PERMANENT PACEMAKERS AND IMPLANTABLE DEFIBRILLATORS Considerations for intensivists

Transcription

1 PERMANENT PACEMAKERS AND IMPLANTABLE DEFIBRILLATORS Considerations for intensivists Craig A. McPherson, MD, FACC Associate Professor of Medicine Constantine Manthous, MD, FACP, FCCP Associate Clinical Professor of Medicine ONLINE DATA SUPPLEMENT

2 Web-based Repository Figure Legends Figure E1.Pacer lead fracture. This 71 year old woman had received a dual chamber pacer several years earlier to treat complete heart block. On the day of this 12-lead ECG recording she presented with syncope and was admitted to the CCU with possible myocardial infarction. The tracing demonstrates sinus rhythm, complete heart block, pacer stimuli that fail to capture (arrows) and a narrow-qrs junctional escape rhythm. The marked T-wave changes are nonspecific. Serum troponin levels did not rise. The chest radiograph revealed a discontinuity in the ventricular lead near the sterno-clavicular junction. A new lead was inserted and the patient recovered. Figure E2. Atrial lead noise: myopotential tracking. This man with healed myocardial infarction and ventricular tachycardia received an ICD two years prior to this recording. At routine ICD interrogation, the device was noted to have logged frequent atrial arrhythmias. This recording was made as the patient was asked to raise his left arm above his head. The atrial channel (middle tracing) demonstrates high frequency, low amplitude noise that likely represents myopotentials. These are sensed by the ICD which emits four paced ventricular beats at rate approaching the upper pacing limit of the device (120/min). Figure E3. Atrial lead noise: mode switching. This tracing, from the same patient as Figure R-2, was stored in device memory as an episode of atrial fibrillation. The upper tracing (RA) is the right atrial lead channel. It depicts high frequency, low amplitude noise punctuated by atrial impulses (A) at approximately 65/min. The right ventricular (RV) channel (middle tracing) and the shock electrogram (lower tracing) demonstrate

3 ventricular pacing at 90/min, which likely represents rate-adaptive, sensor-mediated ventricular pacing. In response to the atrial channel noise, which was perceived as atrial tachyarrhythmia, the device has mode switched to single-chamber ventricular pacing. This results in A-V dissociation, which may diminish cardiac output by as much as 20% in some individuals. The resulting symptoms, which may include fatigue, palpitations, effort intolerance and dyspnea, constitute the pacemaker syndrome. Figure E4. Lead failure following myocardial infarction. This 80 year old man had a dual chamber pacer placed three years earlier for carotid sinus syncope. The system was found to function normally one month prior to this tracing. He was admitted to the cardiac care unit with chest pain, elevated troponin levels and acute inferior wall myocardial infarction (note ST-segment elevation in the inferior leads). Random pacer stimuli (arrows) suggested pacer malfunction. Interrogation demonstrated that the right atrial lead neither sensed nor captured at its highest programmed output (yet, its lead impedance was normal and unchanged from past values, suggesting that lead integrity was not compromised). The chest radiograph revealed stable lead position in the lower portion of the RA and no visible discontinuities. Coronary angiogram demonstrated right coronary artery occlusion proximal the right atrial branch. It was hypothesized that right atrial infarction near the right atrial lead tip resulted in its failure to sense and capture the local myocardium. Figure E5. Syncopal ventricular tachycardia. This patient with ischemic cardiomyopathy, chronic atrial fibrillation and inducible ventricular tachycardia at electrophysiology study two years earlier was admitted to the ICU after an episode of syncope. He reported no ICD shocks. Myocardial infarction was excluded and head CT demonstrated no acute

4 pathology. Telemetry monitoring revealed no spontaneous arrhythmia. He was discharged on his cardiac medications. Interrogation of this device two months later revealed this tracing. The top panel is the description of the event stored in ICD memory. The middle panel shows the ventricular and shock electrograms at the start of an episode of ventricular tachycardia. The bottom panel shows the same tracings. Later in the recording, the ventricular tachycardia has accelerated to 290/min. Though the ventricular tachycardia was terminated by the 23 J biphasic discharge of the ICD, the patient had already lost consciousness. Thus, he did not report feeling the shock. Figure E6. Detection of asymptomatic atrial fibrillation in ICD memory. This recording was retrieved from ICD memory at routine ICD clinic visit of this 54 year old man with diabetes, ischemic cardiomyopathy, complete heart block and sustained ventricular tachycardia. The Cardiac Compass Report in Figure 6A reveals that the patient had atrial fibrillation 24 hours per day from early April 2004 through late May He reported no symptoms during this time. Figure E6B is a recording of an arrhythmia event that was stored on May 15, The upper tracing in each panel is the atrial channel (A) and demonstrated persistent atrial flutter at 300/min. The lower tracing is the ventricular channel (V). In the upper panel the ventricular rate is 220/min due to ventricular tachycardia, which terminates near the end of the panel. In the lower panel, the atrial flutter persists and the ventricle is paced (VP) at 75/min. The patient reported no symptoms at this time. Such protracted episodes of atrial tachyarrhythmia, though asymptomatic, may be a harbinger of stroke, especially in a diabetic patient with dilated atrium and ventricle. Systemic anticoagulation is indicated. Routine interrogation of implanted devices in patients who are admitted to the ICU, often with non-cardiac

5 conditions, provides the opportunity to detect and treat atrial fibrillation risk and perchance prevent a stroke from occurring. Figure E7. Response of ICD to electrocautery at surgery. This tracing was retrieved from the memory of an ICD after the patient had undergone coronary bypass surgery. At the start of surgery, his ICD, which had not been deactivated pre-operatively, discharged as the surgeon was using cautery on the incision. Neither the patient nor the surgeon was harmed (though the later was jolted by surprise). The RV (top tracing) channel reveals high frequency signals that represent detection of the electrocautery unit by the ICD. Though the cautery was used in bursts, the mean rate over this period of time exceeded that which the ICD was programmed to recognize as VT. Thus, it charged and fired. Fortunately the cautery was not being used near any critical structures at the time. This tracing underscores the need to deactivate ICDs prior to any surgery at which electrocautery is to used. Supplementary Explanations for Items Listed in Table 1 of the Primary Manuscript 1 Unexpectedly slow heart rate may result from rate hysteresis. This programmable function allows the PPM to escape (begin pacing) at a slower native rate than that at which it is programmed to stimulate the heart. For example, when the heart rate slows to 50/min, it may begin pacing at 70/min. This feature is most commonly used in singlechamber ventricular pacing to minimize ventricular pacing and maximize the time spent in sinus rhythm (with its attendant atrio-ventricular synchrony). 2. Unexpected lengthening of the AV interval may occur as part of normal PPM function. If the atrial rate of a dual chamber system approaches the upper programmed rate, the

6 AV-interval may begin to lengthen. This phenomenon, referred to as pacemaker Wenckebach behavior, allows the device to track the prevailing atrial rate as much as possible without creating a paced R-R interval that would violate the upper heart rate limit. Some PPMs also have programmable atrio-ventricular search hysteresis. This prompts the PPM to periodically lengthen its AV interval to promote intrinsic AV conduction and minimize right ventricular pacing (which, as noted above, may lead to heart failure in some patients). 3. Unexpected shortening of the AV interval may also occur as part of normal PPM function. One example is ventricular safety pacing. In this instance, detection of a ventricular event shortly after a P-wave prompts the device to deliver a stimulus to the ventricle at a shorter than normal AV interval. The logic is that if the sensed event is noise, the ventricle will be paced and no pause will occur. If the sensed event is a ventricular premature depolarization, the shortened AV interval guarantees that the paced ventricular stimulus falls in, or just after, the QRS when refractory myocardium will not permit capture, rather than in the T-wave where capture might precipitate ventricular tachycardia. Some PPMs are also programmable to rate- adaptive AV interval behavior. This results in shortening of the AV interval as the heart rate increases, to mimic the natural response of the PR-interval during periods of sinus tachycardia.

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