Permanent Cardiac Pacemakers
Carlos Macias
INTRODUCTION
The history of cardiac implantable electrical devices (CIEDs), and specifically cardiac pacemakers indicated for the management of bradyarrhythmias, dates back 60 years to the development of a postoperative external pacing system at the University of Minnesota by Dr Walton Lillehei in collaboration with Earl Bakken, a hospital engineer who later founded Medtronics. The first fully implantable human permanent pacemaker was employed in 1958 when Dr Ake Senning, a thoracic surgeon at Karolinska Hospital in Stockholm, implanted myocardial electrodes and a pulse generator with a rechargeable nickel-cadmium battery in a 40-year-old patient with complete heart block. The first generator lasted 8 hours, and the patient went on to have more than two dozen pulse generator replacements but lived until age 86 years.1,2
It is difficult to imaging modern medicine without these remarkable devices which now number over 1 million implants yearly worldwide with 200,000 in the United States. Implants are projected to continue to increase owing to an aging population, with an estimated 7 million people globally living with CIEDs. Knowledge of the clinical indications, basic function, troubleshooting, reprogramming, perioperative management, risks and complications, new techniques and technologies (physiologic pacing, leadless pacemakers), and future direction of these devices is invaluable for practitioners caring for patients with heart disease.3
TABLE 63.1 Permanent Pacemaker in Sinus Node Dysfunction | ||||
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CLINICAL INDICATIONS
The executive summary from the American College of Cardiology and the American Heart Association guideline for implantation of cardiac pacemakers and anti-arrhythmia devices provides guidance for CIED appropriateness use. Among the most frequently encountered Class I indications in clinical practice are sinus node dysfunction, acquired high-degree atrioventricular (AV) block and tachybrady syndrome. The two most frequent clinical indications remain sinus node dysfunction and acquired high-degree AV block (see Tables 63.1 and 63.2 for guideline recommendations for permanent pacemaker implant).3,4
Cardiac Native Conduction
Intrinsic automaticity is responsible for sinus node cellular depolarization with a subsequent electrical wavefront propagation to the AV node, the bundle of His, and the His-Purkinje system and distally to the right bundle branch and anterior and posterior fascicles of the left bundle branch. Failure at any level interrupts native electrical propagation necessary for normal cardiac contractility and function. A permanent pacemaker system delivers a timed electrical impulse that results
in downstream depolarization, thereby bypassing the region(s) with significant conduction disease.
in downstream depolarization, thereby bypassing the region(s) with significant conduction disease.
TABLE 63.2 Permanent Pacemaker in Acquired Atrioventricular (AV) Conduction Disease | ||||
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PACEMAKER SYSTEM AND BASICS OF PACING
A transvenous pacemaker system is comprised of the pulse generator and the lead(s). The number of the leads gives the device functionality as a single-chamber, dual-chamber (ie, atrium and ventricle), or biventricular pacemaker. The pulse generator is comprised of the battery/energy source, the device circuitry, and the header, which will serve to secure the connection of the lead to the generator. The leads are used for the dual purpose of sensing for intrinsic atrial and ventricular signals and pacing when required. The lead is comprised of the electrode (conductor) with its tip fixation mode (active or passive), the insulation, connection pin, and tie-down sleeves used to secure the lead to the pectoral muscle.
Pacemakers must be able to reliably sense local or near field impulses in a given cardiac chamber (atrium or ventricle). This is known as sensing, which is measured and reported in amplitude as millivolts (mV). For a lead placed in the atrium, the usual atrial sensing amplitude ranges between 1.0 and 5.0 mV, with the majority falling between 2 and 3 mV, which allows for appropriate discrimination of atrial fibrillatory waves and associated device mode switch, will be discussed later. For leads placed in or adjacent to the ventricle, ventricular sensing amplitude ranges between 5 and 15 mV.
Current leads have a bipolar configuration and design but can be programmed to sense and pace in a bipolar or unipolar setting. Bipolar programming is preferred as it decreases the possibility of sensing noncardiac electrical signals causing inappropriate pacing inhibition. A lead programmed in the unipolar setting has the cathode (-) at the tip of the lead and the pulse generator serving as the anode (+), which creates a wider antenna and more susceptible for sensing noncardiac signals. The bipolar lead will have both the cathode (-) and anode (+) located just proximal to the distal end of the lead in the intracardiac chamber which results in a smaller antenna, which is less likely to pick up external electrical potentials. Bipolar leads are the standard of care for newly implanted systems, though some unipolar leads still exist from previously implanted devices. Once a lead is deployed, the stability of the cardiac tissue and lead interface is critical for appropriate and stable sensing and pacing parameters and so, active fixation (deployed helix) is the primary mode of lead delivery to the myocardial tissue for right atrial and right ventricular leads. The use of passive (ie, not active) fixation mechanisms with fixating tines or wings is used in select cases primarily to reduce the risk of cardiac chamber perforation; however, passive leads represent less than 5% of implanted leads in use because of limitations with stability. The exception is the almost exclusive use of passive fixation mechanisms for stability in coronary sinus leads owing to the risk of venous perforation with active mechanisms.1,2,3
FOLLOW-UP PATIENT CARE
The most inquired parameter when discussing pacemaker follow-up care relates to pacing mode and the lower/upper programmed rates.
Programmed Modes and Application
The mode is identified by chamber paced, chamber sensed, response to sensing, rate modulation, and multisite pacing and represented by a combination of three to five capitalized letters (O = none, A = atrium, V = ventricle, D = dual A+V, T = triggered, and I = inhibited). For example, a device programmed DDD will pace both the atrium and the ventricle, sense both atria and ventricle, and based on the sensing will respond with either a triggered (paced event) or inhibited
response to reset the timing for the next pacemaker timing cycle. In comparison, a VVIR programmed pacemaker will pace and sense the ventricle, will be inhibited by a sensed event, and has rate modulation (also referred commonly as rate response) enabled to increase the pacing rate to approximate the appropriate heart rate relative to the activity of the person (Table 63.3).
response to reset the timing for the next pacemaker timing cycle. In comparison, a VVIR programmed pacemaker will pace and sense the ventricle, will be inhibited by a sensed event, and has rate modulation (also referred commonly as rate response) enabled to increase the pacing rate to approximate the appropriate heart rate relative to the activity of the person (Table 63.3).
The VVI mode with or without R (rate response) is reserved for single-chamber ventricular pacemakers in the setting of permanent atrial fibrillation or a dual-chamber system in a person who now has permanent atrial fibrillation without expectation of restoration of sinus rhythm in which case the device can be programmed to a single-chamber mode. AAI mode with a single-chamber device and lead in the right atrium is not frequently implanted in the United States for patients with sinus node dysfunction without AV nodal conduction disease; however, in other parts of the world, it is the preferred mode for isolated sinus node dysfunction (Figure 63.1). However, AAI-DDD programming is frequently employed as a means to primarily pace the right atrium and allow intrinsic conduction to the ventricle to reduce ventricular pacing, which is the ideal programmed mode for those with sinus node dysfunction but intact AV node conduction. All current manufacturers have this programmable feature with a different nomenclature. Although the device is programmed to AAI mode, it surveils for ventricular sensed events following atrial sensing or pacing. If no ventricular sensing is recorded, the device will switch to a DDD mode and scan for native ventricular sensing which, when present, will revert the pacemaker to an AAI mode and scanning for native ventricular sensing starts again. AOO, VOO, or DOO modes are asynchronous pacing for the atrium, ventricular, or both respectably and are rarely used other than for temporary periods such as during electrocautery to prevent oversensing and pacing inhibition and during magnetic resonance imaging.
Rate-Response Programming
Rate-response programming aims at achieving an appropriate rate increase with physical activity and is most beneficial in those with sinus node dysfunction and chronotropic incompetence. This mode is also employed with single-chamber devices with slow ventricular response as a result of atrial fibrillation or complete heart block. Accelerometers embedded in the pulse generator are the most common sensors employed for this purpose, but changes in minute ventilation, thoracic impedance, and cardiac contractility are also employed to assess rate response needs with programmable features on the slope increase and recovery. As noted above, rate response corresponds to the fourth letter of the programmed settings (ie, DDDR).
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