Temporary or permanent cardiac pacing, in which an electrical stimulus depolarizes cardiac tissue, is indicated when bradycardia causes symptoms of cerebral hypoperfusion or hemodynamic decompensation. Occasionally, patients with bradycardia-dependent ventricular tachycardia require pacing to prevent the pauses in rhythm that lead to the tachyarrhythmia (Tables 14–5 and 14–6; see Figure 14–7). Although emergency pacing can be accomplished temporarily by transcutaneous pacing systems, in all but the most critical situations, stable temporary pacing is best ensured by the transvenous insertion of electrodes into the right atrium, right ventricle, or both. Permanent cardiac pacing is also usually performed through the transvenous route; in some circumstances, however, epicardial placement of electrodes via thoracotomy or a subxiphoid approach is still used.
Table 14–6. Common Uses for Temporary Cardiac Pacing ||Download (.pdf)
Table 14–6. Common Uses for Temporary Cardiac Pacing
To provide adequate heart rate in patients with symptomatic bradycardia from sinus node dysfunction or advanced second-degree and complete AV block while awaiting definitive therapy
To terminate some supraventricular and ventricular tachycardias by overdrive suppression or entrainment (eg, atrial flutter, monomorphic ventricular tachycardia)
To prevent advanced second-degree and complete AV block in some patients with acute myocardial infarction and in some patients after cardiac surgery (eg, aortic valve replacement)
To prevent bradycardia-dependent ventricular tachycardia
To determine the site of AV block
For evaluation for optimal type of permanent pacing system
Transmyocardial pacing involves the percutaneous placement of cardiac pacing wires into the ventricular cavity or onto the ventricular wall through a transthoracic needle. The reliability of this technique is poor, and it is a highly invasive procedure with significant potential morbidity. Transmyocardial pacing is performed only in an emergency setting, usually during cardiac arrest, when transvenous pacing cannot be accomplished rapidly or when transcutaneous pacing is unavailable or unsuccessful. The reported incidence of successful capture with transthoracic pacing varies from 5% to 90%; typically, it is 21–40%.
Often, however, because of the clinical circumstances in which this type of pacing is used, electrical capture is not followed by mechanical systole. The major complications of transthoracic pacing include myocardial or coronary artery laceration, pericardial tamponade, pneumothorax, and hepatic or gastric damage. Transthoracic pacing should therefore be reserved for situations of the utmost gravity where no other pacing system is feasible or available. External (transcutaneous) pacing should always be tried first, because it is probably as efficacious (if not more so) and is associated with significantly less morbidity. Transthoracic pacing should never be used in awake or stable patients. The technique is now all but obsolete.
This method, in which electrical current is delivered to the heart through the skin via large surface electrodes, is usually reserved for standby prophylaxis in patients recognized to be at high risk for bradycardia, for example during inferior and large anterior wall acute myocardial infarctions (Table 14–7), and in some patients with suspected sinus node dysfunction who are undergoing elective cardioversion. Because of its ease of use and relative efficacy, this pacing modality has virtually eliminated the need for transmyocardial pacing in emergency situations.
Table 14–7. Conditions Considered Risks for Advanced Second-Degree or Complete Atrioventricular Block during Acute Myocardial Infarction ||Download (.pdf)
Table 14–7. Conditions Considered Risks for Advanced Second-Degree or Complete Atrioventricular Block during Acute Myocardial Infarction
Inferior-wall MI, especially if it involves the interventricular septum, posterior wall, and right ventricle, with first-degree AV block; second-degree AV block, type I (usually intra-AV nodal); or second-degree AV block, type II (often intra-His)
Extensive anteroseptal MI, with new bifascicular block with a normal PR interval or with first-degree AV block; second-degree AV block, type II; first-degree AV block with bifascicular block (not known to be old); or alternating bundle branch block1
The transcutaneous pacing system uses two large, low-impedance surface electrodes placed on the anterior and posterior chest walls. A long duration pacing stimulus output of 20–40 ms (not programmable by the operator) and current output of more than 100 milliamperes (mA) (programmable by the operator) are often necessary to overcome the impedance offered by the chest wall, muscle and bone, and intrathoracic structures. The transcutaneous pacemaker paces the ventricle and inhibits its output when it senses spontaneous ventricular electrical activity, thus functioning in VVI (demand) mode (see later section, Permanent Pacing). Because the pacing pulses are 20–40 ms in duration and the current output is large, they create a deflection of high amplitude on the surface ECG recording that should not be confused with QRS complexes. If ventricular depolarization (capture) is occurring, the pacer output pulse will be followed by a QRS complex that is best seen on the pacemaker generator's oscilloscope and strip-chart recording. Significant distortion, or total obscuration, of the paced QRS complex can exist on the bedside rhythm monitor or surface ECG recording. Ventricular capture should always be verified by confirming the presence of a pulse, either through palpation or through visualizing a proper waveform with pulse oximetry or arterial pressure monitoring. Skeletal muscle twitching occurs at a stimulus output of 30 mA, but ventricular capture does not usually occur until 35–80 mA; sedation of the awake patient is usually required to mitigate the painful muscle contractions.
Transcutaneous cardiac pacing can be effective in up to 70% of patients and has its best use in an emergency situation when pacing of short duration is required or as a bridge to permanent cardiac pacemaker implantation. The majority of pacing failures (specifically, failure to capture) occur in patients during the advanced stages of cardiopulmonary arrest. The likelihood of successful transcutaneous pacing in patients with cardiac arrest of more than 15 minutes in duration is approximately 33–45%. Failure to capture can also occur after prolonged (hours to days) pacing and likely represents increases in impedance; repositioning of the electrodes can restore pacing capability.
Temporary Transvenous Pacing
Although transcutaneous pacing offers ease of use, rapid initiation of pacing therapy, and very low complication rates, transvenous pacing is far more stable and better tolerated if pacing is needed for longer than 20–30 minutes. Transvenous pacing is usually performed by placing an electrode catheter in the right ventricle. In rare cases where temporary atrial pacing is also required, catheters can be positioned in the right atrium or in the proximal portion of the coronary sinus.
Venous access can be obtained by several approaches. The internal jugular, subclavian, and femoral veins are all potential sites for introduction of the pacing catheter into the right heart, although the femoral vein is the least desirable due to the potential for pacing lead dislodgement and infection. The median cubital and basilic veins can also be used, but these sites are also associated with a high incidence of lead dislodgement (because of arm motion) and are rarely, if ever, used today.
Prior to obtaining venous access, the existence of a bleeding diathesis or coagulopathy should be excluded or corrected if possible. If this is not possible, the femoral vein should be considered as the initial access site because it is easier to apply pressure and achieve hemostasis in this region if a complication occurs. Other factors, such as the patient's pulmonary status, location of dialysis shunts, previous neck surgery, or radiation therapy should be taken into account when considering the appropriate site for venous access. The presence of a prosthetic tricuspid valve is a contraindication to right ventricular pacing; in this circumstance, left ventricular pacing can be performed by positioning the pacing catheter in the left ventricular veins via the coronary sinus.
There are two main types of transvenous pacing catheters. The flexible balloon-tipped catheter is advanced into the heart in a similar way as a Swan-Ganz catheter, using blood flow to guide it into the right ventricle; it is important to note that during a cardiac arrest, the inflation of the balloon will be useless because of the lack of circulation. The position of the catheter tip within the heart is confirmed either through assessing the electrogram recorded from the pacing catheter tip (negative pole connected to any precordial lead on an ECG machine) or by observing capture of ventricular tissue. Once the catheter tip crosses the tricuspid valve, the balloon should be deflated to allow advancement into the ideal right ventricular apical position. Balloon-tipped pacing catheters can be inserted at the bedside if necessary. The nonfloating, rigid, fixed-curve catheters are easier to manipulate and are more stable once positioned in the right ventricle; because of their rigid design they are typically placed only under fluoroscopic guidance. In general, temporary transvenous pacing lead positioning should be accomplished using fluoroscopy whenever feasible.
Ventricular capture thresholds should be < 2 mA (or < 2 volts [V] with some pulse generators) and ideally < 1 mA (or < 1 V) in stable lead positions and should not change with coughing or deep breathing. Atrial leads are typically less stable, and capture thresholds around 2 mA (or 1–2 V) are acceptable. The presence of myocardial infarction, ischemia, antiarrhythmic drug therapy, hyperkalemia, and other metabolic derangements can increase capture thresholds. Current or voltage output of the pulse generator should be programmed to at least twice capture threshold.
Sensing thresholds can also be affected by myocardial ischemia or infarction, hyperkalemia, and class I antiarrhythmic agents, leading to undersensing (“failure” to sense). Ectopic ventricular depolarizations are often undersensed because of poor intracardiac signal quality. These considerations need to be borne in mind when setting the sensitivity of the pacemaker; inappropriate pacing occurring because of an undersensed QRS complex can initiate ventricular tachyarrhythmias if the pacing stimulus falls on the terminal portion of the QRS complex or T wave.
A daily chest radiograph and paced 12-lead ECG should be obtained and compared with prior studies to check for possible lead migration. Pacing and sensing thresholds should be checked at least daily, with any significant changes being investigated for possible lead migration, lead disconnection from the pulse generator, or change in the patient's clinical status. Pulse generator battery status should be monitored by the appropriate biomedical personnel, and batteries replaced as needed. Temporary leads and access sites should be changed at least every 3 or 4 days to decrease the risk of infection and venous thrombosis.
Although temporary transvenous pacing is relatively low risk, there are potentially serious complications. Complication rates range from 4% to 20% and include pneumothorax, hemothorax, arterial puncture, air embolism, serious bleeding, myocardial perforation, cardiac tamponade, nerve injury, thoracic duct injury, catheter-related arrhythmias, infection, and thromboembolism. The risk of complications is increased if pacing is initiated in emergent situations. To minimize risk, transvenous pacing should be accomplished when the patient is relatively hemodynamically stable. It is important to remember that if the patient has left bundle branch block (LBBB), pacing catheter manipulation in the area of the right bundle branch can result in complete AV block; in these circumstances, transcutaneous pacing should be in place should rate support be required.
Because of the complexity of pacing system design, an identification code has been developed that describes the function of currently available pacemaker generators. The “mode” code consists of three primary letters. The first letter stands for the chamber in which pacing is occurring: A for atrium, V for ventricle, and D for dual, or both. The second letter stands for the chamber in which sensing of the electrical signal occurs: A, V, D, or O for neither. The third letter refers to the mode of response of the generator to the sensed signal: I for inhibited output, D for both inhibited and triggered output that is delivered in response to a sensed signal (eg, a paced ventricular complex delivered in response to a sensed P wave), and O for not applicable. Currently available pacing systems incorporate one or two sensors that allow the pacing rate to increase and decrease with changes in metabolic need; sensor-based pacing systems thus adapt the pacing rate to the activities of daily living. Pacing systems with this feature add an R following the three primary letters (eg, AAIR, DDDR), indicating the existence of rate-adaptive capability. Current pacemakers have numerous functions that can be altered noninvasively by a programmer; such units are described as having multifunction programmability (Table 14–8). Several of the newer temporary pulse generators also have such features.
Table 14–8. Some Programmable Functions and Parameters of Cardiac Pacemakers ||Download (.pdf)
Table 14–8. Some Programmable Functions and Parameters of Cardiac Pacemakers
Standby rate (base rate, lower rate limit): The rate at which the patient is paced unless the spontaneous rhythm is faster
Upper rate limit: The highest rate at which the ventricles are paced 1:1 in response to the atrial rate
AV interval: The interval between the paced or sensed P wave and the delivery of the ventricular pacing stimulus
Atrial refractory period: The time after a sensed P wave or delivered atrial output during which the atrial channel is refractory to electrical signals; the refractory period that follows a paced QRS complex is referred to as the PVARP
Ventricular refractory period: The time after a sensed QRS or delivered ventricular output during which the ventricular channel is refractory to electrical signals
Sensitivity (atrial and ventricular channels): The amplitude of the intrinsic atrial and ventricular depolarizations that are to be sensed
Energy output (atrial and ventricular channels): Volts, current and pulse duration
Modes of function1: AAI, VVI, AOO, VOO, VDD, DDI, DOO, DDD, OOO
Sensor ("on" or "off"): Rate-adaptive programming either activated or deactivated
Sensor-based parameters: Time to achieve peak pacing rate; time to decline to standby rate; criteria for sensor activation
Mode switch ("on" or "off"): Upon sensing an atrial tachyarrhythmia, a DDD(R)1 device will automatically switch to DDI(R) or VVI(R) mode of function, and will automatically switch back to DDD(R) mode upon sensing normal atrial rhythm
Asynchronous Pacing (VOO, AOO, DOO)
In the asynchronous mode of pacemaker function, no electrical signals are sensed, and the pulse generator delivers output pulses without regard to any electrical activity occurring spontaneously within the heart (Figure 14–14). Because the native cardiac rhythm is not sensed, competitive rhythms (paced and native depolarizations) can result. Asynchronous pacemaker generators are no longer manufactured; however, the asynchronous pacing mode can be programmed. Asynchronous pacing also occurs whenever a magnet is placed over an implanted generator in order to evaluate capture function. With a magnet in place, asynchronous pacing and concomitant occurrence of the spontaneous rhythm result in iatrogenic parasystole (Figure 14–15). At the energy output of today's generators (1.5–7.5 V), induction of repetitive ventricular or atrial rhythms is usually not observed, although this possibility exists, especially if myocardial ischemia or electrolyte imbalance is present.
Schematic illustrations of various pacing modes. (See Permanent Pacing section for explanation of symbols.) A, atrial pacing stimulus; P, spontaneous P wave; R, spontaneous QRS; V, ventricular pacing stimulus.
A VVI pacing system. A: Normal sinus rhythm is present. Sensing function is presumed to be normal because no ventricular pacing artifacts are occurring. B: With a magnet in place over the pulse generator, ventricular pacing stimuli are emitted asynchronously, resulting in a rhythm that competes with the sinus rhythm. The large magnitude of the pacing artifacts indicates that the lead configuration is unipolar. The large unipolar stimulus obscures the resulting QRS complex; however, because T waves are present following some of these pacing stimuli, capture is confirmed. Both sensing and pacing functions are normal. F, true fusion complexes, with ventricular depolarization resulting from both sinus and paced impulses. NC, noncapture because of pacing stimuli falling in the refractory period of ventricular muscle; this has been referred to as “functional” noncapture.
Single-Chamber Demand Pacing [VVI(R), AAI(R)]
Both sensing and pacing circuits are present in these units. When a spontaneous intracardiac signal is sensed, VVI and AAI pulse generators will inhibit their output and no pacemaker stimulus artifact will appear. Electrical signals sensed by demand pacemaker generators can originate not only from the heart but also from the environment (electrocautery, cellular telephones, electronic article surveillance systems, tasers), from the patient (muscle potentials), or from the pacing system itself (lead fracture or insulation breaks). Such sensed signals may cause inhibition of output, leading to pauses in paced rhythm; this phenomenon is termed “oversensing” (Tables 14–9 and 14–10), a problem that can generally be corrected by noninvasive programming or, in the case of lead fracture or insulation break, by replacement of the lead. Current generator design and programming capability have not only helped to reduce problems of oversensing but have also simplified their correction.
Table 14–9. Pacing System Malfunctions and Clues to Their Recognition ||Download (.pdf)
Table 14–9. Pacing System Malfunctions and Clues to Their Recognition
Failure to sense (undersensing)
ECG will show earlier-than-expected appearance of pacing-stimulus artifact
Atrial undersensing: Delivery of atrial pacing stimuli despite occurrence of spontaneous P waves; failure to track intrinsic atrial activity at the programmed AV interval
Ventricular undersensing: Delivery of ventricular pacing stimuli despite occurrence of spontaneous QRS complexes
ECG will show inappropriate inhibition of atrial or ventricular output stimuli; oversensing in the atrial channel causes earlier-thanexpected ventricular pacing stimuli
Failure to capture
Pacing stimuli not followed by atrial or ventricular depolarization (assuming muscle tissue is not refractory)
Failure of output
Absence of pacing stimulus outputs, with oversensing excluded
Table 14–10. Causes of Pacemaker Oversensing ||Download (.pdf)
Table 14–10. Causes of Pacemaker Oversensing
Power transformers, power lines; welding equipment; household appliances such as razors and garage-door openers (unusual with today's pulse generators), microwave ovens operating at high power; rotating radar detectors; metal-detector gates (older generation designs); transcutaneous nerve stimulators; cardioverting and defibrillating devices (external or implanted internally); diathermy; lithotriptors; electrocautery; electrocoagulation; MRI; ionizing radiation; tasers; cellular telephones if used on the side ipsilateral to the pulse generator (some models); electronic article surveillance monitors
Physiologic intracardiac signals
R-wave sensing (AAI1 systems), T-wave sensing (VVI systems), P-wave sensing (VVI systems) (unusual)
Physiologic extracardiac signals
Muscle potentials (eg, diaphragm, pectoral)
Signals generated within the pacing system
Conductor-wire fracture causing a voltage transient; insulation defect
Afterpotential sensing of late portions of the pacing stimulus itself (unusual); component malfunction
The pacing function of a demand pulse generator cannot be evaluated if the patient's spontaneous rhythm exceeds the programmed standby (base) rate of the generator. Applying a magnet over the pulse generator converts it to an asynchronous mode of function, and capture (stimulation) of the atria or ventricles by the pacemaker can be confirmed, provided that the pacing stimuli fall outside the refractory period of the cardiac tissue. Conversely, if the patient's rhythm is continually paced, the sensing function of the generator cannot be evaluated. Programming the device to a lower rate may allow the emergence of a spontaneous cardiac rhythm, which should then be sensed, resulting in inhibition of pacemaker output.
Continuous single-chamber ventricular pacing will result in AV dyssynchrony (unless the atrial rhythm is fibrillation). Although the symptoms attributable to bradycardia are alleviated through ventricular rate support from the pacemaker, these may be replaced by symptoms due to AV dyssynchrony, or pacemaker syndrome. Either single-chamber atrial pacing (with intact AV conduction) or dual-chamber pacing is a solution to avoid pacemaker syndrome.
Single-Lead P-Synchronous Pacing (VDD)
These are systems in which electrodes for both the atrium and the ventricle are located on a single lead. The lead is positioned in the right ventricle where the tip electrodes sense and pace the ventricle; atrial electrodes are located on the lead body, at the level of the atrium and only sense, at least at the present time. When the atrial electrodes sense an electrical signal, a ventricular pacing stimulus is delivered after a programmable AV delay that corresponds to the PR interval. If a spontaneous QRS complex occurs, the ventricular output is inhibited. Tracking of the atrial rhythm in a 1:1 relationship allows the ventricular paced rate to change with the sinus rate. The programmed upper rate is the maximum ventricular paced rate that can occur in a 1:1 relationship to atrial activity, and prevents rapid ventricular paced rates should the atrial rate become too fast. If the atrial rate exceeds the programmed upper rate limit, the paced ventricular rate can become irregular because of an electronic Wenckebach protection, can slow to one-half the programmed upper rate limit, or can fall back gradually until 1:1 tracking can resume. This last feature results in disengagement of the tracking function, which causes transient AV dyssynchrony (Figure 14–16).
Schematic illustration of responses from pulse generators at the atrial-driven upper rate limit. The pacemaker will not allow the ventricular paced rate to exceed this programmed upper rate. Atrial rhythms that can exceed the upper rate limit include sinus tachycardia, atrial tachycardia, atrial flutter, and atrial fibrillation. The pacemaker-mediated tachycardia (see text) will also not exceed the programmed upper rate. A: Lengthening of the interval between the sensed P wave and the triggered ventricular-paced complex so as not to violate the upper rate limit (Wenckebach): the P wave that is not followed by a paced QRS complex falls in the refractory period of the atrial channel and is not sensed, resulting in absence (nondelivery) of the ventricular stimulus output. B: In 2:1 block, alternate P waves fall in the atrial refractory period and are not sensed: they are not followed by a paced ventricular event. C: In fallback, the ventricular paced rate gradually slows once the programmed upper rate has been achieved. During the fallback period, tracking of the atrial rate is disengaged, and AV synchrony is no longer present. The ventricular paced rate will again track the atrial rate once the latter falls below the programmed upper rate. The fallback response avoids abrupt decreases in paced ventricular rate. Pacemakers that function in a rate-adaptive mode can have their sensor-based upper rate limit exceed the previously described upper tracking limit.
If no atrial activity is sensed, as occurs in sinus bradycardia, these pulse generators pace the ventricles on demand at the programmed standby rate; atrial pacing does not occur, at least at the present time. Thus, at slow atrial rates, the pacing system behaves as though it were a VVI system, and AV synchrony is lost (see Figure 14–14). Although this pacing system seems ideal for patients with normal sinus rhythm and AV block, atrial bradycardia, which occurs commonly over ensuing years, either spontaneously or as a result of medications, makes the VDD device ultimately suboptimal for most patients.
Dual-Chamber Pacing [DDD(R)]
These pacing systems are capable of sensing and pacing in both the atrium and the ventricle on demand (see Figure 14–14). They therefore approach the physiology of normal AV conduction. The ability to sense retrograde atrial depolarizations can lead to ventricular stimulus delivery and ventricular pacing in response; if the paced ventricular depolarization travels retrograde to the atrium to depolarize it, the process can become repetitive. This event creates an artificial extra-AV-nodal bypass tract, causing a “pacemaker-mediated tachycardia.” Specific algorithms have been designed to terminate these tachycardias and are automatic once they have been programmed.
Dual-chamber devices depend on a stable atrial rhythm for optimum function. Because of their potential for rapid paced ventricular rates, these systems should not be used with atrial arrhythmias such as chronic fibrillation or flutter, multifocal tachycardia, or refractory automatic tachycardia; single-chamber VVI(R) devices should be used instead.
If the atrial tachyarrhythmias are paroxysmal, however, a programmed “mode switch” feature should be programmed on that automatically changes the mode from DDD(R) to either DDI(R) or VVI(R) modes when a rapid atrial rate is detected; this removes the ability to track the atrial rate as long as the atrial tachyarrhythmia persists (Figure 14–17). Studies have established that in patients with bradycardia, compared with ventricular pacing, atrial-based pacing reduces the incidence of atrial fibrillation and may reduce stroke.
Depiction of mode-switch operation of a dual-chamber pacemaker. In the initial portion of the rhythm strip, tracking of atrial fibrillation is occurring, resulting in a rapid paced ventricular rate. When the algorithm in the pacemaker recognizes the atrial tachyarrhythmia, automatic change of mode of function to VVIR takes place, terminating the rapid paced ventricular rate. On sensing restoration of a normal atrial rhythm, the device will automatically restore its dual-chamber mode of operation.
Rate-adaptive pacing systems are appropriate for patients with permanent atrial arrhythmias with slow ventricular response and for patients whose sinus node dysfunction prevents rate acceleration, but who would benefit from an increase in paced ventricular or atrial rates, respectively, in response to increases in metabolic demand. Current sensors measure body motion and acceleration, minute ventilation, QT interval, or intracardiac impedance; sensors to measure other parameters (eg, right ventricular dP/dt [rate of rise of pressure within the right ventricle]) are under development. Changes within the sensor's established parameters, designed to reflect physiologic needs, result in changes in paced rates. Sensor-based pacing rate depends on the individual sensor used, however; for example, if an activity sensor is being used, the paced rate can increase in response to body vibrations that are unrelated to actual physical activity, such as shivering or tremor. This can cause problems in hospitalized patients, especially those in intensive care units. Several manufacturers, therefore, currently incorporate two sensors into their pacemakers to confirm the need for appropriate changes in pacing rate. For example, the activity sensor input can be confirmed by a more physiologic sensor such as minute ventilation, resulting in a more specific and accurate response to the change in pacing rate for the particular change in metabolic need. Recognition of sensor-based pacing and changing pacing rates is necessary to avoid erroneous diagnoses of pacemaker malfunction.
A growing number of studies have reported that right ventricular pacing can be detrimental, especially in patients with left ventricular systolic dysfunction. The left ventricular dyssynchrony caused by pacing from the right ventricle is thought to induce further cardiomyopathy and systolic heart failure due to functional LBBB. Dyssynchrony-induced cardiomyopathy has also been observed in patients with spontaneous LBBB, where abnormal electrical activation can initiate electrical remodeling that leads to myocardial remodeling; this form of cardiomyopathy can be reversed with cardiac resynchronization therapy through biventricular pacing. When there is preexisting cardiomyopathy, biventricular pacing can address the dyssynchrony caused by unavoidable right ventricular pacing.
In patients who do not need continuous ventricular pacing, a new development in dual-chamber pacing design provides various parameters that can be programmed to minimize unnecessary ventricular pacing. The AV delay can be programmed to automatically extend to allow native AV conduction as much as possible. Another programmable solution is managed ventricular pacing (MVP) mode (Medtronic, Inc., Minneapolis, MN) that maintains AAI(R) mode until AV block is detected, at which time it automatically switches to DDD(R) mode; AAI(R) mode is restored when the pacemaker detects resumption of native AV conduction.
The type of pacing system implanted is indicated on an identification card supplied to the patient by the manufacturer; patients should carry these cards with them at all times. It is important to note, however, that such information does not guarantee the operation of a particular mode of function, rate, or any parameter that can be programmed by the patient's pacemaker physician. As pulse-generator design and function increase in complexity, it is best to assume that the pacemaker is performing normally until proved otherwise (there are, of course, malfunctions and “pseudo” malfunctions; these are addressed in the following sections). Similarly, ECGs in paced patients should be considered to reflect normal device function unless they are interpreted otherwise by personnel experienced in pacemaker ECG.
Unipolar and Bipolar Pacing
Unipolar pacing systems have the cathode (stimulating electrode) in the heart and the anode at the generator. The distance between the cathode and anode in these systems results in the inscription of large pacing artifacts whose direction (pacing-artifact axis) in the frontal plane points toward the anode in analog ECG recorders, but not in digital recorders in which stimulus artifact amplitudes and axes vary due to digital sampling of the pacing stimulus (see below).
Bipolar pacing systems have both lead electrodes within the heart, usually less than 1 cm apart, in either or both atrium and ventricle. Either the distal (tip) electrode or the proximal (ring) electrode of the lead can serve as the cathode. Because of the small interelectrode distance, the pacing artifacts are small and their direction in the frontal plane reflects the direction of current flow (Figure 14–18). It is common for the small pacing artifacts to appear to be absent on ECGs and ECG monitoring strips; even computer-interpreted ECGs may fail to indicate that a pacemaker is present. Identification of paced (as opposed to spontaneous) P waves and QRS complexes must therefore be undertaken; often, magnet application with comparison of paced P and QRS morphologies with the initially recorded complexes is necessary to accomplish this.
Bipolar VVI pacing system. All QRS complexes are paced. Note the small magnitude of the pacing artifacts. The simultaneous recordings indicate that in some leads the pacing stimuli are virtually invisible.
In sum, ECGs recorded on digital rather than analog machines can show marked variations in both amplitude and polarity of pacing artifacts. Because the digital equipment samples the pacing stimuli at specific time intervals and then recreates them on paper, the inscribed stimulus artifacts are not seen in real time. In some ECG leads, the pacing stimuli may not be visible at all, raising the questions of spontaneous wide QRS complex rhythms or even failure of generator output. It is important to recognize this recording artifact in patients with pacemakers to avoid an erroneous diagnosis of pacemaker malfunction. It is equally important to document the morphology of paced complexes so that when the pacing stimuli cannot be seen, normal pacemaker function can be assumed until an accurate evaluation can be made.
Some permanent bipolar pacing systems offer lead polarity that can be programmed to unipolar; therefore, the presence of a bipolar lead on chest radiograph does not ensure bipolar lead function, and the ECG appearance of the pacing artifacts may differ from what is expected.
Electrocardiographic Patterns of Paced Complexes
These patterns depend on how the myocardium is depolarized. Paced atrial complexes reflect the sequence of atrial activation initiated by the pacing impulse and thus, in part, the site of the pacing electrode(s). Because the atrial electrodes can be located in the atrial appendage or screwed into any portion of atrial tissue, paced P wave contours and axes will vary.
Pacing from the right ventricular apex produces paced QRS complexes that have a LBBB configuration (reflecting right ventricular myocardial depolarization before left ventricular depolarization) and a superior mean frontal plane axis (the apex of the heart is depolarized before the base; Figure 14–19). Paced QRS complexes usually have a duration of 120–180 ms; if they are substantially longer, intrinsic myocardial disease, hyperkalemia, or antiarrhythmic drug therapy (eg, amiodarone) should be suspected.
Atrioventricular pacing with ventricular pacing from the area of the right ventricular apex, yielding superiorly directed paced QRS complexes with a left BBB pattern. The paced P-wave morphology and axis are similarly determined by the location of the pacing lead tip.
Pacing from the right ventricular outflow tract also results in QRS complexes that have a LBBB pattern, but the mean frontal plane axis is inferiorly directed (the base of the heart is depolarized before the apex). Occasionally, pacing from the interventricular septum can result in paced QRS complexes that show an indeterminate conduction delay pattern; they can even be narrow and relatively normal-appearing. This reflects almost simultaneous activation of both the right and left sides of the interventricular septum.
Pacing from the left ventricular epicardium produces paced QRS complexes having a right BBB pattern, reflecting left ventricular myocardial activation in advance of right ventricular activation. The mean frontal-plane QRS axis will depend on the location of the epicardial electrodes relative to each other (bipolar system) or to the pulse generator serving as anode (unipolar system).
Over the last decade, left ventricular pacing has been accomplished from the coronary veins approached via the coronary sinus. This technique is used along with simultaneous, or near simultaneous, pacing from the right ventricle in patients with advanced heart failure and wide QRS complexes (≥ 120 ms) in order to “resynchronize” ventricular depolarization-contraction. The biventricular-paced QRS complexes can be narrower and more normal-appearing than the patient's spontaneous QRS complexes, reflecting electrical resynchronization and suggesting a beneficial result of this therapy; electrical synchrony, however, does not necessarily correlate with mechanical synchrony, and a persistently wide QRS complex does not predict failure of therapy. The mean frontal plane axis of the paced complexes will vary with the location of the electrodes. Because the timing of the two ventricular leads can now be programmed separately, and either lead can be activated first by up to 80 ms, biventricular paced QRS complexes can be preceded by tightly coupled double-pacing artifacts (Figure 14–20).
Lead II and V5 in patient with a biventricular pacing system, programmed with a VV timing set to LV first by 60 ms. Two distinct ventricular stimulus output artifacts are seen tightly coupled at the onset of the paced QRS complex, following a sensed P wave.
Spontaneous QRS complexes occurring in patients with pacemakers often show marked T-wave inversion (Figure 14–21). This phenomenon has been explained as “T-wave memory” or the temporary persistence of abnormal repolarization “learned” by the myocardium during pacing. The ECG abnormality should not be interpreted as acute or chronic myocardial disease (including ischemia and infarction) in the absence of clinical indications.
Twelve-lead electrocardiogram in patient with a DDD pacing system, temporarily programmed to a rate of 30 bpm to permit emergence of the native rhythm. The intrinsic rhythm is sinus with complete atrioventricular (AV) block and right bundle branch block. Because no pacing artifacts are occurring, sensing function is normal in both atrium and ventricle. The deeply inverted T waves in the inferior and precordial leads represent a nonspecific abnormality commonly observed in patients with pacemakers; they do not represent myocardial injury.
Pacemakers and Magnetic Resonance Imaging
Traditionally, magnetic resonance imaging (MRI) has been contraindicated in patients with pacemakers. This is based on a number of observed deleterious effects that the strong magnetic field can have on a pacemaker and on a handful of reported deaths possibly associated with MRI scanning. Potential effects range from activation of rate-adaptive sensors causing rapid pacing rates to reverting of the pacemaker generator to a default mode and settings. There is also concern that the magnetic field can induce movement of current in the pacemaker lead, leading to heating at the lead tip-tissue interface with acute rises in capture threshold; in a pacemaker-dependent patient, critical loss of capture could then ensue.
There are instances where the benefits of MRI scanning (eg, early detection of cancer, imaging of the brain) need to be weighed against the potential risks to the patient with a pacemaker. Protocols have been established by different institutions that allow for non–pacemaker-dependent patients to undergo MRI scanning under close observation after making temporary programming changes that will minimize interaction with the magnetic field. Pacemakers implanted in the last 10 years have advanced electromagnetic interference protection that decreases the likelihood of encountering a problem. Pacemakers and leads that are Food and Drug Administration–approved to be used with MRI have recently become available, and MRI compatibility is projected to eventually become a standard feature of pacemakers in the future. MRI compatibility should be part of the discussion with patients prior to pacemaker implantation, and the choice of pacemaker type should be a factor, especially if there are underlying conditions that will likely require future MRI scans (eg, history of cancer, orthopedic problems, neurologic abnormalities).
Pacing System Malfunctions
Pacing system malfunctions fall into four general categories: (1) undersensing, or “failure” to sense; (2) oversensing, or the sensing of unwanted signals; (3) failure to capture and stimulate myocardial tissue; and (4) failure of output. Undersensing of cardiac electrical signals because of poor intrinsic signal quality does not represent sensing failure as such, but rather the inability to detect the suboptimal signal itself; undersensed P waves and QRS complexes are not rare. Premature ventricular complexes (see Table 14–9; Figure 14–22) generate suboptimal signals because they originate from within the myocardium, away from the normal conduction apparatus; they can occur in patients without structural heart disease, during acute myocardial ischemia and infarction, or as a result of drug toxicity and electrolyte imbalance. Undersensed P waves can be caused by changes in atrial volume, ectopic atrial rhythms, or retrograde atrial depolarizations. Undersensing of spontaneous complexes and consequent failure to inhibit output results in the delivery of an earlier-than-expected pacing stimulus, which can, on occasion, induce repetitive rhythms.
Failure to sense spontaneous ventricular complexes in a patient with a VVI pacing system. Because the signal quality of depolarization originating in ventricular tissue is often poor, this is not uncommon. Repetitive ventricular beating induced by the stimulus-on-ST complex is, however, rare in stable patients.
Ventricular pacing artifacts can sometimes occur after the onset of spontaneous QRS complexes that have a right BBB configuration, raising concern of undersensing. This happens because of delayed conduction in the right bundle branch: the wavefront of ventricular depolarization does not reach the lead electrode in the right ventricle (especially the apex) in time to inhibit the output of the pacing stimulus. This phenomenon of stimulus delivery within a QRS complex, called “pseudofusion” (as opposed to true fusion), may also be observed in patients with inferior and right ventricular myocardial infarction and is probably due to the conduction delay resulting from ventricular scarring. The same principles apply to patients who have a left ventricular epicardial electrode and either underlying LBBB or ventricular scarring and to patients who have a right atrial electrode and an intra-atrial conduction delay. Undersensing in these cases is due to intrinsic conduction system disease rather than to a malfunctioning unit. The problem is managed by extending the programmed AV delay (in the case of ventricular pseudofusion), programming a higher sensitivity, or if necessary, increasing the pacing rate to overdrive the native rhythm.
Oversensing refers to sensing of unwanted electrical signals such as T waves, myopotentials, and environmental signals (eg, electrocautery; see Table 14–10). Programming the pulse generator to sense only electrical signals of larger magnitude will often solve the problem. When a programmer is not immediately available, placing a magnet over the pulse generator will temporarily eliminate the oversensing by converting the generator to a nonsensing asynchronous mode. Because competitive rhythms with the magnet in place can induce ventricular tachyarrhythmias, these patients should be in a monitored unit.
Failure to capture exists when pacing stimuli do not depolarize nonrefractory myocardium (Figure 14–23; Table 14–11). This condition may result from poor electrode position; a subthreshold programmed output; output reduction due to battery depletion; or an increase in myocardial stimulation threshold that usually results from acute myocardial infarction, drug toxicity, electrolyte imbalance, cardiopulmonary resuscitation, or fibrosis at the electrode-tissue interface. Pacemaker noncapture can be managed by noninvasive programming of the generator's energy output (voltage and pulse duration), surgical repositioning of the lead, or generator exchange, depending on the underlying problem.
Failure to capture and sense in a patient following cardiac arrest; a temporary transvenous pacing system had been placed in the right ventricular apex. The QRS complexes are spontaneous and occur at a severely slow rate; they do not follow pacing stimuli.
Table 14–11. Causes and Management of Pacemaker Noncapture ||Download (.pdf)
Table 14–11. Causes and Management of Pacemaker Noncapture
Tissue refractoriness: Verify capture during temporal opportunity
Lead dislodgement: Reposition lead, or program lead polarity
Increase in myocardial stimulation threshold: Program higher energy output; treat underlying cause if possible
Lead-insulation break: Repair or replace lead; unipolarize lead
Conductor-wire fracture: Replace lead
Inappropriately low programmed output: Program higher output
Generator end of life: Replace generator
The difference between failure to capture (stimulus artifact is present) and failure of output (lack of stimulus output when such output is expected and indicated) should be recognized. If the pacing stimulus has not been delivered (Table 14–12), capture cannot be ascertained. Applying a magnet will aid in determining the cause for the lack of stimulus output. Asynchronous pacing will result with magnet application if the lack of pacing stimulus output results from inhibition due to oversensing. If there is a true problem with delivery of a stimulus output, no stimulus output and therefore no paced complexes will be seen despite magnet application. The main causes of failure of output are battery depletion and generator component failure. This is to be distinguished from the situation when pulse generator output is occurring normally but the current is not reaching body tissues to depolarize it, due to lead fracture or insulation break, and loose set screw (loss of connection between the lead connector pin and the pacemaker generator). Management of pacemaker failure of output will require replacement of the generator, whereas lead problems usually require lead replacement, and loose set screws are addressed merely by restoring a good connection between the lead connector pin and the generator.
Table 14–12. Causes of Absence of Pacing Stimulus Output and Response to Magnet Application ||Download (.pdf)
Table 14–12. Causes of Absence of Pacing Stimulus Output and Response to Magnet Application
|Cause||Response to Magnet|
Normal inhibition by P waves and QRS complexes
Pacing stimuli will be delivered asynchronously
Pacing stimuli will be delivered asynchronously
Pacing stimuli may not be seen if the break in the wire is complete (current does not reach body tissues); may be seen as multiples of a basing pacing rate, or may be seen intermittently (make–break circuit); may have variable amplitude
Lead–generator disconnection or improper connection
Same as for lead fracture
Battery failure (end of life)
Pacing stimuli at slow rate, no visible pacing stimuli, noncapture, failure to sense
Battery component failure