An 80-year-old undergoes dual-chamber pacemaker placement for CHB. Excellent ventricular and atrial capture thresholds were obtained at the time of the implant. The pacemaker programmed parameters are as follows:
mode, DDD; lower rate, 70 bpm; upper rate, 130 bpm; atrial sensitivity, 0.25 mV (most sensitive setting); ventricular sensitivity, 1.00 mV; AV delay, 175 milliseconds; pace/sense configuration, bipolar. The next day, the following rhythm strip was recorded:
This rhythm strip shows:
Atrial undersensing. This rhythm shows evidence of atrial undersensing. The pacemaker is programmed to DDD. In this mode, an appropriately sensed P wave should cause inhibition of the atrial spike; a ventricular spike is then delivered after the programmed AV interval or inhibited by an intrinsic R wave. In this strip, the P wave is present in each complex. However, in complexes 2, 4, 6, and 8, an atrial spike follows the intrinsic P wave because the intrinsic P wave was not appropriately sensed by the pacemaker. The noncapture of the atrium following the atrial spike on complexes 2, 4, 6, and 8 is anticipated as the atrium would still have been refractory from the preceding P wave. Capture of the atrium on complexes 1, 3, 5, and 7 is suggested by the P wave that is different in morphology (wider) than the intrinsic P wave. Atrial undersensing occurring early after implantation may be the result of lead dislodgment. A CXR should be obtained to assess lead position. Other possibilities include inappropriate programmed sensitivity, which can be assessed on a device check. Finally, inflammation at the lead tip–endocardium interface can result in a decrease in sensing amplitude. This may improve over several weeks as the lead matures and inflammation resolves.
A 50-year-old man with chronic obstructive pulmonary disease related to chronic smoking presents to the emergency room with palpitations. ECG shows narrow QRS tachycardia at 165 bpm. His BP is 125/60 mmHg. Expiratory wheezes are heard on lung examination. His medications include albuterol inhaler and theophylline.
The most appropriate initial treatment includes which of the following?
Verapamil IV bolus. Adenosine is commonly used to terminate SVT. However, this patient is on theophylline, which is an effective blocker of the adenosine receptor. Propafenone might be poorly tolerated by this patient because of its associated β-blocking activity, which might increase airway resistance. Digoxin shortens the refractory period of the atrium and might potentially accelerate an atrial tachycardia. Immediate cardioversion is not needed, as the patient appears hemodynamically stable, and it would be reasonable to attempt pharmacologic therapy initially with verapamil.
A 55-year-old woman returns to the clinic after a recent dual-chamber pacemaker placement. She reports frequent palpitations and fatigue. These episodes last for several minutes before stopping. A Holter monitor recorded the following rhythm (Fig. below): The pacemaker is programmed to mode DDD; lower rate, 80 bpm; upper rate, 150 bpm; AV delay, 200 milliseconds; postventricular atrial RP, 150 milliseconds.
The latter part of this rhythm strip shows
Pacemaker-mediated tachycardia. In this strip, there is evidence of atrial undersensing (fifth complex). As a result, the fifth ventricular-paced beat comes “late” relative to atrial activation. This allows enough time to go by for the AV node to recover its conduction properties. This allows retrograde P-wave conduction following ventricular pacing, which is sensed by the pacer (because of short programmed postventricular atrial refractory period [PVARP]), and results in ventricular triggered pacing, causing a pacemakermediated tachycardia or endless-loop tachycardia. Acute treatment of this condition includes the application of a magnet to inhibit atrial sensing, thereby breaking the tachycardia loop. The spontaneous termination of these episodes in this patient is most probably related to intermittent atrial undersensing, which interrupts the tachycardia loop. Further prevention of these episodes includes reprogramming the PVARP, AV delay, or atrial sensitivity. Pacemaker-mediated tachycardia is an abnormal consequence of normal pacemaker function.
An 82-year-old man receives a dual-chamber pacemaker for SSS. Routine transtelephonic check (without and with magnet) shows the following strips (Fig. below).
Which of the following is true?
The pacing mode is VVI secondary to automatic mode switch. The initial rhythm strip shows background AFib with VVI pacing, most probably related to automatic mode switch. The absence of atrial pacing suggests adequate atrial sensing (of the fibrillation), which resulted in the mode switch behavior. Atrial pacing cannot be determined in the presence of AFib. There is adequate ventricular sensing, as determined on the nonmagnet strip (fifth complex—the small intrinsic QRS is sensed by the pacemaker which results in inhibition of pacing); however, there is intermittent ventricular capture noted (ventricular pacing spike followed by a lack of ventricular depolarization).
The following tracings
is obtained during EP evaluation of AV conduction in different patients. HRA (high right atrium) and HBE (His bundle electrogram) are the intracardiac electrograms, recording from the high right atrium and the His bundle regions, respectively. Which of the following is true for these tracings?
CHB at the level of the AV node. In this tracing, there is NSR with CHB and a narrow escape rhythm that is junctional in origin. This is apparent in the HBE tracing, in which the atrial deflections are completely dissociated from the H–V deflections. Therefore, the atrial impulse entering the AV node is not conducting down to the His bundle (A is not followed by His potential), indicating that the level of block is at the level of the AV node.
Click to expand