Transcutaneous pacing •  Atropine •  Dopamine / Dobutamine •  Treat underlying cause if identified •  If BB or CCB toxicity •  IV glucagon, IV calcium (gluconate, chloride [central]), epinephrine
27. CRM Devices in Anesthesiology Temporary Transvenous Pacing
28. CRM Devices in Anesthesiology Temporary Transvenous Pacing
29. CRM Devices in Anesthesiology Temporary Transvenous Pacemakers (TVPs)
30. CRM Devices in Anesthesiology Temporary Transvenous Pacing
31. CRM Devices in Anesthesiology Temporary Transvenous Pacing •  Temporary Transvenous Pacing Parameters –  Rate [bpm] –  Output [mA] –  Sensitivity [mV] •  Output must be great enough to ensure pacing (“capture”) of the intended chamber − it must be above the pacing “threshold” 1.0 mA 0.9 mA 0.8 mA
32. CRM Devices in Anesthesiology Temporary Transvenous Pacing •  “Sensitivity” is the amplitude above which a cardiac impulse is sensed by the device
33. CRM Devices in Anesthesiology Temporary Transvenous Pacing •  “Sensitivity” is the amplitude above which a cardiac impulse is sensed by the device •  The higher the Sensitivity is, the less sensitive to electrical impulses the device will be •  If the Sensitivity is set to the maximum value, pacing will be asynchronous (e.g. VOO) •  Conversely, if the Sensitivity is set to a very low value, small amplitude noise may be “oversensed” and in turn, erroneously inhibit pacing
34. CRM Devices in Anesthesiology Temporary Transvenous Pacing
35. CRM Devices in Anesthesiology Temporary Transvenous Pacing •  Intermittent failure of (ventricular) capture •  Causes –  The pacing output is too low –  The lead is not well positioned (intermittently good contact with tissue) –  In permanent devices, this may be due to other types of lead failure
36. CRM Devices in Anesthesiology Temporary Transvenous Pacing •  Ventricular undersensing •  Causes –  The Sensitivity is set too high (or pacing is asynchronous) –  The lead is not well positioned (intermittently good contact with tissue) –  May result in pacing on T-wave –  In permanent devices, this may be due to other types of lead failure
37. CRM Devices in Anesthesiology Temporary Transvenous Pacing •  Ventricular oversensing •  Causes –  The Sensitivity is set too low and low-amplitude noise is being inappropriately sensed, inhibiting pacing –  There is excessive noise (e.g. myopotentials, EMF, electrocautery) –  In permanent devices, this may be due to other types of lead failure
38. CRM Devices in Anesthesiology Temporary Transvenous Pacing •  In general: – Undersensing leads to overpacing (as true cardiac impulses are not detected and do not inhibit pacing) – Oversensing leads to underpacing (noise is falsely interpreted as cardiac impulses and inhibits pacing) – Failure to capture is a function of the output being too low, lead positioning being suboptimal, or other lead or generator failure
39. CRM Devices in Anesthesiology Magnet Mode / Need for Programming •  For most pacemakers, placing a device magnet over the pulse generator establishes asynchronous pacing (e.g. DOO or VOO –  This is particularly useful to prevent oversensing of noise due to electrocautery which could inhibit pacing and cause excessive bradycardia / pauses •  For most ICDs, placing a device magnet over the pulse generator disables tachytherapies (e.g. detection of tachyarrhythmias and use of ATP or shocks) –  This is particularly useful to prevent oversensing of noise due to electrocautery which could be misinterpreted by the ICD as VT/ VF and lead to inappropriate tachytherapies (ATP and shocks) •  NOTE that for patients that require pacing from their ICD (particularly if they are pacemaker dependent), the ICD should be programmed (a magnet is not sufficient) to an asynchronous pacing mode and tachytherapies disabled for the duration of the procedure, after which the device should be reprogrammed back to the original settings.
40. CRM Devices in Anesthesiology Device Programmers •  Each CRM device manufacturer has a proprietary programmer and platform
41. CRM Devices in Anesthesiology Device Programmers •  Each CRM device manufacturer has a proprietary programmer and platform •  That said, each provides basically the same functions, including: •  Device interrogation to determine: –  Electrical parameters of each lead (impedance, sensing, threshold) –  History of arrhythmias (lists and often electrogram data) –  History of tachytherapies (ATP and shocks) –  Pacing statistics and rate histograms –  Other data (activity level, thoracic impedance monitoring, etc.) •  Device programming of all pacing and tachytherapy parameters •  Basic EP study / stimulation facilities (e.g. manual ATP) •  Emergency asynchronous pacing / shocks [ICDs]
42. CRM Devices in Anesthesiology Basics of Cardiac Pacing •  Cardiac pacing devices generally have one, two, or three leads, one of which may also have the capability to enable cardioversion/defibrillation
43. CRM Devices in Anesthesiology Basics of Cardiac Pacing •  Basics of Cardiac Pacing Modes •  Abstracted and modified from Medtronic CorePace
44. CRM Devices in Anesthesiology Pacemaker Mode •  Defines the chambers that are paced/sensed •  Defines how the pacemaker will respond to intrinsic events •  Defines if rate modulation is available (i.e., DDDR) Pacing Modes
45. CRM Devices in Anesthesiology NBG Code I II III IV V Chamber(s) Paced Chamber(s) Sensed Response to Sensing Rate Modulation Multisite Pacing O = None A = Atrium V = Ventricle D = Dual (A + V) S = Single (A or V) O = None A = Atrium V = Ventricle D = Dual (A + V) S = Single (A or V) O = None T = Triggered I = Inhibited D = Dual (T + I) O = None R = Rate modulation O = None A = Atrium V = Ventricle D = Dual (A + V) Pacing Modes
46. CRM Devices in Anesthesiology NBG Code – Common Pacing Modes I II III IV V Chamber(s) Paced Chamber(s) Sensed Response to Sensing Rate Modulation Multisite Pacing O = None A = Atrium V = Ventricle D = Dual (A + V) S = Single (A or V) O = None A = Atrium V = Ventricle D = Dual (A + V) S = Single (A or V) O = None T = Triggered I = Inhibited D = Dual (T + I) O = None R = Rate modulation O = None A = Atrium V = Ventricle D = Dual (A + V) •  Common Examples: –  VVI –  AAI –  DDD –  VVIR –  DDDR –  VOO –  DOO –  AOO –  OVO –  ODO Single-chamber demand Dual-chamber AV synchronous Rate-Responsive Asynchronous modes Pacing Disabled Common Pacing Modes
47. CRM Devices in Anesthesiology VVI Mode •  Chamber paced: Ventricle •  Chamber sensed: Ventricle •  Response to sensing: Inhibited –  A ventricular sensed event: •  Inhibits the next scheduled ventricular paced event •  Resets the timer VVI
48. CRM Devices in Anesthesiology VVI Example (VVI 60) •  Chamber paced: Ventricle •  Chamber sensed: Ventricle •  Response to sensing: Inhibition –  VVI 60 = Lower Rate timer of 1000 ms •  Pacing every 1 second if not inhibited V P V P V P Lower Rate Timer 1000 ms Lower Rate Timer 1000 ms Lower Rate Timer …. VVI
49. CRM Devices in Anesthesiology VVI Example 2 (VVI 60) •  Chamber paced: Ventricle –  VVI 60 = Lower Rate timer of 1000 ms •  Pacing every 1 second if not inhibited •  Chamber sensed: Ventricle •  Response to sensing: Inhibition A ventricular sensed event interrupts the pacing interval, resets the lower rate timer, and inhibits the next scheduled paced event (x) V P V S V P V P Lower rate timer 1000 ms x Lower rate timer 1000 ms VVI
50. CRM Devices in Anesthesiology VOO Mode (VOO 60) Chamber paced: Ventricle Chamber sensed: None Response to sensing: None The intrinsic ventricular event cannot be sensed, and thus, does not interrupt the pacing interval. VOO results in asynchronous, fixed-rate pacing in the ventricle. Placing a magnet over the pacemaker usually results in this behavior at known rates, for example, 85 ppm. 1000 ms 1000 ms 1000 ms V P V P V P V P VOO
51. CRM Devices in Anesthesiology DDD Mode •  Chamber paced: Atrium & ventricle •  Chamber sensed: Atrium & ventricle •  Response to sensing: Triggered & inhibited –  An atrial sensed event: •  Inhibits the next scheduled atrial paced event •  Re-starts the lower rate timer •  Triggers an AV interval (called a Sensed AV Interval or SAV) –  An atrial paced event: •  Re-starts the lower rate timer •  Triggers an AV delay timer (the Paced AV or PAV) –  A ventricular sensed event: •  Inhibits the next scheduled ventricular paced event DDD
52. CRM Devices in Anesthesiology DDD Mode •  Given that both the Atrium and Ventricle can be either sensed or paced, there are four types of pacing behavior in DDD mode: •  A-paced, V-paced •  A-paced, V-sensed •  A-sensed, V-paced •  A-sensed, V-sensed •  The AV delays (SAV and PAV) are a bit like the PR interval and are helpful in maintaining physiologic AV synchrony DDD
53. CRM Devices in Anesthesiology DDD Examples (A-paced, V-paced) •  Atrial and ventricular pacing –  Atrial paced event re-starts the lower rate timer and triggers an AV delay timer (PAV) •  The PAV expires without being inhibited by a ventricular sensed event, resulting in a ventricular paced event A P A P V P V P DDD
54. CRM Devices in Anesthesiology DDD Examples (A-paced, V-sensed) •  Atrial pacing and ventricular sensing –  An atrial paced event restarts the lower rate timer and triggers an AV delay timer (PAV) •  Before the PAV can expire, it is inhibited by an intrinsic ventricular sensed event (R-wave) A P A P V S V S DDD
55. CRM Devices in Anesthesiology DDD Examples (A-sensed, V-paced) •  Atrial sensing, ventricular pacing –  The intrinsic atrial sensed event (P-wave) inhibits the lower rate timer and triggers an AV delay timer (SAV) •  The SAV expires without being inhibited by an intrinsic sensed ventricular event, resulting in a ventricular paced event A S A S V P V P DDD
56. CRM Devices in Anesthesiology DDD Examples (A-sensed, V-sensed) •  Atrial and ventricular sensing –  The intrinsic atrial sensed event (P-wave) inhibits the lower rate timer and triggers an AV delay timer (SAV) •  Before the SAV can expire, it is inhibited by an intrinsic ventricular event (R-wave) A S A S V S V S DDD
57. CRM Devices in Anesthesiology •  Designed to prevent bradycardia and to maintain AV synchrony DDD Mode DDD Ap-Vp As-Vp Ap-Vs As-Vs
58. CRM Devices in Anesthesiology DDD Mode •  Lower Rate Limit –  Minimum pacing rate maintained by the device under normal circumstances •  Maximum Tracking Rate –  Fastest rate that the ventricles will be paced 1:1 in response to atrial activity •  DDD 60-120 (LRL-MTR) DDD
59. CRM Devices in Anesthesiology DDD Mode •  Upper rate behavior –  Occurs when the atrial rate begins to exceed the MTR –  “Pacemaker Wenckebach” DDD
60. CRM Devices in Anesthesiology DDD Mode •  Atrial Mode-Switch Rate –  Usually set to a high value (~170 bpm) –  Useful for detecting and handling atrial arrhythmias (AT/AF/AFL) –  Switches mode to DDI/DDIR, preventing rapid ventricular pacing •  In DDI mode: –  The atrial pacing is akin to AAI pacing –  The ventricular pacing is akin to VVI pacing, unless there there is an atrial-paced event, in which case ventricular pacing can follow by a paced AV delay DDD
61. CRM Devices in Anesthesiology DDDR Mode (Rate Responsive Mode) •  Lower Rate Limit –  Minimum pacing rate maintained by the device under normal circumstances •  Maximum Tracking Rate –  Fastest rate that the ventricles will be paced 1:1 in response to atrial activity •  Maximum Sensor Rate –  Fastest pacing rate (LRL) established in response to activity (e.g. measured by an accelerometer) •  DDDR 60-130 DDD
62. CRM Devices in Anesthesiology DDDR Mode •  DDDR 60-120 (LRL 60, MSR 120, MTR 100) DDD
63. CRM Devices in Anesthesiology •  Permanent Pacing Guidelines •  Many guidelines for various conditions •  Sinus Node Dysfunction •  Symptomatic sinus bradycardia •  Chronotropic incompetence •  Tachy-brady syndrome (SND / paroxysmal atrial tachyarrhythmias) •  Acquired AV Block •  Complete heart block / high-grade AV block •  Mobitz II AV block •  (Infrequently) Mobitz I AV block •  Carotid sinus syndrome / Neurocardiogenic syncope with a cardioinhibitory response •  Virtually all indications require symptomatic bradycardia ACCF/AHA/HRS PPM Guidelines
64. CRM Devices in Anesthesiology exercise in bradycardia patients with pacemaker sensors seems logical, a clinical benefit on a population scale has not been demonstrated in large randomized controlled trials of pacemaker therapy (52). These rapidly evolving areas of clinical investigation should inform the choice of pacing system in SND (see Section 2.6, “Selection of Pacemaker Device”). Recommendations for Permanent Pacing in Sinus Node Dysfunction CLASS I 1. Permanent pacemaker implantation is indicated for SND with documented symptomatic bradycardia, including frequent si- nus pauses that produce symptoms. (Level of Evidence: C) (53–55) 2. Permanent pacemaker implantation is indicated for symp- tomatic chronotropic incompetence. (Level of Evidence: C) (53–57) 3. Permanent pacemaker implantation is indicated for symptom- atic sinus bradycardia that results from required drug therapy for medical conditions. (Level of Evidence: C) CLASS IIa 1. Permanent pacemaker implantation is reasonable for SND with heart rate less than 40 bpm when a clear association between significant symptoms consistent with bradycardia and the actual presence of bradycardia has not been documented. (Level of Evidence: C) (53–55,58–60) 2. Permanent pacemaker implantation is reasonable for syncope of unexplained origin when clinically significant abnormalities of sinus node function are discovered or provoked in electro- physiological studies. (Level of Evidence: C) (61,62) QRS. Type I second-degree AV block is characterized by progressive prolongation of the PR interval before a noncon- ducted beat and a shorter PR interval after the blocked beat. Type II second-degree AV block is characterized by fixed PR intervals before and after blocked beats and is usually associated with a wide QRS complex. When AV conduction occurs in a 2:1 pattern, block cannot be classified unequivo- cally as type I or type II, although the width of the QRS can be suggestive, as just described. Advanced second-degree AV block refers to the blocking of 2 or more consecutive P waves with some conducted beats, which indicates some preserva- tion of AV conduction. In the setting of AF, a prolonged pause (e.g., greater than 5 seconds) should be considered to be due to advanced second-degree AV block. Third-degree AV block (complete heart block) is defined as absence of AV conduction. Patients with abnormalities of AV conduction may be asymptomatic or may experience serious symptoms related to bradycardia, ventricular arrhythmias, or both. Decisions re- garding the need for a pacemaker are importantly influenced by the presence or absence of symptoms directly attributable to bradycardia. Furthermore, many of the indications for pacing have evolved over the past 40 years on the basis of experience without the benefit of comparative randomized clinical trials, in part because no acceptable alternative options exist to treat most bradycardias. Nonrandomized studies strongly suggest that permanent pacing does improve survival in patients with third-degree AV block, especially if syncope has occurred (63–68). Although there is little evidence to suggest that pacemakers improve survival in patients with isolated first-degree AV block (69), it is now recognized that marked (PR more than Downloaded From: http://content.onlinejacc.org/ by William Kostis on 12/31/2012 trained athletes. Such individuals may have heart rates of 40 to 50 bpm while at rest and awake and may have a sleeping rate as slow as 30 bpm, with sinus pauses or progressive sinus slowing accompanied by AV conduction delay (PR prolon- gation), sometimes culminating in type I second-degree AV block (34,35). The basis of the distinction between physio- logical and pathological bradycardia, which may overlap in ECG presentation, therefore pivots on correlation of episodic bradycardia with symptoms compatible with cerebral hypo- perfusion. Intermittent ECG monitoring with Holter monitors and event recorders may be helpful (36,37), although the duration of monitoring required to capture such evidence may be very long (38). The use of insertable loop recorders offers the advantages of compliance and convenience during very long-term monitoring efforts (39). The optimal pacing system for prevention of symptomatic bradycardia in SND is unknown. Recent evidence suggests that ventricular desynchronization due to right ventricular apical (RVA) pacing may have adverse effects on left ventricular (LV) and left atrial structure and function (40–47). These adverse effects likely explain the association of RVA pacing, independent of AV synchrony, with increased risks of AF and heart failure in randomized clinical trials of pace- maker therapy (45,48,49) and, additionally, ventricular ar- rhythmias and death during ICD therapy (50,51). Likewise, although simulation of the normal sinus node response to exercise in bradycardia patients with pacemaker sensors seems logical, a clinical benefit on a population scale has not been demonstrated in large randomized controlled trials of pacemaker therapy (52). These rapidly evolving areas of clinical investigation should inform the choice of pacing system in SND (see Section 2.6, “Selection of Pacemaker Device”). Recommendations for Permanent Pacing in Sinus Node Dysfunction CLASS I CLASS IIb 1. Permanent pacemaker implantation may be considered in minimally symptomatic patients with chronic heart rate less than 40 bpm while awake. (Level of Evidence: C) (53,55,56, 58–60) CLASS III 1. Permanent pacemaker implantation is not indicated for SND in asymptomatic patients. (Level of Evidence: C) 2. Permanent pacemaker implantation is not indicated for SND in patients for whom the symptoms suggestive of bradycardia have been clearly documented to occur in the absence of bradycardia. (Level of Evidence: C) 3. Permanent pacemaker implantation is not indicated for SND with symptomatic bradycardia due to nonessential drug ther- apy. (Level of Evidence: C) 2.1.2. Acquired Atrioventricular Block in Adults AV block is classified as first-, second-, or third-degree (complete) block; anatomically, it is defined as supra-, intra-, or infra-His. First-degree AV block is defined as abnormal prolongation of the PR interval (greater than 0.20 seconds). Second-degree AV block is subclassified as type I and type II. Type I second-degree AV block is characterized by progres- sive prolongation of the interval between the onset of atrial (P wave) and ventricular (R wave) conduction (PR) before a nonconducted beat and is usually seen in conjunction with QRS. Type I second-degree AV block is characterized by progressive prolongation of the PR interval before a noncon- ducted beat and a shorter PR interval after the blocked beat. Type II second-degree AV block is characterized by fixed PR intervals before and after blocked beats and is usually associated with a wide QRS complex. When AV conduction occurs in a 2:1 pattern, block cannot be classified unequivo- cally as type I or type II, although the width of the QRS can be suggestive, as just described. Advanced second-degree AV block refers to the blocking of 2 or more consecutive P waves with some conducted beats, which indicates some preserva- tion of AV conduction. In the setting of AF, a prolonged 9 JACC Vol. 61, No. 13, 2013 Epstein et al. January 22, 2013:xxx–xxx Device Guideline: 2012 Update Incorporated Sinus node dysfunction with Symptomatic bradycardia +/- chronotropic incompetence ACCF/AHA/HRS PPM Guidelines
65. CRM Devices in Anesthesiology ression 73–75), mptom- ation is ree AV ), espe- oms are sion to 75,79). e QRS se and ence of termine luation, ranodal -degree ntra- or ould be d their fatigue to ac- at may -degree sidered because was not escape site of the His . If not circum- system may warrant pacemaker implantation because of the pos- sibility of disease progression even if the AV block reverses transiently (e.g., sarcoidosis, amyloidosis, and neuromuscular diseases). Finally, permanent pacing for AV block after valve surgery follows a variable natural history; therefore, the decision for permanent pacing is at the physician’s discretion (84). Recommendations for Acquired Atrioventricular Block in Adults CLASS I 1. Permanent pacemaker implantation is indicated for third- degree and advanced second-degree AV block at any anatomic level associated with bradycardia with symptoms (including heart failure) or ventricular arrhythmias presumed to be due to AV block. (Level of Evidence: C) (59,63,76,85) 2. Permanent pacemaker implantation is indicated for third- degree and advanced second-degree AV block at any anatomic level associated with arrhythmias and other medical conditions that require drug therapy that results in symptomatic bradycar- dia. (Level of Evidence: C) (59,63,76,85) 3. Permanent pacemaker implantation is indicated for third- degree and advanced second-degree AV block at any anatomic level in awake, symptom-free patients in sinus rhythm, with documented periods of asystole greater than or equal to 3.0 seconds (86) or any escape rate less than 40 bpm, or with an escape rhythm that is below the AV node. (Level of Evidence: C) (53,58) 4. Permanent pacemaker implantation is indicated for third- degree and advanced second-degree AV block at any anatomic level in awake, symptom-free patients with AF and bradycardia with 1 or more pauses of at least 5 seconds or longer. (Level of Evidence: C) n 12/31/2012 5. Permanent pacemaker implantation is indicated for third- degree and advanced second-degree AV block at any anatomic level after catheter ablation of the AV junction. (Level of Evidence: C) (87,88) 6. Permanent pacemaker implantation is indicated for third- degree and advanced second-degree AV block at any anatomic level associated with postoperative AV block that is not expected to resolve after cardiac surgery. (Level of Evidence: C) (84,85,89,90) 7. Permanent pacemaker implantation is indicated for third- degree and advanced second-degree AV block at any anatomic level associated with neuromuscular diseases with AV block, such as myotonic muscular dystrophy, Kearns-Sayre syndrome, Erb dystrophy (limb-girdle muscular dystrophy), and peroneal muscular atrophy, with or without symptoms. (Level of Evi- dence: B) (91–97) 8. Permanent pacemaker implantation is indicated for second- degree AV block with associated symptomatic bradycardia regardless of type or site of block. (Level of Evidence: B) (74) 9. Permanent pacemaker implantation is indicated for asymptom- atic persistent third-degree AV block at any anatomic site with average awake ventricular rates of 40 bpm or faster if cardio- megaly or LV dysfunction is present or if the site of block is below the AV node. (Level of Evidence: B) (76,78) 10. Permanent pacemaker implantation is indicated for second- or third-degree AV block during exercise in the absence of myocardial ischemia. (Level of Evidence: C) (81,82) CLASS IIa 1. Permanent pacemaker implantation is reasonable for persis- tent third-degree AV block with an escape rate greater than 40 bpm in asymptomatic adult patients without cardiomegaly. (Level of Evidence: C) (59,63,64,76,82,85) 2. Permanent pacemaker implantation is reasonable for asymp- tomatic second-degree AV block at intra- or infra-His levels found at electrophysiological study. (Level of Evidence: B) (74,76,78) 3. Permanent pacemaker implantation is reasonable for first- or second-degree AV block with symptoms similar to those of CLASS III 1. Permanent pa tomatic first-d Section 2.1.3 2. Permanent pa tomatic type node) level o Hisian. (Level 3. Permanent p block that is e (e.g., drug to vagal tone or absence of sy 2.1.3. Chroni Bifascicular bl conduction belo Alternating bun bundle-branch b evidence for b successive ECG and left bundle bundle-branch block on 1 ECG on another EC association wit vanced AV blo tial incidence degree AV blo block, there is bifascicular blo Furthermore, n including bifas of death due bundle-branch Syncope is c Although synco an increased in JACC Vol. 61, No. 13, 2013 January 22, 2013:xxx–xxx D Symptomatic AV block ACCF/AHA/HRS PPM Guidelines
66. CRM Devices in Anesthesiology atic persistent third-degree AV block at any anatomic site with average awake ventricular rates of 40 bpm or faster if cardio- megaly or LV dysfunction is present or if the site of block is below the AV node. (Level of Evidence: B) (76,78) 10. Permanent pacemaker implantation is indicated for second- or third-degree AV block during exercise in the absence of myocardial ischemia. (Level of Evidence: C) (81,82) CLASS IIa 1. Permanent pacemaker implantation is reasonable for persis- tent third-degree AV block with an escape rate greater than 40 bpm in asymptomatic adult patients without cardiomegaly. (Level of Evidence: C) (59,63,64,76,82,85) 2. Permanent pacemaker implantation is reasonable for asymp- tomatic second-degree AV block at intra- or infra-His levels found at electrophysiological study. (Level of Evidence: B) (74,76,78) 3. Permanent pacemaker implantation is reasonable for first- or second-degree AV block with symptoms similar to those of pacemaker syndrome or hemodynamic compromise. (Level of Evidence: B) (70,71) 4. Permanent pacemaker implantation is reasonable for asymp- tomatic type II second-degree AV block with a narrow QRS. When type II second-degree AV block occurs with a wide QRS, including isolated right bundle-branch block, pacing becomes a Class I recommendation. (See Section 2.1.3, “Chronic Bifas- cicular Block.”) (Level of Evidence: B) (70,76,80,85) CLASS IIb 1. Permanent pacemaker implantation may be considered for neuromuscular diseases such as myotonic muscular dystrophy, Erb dystrophy (limb-girdle muscular dystrophy), and peroneal muscular atrophy with any degree of AV block (including first-degree AV block), with or without symptoms, because there may be unpredictable progression of AV conduction disease. (Level of Evidence: B) (91–97) 2. Permanent pacemaker implantation may be considered for AV block in the setting of drug use and/or drug toxicity when the block is expected to recur even after the drug is withdrawn. (Level of Evidence: B) (98,99) successive ECGs. Examples are right bundle-branch block and left bundle-branch block on successive ECGs or right bundle-branch block with associated left anterior fascicular block on 1 ECG and associated left posterior fascicular block on another ECG. Patients with first-degree AV block in association with bifascicular block and symptomatic, ad- vanced AV block have a high mortality rate and a substan- tial incidence of sudden death (64,101). Although third- degree AV block is most often preceded by bifascicular block, there is evidence that the rate of progression of bifascicular block to third-degree AV block is slow (102). Furthermore, no single clinical or laboratory variable, including bifascicular block, identifies patients at high risk of death due to a future bradyarrhythmia caused by bundle-branch block (103). Syncope is common in patients with bifascicular block. Although syncope may be recurrent, it is not associated with an increased incidence of sudden death (73,102–112). Even though pacing relieves the neurological symptoms, it does not reduce the occurrence of sudden death (108). An electrophys- iological study may be helpful to evaluate and direct the treatment of inducible ventricular arrhythmias (113,114) that are common in patients with bifascicular block. There is convincing evidence that in the presence of permanent or transient third-degree AV block, syncope is associated with an increased incidence of sudden death regardless of the results of the electrophysiological study (64,114,115). Fi- nally, if the cause of syncope in the presence of bifascicular block cannot be determined with certainty, or if treatments used (such as drugs) may exacerbate AV block, prophylactic perma- nent pacing is indicated, especially if syncope may have been due to transient third-degree AV block (102–112,116). Of the many laboratory variables, the PR and HV intervals have been identified as possible predictors of third-degree AV block and sudden death. Although PR-interval prolongation is common in patients with bifascicular block, the delay is often at the level of the AV node. There is no correlation between the PR and HV intervals or between the length of the PR interval, progression to third-degree AV block, and sudden Downloaded From: http://content.onlinejacc.org/ by William Kostis on 12/31/2012 5. Permanent pacemaker implantation is indicated for third- degree and advanced second-degree AV block at any anatomic level after catheter ablation of the AV junction. (Level of Evidence: C) (87,88) 6. Permanent pacemaker implantation is indicated for third- degree and advanced second-degree AV block at any anatomic level associated with postoperative AV block that is not expected to resolve after cardiac surgery. (Level of Evidence: C) (84,85,89,90) 7. Permanent pacemaker implantation is indicated for third- degree and advanced second-degree AV block at any anatomic level associated with neuromuscular diseases with AV block, such as myotonic muscular dystrophy, Kearns-Sayre syndrome, Erb dystrophy (limb-girdle muscular dystrophy), and peroneal muscular atrophy, with or without symptoms. (Level of Evi- dence: B) (91–97) 8. Permanent pacemaker implantation is indicated for second- degree AV block with associated symptomatic bradycardia regardless of type or site of block. (Level of Evidence: B) (74) 9. Permanent pacemaker implantation is indicated for asymptom- atic persistent third-degree AV block at any anatomic site with average awake ventricular rates of 40 bpm or faster if cardio- megaly or LV dysfunction is present or if the site of block is below the AV node. (Level of Evidence: B) (76,78) 10. Permanent pacemaker implantation is indicated for second- or third-degree AV block during exercise in the absence of myocardial ischemia. (Level of Evidence: C) (81,82) CLASS IIa 1. Permanent pacemaker implantation is reasonable for persis- tent third-degree AV block with an escape rate greater than 40 bpm in asymptomatic adult patients without cardiomegaly. (Level of Evidence: C) (59,63,64,76,82,85) 2. Permanent pacemaker implantation is reasonable for asymp- tomatic second-degree AV block at intra- or infra-His levels found at electrophysiological study. (Level of Evidence: B) (74,76,78) 3. Permanent pacemaker implantation is reasonable for first- or second-degree AV block with symptoms similar to those of CLASS III 1. Permanent pacemaker implantation is not indicated for asymp- tomatic first-degree AV block. (Level of Evidence: B) (69) (See Section 2.1.3, “Chronic Bifascicular Block.”) 2. Permanent pacemaker implantation is not indicated for asymp- tomatic type I second-degree AV block at the supra-His (AV node) level or that which is not known to be intra- or infra- Hisian. (Level of Evidence: C) (74) 3. Permanent pacemaker implantation is not indicated for AV block that is expected to resolve and is unlikely to recur (100) (e.g., drug toxicity, Lyme disease, or transient increases in vagal tone or during hypoxia in sleep apnea syndrome in the absence of symptoms). (Level of Evidence: B) (99,100) 2.1.3. Chronic Bifascicular Block Bifascicular block refers to ECG evidence of impaired conduction below the AV node in the right and left bundles. Alternating bundle-branch block (also known as bilateral bundle-branch block) refers to situations in which clear ECG evidence for block in all 3 fascicles is manifested on successive ECGs. Examples are right bundle-branch block and left bundle-branch block on successive ECGs or right bundle-branch block with associated left anterior fascicular block on 1 ECG and associated left posterior fascicular block on another ECG. Patients with first-degree AV block in association with bifascicular block and symptomatic, ad- vanced AV block have a high mortality rate and a substan- tial incidence of sudden death (64,101). Although third- degree AV block is most often preceded by bifascicular block, there is evidence that the rate of progression of bifascicular block to third-degree AV block is slow (102). Furthermore, no single clinical or laboratory variable, including bifascicular block, identifies patients at high risk of death due to a future bradyarrhythmia caused by bundle-branch block (103). Syncope is common in patients with bifascicular block. Although syncope may be recurrent, it is not associated with an increased incidence of sudden death (73,102–112). Even 11 JACC Vol. 61, No. 13, 2013 Epstein et al. January 22, 2013:xxx–xxx Device Guideline: 2012 Update Incorporated More symptomatic AV block and high-risk for progressive block ACCF/AHA/HRS PPM Guidelines
67. CRM Devices in Anesthesiology death (107,109,116). Although most patients with chronic or intermittent third-degree AV block demonstrate prolongation of the HV interval during anterograde conduction, some investigators (110,111) have suggested that asymptomatic patients with bifascicular block and a prolonged HV interval should be considered for permanent pacing, especially if the HV interval is greater than or equal to 100 milliseconds (109). Although the prevalence of HV-interval prolongation is high, the incidence of progression to third-degree AV block is low. Because HV prolongation accompanies advanced cardiac disease and is associated with increased mortality, death is often not sudden or due to AV block but rather is due to the underlying heart disease itself and nonarrhythmic cardiac causes (102,103,108,109,111,114–117). Atrial pacing at electrophysiological study in asymptom- atic patients as a means of identifying patients at increased risk of future high- or third-degree AV block is controver- sial. The probability of inducing block distal to the AV node (i.e., intra- or infra-His) with rapid atrial pacing is low (102,110,111,118–121). Failure to induce distal block cannot be taken as evidence that the patient will not develop third-degree AV block in the future. However, if atrial pacing induces nonphysiological infra-His block, some consider this an indication for pacing (118). Nevertheless, infra-His block that occurs during either rapid atrial pacing or programmed stimulation at short coupling intervals may be physiological and not pathological, simply reflecting disparity between refractoriness of the AV node and His-Purkinje systems (122). Recommendations for Permanent Pacing in Chronic Bifascicular Block CLASS I 1. Permanent pacemaker implantation is indicated for advanced second-degree AV block or intermittent third-degree AV block. (Level of Evidence: B) (63–68,101) 2. Permanent pacemaker implantation is indicated for type II second-degree AV block. (Level of Evidence: B) (73,75,79,123) 3. Permanent pacemaker implantation is indicated for alternating bundle-branch block. (Level of Evidence: C) (124) CLASS IIa peroneal muscular atrophy with bifascicular block or any fas- cicular block, with or without symptoms. (Level of Evidence: C) (91–97) CLASS III 1. Permanent pacemaker implantation is not indicated for fascic- ular block without AV block or symptoms. (Level of Evidence: B) (103,107,109,116) 2. Permanent pacemaker implantation is not indicated for fascic- ular block with first-degree AV block without symptoms. (Level of Evidence: B) (103,107,109,116) 2.1.4. Pacing for Atrioventricular Block Associated With Acute Myocardial Infarction Indications for permanent pacing after myocardial infarction (MI) in patients experiencing AV block are related in large measure to the presence of intraventricular conduction de- fects. The criteria for patients with MI and AV block do not necessarily depend on the presence of symptoms. Further- more, the requirement for temporary pacing in AMI does not by itself constitute an indication for permanent pacing (see “ACC/AHA Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction” (6)). The long-term prognosis for survivors of AMI who have had AV block is related primarily to the extent of myocardial injury and the character of intraventricular conduction disturbances rather than the AV block itself (66,126–130). Patients with AMI who have intraventricular conduction defects, with the excep- tion of isolated left anterior fascicular block, have an unfa- vorable short- and long-term prognosis and an increased risk of sudden death (66,79,126,128,130). This unfavorable prog- nosis is not necessarily due to development of high-grade AV block, although the incidence of such block is higher in postinfarction patients with abnormal intraventricular con- duction (126,131,132). When AV or intraventricular conduction block compli- cates AMI, the type of conduction disturbance, location of infarction, and relation of electrical disturbance to infarction must be considered if permanent pacing is contemplated. Even with data available, the decision is not always straight- forward, because the reported incidence and significance of various conduction disturbances vary widely (133). Despite 12 Epstein et al. JACC Vol. 61, No. 13, 2013 Device Guideline: 2012 Update Incorporated January 22, 2013:xxx–xxx induces nonphysiological infra-His block, some consider this an indication for pacing (118). Nevertheless, infra-His block that occurs during either rapid atrial pacing or programmed stimulation at short coupling intervals may be physiological and not pathological, simply reflecting disparity between refractoriness of the AV node and His-Purkinje systems (122). Recommendations for Permanent Pacing in Chronic Bifascicular Block CLASS I 1. Permanent pacemaker implantation is indicated for advanced second-degree AV block or intermittent third-degree AV block. (Level of Evidence: B) (63–68,101) 2. Permanent pacemaker implantation is indicated for type II second-degree AV block. (Level of Evidence: B) (73,75,79,123) 3. Permanent pacemaker implantation is indicated for alternating bundle-branch block. (Level of Evidence: C) (124) CLASS IIa 1. Permanent pacemaker implantation is reasonable for syncope not demonstrated to be due to AV block when other likely causes have been excluded, specifically ventricular tachycar- dia (VT). (Level of Evidence: B) (102–111,113–119,123,125) 2. Permanent pacemaker implantation is reasonable for an inci- dental finding at electrophysiological study of a markedly prolonged HV interval (greater than or equal to 100 millisec- onds) in asymptomatic patients. (Level of Evidence: B) (109) 3. Permanent pacemaker implantation is reasonable for an incidental finding at electrophysiological study of pacing- induced infra-His block that is not physiological. (Level of Evidence: B) (118) CLASS IIb 1. Permanent pacemaker implantation may be considered in the setting of neuromuscular diseases such as myotonic muscular dystrophy, Erb dystrophy (limb-girdle muscular dystrophy), and ST-Elevation Myocardial Infarction” (6)). The long-term prognosis for survivors of AMI who have had AV block is related primarily to the extent of myocardial injury and the character of intraventricular conduction disturbances rather than the AV block itself (66,126–130). Patients with AMI who have intraventricular conduction defects, with the excep- tion of isolated left anterior fascicular block, have an unfa- vorable short- and long-term prognosis and an increased risk of sudden death (66,79,126,128,130). This unfavorable prog- nosis is not necessarily due to development of high-grade AV block, although the incidence of such block is higher in postinfarction patients with abnormal intraventricular con- duction (126,131,132). When AV or intraventricular conduction block compli- cates AMI, the type of conduction disturbance, location of infarction, and relation of electrical disturbance to infarction must be considered if permanent pacing is contemplated. Even with data available, the decision is not always straight- forward, because the reported incidence and significance of various conduction disturbances vary widely (133). Despite the use of thrombolytic therapy and primary angioplasty, which have decreased the incidence of AV block in AMI, mortality remains high if AV block occurs (130,134–137). Although more severe disturbances in conduction have generally been associated with greater arrhythmic and non- arrhythmic mortality, (126–129,131,133) the impact of pre- existing bundle-branch block on mortality after AMI is controversial (112,133). A particularly ominous prognosis is associated with left bundle-branch block combined with advanced second- or third-degree AV block and with right bundle-branch block combined with left anterior or left posterior fascicular block (105,112,127,129). Regardless of whether the infarction is anterior or inferior, the development of an intraventricular conduction delay reflects extensive myocardial damage rather than an electrical problem in isolation (129). Although AV block that occurs during inferior MI can be associated with a favorable long-term Downloaded From: http://content.onlinejacc.org/ by William Kostis on 12/31/2012 ronic or ngation n, some tomatic interval y if the s (109). is high, k is low. peroneal muscular atrophy with bifascicular block or any fas- cicular block, with or without symptoms. (Level of Evidence: C) (91–97) CLASS III 1. Permanent pacemaker implantation is not indicated for fascic- ular block without AV block or symptoms. (Level of Evidence: B) (103,107,109,116) 2. Permanent pacemaker implantation is not indicated for fascic- JACC Vol. 61, No. 13, 2013 January 22, 2013:xxx–xxx Even more symptomatic AV block and high-risk for progressive block ACCF/AHA/HRS PPM Guidelines
68. CRM Devices in Anesthesiology MI with a left ventricular ejection fraction (LVEF) less than or equal to 35% and an indication for permanent pacing, consideration may be given to use of an ICD, a CRT device that provides pacing but not defibrillation capability (CRT-P), or a CRT device that incorporates both pacing and defibril- lation capabilities (CRT-D) when improvement in LVEF is not anticipated. Recommendations for Permanent Pacing After the Acute Phase of Myocardial Infarction* CLASS I 1. Permanent ventricular pacing is indicated for persistent second-degree AV block in the His-Purkinje system with alter- nating bundle-branch block or third-degree AV block within or below the His-Purkinje system after ST-segment elevation MI. (Level of Evidence: B) (79,126–129,131) 2. Permanent ventricular pacing is indicated for transient ad- vanced second- or third-degree infranodal AV block and asso- ciated bundle-branch block. If the site of block is uncertain, an electrophysiological study may be necessary. (Level of Evi- dence: B) (126,127) 3. Permanent ventricular pacing is indicated for persistent and symptomatic second- or third-degree AV block. (Level of Evi- dence: C) CLASS IIb 1. Permanent ventricular pacing may be considered for persistent second- or third-degree AV block at the AV node level, even in the absence of symptoms. (Level of Evidence: B) (58) CLASS III 1. Permanent ventricular pacing is not indicated for transient AV block in the absence of intraventricular conduction defects. (Level of Evidence: B) (126) 2. Permanent ventricular pacing is not indicated for transient AV block in the presence of isolated left anterior fascicular block. (Level of Evidence: B) (128) 3. Permanent ventricular pacing is not indicated for new bundle- branch block or fascicular block in the absence of AV block. (Level of Evidence: B) (66,126) 4. Permanent ventricular pacing is not indicated for persistent asymptomatic first-degree AV block in the presence of bundle- branch or fascicular block. (Level of Evidence: B) (126) 2.1.5. Hypersensitive Carotid Sinus Syndrome and Neurocardiogenic Syncope The hypersensitive carotid sinus syndrome is defined as Before concluding that permanent pacing is clinically indicated, the physician should determine the relative contri- bution of the 2 components of carotid sinus stimulation to the individual patient’s symptom complex. Hyperactive response to carotid sinus stimulation is defined as asystole due to either sinus arrest or AV block of more than 3 seconds, a substantial symptomatic decrease in systolic blood pressure, or both (140). Pauses up to 3 seconds during carotid sinus massage are considered to be within normal limits. Such heart rate and hemodynamic responses may occur in normal subjects and patients with coronary artery disease. The cause-and-effect relation between the hypersensitive carotid sinus and the patient’s symptoms must be drawn with great caution (141). Spontaneous syncope reproduced by carotid sinus stimulation should alert the physician to the presence of this syndrome. Minimal pressure on the carotid sinus in elderly patients may result in marked changes in heart rate and blood pressure yet may not be of clinical significance. Permanent pacing for patients with an excessive cardioinhibitory response to ca- rotid stimulation is effective in relieving symptoms (142,143). Because 10% to 20% of patients with this syndrome may have an important vasodepressive component of their reflex response, it is desirable that this component be defined before one concludes that all symptoms are related to asystole alone. Among patients whose reflex response includes both car- dioinhibitory and vasodepressive components, attention to the latter is essential for effective therapy in patients undergoing pacing. Carotid sinus hypersensitivity should be considered in elderly patients who have had otherwise unexplained falls. In 1 study, 175 elderly patients who had fallen without loss of consciousness and who had pauses of more than 3 seconds during carotid sinus massage (thus fulfilling the diagnosis of carotid sinus hypersensitivity) were randomized to pacing or nonpacing therapy. The paced group had a significantly lower likelihood of subsequent falling episodes during follow-up (144). Neurocardiogenic syncope and neurocardiogenic syn- dromes refer to a variety of clinical scenarios in which triggering of a neural reflex results in a usually self-limited episode of systemic hypotension characterized by both bra- dycardia and peripheral vasodilation (145,146). Neurocardio- genic syncope accounts for an estimated 10% to 40% of syncope episodes. Vasovagal syncope is a term used to denote one of the most common clinical scenarios within the category of neurocardiogenic syncopal syndromes. Patients symptoms. Although spontaneous or provoked prolonged pauses are a concern in this population, the prognosis without pacing is excellent (151). The evaluation of patients with syncope of undetermined origin should take into account clinical status and should not overlook other, more serious causes of syncope, such as ventricular tachyarrhythmias. Recommendations for Permanent Pacing in Hypersensitive Carotid Sinus Syndrome and Neurocardiogenic Syncope CLASS I 1. Permanent pacing is indicated for recurrent syncope caused by spontaneously occurring carotid sinus stimulation and carotid 12 months (159 implantation is dia and syncop associated with system. Posttran AV block with have permanen the atrial rate c tropic compete status. When re tation, pacemak repeated negativ cardia are often transplant vascu Downloaded From: http://content.onlinejacc.org/ by William Kostis on 12/31/2012 bodily functions, or crowded conditions). Typically, no evi- dence of structural heart disease is present. Other causes of syncope such as LV outflow obstruction, bradyarrhythmias, and tachyarrhythmias should be excluded. Head-up tilt-table testing may be diagnostic. The role of permanent pacing in refractory neurocardio- genic syncope associated with significant bradycardia or asystole remains controversial. Approximately 25% of pa- tients have a predominant vasodepressor reaction without significant bradycardia. Many patients will have a mixed vasodepressive/cardioinhibitory cause of their symptoms. It has been estimated that approximately one third of patients will have substantial bradycardia or asystole during head-up tilt testing or during observed and recorded spontaneous episodes of syncope. Outcomes from clinical trials have not been consistent. Results from a randomized controlled trial (147) in highly symptomatic patients with bradycardia dem- onstrated that permanent pacing increased the time to the first syncopal event. Another study demonstrated that DDD (a dual-chamber pacemaker that senses/paces in the atrium/ ventricle and is inhibited/triggered by intrinsic rhythm) pac- ing with a sudden bradycardia 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 (148). In VPS (Vasovagal Pacemaker Study) (149), the actuarial rate of recurrent syncope at 1 year was 18.5% for pacemaker patients and 59.7% for control patients. However, in VPS-II (Vasova- gal Pacemaker Study II) (150), a double-blind randomized trial, pacing therapy did not reduce the risk of recurrent syncopal events. In VPS-II, all patients received a permanent pacemaker and were randomized to therapy versus no therapy sinus pressure that induces ventricular asystole of more than 3 seconds. (Level of Evidence: C) (142,152) CLASS IIa 1. Permanent pacing is reasonable for syncope without clear, provocative events and with a hypersensitive cardioinhibitory response of 3 seconds or longer. (Level of Evidence: C) (142) CLASS IIb 1. Permanent pacing may be considered for significantly symp- tomatic neurocardiogenic syncope associated with bradycar- dia documented spontaneously or at the time of tilt-table testing. (Level of Evidence: B) (147,148,150,153) CLASS III 1. Permanent pacing is not indicated for a hypersensitive car- dioinhibitory response to carotid sinus stimulation without symptoms or with vague symptoms. (Level of Evidence: C) 2. Permanent pacing is not indicated for situational vasovagal syncope in which avoidance behavior is effective and preferred. (Level of Evidence: C) 2.2. Pacing for Specific Conditions The following sections on cardiac transplantation, neuromus- cular diseases, sleep apnea syndromes, and infiltrative and inflammatory diseases are provided to recognize develop- ments in these specific areas and new information that has been obtained since publication of prior guidelines. Some of the information has been addressed in prior sections but herein is explored in more detail. 2.2.1. Cardiac Transplantation 14 Epstein et al. JACC Vol. 61, No. 13, 2013 Device Guideline: 2012 Update Incorporated January 22, 2013:xxx–xxx Post-MI AV block Carotid sinus syndrome + Neurocardiogenic syncope ACCF/AHA/HRS PPM Guidelines
69. CRM Devices in Anesthesiology Implantable Cardioverter Defibrillators (ICDs) •  Implantable Cardioverter Defibrillators (ICDs) •  Devices designed to prevent sudden cardiac death (SCD) •  Able to detect ventricular tachyarrhythmias and terminate them in one of two ways: •  HV Shock (Cardioversion / Defibrillation) •  Anti-tachycardia Pacing •  Ventricular overdrive pacing with the goal of terminating VT •  May accelerate VT •  Tachytherapies are programmed in zones by rate •  (May use morphologic and other criteria to discriminate VT from SVT)
70. CRM Devices in Anesthesiology ICD Guidelines •  ICD Implantation Guidelines •  ICD Implantation is considered for: •  Secondary Prevention of Sudden Cardiac Death (SCD) •  Survivor of SCD, sustained hemodynamically significant VT •  (Without reversible cause) •  Primary Prevention of Sudden Cardiac Death •  People at significantly increased risk of SCD •  Ischemic or nonischemic cardiomyopathy with low LVEF (generally <35%) •  No transient cause, on GDMT for >3 months, no revascularization < 3 months •  Genetic/acquired cardiomyopathies / channelopathies AND high-risk features •  HCM, ARVC, LQTS •  Brugada, CPVT •  Cardiac sarcoid •  Chagas •  GCM •  LVNC
71. CRM Devices in Anesthesiology ACCF/AHA/HRS ICD Guidelines ation and optimal lead placement may status or better for both function and point prevention of sudden death again goal. Information on this group is limited f the almost 4,000 patients in resynchro- had Class IV symptoms. In the COM- , there were Class IV patients for whom mproved QOL and reduced rehospitaliza- owever, these patients had been stable at ntry and may not represent typical Class in this selected group, there was no survival between CRT patients with and ator feature (230). In patients with Class hom resynchronization is inadequate to lity, the presence of a defibrillator often ending transition to end-of-life care. for Implantable Cardioverter on refers to the prevention of SCD in have survived a prior cardiac arrest or ry prevention refers to the prevention of without a history of cardiac arrest or ents with cardiac conditions associated f sudden death who have unexplained y to be due to ventricular arrhythmias are a secondary indication. s for consideration of ICD therapy, par- rimary prevention, apply only to patients optimal medical therapy and have a ion of survival with a good functional among the commonly used clinical techniques of LVEF determination. All clinical methods of LVEF determination lack precision and the accuracy of techniques varies amongst laboratories and institutions. Based on these considerations, this writing committee recommends that the clinician use the LVEF determination that they feel is the most clinically accurate and appropriate in their institution. CLASS I 1. ICD therapy is indicated in patients who are survivors of cardiac arrest due to VF or hemodynamically unstable sus- tained VT after evaluation to define the cause of the event and to exclude any completely reversible causes. (Level of Evi- dence: A) (16,319–324) 2. ICD therapy is indicated in patients with structural heart disease and spontaneous sustained VT, whether hemodynam- ically stable or unstable. (Level of Evidence: B) (16,319–324) 3. ICD therapy is indicated in patients with syncope of undeter- mined origin with clinically relevant, hemodynamically signifi- cant sustained VT or VF induced at electrophysiological study. (Level of Evidence: B) (16,322) 4. ICD therapy is indicated in patients with LVEF less than or equal to 35% due to prior MI who are at least 40 days post-MI and are in NYHA functional Class II or III. (Level of Evidence: A) (16,333) 5. ICD therapy is indicated in patients with nonischemic DCM who have an LVEF less than or equal to 35% and who are in NYHA functional Class II or III. (Level of Evidence: B) (16,333,369,379) 6. ICD therapy is indicated in patients with LV dysfunction due to prior MI who are at least 40 days post-MI, have an LVEF less nt.onlinejacc.org/ by William Kostis on 12/31/2012 than or equal to 30%, and are in NYHA functional Class I. (Level of Evidence: A) (16,332) 7. ICD therapy is indicated in patients with nonsustained VT due to prior MI, LVEF less than or equal to 40%, and inducible VF or sustained VT at electrophysiological study. (Level of Evidence: B) (16,327,329) CLASS IIa 1. ICD implantation is reasonable for patients with unexplained syncope, significant LV dysfunction, and nonischemic DCM. 2. ICD therapy is not indicated for patients VF. (Level of Evidence: C) 3. ICD therapy is not indicated in patients wi ric illnesses that may be aggravated by that may preclude systematic follow-up. ( 4. ICD therapy is not indicated for NYHA C drug-refractory congestive heart failure w for cardiac transplantation or CRT-D. (Le 5. ICD therapy is not indicated for syncope o in a patient without inducible ventricular JACC Vol. 61, No. 13, 2013 January 22, 2013:xxx–xxx Device Guideline: 2012 Update Class I Secondary Prevention (exclude completely reversible causes) Structural HD + Sustained VT Unexplained Syncope + Inducible VT/VF MI + LVEF ≤ 35%, NYHA II-III >40 days post-MI NIDCM + LVEF ≤ 35%, NYHA II-III MI + LVEF ≤ 30%, NYHA I >40 days post-MI MI + LVEF ≤ 40%, NSVT + Inducible VT/VF
72. CRM Devices in Anesthesiology than or equal to 30%, and are in NYHA functional Class I. (Level of Evidence: A) (16,332) 7. ICD therapy is indicated in patients with nonsustained VT due to prior MI, LVEF less than or equal to 40%, and inducible VF or sustained VT at electrophysiological study. (Level of Evidence: B) (16,327,329) CLASS IIa 1. ICD implantation is reasonable for patients with unexplained syncope, significant LV dysfunction, and nonischemic DCM. (Level of Evidence: C) 2. ICD implantation is reasonable for patients with sustained VT and normal or near-normal ventricular function. (Level of Evi- dence: C) 3. ICD implantation is reasonable for patients with HCM who have 1 or more major† risk factors for SCD. (Level of Evidence: C) 4. ICD implantation is reasonable for the prevention of SCD in patients with ARVD/C who have 1 or more risk factors for SCD. (Level of Evidence: C) 5. ICD implantation is reasonable to reduce SCD in patients with long-QT syndrome who are experiencing syncope and/ or VT while receiving beta blockers. (Level of Evidence: B) (349–354) 6. ICD implantation is reasonable for nonhospitalized patients awaiting transplantation. (Level of Evidence: C) 7. ICD implantation is reasonable for patients with Brugada syndrome who have had syncope. (Level of Evidence: C) 8. ICD implantation is reasonable for patients with Brugada syndrome who have documented VT that has not resulted in cardiac arrest. (Level of Evidence: C) 9. ICD implantation is reasonable for patients with catecholaminer- gic polymorphic VT who have syncope and/or documented sus- tained VT while receiving beta blockers. (Level of Evidence: C) 10. ICD implantation is reasonable for patients with cardiac sarcoidosis, giant cell myocarditis, or Chagas disease. (Level of Evidence: C) CLASS IIa 1. ICD therapy may be considered in patients with nonischemic heart disease who have an LVEF of less than or equal to 35% and who are in NYHA functional Class I. (Level of Evidence: C) 2. ICD therapy is not indicated for patients wit VF. (Level of Evidence: C) 3. ICD therapy is not indicated in patients with s ric illnesses that may be aggravated by devi that may preclude systematic follow-up. (Leve 4. ICD therapy is not indicated for NYHA Clas drug-refractory congestive heart failure who a for cardiac transplantation or CRT-D. (Level 5. ICD therapy is not indicated for syncope of un in a patient without inducible ventricular tac without structural heart disease. (Level of E 6. ICD therapy is not indicated when VF or V surgical or catheter ablation (e.g., atrial ar ated with the Wolff-Parkinson-White syndro flow tract VT, idiopathic VT, or fascicular VT structural heart disease). (Level of Evidence 7. ICD therapy is not indicated for patients tachyarrhythmias due to a completely revers absence of structural heart disease (e.g., ance, drugs, or trauma). (Level of Evidence: 3.3. Implantable Cardioverter-Defi Children, Adolescents, and Patien Congenital Heart Disease The indications for ICD implantation in young with congenital heart disease have evolved ove based on data derived primarily from adult ra trials. Similar to adults, ICD indications have secondary prevention of SCD to the treatmen sustained ventricular arrhythmias to the curren primary prevention in patients with an increa However, in contrast to adults, there are min data regarding ICD survival benefit, because all ICDs are implanted in pediatric or congen patients (439). Considerations such as the cu risk of SCD in high-risk patients and the nee antiarrhythmic therapy make the ICD an im option for young patients. SCD in childhood and adolescence is a principal forms of cardiovascular disease: 1) January 22, 2013:xxx–xxx Device Guideline: 2012 Update Inco Class IIa Unexplained Syncope + NIDCM, Significant LVD Sustained VT + ~Normal EF HCM + ≥1 risk fx for SCD ARVC + ≥1 risk fx for SCD LQTS + Syncope/VT on BB Pre-Transplant Outpatients Brugada + Syncope Brugada + VT CPVT + Syncope/VT on BB Cardiac Sarcoid, GCM, Chagas ACCF/AHA/HRS ICD Guidelines
73. CRM Devices in Anesthesiology syndrome who have had syncope. (Level of Evidence: C) 8. ICD implantation is reasonable for patients with Brugada syndrome who have documented VT that has not resulted in cardiac arrest. (Level of Evidence: C) 9. ICD implantation is reasonable for patients with catecholaminer- gic polymorphic VT who have syncope and/or documented sus- tained VT while receiving beta blockers. (Level of Evidence: C) 10. ICD implantation is reasonable for patients with cardiac sarcoidosis, giant cell myocarditis, or Chagas disease. (Level of Evidence: C) CLASS IIa 1. ICD therapy may be considered in patients with nonischemic heart disease who have an LVEF of less than or equal to 35% and who are in NYHA functional Class I. (Level of Evidence: C) 2. ICD therapy may be considered for patients with long-QT syndrome and risk factors for SCD. (Level of Evidence: B) (16,349–354) 3. ICD therapy may be considered in patients with syncope and advanced structural heart disease in whom thorough invasive and noninvasive investigations have failed to define a cause. (Level of Evidence: C) 4. ICD therapy may be considered in patients with a familial cardiomyopathy associated with sudden death. (Level of Evi- dence: C) 5. ICD therapy may be considered in patients with LV noncompac- tion. (Level of Evidence: C) CLASS III 1. ICD therapy is not indicated for patients who do not have a reasonable expectation of survival with an acceptable func- tional status for at least 1 year, even if they meet ICD implantation criteria specified in the Class I, IIa, and IIb recommendations above. (Level of Evidence: C) based on data derived primarily from adult rand trials. Similar to adults, ICD indications have e secondary prevention of SCD to the treatment sustained ventricular arrhythmias to the current primary prevention in patients with an increase However, in contrast to adults, there are mini data regarding ICD survival benefit, because fe all ICDs are implanted in pediatric or congeni patients (439). Considerations such as the cum risk of SCD in high-risk patients and the need antiarrhythmic therapy make the ICD an imp option for young patients. SCD in childhood and adolescence is ass principal forms of cardiovascular disease: 1) disease, 2) cardiomyopathies, and 3) genetic dromes (440,441). Prospective identification a young patients at risk for sudden death is compared with adults, a very low percentage of going resuscitation survive to hospital discharg The indications for ICD therapy in pediatr have been resuscitated or who are at high ri similar to those for adults. Data from nonrand provide support for the Class I recommenda patients who have been resuscitated from S dergo ICD implantation after a careful evalua any potentially reversible causes (440,443–4 ous sustained VT or unexplained syncope sustained hypotensive VT in patients with c disease are also considered Class I ICD in other remediable causes (hemodynamic or ar been excluded (446). Catheter ablation or su may provide an alternative to use of an ICD congenital heart disease and recurrent VT (44 Downloaded From: http://content.onlinejacc.org/ by William Kostis on 12/31/2012 Class IIb NIDCM + LVEF ≤ 35%, NYHA I LQTS + ≥1 risk fx for SCD Syncope + Structural HD + No Cause Familial CM associated with SCD LV Noncompaction ACCF/AHA/HRS ICD Guidelines
74. CRM Devices in Anesthesiology advanced structural heart disease in whom thorough invasive and noninvasive investigations have failed to define a cause. (Level of Evidence: C) 4. ICD therapy may be considered in patients with a familial cardiomyopathy associated with sudden death. (Level of Evi- dence: C) 5. ICD therapy may be considered in patients with LV noncompac- tion. (Level of Evidence: C) CLASS III 1. ICD therapy is not indicated for patients who do not have a reasonable expectation of survival with an acceptable func- tional status for at least 1 year, even if they meet ICD implantation criteria specified in the Class I, IIa, and IIb recommendations above. (Level of Evidence: C) going resuscitation survive to hospital discharge The indications for ICD therapy in pediatri have been resuscitated or who are at high ris similar to those for adults. Data from nonrand provide support for the Class I recommendat patients who have been resuscitated from SC dergo ICD implantation after a careful evalua any potentially reversible causes (440,443–4 ous sustained VT or unexplained syncope sustained hypotensive VT in patients with c disease are also considered Class I ICD ind other remediable causes (hemodynamic or ar been excluded (446). Catheter ablation or sur may provide an alternative to use of an ICD i congenital heart disease and recurrent VT (44 Downloaded From: http://content.onlinejacc.org/ by William Kostis on 12/31/2012 l to 30%, and are in NYHA functional Class I. (Level A) (16,332) is indicated in patients with nonsustained VT due VEF less than or equal to 40%, and inducible VF or T at electrophysiological study. (Level of Evidence: 329) ation is reasonable for patients with unexplained gnificant LV dysfunction, and nonischemic DCM. dence: C) ation is reasonable for patients with sustained VT or near-normal ventricular function. (Level of Evi- tion is reasonable for patients with HCM who have ajor† risk factors for SCD. (Level of Evidence: C) ation is reasonable for the prevention of SCD in h ARVD/C who have 1 or more risk factors for SCD. dence: C) ation is reasonable to reduce SCD in patients T syndrome who are experiencing syncope and/ receiving beta blockers. (Level of Evidence: B) ation is reasonable for nonhospitalized patients nsplantation. (Level of Evidence: C) ation is reasonable for patients with Brugada ho have had syncope. (Level of Evidence: C) ation is reasonable for patients with Brugada 2. ICD therapy is not indicated for patients with incessant VT or VF. (Level of Evidence: C) 3. ICD therapy is not indicated in patients with significant psychiat- ric illnesses that may be aggravated by device implantation or that may preclude systematic follow-up. (Level of Evidence: C) 4. ICD therapy is not indicated for NYHA Class IV patients with drug-refractory congestive heart failure who are not candidates for cardiac transplantation or CRT-D. (Level of Evidence: C) 5. ICD therapy is not indicated for syncope of undetermined cause in a patient without inducible ventricular tachyarrhythmias and without structural heart disease. (Level of Evidence: C) 6. ICD therapy is not indicated when VF or VT is amenable to surgical or catheter ablation (e.g., atrial arrhythmias associ- ated with the Wolff-Parkinson-White syndrome, RV or LV out- flow tract VT, idiopathic VT, or fascicular VT in the absence of structural heart disease). (Level of Evidence: C) 7. ICD therapy is not indicated for patients with ventricular tachyarrhythmias due to a completely reversible disorder in the absence of structural heart disease (e.g., electrolyte imbal- ance, drugs, or trauma). (Level of Evidence: B) (16) 3.3. Implantable Cardioverter-Defibrillators in Children, Adolescents, and Patients With Congenital Heart Disease The indications for ICD implantation in young patients and those with congenital heart disease have evolved over the past 15 years based on data derived primarily from adult randomized clinical 39 , 2013 Epstein et al. x–xxx Device Guideline: 2012 Update Incorporated Class III Survival or Functional Status < 1 year Incessant VT/VF Significant Psychiatric Dz NYHA IV on tx + Not candidates for OHT or CRT-D Unexplained Syncope Without Structural dz or Inducible VT/VF VT/VF Amenable to Surgical or Catheter Ablation VT/VF Due to Reversible Cause in Absence of Structural dz ACCF/AHA/HRS ICD Guidelines
75. CRM Devices in Anesthesiology Cardiac Rhythm Management Devices •  Common Cardiac Rhythm Management Devices •  Temporary Transvenous Pacemaker (TVP) •  Permanent Pacemaker (PPM) •  Transvenous PPM •  Leadless PPM •  Implantable Cardioverter Defibrillator (ICD) •  Transvenous ICD •  Subcutaneous ICD •  Cardiac Resynchronization Therapy Devices (CRT) •  CRT-D •  CRT-P •  Implantable Loop Recorder (ILR) •  Ambulatory Monitor (e.g. Holter, Patch Monitor)
76. CRM Devices in Anesthesiology •  Permanent Pacemakers (PPMs) –  Prevent bradycardia via pacing •  Single-chamber, dual-chamber, or CRT pacing –  Promote AV synchrony •  Dual-chamber or CRT devices –  Provide rate and EGM data and other diagnostics –  About 10-15 years longevity –  Some devices include therapies for pace-termination of atrial arrhythmias Permanent Pacemakers (PPMs)
77. CRM Devices in Anesthesiology Transvenous PPMs
78. CRM Devices in Anesthesiology Transvenous PPMs
79. CRM Devices in Anesthesiology Transvenous PPMs
80. CRM Devices in Anesthesiology Transvenous PPMs
81. CRM Devices in Anesthesiology Transvenous PPMs
82. CRM Devices in Anesthesiology Transvenous PPMs
83. CRM Devices in Anesthesiology Leadless PPMs •  Leadless Pacemakers (Leadless PPMs) –  Prevent bradycardia via pacing –  Currently single-chamber RV devices –  Originally for VVI/VVIR Pacing Only –  Can now function in A-sensed, V-paced mode to promote AV synchrony –  Provide rate and EGM data and other diagnostics –  About 10-15 years longevity –  Other technology for dual-chamber pacing is in development
84. CRM Devices in Anesthesiology Leadless PPMs
85. CRM Devices in Anesthesiology Leadless PPMs
86. CRM Devices in Anesthesiology Leadless PPMs
87. CRM Devices in Anesthesiology •  Transvenous ICDs –  Restore sinus rhythm in the presence of ventricular tachyarrhythmias •  Cardioversion •  Defibrillation •  Anti-Tachycardia Pacing (ATP) –  Provide pacing •  Single-chamber, dual-chamber, or CRT pacing –  Provide rate and EGM data and other diagnostics –  About 5-15 years longevity –  There are also devices designed to terminate AT/AF via ATP or cardioversion in addition to standard ICD therapies Transvenous ICDs
88. CRM Devices in Anesthesiology Transvenous ICDs
89. CRM Devices in Anesthesiology Transvenous ICDs
90. CRM Devices in Anesthesiology Transvenous ICDs
91. CRM Devices in Anesthesiology Transvenous ICDs
92. CRM Devices in Anesthesiology •  Subcutaneous ICDs –  Restore sinus rhythm in the presence of ventricular tachyarrhythmias •  Cardioversion •  Defibrillation •  No Anti-Tachycardia Pacing (ATP) –  No pacing for bradycardia •  Post-shock pacing: VVI 50 for up to 30 seconds •  Similar to transcutaneous pacing –  Provide rate and EGM data and other diagnostics –  About 7 years longevity –  Possibility of fewer long-term complications S-ICDs
93. CRM Devices in Anesthesiology S-ICDs
94. CRM Devices in Anesthesiology S-ICDs
95. CRM Devices in Anesthesiology S-ICDs
96. CRM Devices in Anesthesiology •  Cardiac Resynchronization Therapy –  Accompanies ICD (CRT-D) or PPM (CRT-P) –  Restore ventricular synchrony via LV pacing •  Biventricular pacing (RV and LV) •  LV pacing –  The LV lead is placed transvenously via the coronary sinus into a coronary venous branch, typically overlying the posterolateral wall of the LV –  Epicardial lead placement is an option –  Provide rate and EGM data and other diagnostics –  About 5-10 years longevity CRT
97. CRM Devices in Anesthesiology Mechanical Effects of LBBB Leyva F, JACC 2014;64(10):1047-1058 CRT-D reduced all-cause mortality in NYHA ctional class IV patients (20). The CARE-HF (Cardiac Resynchronization-Heart ure) study (21), which randomized patients OPT with or without CRT-P, showed that CRT-P uced death from any cause or unplanned hospital- ions for major cardiovascular events, as well as al mortality after 29 months. In addition, CRT-P proved quality of life and LVEF, induced LV erse remodeling, and reduced mitral regurgitation. The COMPANION trial (19) and the CARE-HF study established CRT as a treatment for HF (NYHA ctional class III or IV), impaired LV function, and a e QRS complex. Although the characteristics of ice-treated patients were similar, the control up was ICD plus OPT in the COMPANION trial and T only in the CARE-HF study. This may account for apparently lower efficacy of CRT-P in the MPANION trial. Although some would argue on the is of the COMPANION trial that the treatment ect of CRT-D is superior to that of CRT-P, others pose that a definitive comparison is still required ause CRT-D and CRT-P were not compared. T IN MILD HF efficacy of CRT-D in mild HF was suggested by the NTAK CD study, which demonstrated LV reverse modeling across NYHA functional classes II to IV . In the MIRACLE ICD II study (23), which included ients in NYHA functional class II, CRT-D induced LV erse remodeling compared with ICD. Subsequently, the MADIT-CRT (Multicenter Automatic Defibril- or Implantation Trial with Cardiac Resynchroniza- n Therapy) (24), which randomized 1,820 patients NYHA functional class I and II to CRT-D or ICD, T-D reduced total mortality or HF events by 34%. s endpoint was mainly driven by reductions in The failure of the MADIT-CRT and the REVERSE study to demonstrate an independent effect on mor- tality reflects the low background mortality (2% to 3%) in NYHA functional classes I and II. However, in 0 20 40 60 80 100 +5 0 -5 0 200 400 Time (ms) NORMAL CONDUCTION LBBB LATERAL SEPTAL Strain (%) Activation Time (ms) -10 120 FIGURE 1 Mechanical Effects of LBBB Three-dimensional representation of ventricular activation (top) and strain (bottom) during normal activation and left bundle branch block (LBBB) in a canine heart showing how early septal activation (blue circles) leads to early shortening (blue tracing) and late lateral wall activation (red circle) leads to stretching in early systole followed by shortening during the ejection phase. Gray tracings denote mean left ventricular strain. Adapted with permission from Prinzen et al. (86) and derived from De Boeck et al. (87) and Mills et al. (88). C V O L . 6 4 , N O . 1 0 , 2 0 1 4 Leyva et al. T E M B E R 9 , 2 0 1 4 : 1 0 4 7 – 5 8 20 Years of CRT 1049
98. CRM Devices in Anesthesiology MADIT-CRT Moss AJ, NEJM 2009;361:1329-1338. diac Resynchronization for Heart-Failure Prevention dditional primary analyses onal-hazards regression for d for death at any time and ecified categorical subgroups ctions. The homogeneity of ording to time period was l P values are two-tailed and d for the stopping rule, ex- end-point analysis. ts were used to evaluate the eft ventricular volumes and (as seen on echocardiogra- and 1-year follow-up in pa- dy group who had paired th recordings. mittee stopped the trial on after the 9th of 20 planned mmendation of the indepen- monitoring board, since the ad reached the prespecified ig. 1). Study-group assign- inded, and all analyses were curring before trial termi- o the prespecified primary a plan for secondary analy- ng heart-failure events and a patients who were assigned to the CRT–ICD group (7.5%) received an ICD-only device during the trial because of technical difficulties in positioning the 22p3 1.0      
      
       0.8 0.9 0.7 0.6 0.0 0 1 2 3 4 CRT–ICD ICD only  ** ("(# ' , (    *&       ICD only CRT–ICD 731 1089 621 (0.89) 985 (0.92) 379 (0.78) 651 (0.86) 173 (0.71) 279 (0.80) 43 (0.63) 58 (0.73) AUTHOR: FIGURE: JOB: 4-C H/T RETAKE ! ICM CASE EMail Line H/T Combo Revised 
    $ %*( # +((# )%*( *   *"%"&"   REG F Enon 1st 2nd 3rd Moss 2 of 4 10-01-09 ARTIST: ts 36114 ISSUE: P<0.001 Figure 2. Kaplan–Meier Estimates of the Probability of Survival Free of Heart Failure. There was a significant difference in the estimate of survival free of heart failure between the group that received cardiac-resynchronization therapy plus an implantable cardioverter–defibrillator (CRT–ICD) and the group that received an ICD only (unadjusted P<0.001 by the log-rank test).
99. CRM Devices in Anesthesiology MADIT-CRT by QRS Morphology Zareba W, Circulation 2011;123(10):1061-72. Clinical and Echocardiographic Data Collection Baseline clinical information included patient demographics; data regarding the cause of the cardiomyopathy (ischemic or nonis- chemic); NYHA class; QRS duration; history of diabetes, hyper- Analyses evaluating the effects of CRT-D versus ICD-only in subgroups of LBBB and non-LBBB patients were performed without adjustment. All analyses were on an intention-to-treat basis, with end points collected by June 23, 2009. Interaction Figure 1. Cumulative probability of heart failure (HF) event or death (top) and of death (bottom) according to QRS morphology in the implantable cardioverter defibrillator (ICD) arm and cardiac resynchronization therapy with defibrillator (CRT-D) arm of the Multicenter Automatic Defibrillator Implantation Trial–Cardiac Resynchronization Therapy (MADIT-CRT). LBBB indicates left bundle-branch block; RBBB, right bundle-branch block; and IVCD, intraventricular conduction disturbances. Zareba et al Cardiac Resynchronization Therapy and BBB 1063 Heart Failure Event or Death by QRS Morphology and ICD vs. CRT-D
100. CRM Devices in Anesthesiology MADIT-CRT Long-Term Survival Goldenberg I, NEJM 2014;370:1694-1701. The new engl and jour nal of medicine rated at the time of enrollment, and the separa- tion was maintained (Fig. S1 in the Supplementary Appendix). The unadjusted and adjusted hazard ratios for signed to CRT-D therapy, as compared with those randomly assigned to ICD therapy alone. For the secondary end point of a nonfatal heart-failure event, the adjusted hazard ratio of 0.38 indicated a reduction in risk of 62% with CRT-D (Table 2). The effects of CRT-D therapy on mortality among patients with left bundle-branch block in seven prespecified subgroups are shown in Fig- ure 3. The survival benefit with CRT-D was con- sistent in each subgroup analyzed, including pa- tients with ischemic cardiomyopathy and those with nonischemic cardiomyopathy, men and women, and patients with a longer QRS duration (≥150 msec) and those with a shorter QRS dura- tion (<150 msec); there were no significant treat- ment-by-subgroup interactions. The survival ben- efit provided by CRT-D in patients with left bundle-branch block was independent of the QRS duration, even when the QRS duration was further categorized into quartiles (Fig. S2 in the Supplementary Appendix). CRT-d IN PATIENTS WITHOUT LEFT BUNDLE-BRANCH BLOCK Among patients without left bundle-branch block, Kaplan–Meier survival analysis did not show a significant difference between the two treatment groups in the cumulative probability of death from any cause during the period from enrollment through 7 years of follow-up (P = 0.21 by the log- rank test without adjustment) (Fig. 2B). Similarly, the cumulative probability of a nonfatal heart- failure event during 7 years of follow-up did not differ significantly between the ICD-only group and the CRT-D group (P = 0.58 by the log-rank test without adjustment) (Fig. S3 in the Supple- mentary Appendix). Cox proportional-hazards regression model- ing consistently showed a lack of benefit associ- ated with CRT-D in patients without left bundle- branch block, with a trend toward an increased risk of death observed only after multivariate adjustment (Table 2). The differential effect of CRT-D on outcomes according to QRS morpho- logic findings was significant for all end points Probability of Death 0.00 0 1 2 3 4 5 7 Follow-up (yr) B Patients without Left Bundle-Branch Block A Patients with Left Bundle-Branch Block P=0.002 No. at Risk ICD only CRT-D 520 761 488 734 463 714 40 636 326 527 254 425 41 70 6 94 157 0.30 0.20 0.25 0.15 0.10 0.05 0.00 0 1 2 3 4 5 7 6 ICD only CRT-D 0.35 0.30 0.20 0.25 0.15 0.10 0.05 0.00 0 1 2 3 4 5 7 6 CRT-D ICD only Probability of Death 0.80 0.40 0.60 1.00 0.20 0.10 0.30 0.50 0.70 0.90 0.80 0.40 0.60 1.00 0.20 0.10 0.30 0.50 0.70 0.90 0.00 0 1 2 3 4 5 7 Follow-up (yr) P=0.205 No. at Risk ICD only CRT-D 209 328 197 312 189 292 156 240 115 182 95 136 10 13 6 24 39 Figure 2. Kaplan–Meier Estimates of the Cumulative Probability of Death from Any Cause among Patients with and Those without Left Bundle- Branch Block. CRT-D denotes cardiac-resynchronization therapy with defibrillator, and ICD implantable cardioverter–defibrillator. The insets show the same data on an enlarged y axis.
101. CRM Devices in Anesthesiology MADIT-CRT Long-Term Survival Goldenberg I, NEJM 2014;370:1694-1701. Survival with CRT in Mild Heart Failure ing right bundle-branch block or intraventricular conduction delay (Fig. S4 in the Supplementary Appendix). POST-TRIAL ANALYSIS To further validate the consistency of our find- ings, we carried out a post-trial landmark analy- sis (i.e., with the follow-up time beginning after trial closure). The landmark multivariate Cox model showed similar findings: among patients ventricular dysfunction and an ECG pattern show- ing left bundle-branch block. However, there were no beneficial effects on long-term outcomes in patients without left bundle-branch block. Cardiac-resynchronization therapy (CRT) with or without a defibrillator is associated with re- verse remodeling and has been shown to reduce heart-failure symptoms and rates of hospitaliza- tion and death among patients with NYHA class III or IV heart failure.4-7 MADIT-CRT and the Table 2. Hazard Ratios for End Points with CRT-D versus ICD Alone, According to the Presence or Absence of Left Bundle-Branch Block. End Point No. of Events No. of Patients Left Bundle-Branch Block Non–Left Bundle-Branch Block P Value for Interaction* Hazard Ratio (95% CI) P Value Hazard Ratio (95% CI) P Value Death from any cause Unadjusted analysis 292 1818 0.63 (0.47–0.84) 0.002 1.31 (0.87–1.96) 0.19 0.004 Adjusted analysis† 267 1681 0.59 (0.43–0.80) <0.001 1.57 (1.03–2.39) 0.04 <0.001 Nonfatal heart-failure event Unadjusted analysis 442 1818 0.42 (0.33–0.52) <0.001 1.10 (0.79–1.53) 0.59 <0.001 Adjusted analysis† 405 1681 0.38 (0.30–0.48) <0.001 1.13 (0.80–1.60) 0.48 <0.001 Nonfatal heart-failure event or death Unadjusted analysis 577 1818 0.50 (0.41–0.61) <0.001 1.21 (0.90–1.63) 0.21 <0.001 Adjusted analysis† 530 1681 0.45 (0.37–0.56) <0.001 1.27 (0.94–1.73) 0.12 <0.001 * The P value for interaction represents the likelihood that the difference between the treatment effect on patients with left bundle-branch block and the treatment effect on those without left bundle-branch block occurred by chance alone. † Models were adjusted for the following covariates: age at enrollment, serum creatinine level of 1.4 mg per deciliter (120 µmol per liter) or more, smoking status at enrollment, presence or absence of diabetes mellitus, cause of cardiomyopathy (ischemic vs. nonischemic), left ventricular end- systolic volume at baseline indexed by body-surface area, QRS duration at baseline (≥150 msec vs. <150 msec), and NYHA class III or IV more than 3 months before enrollment (yes vs. no). Covariates were identified from a best-subset regression analysis.
102. CRM Devices in Anesthesiology ACCF/AHA/HRS CRT Guidelines Class I in the class of recommendations, on the basis of perceived differential benefit by functional class, QRS morphology, and QRS duration. Recommendations for Cardiac Resynchronization Therapy See Appendix 6, “Indications for CRT Therapy–Algorithm.” CLASS I 1. CRT is indicated for patients who have LVEF less than or equal to 35%, sinus rhythm, LBBB with a QRS duration greater than or equal to 150 ms, and NYHA class II, (546,547) III, or ambulatory IV (542–545); symptoms on GDMT. (Level of Evidence: A for NYHA class III/IV; Level of Evidence: B for NYHA class II) CLASS IIa 1. CRT can be useful for patients who have LVEF less than or equal to 35%, sinus rhythm, LBBB with a QRS duration 120 to 149 ms, and NYHA class II, III, or ambulatory IV symptoms on GDMT (542–544,546–548). (Level of Evidence: B) 2. CRT can be useful for patients who have LVEF less than or equal to 35%, sinus rhythm, a non-LBBB pattern with a QRS duration greater than or equal to 150 ms, and NYHA class III/ ambulatory class IV symptoms on GDMT (542–544,547). (Level of Evidence: A) 3. CRT can be useful in patients with atrial fibrillation and LVEF less than or equal to 35% on GDMT if a) the patient requires ventricular pacing or otherwise meets CRT criteria and b) AV nodal ablation or pharmacologic rate control will allow near 100% ventric- ular pacing with CRT (549–553,575). (Level of Evidence: B) 4. CRT can be useful for patients on GDMT who have LVEF less than or equal to 35% and are undergoing new or replacement device placement with anticipated requirement for significant (>40%) ventricular pacing (551,554,555,556). (Level of Evi- dence: C) 2.4.2. Obstructive Hypertrophic Card Early nonrandomized studies demonstrate outflow gradient with dual-chamber paci delay and symptomatic improvement in obstructive HCM (232–235). One long-te patients supported the long-term benefi pacing in this group of patients. The ou reduced even after cessation of pacing, w some ventricular remodeling had occurre of pacing. Two randomized trials (235, subjective improvement in approximate participants, but there was no correlat reduction, and a significant placebo effe third randomized, double-blinded trial (23 strate any overall improvement in QOL wi there was a suggestion that elderly patie years of age) may derive more benefit fro In a small group of patients with sy tensive cardiac hypertrophy with cavity pacing with premature excitation stati exercise capacity, cardiac reserve, and (239). Dual-chamber pacing may impro LV outflow gradient in pediatric patien atrial rates, rapid AV conduction, and valve abnormalities may preclude effect patients (240). There are currently no data availab contention that pacing alters the clinical co or improves survival or long-term QOL i routine implantation of dual-chamber pac be advocated in all patients with sympt HCM. Patients who may benefit the m significant gradients (more than 30 mm than 50 mm Hg provoked). (235,241–24 block can develop after transcoronary a Downloaded From: http://content.onlinejacc.org/ by William Kostis on 12/31/2012 LVEF ≤ 35%, SR LBBB, QRSd ≥ 150 ms NYHA II, III, ambulatory IV
103. CRM Devices in Anesthesiology Class IIa ACCF/AHA/HRS CRT Guidelines CLASS I 1. CRT is indicated for patients who have LVEF less than or equal to 35%, sinus rhythm, LBBB with a QRS duration greater than or equal to 150 ms, and NYHA class II, (546,547) III, or ambulatory IV (542–545); symptoms on GDMT. (Level of Evidence: A for NYHA class III/IV; Level of Evidence: B for NYHA class II) CLASS IIa 1. CRT can be useful for patients who have LVEF less than or equal to 35%, sinus rhythm, LBBB with a QRS duration 120 to 149 ms, and NYHA class II, III, or ambulatory IV symptoms on GDMT (542–544,546–548). (Level of Evidence: B) 2. CRT can be useful for patients who have LVEF less than or equal to 35%, sinus rhythm, a non-LBBB pattern with a QRS duration greater than or equal to 150 ms, and NYHA class III/ ambulatory class IV symptoms on GDMT (542–544,547). (Level of Evidence: A) 3. CRT can be useful in patients with atrial fibrillation and LVEF less than or equal to 35% on GDMT if a) the patient requires ventricular pacing or otherwise meets CRT criteria and b) AV nodal ablation or pharmacologic rate control will allow near 100% ventric- ular pacing with CRT (549–553,575). (Level of Evidence: B) 4. CRT can be useful for patients on GDMT who have LVEF less than or equal to 35% and are undergoing new or replacement device placement with anticipated requirement for significant (>40%) ventricular pacing (551,554,555,556). (Level of Evi- dence: C) reduced even after cessation of pacing, wh some ventricular remodeling had occurred a of pacing. Two randomized trials (235,23 subjective improvement in approximately participants, but there was no correlatio reduction, and a significant placebo effect third randomized, double-blinded trial (238) strate any overall improvement in QOL with there was a suggestion that elderly patient years of age) may derive more benefit from In a small group of patients with symp tensive cardiac hypertrophy with cavity ob pacing with premature excitation statist exercise capacity, cardiac reserve, and cli (239). Dual-chamber pacing may improve LV outflow gradient in pediatric patients. atrial rates, rapid AV conduction, and c valve abnormalities may preclude effective patients (240). There are currently no data available contention that pacing alters the clinical cour or improves survival or long-term QOL in H routine implantation of dual-chamber pacem be advocated in all patients with symptom HCM. Patients who may benefit the most significant gradients (more than 30 mm Hg than 50 mm Hg provoked). (235,241–243). block can develop after transcoronary alc Downloaded From: http://content.onlinejacc.org/ by William Kostis on 12/31/2012 LVEF ≤ 35%, SR LBBB, 120 ≤ QRSd ≤ 149 ms NYHA II, III, ambulatory IV LVEF ≤ 35%, SR non-LBBB, QRSd ≥ 150 ms NYHA III, ambulatory IV LVEF ≤ 35%, AF a) needs V-pacing b) AVNA/Rx è near 100% Vp LVEF ≤ 35% Antcipated > 40% Vp
104. CRM Devices in Anesthesiology Class IIb ACCF/AHA/HRS CRT Guidelines the pivotal trials demonstrating the efficacy ce in centers that provided expertise in device both at implantation and during long-term ganizational guidelines by the Heart Failure erica (588) and the European Society of ) have recently been published that address CRT. For the patient categories in common rt Failure Society of America document and sed update, there was a good deal of concor- h there are many areas of agreement, some t between the present guideline and the y of Cardiology document. One difference is nt guideline, CRT is recommended in NYHA who have LVEF Յ30%, have ischemic heart inus rhythm, and have a LBBB with a QRS ms (Class IIb; LOE: C) (546,547). There is no endation in the European Society of Cardiol- The European Society of Cardiology recom- ude patients with QRS duration Ͻ120 ms. We mmended CRT for any functional class or with QRS durations Ͻ120 ms. We also have der the presence of LBBB versus non-LBBB ecommendations, on the basis of perceived fit by functional class, QRS morphology, and ons for Cardiac ion Therapy “Indications for CRT Therapy–Algorithm.” ed for patients who have LVEF less than or equal CLASS IIa 1. CRT may be considered for patients who have LVEF less than or equal to 30%, ischemic etiology of heart failure, sinus rhythm, LBBB with a QRS duration of greater than or equal to 150 ms, and NYHA class I symptoms on GDMT (546,547). (Level of Evidence: C) 2. CRT may be considered for patients who have LVEF less than or equal to 35%, sinus rhythm, a non-LBBB pattern with QRS duration 120 to 149 ms, and NYHA class III/ambulatory class IV on GDMT (547,557). (Level of Evidence: B) 3. CRT may be considered for patients who have LVEF less than or equal to 35%, sinus rhythm, a non-LBBB pattern with a QRS duration greater than or equal to 150 ms, and NYHA class II symptoms on GDMT (546,547). (Level of Evidence: B) CLASS III: NO BENEFIT 1. CRT is not recommended for patients with NYHA class I or II symptoms and non-LBBB pattern with QRS duration less than 150 ms (546,547,557). (Level of Evidence: B) 2. CRT is not indicated for patients whose comorbidities and/or frailty limit survival with good functional capacity to less than 1 year (545). (Level of Evidence: C) 2.4.2. Obstructive Hypertrophic Cardiomyopathy Early nonrandomized studies demonstrated a fall in the LV outflow gradient with dual-chamber pacing and a short AV delay and symptomatic improvement in some patients with obstructive HCM (232–235). One long-term study (236) in 8 patients supported the long-term benefit of dual-chamber pacing in this group of patients. The outflow gradient was reduced even after cessation of pacing, which suggests that some ventricular remodeling had occurred as a consequence of pacing. Two randomized trials (235,237) demonstrated et al. JACC Vol. 61, No. 13, 2013 uideline: 2012 Update Incorporated January 22, 2013:xxx–xxx ICM, LVEF ≤ 30%, SR LBBB, QRSd ≥ 150 ms NYHA I LVEF ≤ 35%, SR non-LBBB, 120 ≤ QRSd ≤ 149 ms NYHA III, ambulatory IV ICM, LVEF ≤ 30%, SR non-LBBB, QRSd ≥ 150 ms NYHA II
105. CRM Devices in Anesthesiology Class III ACCF/AHA/HRS CRT Guidelines CRT. For the patient categories in common art Failure Society of America document and sed update, there was a good deal of concor- h there are many areas of agreement, some t between the present guideline and the y of Cardiology document. One difference is nt guideline, CRT is recommended in NYHA who have LVEF Յ30%, have ischemic heart inus rhythm, and have a LBBB with a QRS ms (Class IIb; LOE: C) (546,547). There is no endation in the European Society of Cardiol- The European Society of Cardiology recom- ude patients with QRS duration Ͻ120 ms. We mmended CRT for any functional class or with QRS durations Ͻ120 ms. We also have der the presence of LBBB versus non-LBBB ecommendations, on the basis of perceived fit by functional class, QRS morphology, and ons for Cardiac ion Therapy , “Indications for CRT Therapy–Algorithm.” ed for patients who have LVEF less than or equal rhythm, LBBB with a QRS duration greater than 50 ms, and NYHA class II, (546,547) III, or V (542–545); symptoms on GDMT. (Level of or NYHA class III/IV; Level of Evidence: B for ) seful for patients who have LVEF less than or sinus rhythm, LBBB with a QRS duration 120 to NYHA class II, III, or ambulatory IV symptoms on 44,546–548). (Level of Evidence: B) eful for patients who have LVEF less than or equal rhythm, a non-LBBB pattern with a QRS duration or equal to 150 ms, and NYHA class III/ ass IV symptoms on GDMT (542–544,547). ence: A) equal to 35%, sinus rhythm, a non-LBBB pattern with QRS duration 120 to 149 ms, and NYHA class III/ambulatory class IV on GDMT (547,557). (Level of Evidence: B) 3. CRT may be considered for patients who have LVEF less than or equal to 35%, sinus rhythm, a non-LBBB pattern with a QRS duration greater than or equal to 150 ms, and NYHA class II symptoms on GDMT (546,547). (Level of Evidence: B) CLASS III: NO BENEFIT 1. CRT is not recommended for patients with NYHA class I or II symptoms and non-LBBB pattern with QRS duration less than 150 ms (546,547,557). (Level of Evidence: B) 2. CRT is not indicated for patients whose comorbidities and/or frailty limit survival with good functional capacity to less than 1 year (545). (Level of Evidence: C) 2.4.2. Obstructive Hypertrophic Cardiomyopathy Early nonrandomized studies demonstrated a fall in the LV outflow gradient with dual-chamber pacing and a short AV delay and symptomatic improvement in some patients with obstructive HCM (232–235). One long-term study (236) in 8 patients supported the long-term benefit of dual-chamber pacing in this group of patients. The outflow gradient was reduced even after cessation of pacing, which suggests that some ventricular remodeling had occurred as a consequence of pacing. Two randomized trials (235,237) demonstrated subjective improvement in approximately 50% of study participants, but there was no correlation with gradient reduction, and a significant placebo effect was present. A third randomized, double-blinded trial (238) failed to demon- strate any overall improvement in QOL with pacing, although there was a suggestion that elderly patients (more than 65 years of age) may derive more benefit from pacing. In a small group of patients with symptomatic, hyper- tensive cardiac hypertrophy with cavity obliteration, VDD pacing with premature excitation statistically improved exercise capacity, cardiac reserve, and clinical symptoms (239). Dual-chamber pacing may improve symptoms and LV outflow gradient in pediatric patients. However, rapid atrial rates, rapid AV conduction, and congenital mitral valve abnormalities may preclude effective pacing in some non-LBBB, QRSd < 150 ms NYHA I-II Survival or Functional Status < 1 year
106. CRM Devices in Anesthesiology CRT-D
107. CRM Devices in Anesthesiology CRT-D
108. CRM Devices in Anesthesiology CRT-P
109. CRM Devices in Anesthesiology CRT-P
110. CRM Devices in Anesthesiology Other Mechanism for Prevention of SCD §  There is another mechanism by which ICDs can prevent sudden death...
111. CRM Devices in Anesthesiology Other Mechanism for Prevention of SCD
112. CRM Devices in Anesthesiology •  Implantable Loop Recorders (ILRs) –  Provide ability to detect a variety of arrhythmias –  Bradyarrhythmias and pauses –  Tachyarrhythmias (including SVT, VT, and VF) –  Atrial Fibrillation –  Recordings can be due to automatically detected arrhythmias or due to patient-triggered events Implantable Loop Recorders (ILRs)
113. CRM Devices in Anesthesiology ILRs
114. CRM Devices in Anesthesiology •  Holter Monitors (24-48 hours) •  Loop Recorders (2-4 weeks) •  Patch Monitors (2-4 weeks) –  Provide ability to detect a variety of arrhythmias –  Recordings can be due to automatically detected arrhythmias or due to patient-triggered events Other Ambulatory Monitors
115. CRM Devices in Anesthesiology •  Examples of output of device interrogations Device Interrogation
116. CRM Devices in Anesthesiology Device Interrogation Device Interrogation Case 1
117. CRM Devices in Anesthesiology Device Interrogation
118. CRM Devices in Anesthesiology Device Interrogation
119. CRM Devices in Anesthesiology Device Interrogation
120. CRM Devices in Anesthesiology Device Interrogation
121. CRM Devices in Anesthesiology Device Interrogation
122. CRM Devices in Anesthesiology Device Interrogation
123. CRM Devices in Anesthesiology Device Interrogation
124. CRM Devices in Anesthesiology Device Interrogation
125. CRM Devices in Anesthesiology Device Interrogation Device Interrogation Case 2
126. CRM Devices in Anesthesiology Device Interrogation
127. CRM Devices in Anesthesiology Device Interrogation
128. CRM Devices in Anesthesiology Device Interrogation
129. CRM Devices in Anesthesiology Device Interrogation
130. CRM Devices in Anesthesiology Device Interrogation
131. CRM Devices in Anesthesiology Device Interrogation
132. CRM Devices in Anesthesiology Device Interrogation
133. CRM Devices in Anesthesiology Device Interrogation
134. CRM Devices in Anesthesiology Device Interrogation
135. CRM Devices in Anesthesiology Device Interrogation Device Interrogation Case 3
136. CRM Devices in Anesthesiology Device Interrogation
137. CRM Devices in Anesthesiology Device Interrogation
138. CRM Devices in Anesthesiology Device Interrogation
139. CRM Devices in Anesthesiology Device Interrogation Device Interrogation Case 4
140. CRM Devices in Anesthesiology Device Interrogation
141. CRM Devices in Anesthesiology Device Interrogation
142. CRM Devices in Anesthesiology Device Interrogation
143. CRM Devices in Anesthesiology Device Interrogation Device Interrogation Case 5
144. CRM Devices in Anesthesiology Device Interrogation
145. CRM Devices in Anesthesiology Device Interrogation
146. CRM Devices in Anesthesiology Device Interrogation
147. CRM Devices in Anesthesiology Device Interrogation Device Interrogation Case 6
148. CRM Devices in Anesthesiology Device Interrogation
149. CRM Devices in Anesthesiology Device Interrogation
150. CRM Devices in Anesthesiology Thank You