Cardiac Pacing and Pacemaker Rhythms


Pacemaker rhythms

Cardiac pacing systems are described by a three- or four-letter code. The first letter indicates the chamber in which pacing stimuli are delivered (atrium, A; ventricle, V; or both, D). The second letter indicates the chamber in which sensing of the intracardiac electrical signal is occurring (atrium, A; ventricle, V; or both, D). The third letter indicates the response of the device to a sensed signal (inhibition of pacing stimulus output, I; triggering [causing to occur] of stimulus output, T; or both, D). The fourth letter, R, indicates that the device is rate adaptive—that is, it uses one or more sensors to achieve increases and decreases in pacing rate to mimic normal physiologic responses to changes in metabolic need. Commonly used sensors are body motion sensors (e.g., accelerometers) and minute ventilation sensors; one or more sensors can be programmed to be used simultaneously (“blended” sensors).

From Olshansky B, Chung M, Pogwizd S, Goldschlager N. Arrhythmia Essentials. Sudbury, MA: Jones & Bartlett Learning; 2012:241.

The usual pacing system implanted in patients who do not have chronic atrial fibrillation (AF) is DDD(R), in which both sensing and pacing occur in both atria and ventricles; AAI(R) systems ( Fig. 7.1 ), which sense and pace only in the atrium, are still in use for patients with sinus node dysfunction and atrioventricular (AV) conduction, and there are systems that can switch between AAI(R) and DDD(R), or AAI(R) and VVI. VVI(R) systems ( Fig. 7.2 ), which sense and pace only in the ventricles, are generally reserved for patients with chronic atrial fibrillation or very old, infirm patients, although they may be used in some young patients with the rare need for backup pacing. Examples of standard dual-chamber pacemakers are shown in Figs. 7.1 , 7.3 , and 7.4 .

Figure 7.1, Normal atrial pacing (AAI or AAI[R]).

Figure 7.2, Normal ventricular pacing (VVI or VVI[R]).

Figure 7.3, Dual-chamber pacing: Atrial and ventricular paced.

Figure 7.4, Dual-chamber pacing: Atrial sensed, ventricular paced.

The base rate (lower rate limit, standby rate) of a pacing system is that programmed rate at which pacing will occur if there is no spontaneous cardiac depolarization. In devices programmed to rate responsiveness, the base rate is the lowest programmed rate at rest. The upper rate limit , which is either atrial (native P wave) based or sensor based, is the programmed maximum pacing rate that can occur. The maximum tracking rate is that rate at which ventricular pacing will be triggered by native P waves in a 1:1 relationship (atrial based); the maximum sensor-based rate is the highest programmed rate dictated by sensor input to the pulse generator. Whereas these rates are often programmed to be the same, the sensor-based rate can be programmed to exceed the tracking rate in response to exercise, thereby avoiding rapid ventricular paced rates triggered by supraventricular tachycardias.

The magnet rate (designated AOO, VOO, or DOO, as sensing, and therefore response to a sensed signal, do not occur; thus, the letter “O”—an asynchronous mode) is that nonprogrammable rate that occurs when a magnet is placed over the pulse generator. It varies with the manufacturer; several manufacturers set a constant magnet rate well above the expected spontaneous rate (e.g., 100 beats per minute) in order to allow myocardial depolarization (pacing) to be confirmed ( Fig. 7.5A ); other manufacturers set a rapid magnet rate for a specific number of cycles, followed by a slower rate (see Fig. 7.5B ). Because magnet placement eliminates sensing, pacing output occurs despite the existence of a spontaneous cardiac rhythm; repetitive atrial or ventricular beating is only very rarely a clinical consequence.

Figure 7.5, Examples of two different magnet rates and AV intervals.

The programmed AV or PV intervals, independently programmable, define the interval between an atrial and ventricular stimulus or a sensed P wave (atrial electrogram) and the triggered ventricular stimulus, respectively. In DOO mode, the AV interval is generally shortened in order to usurp intact AV conduction and allow confirmation of ventricular pacing; some manufacturers design a lengthening of this interval after a specified number of cycles in order to assess native AV conduction (see Fig. 7.5B ).

After a sensed or paced event, an independently programmable refractory period ensues in each channel (atrial, ARP; and ventricular, VRP), during which the device will not respond to electrical signals. In DDD pacing systems, a programmable postventricular atrial refractory period (PVARP) is designed to prevent tracking of early P waves, which can be retrogradely conducted, thus avoiding “pacemaker-mediated tachycardia” and rapid paced ventricular rates.

Failure to capture, noncapture ( Fig. 7.6 ) indicates that a pacing stimulus output does not depolarize myocardial tissue. This can occur because of too low a programmed voltage output, an increase in myocardial stimulation threshold (such as occurs during hyperkalemia or flecainide treatment), pacing lead insulation break or fracture, lead dislodgement, or battery end of life; failure to capture may also be “functional” due to refractoriness of the myocardial tissue. Pacing system interrogation through manufacturer-specific programmers is often necessary to define the nature of the problem.

Figure 7.6, Failure to capture (ventricle).

Undersensing ( Fig. 7.7 ) refers to failure to sense the intracardiac signal and is usually due to a poor signal rather than a pacing system failure; it can often be corrected by appropriate programming. Undersensing can also result from lead fracture or insulation break or lead dislodgment; interrogation will be necessary to confirm this diagnosis; if present, lead revision will be required.

Figure 7.7, Undersensing (Failure to sense and failure to capture).

Oversensing ( Fig. 7.8 ) is the sensing of electrical signals that are not actually generated within the cardiac chamber, or sensing unwanted signals, such as a T wave in the ventricle. The oversensed signal can come from the patient (e.g., myopotentials; Fig. 7.9 ), the environment (e.g., electronic article surveillance devices, electrocautery, ionizing radiation), and the pacing system itself (e.g., a lead insulation break or fracture that generates electrical signals due to potential differences within the leads). The oversensed signals will cause inhibition of pacing output or, if occurring in the atrial channel in DDD systems, triggering of an earlier-than-expected ventricular pacing stimulus.

Figure 7.8, Oversensing (and undersensing).

Figure 7.9, Myopotential inhibition.

Rapid paced ventricular rates generally occur in response to supraventricular tachycardias ( Fig. 7.10 ), in which the sensed atrial signals trigger ventricular pacing; this can cause hemodynamic compromise and may need to be emergently managed by programming or by placing a magnet over the pulse generator to eliminate sensing. Devices in use today have a programmable function that changes the mode of pacemaker function from DDD(R) to DDI(R) or VVI(R) or VDI(R) in response to sensing of rapid atrial rates (automatic mode switch) to prevent this complication, but the function must be programmed “on” and the parameters for the mode switch programmed; device interrogation is necessary to assess all programmed parameters and functions.

Figure 7.10, Upper rate pacing with atrial tachycardia.

Occasionally, a rapid paced ventricular rate can result from pacemaker-mediated tachycardia (PMT) ( Fig. 7.11 ). In this circumstance, a paced ventricular depolarization is conducted retrogradely to the atrium, and the sensed atrial electrical signal triggers another ventricular paced event, which leads again to retrograde ventriculoatrial (VA) conduction and subsequent triggering of a ventricular paced event and so forth. The rapid paced ventricular rate, as well as the VA conduction, can cause unwanted hemodynamic consequences; application of a magnet will prevent sensing and thus terminate the PMT. Subsequent pacemaker programming to eliminate sensing of the retrograde P wave (increase in PVARP) can resolve the problem.

Figure 7.11, Pacemaker-mediated tachycardia.

Paced QRS complexes resulting from right ventricular outflow tract or apical pacing sites are generally broad (> 120 ms) and have an left bundle branch block (LBBB) pattern as depolarization is originating from the right ventricle. The frontal plane axis will be inferiorly directed if the outflow tract is being paced and superiorly directed if the apex is being paced. Unintended left ventricle (LV) pacing is suggested by paced complexes with a right bundle branch block (RBBB) pattern ( Fig. 7.12A and B ).

Figure 7.12, Unintended left ventricular pacing.

Biventricular pacing systems ( Fig. 7.13 ), in which right and left ventricles are stimulated simultaneously or in proximity, will be narrower and may have a rightward axis due to the LV stimulation; they may also have RBBB morphology. Morphology in biventricular pacing is dependent on lead location and the programmed relative timing of right and left ventricular pacing impulses.

Figure 7.13, Biventricular pacing.

All pacing systems can store in memory episodes of rapid heart rates, provided they are appropriately programmed to do so. High rates in either atrium or ventricle can be interrogated, and stored intracardiac electrograms can be viewed for confirmation of the rhythm and appropriate management undertaken. Pacing devices also store other clinically relevant information, such as heart rate histograms, percentage of atrial and ventricular pacing and sensing, and number of mode switches. Evaluation of such data can have direct effects on patient management.

Pacemakers nearing end of life from battery depletion can present with marked slowing of the paced rate ( Fig. 7.14 ). Interrogation of the device often alerts the clinician to this problem via text on the programmer’s screen; inability to interrogate due to insufficient battery voltage and current is also a clue to end of life. If interrogation can be accomplished, pulse generators nearing end of life (“elective replacement time”) will display a warning.

Figure 7.14, Pacemaker malfunction: End of life.

Indications for pacing

Indications for Temporary Transvenous Cardiac Pacing

  • In patients with medically refractory symptomatic bradycardia or high risk of bradycardia of any etiology

  • In patients in whom a permanent cardiac pacing system is necessary but cannot be implanted expeditiously

  • In patients with LBBB in whom a right heart catheter is to be inserted (risk of development of complete AV block due to catheter-induced trauma to the right bundle)

  • In patients with new AV block, including progressive first-degree AV block, developing during infections (e.g., aortic valve endocarditis, Lyme disease)

  • In patients undergoing electrical cardioversion who have known sinus node dysfunction

  • In patients for whom only temporary pacing is needed (drug-induced bradycardia, transient heart block post inferior myocardial infarction [MI], preoperatively in a patient who needs a valve replacement, endocarditis, lead extraction)

  • In patients with pause-dependent ventricular tachycardia (VT) for treatment and prevention

  • In high-risk, post-MI patients (uncommon in current MI treatment era) with medically refractory symptomatic bradycardia

  • Hemodynamically destabilizing AV block at any level (use caution in patients undergoing percutaneous intervention due to bleeding risk; pacing lead should be placed prior to the percutaneous coronary intervention (PCI)

  • New bundle branch block (BBB) with Mobitz type II second-degree AV block

  • Alternating BBB or fascicular block

Indications for Permanent Cardiac Pacing

Atrioventricular Block

  • Advanced second-degree or complete AV block with symptoms of bradycardia or if due to medications that are needed for some other reason

  • Advanced second-degree or complete AV block occurring below the AV node

  • Advanced second-degree or complete AV block with an escape pacemaker with rate of < 40 bpm

  • Asystolic periods of more than 3 seconds that recur and are unpredictable and are unrelated to hypervagotonic states

  • Second-degree, advanced, or complete AV block developing during exercise

  • After ablation of the AV junction performed to control ventricular rate in AF

  • Post-op AV block (usually aortic valve surgery) that is not expected to resolve

  • Second-degree AV block found at electrophysiologic study to be infra-AV nodal

  • Neuromuscular disease (e.g., myotonic muscular dystrophy, Kearns-Sayre syndrome), because progression to advanced or complete AV block is unpredictable

  • First-degree AV block causing symptoms due to suboptimal AV relationships

Sinus Node Dysfunction

  • Symptomatic bradycardia or pauses in rhythm, including chronotropic incompetence (inability to increase sinus rate in response to metabolic needs)

  • Symptomatic bradycardia resulting from medications otherwise necessary to treat other conditions

  • Questionably symptomatic bradycardia, but with a rate of < 40 bpm

  • Syncope of unclear etiology with evidence for sinus node dysfunction

  • Prolonged pauses occurring on termination of atrial arrhythmias, such as atrial fibrillation

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