Cardiac Pacemaker

CARDIAC PACEMAKER

23.3.1 Pacemaker Principles

We have noted previously the differences in stimulation of cardiac tissue in contrast to that of nervous tissue. Basically since the heart is an electric syncytium, excitation in any suitable region readily spreads throughout the entire heart. Furthermore, since the heart is a very large organ, the stimulating electrodes require no special design. And since there is a good separation from other excitable tissue, whatever necessary stimulation thresholds are required (times a safety factor), they can normally be fulfilled without excitation of other organs. The engineering challenges thus lie primarily in areas other than the classical electrophysiology described in previous chapters. These critical areas have to do, mainly, with logical decisions to provide or withhold pulses and/or to adjust their timing to make them as physiological as possible. The following sections are devoted to a description of the various practical aspects of pacemaker design and an elucidation of the points raised above. We consider the following topics:

Control of impulses Site of stimulation Excitation parameters and configuration Implantable energy sources Electrodes.

23.3.2 Control of Impulses

The earliest implantable pacemakers were designed to control the Stokes-Adams syndrome and for this purpose the simplest design is one where the ventricle is continuously stimulated at a safe rate. The pulse generator design required simply the generation of transthreshold pulses at the desired fixed heart rate. A pulse of about 2 ms duration, amplitude (essentially the battery voltage) of 5-8 V, and a frequency of 72 beats per minute were typically used. In general, the electrodes were sutured to the ventricle, and both electrodes and generator were implanted following a thoracotomy. This system has a number of shortcomings. First, it does not respond to the physiological needs for a variable heart rate depending on the body's oxygen requirements. (For example, these increase during exercise). Second, the patient may have only sporadic periods of Stokes-Adams syndrome. By pacing during regular ventricular activation, not only is there an unnecessary drain on implanted batteries but there is no coordination between the artificial stimulus and the naturally occurring one (in fact, this type of stimulation is called asynchronous). One potentially dangerous consequence is that the artificial stimulus might fall into the naturally occurring T-wave vulnerable period initiating tachycardia or fibrillation. Particularly with the advent of integrated circuits it became possible to implant electronics that could sense the presence of an atrial and/or ventricular signal and to respond in an appropriate physiological way. For example, if the pathology is solely complete heart block, then the atrial pulse can be normal. An improved pacemaker design is one that senses the atrial excitation and delivers a ventricular pacing stimuli after a suitable delay (around 0.1 ms). An alternative was to sense the ectopic ventricular excitation, when it occurred. In its presence, an artificial stimulus was inhibited (or timed to coincide with the R wave). In the absence of a ventricular pulse, after a maximum acceptable delay, an artificial ventricular pulse was generated. Such pacemakers were termed a "demand" type. In the mid-1970s pacemakers were being developed with programmable logic of this kind. A nomenclature code was developed to describe the particular logical pacemaker design implemented; this is reproduced in Table 23.2. (Although this code has been superseded by a more sophisticated one, it is still referred to in some current literature, and for this reason is included here.) The code consists of three letters: the first, giving the chamber paced (A = atrial, V = ventricular, and D = both, i.e., dual); the second, the chamber sensed; and the third, the type of response. Thus the asynchronous, fixed-rate, early type with ventricular pacing is simply V00. VVI describes the situation where a ventricular stimulus is inhibited if an acceptable intrinsic ventricular beat is sensed. In VAT, the atrial electrophysiology is normal; thus the atria is sensed and the ventricle triggered (after a suitable delay).

Table 23.2. ICHD nomenclature code for implantable cardiac pacemaker (Parsonnet, Furman, and Smyth, 1974)

Chamber paced Chamber sensed Response Description of mechanism

V 0 0 Fixed-rate ventricular pacing A 0 0 Fixed-rate atrial pacing D 0 0 Fixed-rate AV pacing V V I Ventricular sensing and pacing, inhibited mode V V T Ventricular sensing and pacing, triggered mode A A I Atrial sensing and pacing, inhibited mode A A T Atrial sensing and pacing, triggered mode V A T Atrial sensing, ventricular pacing, triggered mode D V I Ventricular sensing, AV pacing, inhibited

23.3.3 Dual Chamber Multiprogrammable

The continued improvement in technology has made possible the implantation of microprocessors. This, coupled with improved technology, has permitted the placement of sensing/pacing leads routinely in both atria and ventricles. An important aspect of this improvement is in the power source, mainly the lithium battery, which significantly improves the available energy. The result is a much greater repertoire of electrophysiological behavior. An indication of this increased sophistication is the current pacemaker code. This consists of five letters. The first three are similar to the original ICHD code described in Table 23.2. The fourth and fifth letters are described in Table 23.3. These describe two additional functions of implantable pacemakers that have become possible with present technology.

Table 23.3. Fourth and fifth letter of NASPE/BPEG pacemaker code

Fourth letter: Fifth letter: rate modulation antiarrhythmia function

0 = none 0 = none

P = Pacing (anti- P = Simple Programmable tachyarrhythmia)

M = Multiprogrammable S = Shock

C = Communicating D = Dual (i.e., P and S)

R = Rate modulation

Note: First, second, third letters as in Table 23.2 Source: Bernstein, et al. (1987)

23.3.4 Rate Modulation

The natural heart rate is modulated by the sympathetic and parasympathetic central nervous systems. These respond to baroreceptor activity in the cardiovascular system, hypoxia, exercise, circulating catecholamines, and so on. Although it is impossible to devise a system that could respond to all of these, physiological control signals have been introduced that are believed significantly to evaluate the desired cardiac output. These include oxygen saturation (using optical methods), physical body movement, respiration rate, temperature, and so on. The introduction of rate modulation is, in effect, adaptive pacing to achieve more realistic physiological behavior and represents a higher level of sophistication than heretofore available. The goal is to keep the system as a whole in a reasonable physiological state. The fourth position in the NASPE/BPEG Code (Table 23.3) shows R if the system is capable of rate modulation, as described in the previous paragraph. When this feature is not present, this position describes the extent to which the pulse generator's operating values can be modified noninvasively. S (= Simple programmable) refers to the capability of adjusting the rate, output, or both; M (= Multiprogrammable) describes more extensive program capability; and C (= Communicating) the presence of some degree of telemetry. This degree of sophistication implies a multiprogrammable system. Similarly R (= Rate modulation) normally implies some degree of telemetry.

23.3.5 Anti-Tachycardia/Fibrillation

As we have seen, the pacemaker was originally devised to benefit patients with Stokes-Adams syndrome. The design requirements were simple and could be met with a fixed-rate pulse generator (mode V00). With the advent of increasingly sophisticated technology, the pacemaker functions were broadened and extended to patients with such conditions as sick sinus syndrome. An important additional category is patients with malignant tachycardia. These patients have occasional periods of tachycardia which can, if not treated, lead to fibrillation and death. Two main approaches are available. One consists of a set of rapid pacemaker pulses (approximately 20-30% faster than the tachycardia) delivered to the atria or ventricles. This may terminate the arrhythmia. The second approach entails the application of a shock of high energy with cardiac currents comparable to that present with external defibrillation. (A description of defibrillation systems, including implantable defibrillators, constitutes the material of Chapter 24). In the fifth position of the NASPE/BPEG code (Table 23.3), the anti-tachyarrhythmia function of the pacemaker is described. With P (= Pacing), low-energy stimulation (noted above), which is in the form of bursts, is present. S (= Shock) reflects the existence of a high-energy anti-tachyarrhythmia intervention capability for cardioversion or defibrillation. D (= Dual) describes both high- and low-energy intervention. Many believe that permanent pacing for ventricular tachycardia is too hazardous since it can lead to unstable ventricular tachycardia or even ventricular fibrillation. For these possibilities a shock backup presence is deemed essential. (An exception is physician-activated pacing which, in the presence of the physician, is used as an adjunctive therapy for sustained ventricular tachycardia.) For this purpose noninvasive activation is achieved by a magnet or rf telemetry.

23.4 SITE OF STIMULATION

In the early pacemaker models, electrodes were sutured directly to the heart and the wires led to the pulse generators which were placed in a thoracic or abdominal pocket. But to avoid the trauma of a thoracotomy electrodes were increasingly placed in the heart cavities through a transvenous route. (The term transvenous while very popular, is a misnomer since it actually refers to the threading of electrodes through a vein into the right atria and/or ventricle). At present, around 95% of pacemaker electrodes areendocardial. Several veins are and have been used, including, typically, the subclavian, cephalic, and external jugular. The electrodes are manipulated by a stiff stylet wire from the distal end under fluoroscopic visualization. The right atrial electrode is hooked into the right atrial appendage, whereas the right ventricular electrode lies at the right ventricular apex position. The electrode tips are fabricated with tines that lodge in the right ventricular trabeculation and the right atrial appendage for stabilization. (Also, after removal of the stylet wire, the atrial lead curves into a J shape that adds additional stabilization.) The pulse generator is usually placed in a prepectoral location. From an electrophysiological standpoint, the actual location of the ventricular myocardial or endocardial electrode is not important. From the right heart position the activation wave must resemble that in left bundle branch block and reflect mainly cell-to-cell conduction. The hemodynamic consequence is that a satisfactory cardiac output is achieved. Experiments also show that the threshold stimulating currents do not vary widely, suggesting a certain symmetry between current source and depolarization achieved.

(Taken from Jaakko Malmivuo & Robert Plonsey: Bioelectromagnetism - Principles and Applications of Bioelectric and Biomagnetic Fields, Oxford University Press, New York, 1995, available online at http://www.bem.fi/book/index.htm)