The simplest pacemaker is a single chamber, asynchronous device. The device is usually implanted subcutaneously in the pectoral area, and the lead traverses the subclavian vein with the tip embedded in the chamber wall. Modern day leads are almost always bipolar, which means the signal picked up or delivered by the lead is the difference in voltage between the tip lead and the ring electrode 1–2 cm proximal (Fig. 24.1). Asynchronous pacing is designated as either AOO or VOO, for atrial and ventricular asynchronous pacing, respectively. Such a setting is not used in the long term, since most patients have some degree of intrinsic rhythm, even if it is just an occasional ectopic beat. The pacemaker must detect such events and delay the next pacing impulse accordingly. Inhibition of pacing when the patient is self-generating an adequate rhythm is called “demand” pacing. For a ventricular pacemaker, demand mode would be designated as VVI (demand pacing, where the ventricle is paced, sensing occurs in the ventricle, a sensed event inhibits pacing). There are only a few controls, specifically base rate, pulse amplitude, and pulse duration. The base rate, also referred to as the lower rate limit, will dictate the soonest a paced beat would occur. For example, a base rate of 60 beats per minute (bpm) means a paced beat would occur no later than 1000 msec after the last beat, regardless of whether that last beat was sensed or paced. If the device senses a spontaneous depolarization in the chamber before the timer times out, the timer resets and once again must wait the full interval before an impulse could be delivered. In this example, so long as a sensed beat always occurs before the 1000 msec ran out, there would never be a paced beat. Atrial-only pacing is typically used when there is sinoatrial (SA) node dysfunction, but the conduction system functions normally. Ventricular-only pacing may be found in ICDs when the patient normally has no need for pacing or if there is no point in monitoring or pacing the atrium, for example, if the patient is in chronic atrial fibrillation.

Whenever possible, it is beneficial to maintain synchrony between the atria and the ventricles. The atrial “kick” contributes to ventricular filling, and if the SA node is functioning normally, it would be best to let its activity control the heart rate. This goal is achieved with leads in both the atrium and ventricle. The pacing mode is usually DDD, which requires some explanation. The device first “looks” for an atrial depolarization. If the device is counting down the time to a required ventricular depolarization, then the device expects to see an atrial depolarization no later than the AV delay time before the ventricular depolarization is expected. For example, with a base rate of 60, the device expects to see a ventricular depolarization by no later than 1000 ms after the last ventricular depolarization. If the AV delay is programmed at 150 ms, then the device expects to see a spontaneous atrial depolarization by 850 ms after the last ventricular depolarization. If no atrial depolarization is observed, then an electrical impulse is delivered to the atrium. Regardless of whether the atrium depolarized by itself or by a paced impulse, the device expects to see a ventricular depolarization by no later than end of the AV delay . If it does, the 1000 ms clock is reset and the whole process starts over. If no ventricular depolarization is seen, then an electrical impulse is delivered to the ventricle. Therefore, with a DDD device, there are four possible basic rhythms that could be observed (where A = atrium, V = ventricle, S = sensed, and P = paced; see also Fig. 24.2).

The option of AS-VP is an example of “triggering,” where a sensed beat (in the atrium) “triggers” a ventricular depolarization. AS-VP is also referred to as “tracking” because the pacing impulses to the ventricle follow, or track, the atrial activity. This pattern would be the norm in a patient with complete heart block but a normally functioning SA node. When this pattern is observed, practitioners can be confused because they may see the ventricle being paced at a rate much higher than the base rate. It is not device malfunction: the device is just trying to maintain AV synchrony.

Tracking typically has an upper bound, a rate above which the atrial event will not lead to a paced ventricular beat. In an older, sedentary patient, that “upper tracking rate” might be as low as 120 but would be higher in a more active patient. The determination to pace the ventricle is made on a beat-to-beat basis. If the atrial rate exceeds the upper tracking rate, then the AV delay will be extended in order to pace the ventricle at the upper tracking rate for as long as possible. Eventually, though, an atrial beat will occur too early to permit a ventricular paced beat and the rhythm will mimic Mobitz type I block (pacemaker Wenckebach).

Allowing a device to trigger a ventricular impulse after an atrial sense can lead to undesired tachycardias. Atrial fibrillation or flutter would cause very fast ventricular pacing if the device paced the ventricle after each atrial depolarization. Although the upper tracking rate described in the previous paragraph would limit how fast the ventricle was paced, a better strategy is to break the link between atrial activity and ventricular pacing. This goal is accomplished with a feature referred to as mode switching . If the device detects a very rapid atrial rate, then the device switches its pacing mode, typically to DDI. Note that the third letter indicates that a sensed beat can only inhibit pacing. There is no more “triggering.” Of the four basic rhythms mentioned above, AS-VP is no longer an option. Assuming there is no intrinsic conduction to the ventricle, if the atrium is beating faster than the base rate, the ventricle will still be paced at the base rate (Fig. 24.3).

Another troubling event with the triggering feature is a phenomenon known as pacemaker-mediated tachycardia (PMT) or pacemaker-induced tachycardia (PIT) . In the event a ventricular depolarization finds the conduction system in a non-refractory state, the depolarization could conduct in a retrograde fashion into the atrium. The ensuing atrial depolarization would be detected by the device, and in turn would lead to a ventricular pace after the AV delay (Fig. 24.4). By the time the ventricle depolarizes, the AV node/bundle of His would likely be non-refractory. The (paced) ventricular depolarization would once again conduct in a retrograde fashion to the atrium and the process would repeat. Given typical paced AV delay times, the time for the retrograde conduction and the time to detect the atrial depolarization, the entire cycle commonly takes about 0.5 s and so would result in a heart rate in the 120 bpm range. Prevention of PMT is primarily achieved by PVARP , a feature present in all dual-chamber devices. PVARP stands for post-ventricular atrial refractory period. During PVARP, the device will continue to monitor for atrial depolarization, but will not use an atrial depolarization to trigger a ventricular depolarization. A common programmed duration of PVARP is 250 msec. In the case shown in Fig. 24.4, the retrograde conduction was so slow that the tail end of the retrograde P wave fell just beyond the end of the PVARP , allowing for an atrial sense that could trigger a ventricular depolarization.

When people exercise , the heart rate normally increases to enhance cardiac output. Patients with chronotropic insufficiency may have little or no increase in heart rate with exercise and therefore have significant exertional limitations. The rate-response feature of CIEDs is designed to sense patient activity and ramp up the heart rate accordingly. There are several methods that can be used to sense when the patient is active. The most common method, the accelerometer, is found in almost all devices. A piezoelectric crystal in the device detects movement in the form of acceleration and will increase the pacing rate to a value in proportion to the magnitude of the acceleration, but not above a programmed upper limit. As with all demand pacing, if the patient’s intrinsic rate is higher than what is dictated by the rate-response, then pacing will be inhibited.

Another method for varying pacing rate with activity involves bioimpedance . The resistance (impedance) between a lead tip and the device itself will change with respiration because of the change in lung volume. This measurement provides respiratory rate, and the magnitude of the impedance change is used to reflect tidal volume, hence the method being labeled as a minute ventilation sensor. At present, only pacemakers made by Boston Scientific/Guidant have this specific feature. An alternative bioimpedance method is present in some Biotronik devices. Changes in sympathetic nervous system stimulation of the cardiac muscle cause small changes in lead impedance. These changes are used to increase the minimum pacing rate of the device, with programmable gain and upper rate limits just as with the other rate-response methods.

Rate-response is not used on every patient, but when it is, the three-letter code becomes a four-letter code with an “R” at the end. For example, VVIR would indicate ventricular demand pacing that includes a rate-response feature.

The goal of CRT is to provide for a more synchronized contraction of the left ventricle. In severe left ventricular enlargement and muscle hypertrophy, the left bundle often fails. Left ventricular depolarization must now initiate in the right ventricle, reaching the septum first and then spreading around the left ventricle making the lateral (free) wall of the left ventricle the last to be depolarized. Septal contraction may cause the free wall to bulge out because the free wall is still relaxed. By the time the free wall is at its peak of contraction, the septum is relaxing so the septum bulges into the right ventricle. In short, each wall “ejects” partly into the other wall, and stroke volume is compromised. Placing a pacing lead on the free wall permits most of the left ventricle to begin contraction at the same time. In CRT, it is disadvantageous to permit the native conduction from the atrium to the right ventricle because it may lead to a pattern of depolarization different from one initiated by the right and left ventricular pacing leads. For this reason, the PR interval is deliberately set to a short duration so that the pacing spikes are delivered before any intrinsic activation occurs. The EKG or rhythm strip will reveal nothing but ventricular paced beats, but the observer should not automatically assume the patient is pacing-dependent. There may well be conduction to the right ventricle if the pacing is suppressed, but there is no way to tell just from looking at the EKG.