Pacemaker Programming and Troubleshooting

Pacing Mode

Recommendations for pacing mode selection according to device indication and patient profile have been made, both by the US/Canadian (HRS/ACCF) and the European (ESC) cardiological societies. The recommendations are very similar, and a summary of the pacing modes from the 2013 ESC guidelines is shown in Figure 37-1 .

ADI(R)

This pacing mode, in conjunction with a switch to the DDD(R) mode, constitutes the basis of several algorithms designed to reduce RV pacing (see Chapter 13 ). These algorithms are designated by different names: AAI(R)/DDD(R) or Managed Ventricular Pacing by Medtronic (Minneapolis, MN), AAI(R) with VVI backup or RYTHMIQ by Boston Scientific (Marlborough, MA), AAI Safe R by Sorin (Milan, Italy), and ADI(R)/DDD(R) mode by Biotronik (Berlin, Germany). The device functions in an ADI(R) mode until blocked P waves occur repeatedly, resulting in a switch to a DDD(R) mode for a specified duration, followed by an AV conduction check ( Fig. 37-2 ). Algorithms from different companies have slight differences but all allow pauses with long-short sequences to occur. Although they reduce ventricular pacing effectively, it may be better to avoid this algorithm in (1) patients with permanent complete AV block (in whom they are ineffective), (2) patients with symptomatic first degree AV block ( Fig. 37-3 ), (3) pacemaker-dependent patients who do not tolerate slow rates (as dizzy spells may occur during the conduction search tests), and (4) cases with a long QT interval or history of torsades de pointes. Even though these algorithms are safe and well-tolerated by the great majority of patients, there has been concern for ventricular proarrhythmia of the long-short pacing sequences.

Baseline and Upper Rates

Many pacemakers are shipped with the default setting of pacing rates of 60 to 120 bpm. In patients who do not have sinus node dysfunction, programming a lower baseline rate (e.g., 40 to 50 beats per minute [bpm]) is useful to avoid unnecessary atrial pacing, which in turn will prolong battery life and may avoid atrial arrhythmias (due to atrial conduction delay resulting from pacing). Avoidance of atrial pacing may also avoid unnecessary ventricular pacing, as AV intervals may be substantially longer with atrial pacing than with atrial sensing (again due to atrial conduction delay). In patients with chronic atrial fibrillation (AF) and bradycardia, baseline rates are often programmed to 60 to 70 bpm in clinical practice. Night heart rates and rate hysteresis may also be useful to avoid unnecessary pacing.

Upper tracking rates should be tailored to the patient's individual profile, and are usually programmed in the range of 110 to 160 bpm. In some studies, the upper tracking rate was programmed according to the formula 220 minus age (which is the theoretical maximum heart rate). Even though this formula may be used as a guide for programming, other factors should also be taken into account. Patients with coronary artery disease and angina, for instance, should have lower programmed rates (e.g., 110 to 120 bpm). Sensor-driven rates should be programmed to approximately 80% of 220 minus age, which provides maximum cardiac output.

Rate Response

A detailed description of sensor technology is given in Chapter 10 . Rate response should only be activated in patients with symptomatic chronotropic insufficiency. Even though sensor technology and programming varies between manufacturers, the two main parameters that are commonly programmed are threshold and slope ( Fig. 37-4 ).

It is usually better to change one single parameter at a time ( Fig. 37-5 ) unless the rate histograms clearly indicate otherwise, or the device has a modelling feature that allows simulating rate response at different settings for recorded sensor data. Patient history is of course essential, and modifying sensor settings is only warranted in case of symptoms.

Pacing Output

With modern steroid-eluting pacing leads, capture thresholds are usually low and stable over time. Nevertheless, about 4% of patients will have chronic ventricular thresholds greater than 2.5 V @ 0.4 msec. Pacing polarity may be programmed to either unipolar or to bipolar (as long as the pacing lead is bipolar, which is the case in almost all transvenous endocardial leads implanted today). The former has the advantage that pacing artefacts are easily visible on the surface electrocardiogram (ECG) and facilitates the interpretation of tracings. Also, it does not rely on the outer conductor coil avoiding any issues with damage to this component of the circuit or to outer insulation defects. The downsides of a unipolar pacing configuration are that the impedance is usually lower, resulting in more current drain, and that there may be pectoral muscle capture in case of high programmed output as the pacemaker generator acts as the anode and is electrically active (some devices are coated on one side to avoid this). Automatic impedance measurements are often performed in the pacing polarity that is permanently programmed, which in case of unipolar pacing will not reflect lead integrity of the outer conductor coil (which is part of the circuit if sensing is programmed to bipolar).

In order to have a 100% safety margin, pacing output should in general be programmed at twice the capture threshold. This corresponds to twice the threshold amplitude (in V) at a given pulse width, or three times the duration (in msec) at a given amplitude. This margin may be lower (e.g., 1.5 to 2×) in devices which perform daily automatic threshold measurements and adapt output accordingly, or in patients with automatic capture algorithms, which pace with a safety margin of only 0.25 to 0.5 V, but verify capture on a beat-to-beat basis with backup pacing in case of loss of capture (see Chapter 14 ). In addition to patient safety, device longevity should be borne in mind when programming pacing output. It should be remembered that Energy = (V ² t)/R. Therefore battery longevity will be more affected by increasing output voltage than duration. Doubling the voltage will result in multiplying the energy by four, whereas doubling the pulse width results in a doubling of the energy. Some devices will plot a strength-duration curve based upon manual thresholds ( Fig. 37-6 ), which may be useful for choosing the best combination of voltage and duration (with the most energy efficient point approximating to the chronaxie). However, battery voltage is an important factor that also needs to be taken into account. As soon as the programmed output voltage exceeds that of the battery, voltage multipliers will come into play with considerable loss of energy. It is therefore usually advantageous to program the voltage amplitude to below that of the battery (which may be 2.7 to 3.1 V, depending on the model) and is therefore often programmed as a default value of 2.5 V @ 0.4 msec in clinical practice. Gain in battery longevity is usually minimal below 2.0 to 2.5 V. In cases of high thresholds, automatic beat-to-beat capture verification algorithms are particularly useful, because they significantly reduce the safety margin and may therefore avoid having to pace above the battery voltage ( Case Study 37-1 ). Other factors that should be borne in mind when programming the safety margin and pacing output are pacemaker dependency, percentage of ventricular pacing, lead impedance (which also affects current consumption), previous fluctuations in capture threshold, and introduction of drugs which may affect capture thresholds (e.g., flecainide). Automatic threshold or capture algorithms have been shown to be reliable and not only have the potential to increase patient safety and device longevity, but are also very convenient for device follow-up, both in-office and remotely. Many physicians choose to activate them routinely, at least for monitoring thresholds over time, if not for automatically adjusting pacing output (however, in current St. Jude Medical [St. Paul, MN] pacemakers, the AutoCapture algorithm cannot be programmed to a “monitoring only” mode).

Case Study 37-1

Management of High Ventricular Pacing Threshold in Patients with Intact Ventricular Leads

A 41-year-old gentleman received a VVI pacemaker because of sick sinus syndrome (SSS) with dizzy spells. A family history of early-onset SSS and pacemaker implantation was well known.

Pacemaker syndrome occurred after 2 years followed by an upgrade to DDDR; because the right ventricular (RV) pacing threshold was 3 V @ 0.4 msec, a new RV lead was inserted. The pacemaker was replaced after 7 years at end of service, in January 2008, because secondary atrioventricular block (AVB) had developed. A Sensia DDDR pacemaker by Medtronic was chosen to enable increased longevity, given the patient's life expectancy.

Atrial capture management could not work due to the coexistence of SSS and AVB, ¹ whereas RV stimulation was elicited by ventricular capture management (VCM), which is an autothreshold algorithm. ² RV output was programmed with a 1.5× threshold safety margin and threshold measurements every 12 hours. ³

One year after replacement in January 2009 ( Fig. E37-1 ) a slight increase of RV threshold from 0.875 V to 1.25 V at 0.4 msec had occurred. On November 2009 RV threshold had increased further, ranging from 1.7 to 2 V @ 0.4 msec; RV output was adapted accordingly ( Fig. E37-2 ). Lead impedance was within normal range and had never changed since implantation (see Figs. E37-1 and E37-2 ). Frequent atrial fibrillation episodes were recorded.

In March 2010 the patient was seen at the emergency room because of dizzy spells: intermittent ventricular exit block was observed ( Fig. E37-3 ). The RV threshold measured during the night was 1.75 V, but had increased to 2.75 V at noon when the RV output was still set at 2.75 until the next threshold update, thereby causing the erratic ventricular capture. In the evening the threshold was back at 2.25 V. VCM setting was changed to threshold measurements every 6 hours. The chest x-rays did not show any lead issues. The RV threshold ranged between 2 and 2.5 V in the following 6 months ( Fig. E37-4 ) and the patient was doing well. The device was re-programmed in VVIR mode because of permanent atrial fibrillation (AF).

In August 2012 the patient had syncope and dizzy spells in the early morning. Ventricular exit block with ventricular escape rhythm was recorded ( Fig. E37-5 ); RV threshold during the night time was 2 V but had increased to 3 V in the following 5 hours. Soon after admission, threshold measurement occurred and the RV output automatically reverted to 5 V @ 1 msec on detection of a pacing threshold greater than 2.5 V.

Pacemaker longevity became a trade-off with patient safety: VCM was set to monitor, and a fixed output as 5 V @ 0.4 msec was programmed to avoid continuous pacing at 5 V @ 1 msec. The patient was followed closely, and a stable RV threshold around 2.5 V @ 0.4 msec over 2 years was recorded ( Fig. E37-6 ); slight improvement (2.25 V) was observed when testing at 1-msec pulse width. Device replacement can be foreseen by the third quarter of 2016 (8.6 years overall longevity).

This case highlights the limitations of autothreshold algorithms compared with beat-to-beat verification of capture with back-up pulse delivery. The future management of this patient offers several hints for discussion; a device with beat-to-beat capture verification will be chosen to increase safety and at the same time enabling superior longevity. The choice of such an algorithm among the three available should stand on the following considerations, based on a 500-ohm pacing impedance such as in this patient:

	Dedicated Leads Needed	Maximum Adapted Threshold	Energy Drained at 4 V@ 0.4 msec Pacing Threshold
Biotronik	No	4.8 V @ 0.4 msec	16 µJ
Boston Scientific	No	3.0 V @ 0.4 msec	50 µJ
St. Jude Medical	Low polarization	3.875 V @ 1.5 msec	20 µJ

A new lead addition poses the risk of complications and infections ⁴ and does not warrant a persistent low pacing threshold at long term.

References

• 1.

  Biffi M, Spitali G, Silvetti MS, et al: Atrial threshold variability: implications for automatic atrial stimulation algorithms. Pacing Clin Electrophysiol 30(12):1445–1454, 2007.

• 2.

  Biffi M, Sperzel J, Martignani C, et al: Evolution of pacing for bradycardia: autocapture. Eur Heart J 9(Suppl 1):I23–I32, 2007.

• 3.

  Biffi M, Bertini M, Mazzotti A, et al: Long-term RV threshold behavior by automated measurements: safety is the standpoint of pacemaker longevity! Pacing Clin Electrophysiol 34(1):89–95, 2011.

• 4.

  Poole JE, Gleva MJ, Mela T, REPLACE Registry Investigators, et al: Complication rates associated with pacemaker or implantable cardioverter-defibrillator generator replacements and upgrade procedures: results from the REPLACE registry. Circulation 122:1553–1561, 2010.

Errors or inability to measure capture thresholds ( Fig. 37-7 ) may result in the device pacing at a high (e.g., 4.5 V) output amplitude, which may have a detrimental effect on device longevity. In a recent report, issues (high variability or out-of-range values) in AutoCapture threshold measurements were found in almost half of patients, and were more frequent in patients with atrial fibrillation or infrequent (<25%) ventricular pacing.

Sensitivity

Sensitivity levels in most pacemakers are programmed to a constant value, although some systems are designed with an implantable cardioverter-defibrillator (ICD) platform and have adaptive sensitivity. Bipolar sensitivity levels are typically set to 0.3 to 0.5 mV for the atrium and to 2.0 to 2.8 mV for the ventricle. Unipolar sensitivity levels are typically set higher (less sensitive) to reduce oversensing of far-field cardiac and extracardiac signals that can lead to inappropriate pacemaker inhibition or tracking. Sensing should always be set to a bipolar configuration in bipolar leads unless there is an issue with that lead (e.g., fracture of the outer conduction coil or outer insulation defect resulting in artefacts).

Ventricular sensitivity should be programmed with a safety margin of at least 2 : 1. However, there is probably little rationale for making the ventricular channel less sensitive (i.e., with a higher value) than 3.0 mV for bipolar sensing, as there is little risk of oversensing at this setting. However, programming lower sensitivity (e.g., 4.0 mV) may lead to undersensing of ventricular premature beats, the amplitude of which may be low (e.g., if the vector of the ventricular arrhythmia is perpendicular to the axis of the electrode bipole). Many pacemakers are currently able to perform automatic atrial and ventricular sensing measurements on a daily basis and to record them as trends over time. This feature can be very useful for inpatient and remote device follow-up. The devices may also be programmed to automatically adjust sensitivity levels according to daily measurements of sensing amplitude. However, when programming automatic sensitivity, care should be taken to limit the upper value (lowest sensitivity) of the sensitivity range, because very low sensitivities (e.g., 5.6 mV for the ventricle) may result from automatic settings. This may lead to undersensing of ventricular premature beats and pacing on their T waves, with a risk of proarrhythmia.

Sensing amplitudes during acutely induced atrial fibrillation have been found to be about a third when compared with sinus rhythm, and even though there was a significant correlation between the amplitudes, interindividual variability was high. Based upon these findings, it is wise to program a 4 : 1 atrial sensing safety margin relative to the atrial sensing amplitude in sinus rhythm in order to detect atrial fibrillation, the signal amplitude of which may decrease with time due to electrical remodeling of the atria. Routine programming of very high atrial sensitivities (e.g., 0.1 mV) may, however, lead to oversensing of high-frequency fragmented signals and to noise reversion ( Fig. 37-8 ).

Atrioventricular Delay

It is important to adequately program the AV delay because this will have hemodynamic consequences by affecting ventricular filling in addition to determining the percentage of ventricular pacing (which will also affect battery longevity). As detailed in Chapter 36 , the paced AV delay is programmed longer than the sensed AV delay, with an offset of around 30 to 50 msec. Default values of AV delays vary between manufacturers but are usually in the range of 100 to 150 msec for the sensed AV delay and 120 to 200 msec for the paced AV delay, and may or may not be rate-adaptive (i.e., shorten at higher rates).

There is ample evidence to indicate that unnecessary ventricular pacing should be avoided to prevent heart failure and atrial fibrillation (see Chapter 13 ). Before the advent of specific algorithms, this was achieved simply by programming a long AV delay, which is of limited efficacy. In a study evaluating patients with sick sinus syndrome, patients with an AV delay programmed to 300 msec still had on average of 18% ventricular pacing. This measure is often ineffective in patients with right bundle branch block (RBBB) as the depolarization wavefront reaches the RV lead late (about 40 to 80 msec after the onset of the QRS complex).

Drawbacks with programming a long AV delay are (1) symptomatic first-degree AV block with “P on T” phenomenon resulting in reduced ventricular filling and increased left atrial pressures (see Fig. 37-3 ), (2) limited maximum tracking rate (due to the total atrial refractory period [TARP]—see Chapter 36 ), (3) proarrhythmia in case of pacing on the T wave, resulting from functional ventricular undersensing when a ventricular premature beat falls during the postatrial ventricular blanking period (PAVB) (see Fig. 37-20 ), (4) endless loop tachycardia (see Fig. 37-41 ), and (5) nonreentrant AV synchrony (see Fig. 37-50 ). Algorithms to avoid ventricular pacing include the ADI(R)/DDD(R) pacing mode and AV hysteresis (see Chapter 13 ). Sorin devices have additional features for AV delay management, which avoid excessively long AV delays at rest and/or exercise, and also limit the maximum duration of pauses to programmable values.

Patients requiring ventricular pacing who have inter-atrial conduction delay are a challenge because they may require programming long AV delays (that are longer than default settings) to avoid left AV dyssynchrony with truncation of the A wave (see Chapter 14 ). Several methods have been used to optimize AV delays in patients with AV block. The Ritter method to calculate the optimal AV interval (AVopt) evaluates transmitral flow using pulsed-wave Doppler and measuring intervals between the onset of the QRS and the end of the A wave (QA interval) with a long (AVlong) and a short (AVshort) programmed AV interval. The formula states that AVopt = AVshort + ([AVlong + QAlong] − [AVshort + QAshort]).

This may be mathematically simplified to AVopt = AVlong − (QAshort-QAlong). The issues with this algorithm are that different AVshort will yield different values for AVopt and that the results may not be reproducible.

Analyzing the surface ECG may be a simpler means of evaluating suboptimal AV intervals. As has been shown for CRT, optimal AV delays may be approximated by evaluating the surface ECG and timing ventricular pacing to about 40 msec after the end of the P wave. This corresponds roughly to another study, which optimized AV delays by timing a delay of 100 msec from the end of the P wave to the peak or nadir of the paced QRS complex (which approximates timing of mitral valve closure).

Routine AV delay optimization in pacemaker patients is not warranted because there is no proof that this affects outcome, but it may nevertheless be useful to evaluate transmitral flow and to check for absence of A-wave truncation if the patient undergoes echocardiography. Standard factory settings are usually appropriate for the great majority of patients unless inter-atrial conduction delay is present (which may be evaluated by a surface P-wave duration of >120 msec).

Electrocardiograms in Patients with Pacemakers

Interpreting surface ECG or Holter recordings in pacemaker patients may be challenging, because simultaneous device telemetry with intracardiac electrograms (EGMs) and marker events are usually not available.

Pacing Pulse Artifacts

Pacing pulses programmed in the unipolar mode are usually readily visible on the surface ECG. The amplitude of the pulse may vary according to the ECG lead because of the orientation of the pacing vector with that lead (much as it does for the P-QRS-T waveforms). However, pacing pulses programmed in the bipolar configuration are often difficult to visualize on the surface ECG ( Fig. 37-9 ). The pacing pulse may be even less visible if artifact filters (e.g., the low-pass 40 Hz filter) are activated. Many modern electrocardiographs and Holter recorders have algorithms, which detect pacing pulses and reconstruct them as spikes on the tracing in order to facilitate interpretation. Although these algorithms may be very useful, one must be aware that they may be inaccurate. Undersensing of the pacing pulse may occur, especially if the sampling rate is not high enough (i.e., the pacing pulse is not detected and a reconstructed spike is not displayed, but the P/PQRS complexes are identical in morphology to those which are clearly paced [ Fig. 37-10 ]). Oversensing may also occur due to artifacts generated by loose electrodes, minute-ventilation pulses, or electromagnetic interference, which may be interpreted as pacing spikes by the electrocardiograph. In a report evaluating automatic recognition of pacing artefacts, 17% of paced ECGs had inaccuracies by the algorithm despite using an electrocardiograph with a high sampling rate.

Paced QRS Morphology

For the QRS complex, pacing from the right ventricular apex or mid/low septum yields a QRS axis in the north-east quadrant (see Fig. 37-9 ). The QRS axis is inferior when the lead is positioned in the right ventricular outflow tract (RVOT). There is no specific ECG feature that is able to reliably identify RV septal pacing. A common misconception is that a negative QRS complex in lead I indicates pacing from the interventricular septum, or is specific for pacing from the left ventricle (LV). However, this is also possible when pacing from the RV anterior free wall (where leads intended for the septum often end up being inadvertently placed). Also, a “pseudo-RBBB” pattern in lead V1 (suggesting LV capture) may be observed in 8% to 20% of the patients during RV pacing. Electrode malposition may in part explain this finding, as it has been shown that placing the V1 and V2 electrodes in the second or third instead of the fourth intercostal space accentuates the phenomenon ( Fig. 37-11 ), but it may also be related to ventricular geometry (e.g., in case of a dilated RV) and scar (producing lines of conduction block). A pseudo-RBBB pattern may also be observed in case of LV capture because of the lead being positioned in a coronary sinus tributary, or if the lead is placed in the LV via a patent foramen ovale or an atrial/ventricular septal defect ( Fig. 37-12 ). Finally, a RBBB pattern may also be observed in pseudo-fusion when there is intrinsic AV conduction in patients with underlying RBBB (see Fig. 37-9 ).