CARDIAC PACING IN BRADYARRHYTHMIAS^2,3

ELECTRODES

UNIPOLAR (Figure 19.1)

The pacing lead has only one conducting wire and electrode. Electric current returns to the pacemaker via the body fluids. A unipolar lead is rarely used for temporary pacing, as a skin electrode is also needed for the return current pathway, which may cause muscle twitching. Unipolar systems are sometimes used for permanent pacing. Oversensing of electromagnetic interference (EMI) or skeletal muscle potentials may be a significant problem.

Figure 19.1 Unipolar pacing lead. P, pacemaker.

BIPOLAR (Figure 19.2)

A bipolar lead has two conducting wires surrounded by a layer of insulation. Electric current travels down one wire to an electrode (usually the distal), passes through cardiac tissue to cause depolarisation, and returns to the pacemaker via the second electrode. Inappropriate sensing of EMI or myopotentials is uncommon. Bipolar pacing is the method of choice for temporary pacing. If one limb fails, a bipolar system can be converted to a unipolar system (see Figure 19.1) by connecting the other limb to one pacemaker pole (usually positive). The other pole (usually negative) is connected to an electrocardiogram (ECG) skin electrode to complete a unipolar pacing circuit.

Figure 19.2 Bipolar pacing lead. P, pacemaker.

SPECIFIC PACING MODES

The three-position code (Figure 19.3) is adequate to describe emergency temporary pacing and most forms of permanent pacing in the intensive care unit (ICU) (Table 19.2).

Figure 19.3 Examples of pacemaker modes and their three-position (letter) codes. P, pacemaker; S, sensing.

SINGLE-CHAMBER PACING

1 AOO and VOO (asynchronous atrial and ventricular) pacing. There is no ability to sense cardiac activity (Figure 19.4). Such pacing is virtually obsolete, except in some pacing emergencies (see later).

2 AAI (atrial demand) pacing. This is indicated for sinus bradycardia provided AV conduction is intact (to maintain AV synchrony).

3 VVI (ventricular demand) pacing (Figure 19.5). This is the most commonly used mode and the mode of choice in life-threatening bradyarrhythmias. Spontaneous cardiac rhythm is sensed, and there is minimal danger of pacemaker-induced ventricular tachyarrhythmia (Figure 19.6). AV synchrony is, however, lost and there is no ‘speed-up for need’.

Figure 19.4 Fixed-rate ventricular pacing VOO. P, pacemaker.

Figure 19.5 Ventricular demand pacing VVI. P, pacemaker; S, sensing.

Figure 19.6 Non-sensing of QRS (see first two beats). Pacing spikes (arrows) fall on the T-wave with subsequent pacemaker-induced ventricular tachycardia.

DUAL-CHAMBER PACING

Two sets of electrodes are required (atrial and ventricular).

DVI (AV SEQUENTIAL) PACING

Atria and ventricles are paced in sequence (Figure 19.7). After a stimulus is delivered to the atrium, there is a delay and an impulse is then delivered after atrial stimulation, to the ventricles. If AV conduction is successful, the ventricular output of the pacemaker is inhibited; otherwise the ventricle is paced. The advantage of this mode is that the atria and ventricles usually contract in sequence. To maintain AV synchrony in the absence of atrial sensing, the pacemaker discharge rate must be greater than the spontaneous atrial rate; asynchronous atrial pacing can precipitate AF. Self-inhibition (‘cross-talk’) can occasionally occur, that is, inappropriate detection of the atrial pacing stimulus by the ventricular channel. If there is no escape rhythm, asystole may result. DVI pacing is indicated when there is impaired AV conduction with an atrial bradycardia. It is of no value when atrial tachyarrhythmias are present.

Figure 19.7 Atrioventricular sequential demand pacing DVI. P, pacemaker; S, sensing.

VDD (ATRIAL SYNCHRONOUS VENTRICULAR INHIBITED) PACING

This mode paces only the ventricle. Sensing takes place in both atrium and ventricle. A sensed P-wave triggers ventricular pacing. VDD pacing is used in some permanent pacemaker systems as a single-lead system capable of pacing the ventricle in response to atrial sensing (from an electrode situated in the intra-atrial part of the lead) with ventricular electrodes at the apex of the RV.

DDD PACING

There is pacing and sensing in both chambers (Figure 19.8). An atrial impulse will trigger a ventricular output and simultaneously inhibit an atrial output. If the impulse is conducted normally to the ventricle, the ventricular output is then inhibited, as with the DVI mode. Upper rate-limiters prevent the pacemaker from following excessive atrial activity with paced ventricular responses. DDD pacemaker function depends on the underlying cardiac rhythm:

1 atrial bradycardia with intact AV conduction – atrial pacing

2 normal sinus rhythm with high-degree AV block – tracking of P-waves with synchronised ventricular pacing

3 sinus bradycardia with AV block – pacing the atria and ventricles sequentially

4 normal sinus rhythm and AV conduction – inhibition of both atrial and ventricular pacing

Figure 19.8 DDD pacing. P, pacing; S, sensing.

Self-inhibition can be prevented by introducing a ventricular blanking (refractory) period coinciding with the atrial pacing stimulus. With DDD and VDD pacing, re-entry pacemaker-mediated ‘endless-loop’ tachycardias are possible.⁷ These are commonly initiated by a ventricular premature beat (Figure 19.9) conducted retrogradely to the atria, where it is sensed and ventricular pacing is triggered with an endless loop: the circuit’s anterograde limb is the pacemaker, and the retrograde limb is via the AV node. Conversion to asynchronous (non-sensing) mode or DDI or increasing the postventricular atrial refractory period (PVARP) will prevent endless-loop tachycardia.

Figure 19.9 Pacemaker-mediated ‘endless-loop’ tachycardia: (i) under normal conditions (first beat) there is no conduction from the ventricles to the atria because of ventriculoatrial block or because the atrial and ventricular impulses collide and extinguish each other in the atrioventricular node; (ii) if a ventricular premature beat (VPB) is conducted retrogradely to the atria (second beat), inducing an inverted ‘p’-wave, this may be sensed by the pacemaker (P) which then triggers a ventricular paced beat (third beat); (iii) if the paced ventricular beat is then retrogradely conducted from the ventricle to the atria and sensed, an ‘endless loop’ may occur (beats 4, 5); that is, pace ventricle VA conduction ‘p’ wave (sensed) ventricular pace, and so forth.

DDI PACING (AV SEQUENTIAL, NON-P-WAVE SYNCHRONOUS)

Sensing occurs in both atria and ventricle, but sensed atrial events do not trigger ventricular pacing. This mode prevents endless-loop tachycardias or tracking of SVTs. It is also useful in patients with SA node dysfunction and episodes of atrial tachyarrhythmias, although DDD (R) with mode switching (ability to change to DDI, DDIR, DVI or DVIR with the onset of an atrial tachyarrhythmia) is preferable. During atrial tachyarrhythmias, the DDI pacemaker will simply pace the ventricle at its back-up rate and not track the tachycardia.

HAEMODYNAMICS OF CARDIAC PACING

In the normal heart, cardiac output increases three- to fourfold during exercise, due mainly to increased heart rate and increases in stroke volume. Atrioventricular synchrony – the normal activation sequence of the heart in which the atria contract first and then, after an appropriate delay, the ventricles contract – contributes only about 20% of cardiac output.⁸ Thus the ability of pacemakers to increase heart rate is paramount, although AV synchrony may on occasions be vital (e.g. in low-cardiac-output states). Many permanent pacemakers are rate-adaptive. When temporary pacing is used, the arbitrary back-up rate of 70–80 beats/min may need to be increased if oxygen delivery is inadequate. For life-threatening bradyarrhythmias, increasing heart rate with VVI mode pacing is the treatment of choice. Permanent VVIR pacing (most commonly using an activity or respiration sensor) will allow heart rate modulation. However, in the ICU, adaptive rate changes may not occur. For example, no activity will be sensed in a patient with septic shock, even when the cardiac output is low.

During VVI and VVIR pacing the atria and ventricles beat independently and AV synchrony is lost. Occasionally this can have deleterious effects and cause a ‘pacemaker syndrome’.⁹ The pacemaker syndrome is, however, a complex of clinical signs and symptoms associated with loss of AV synchrony. A fall in blood pressure coinciding with the onset of ventricular pacing is consistent with the pacemaker syndrome. It was initially recognised with VVI pacing but can occur with any pacing mode if there is AV dissociation, and can be compared to the effects in patients with complete heart block and AV dissociation. The atria contract against closed AV valves with significant regurgitation of blood into the pulmonary and systemic circulation. Blood pressure, stroke volume and cardiac output may fall. The pacemaker syndrome can be eliminated by restoring AV synchrony.

Emergency and long-term haemodynamic effects of DDD or AAI pacing are generally superior to VVI pacing. In studies of patients with permanent pacing, there is a consistent lower mortality with DDD or AAI pacing compared to VVI pacing, and a significantly lower incidence of AF.² DDD and/or DVI pacing requires two pacing leads, one each in the RA and RV. Under appropriate conditions AAI and DVI pacing provide AV synchrony but not rate adaptation. DDD pacing will usually ensure AV synchrony and heart rate responsiveness, provided the SA node is normal.

Dual-chamber pacemakers require the AV interval to be set as close as possible to the normal P-R interval (140–200 ms). Traditionally, the pacing AV interval is arbitrarily set at about 150–200 ms. If interatrial conduction time (between the RA and LA) is significantly prolonged, the LV may contract before or at the same time as the LA, causing DDD pacemaker syndrome¹⁰ with decreased stroke volume and cardiac output (due to LA contraction against a closed mitral valve). Hence, if there is evidence of inadequate cardiac output or impaired oxygen delivery, the AV interval may need to be increased appropriately, or optimised using thermodilution cardiac output or echocardiographic techniques at various AV intervals.

INDICATIONS FOR CARDIAC PACING IN BRADYARRHYTHMIAS

ELECTROMAGNETIC INTERFERENCE

Any signal that can be sensed by the pacemaker, or ICD, constitutes EMI and can cause pacing problems such as failure to pace (inappropriate sensing), asynchronous pacing (‘safety pacing’ when excess ‘noise’ is detected), pacemaker reprogramming and occasionally damage to the pacemaker (DC shock, diathermy) or the heart itself. The most important source of potentially harmful electromagnetic radiation in hospitals is magnetic resonance imaging (MRI). MRI is generally considered to be contraindicated in patients with a pacemaker or ICD. Recently, several studies have demonstrated the potential for MRI to be performed in pacemaker or ICD patients.²⁰ The risks presented by MRI must be outweighed by the diagnostic benefit of this powerful imaging modality on a case-by-case assessment.

In critically ill patients, potential EMI sources include DC shocks, diathermy and possibly mobile telephones. In general, mobile telephones, especially analogue systems, are reasonably safe. Digital telephones have a greater theoretical risk for EMI and it is recommended that telephones do not come into close contact with the pacemaker, for example the mobile telephone should not be rested on the skin over the implanted device. If there is any doubt the pacemaker (or ICD) should be checked and reprogrammed.

CARDIOVERSION/DEFIBRILLATION IN PATIENTS WITH A PERMANENT PACEMAKER (OR ICD)

Place paddles in the anterior–posterior position, at least 10 cm from the unit. Make sure a suitable programmer is available and check the pacemaker (or ICD) afterwards. In patients with a temporary transvenous pacemaker, keep the external unit and the leads well away from the paddles.

DIATHERMY

Bipolar diathermy should be used whenever possible. When diathermy is used in pacemaker-dependent patients, it may be safer to change the mode to asynchronous pacing. This can be achieved in permanent pacemakers by reprogramming the pacemaker: close liaison with the patient’s cardiologist is very important. In an emergency (e.g. asystole in a patient whose pacemaker is inhibited by diathermy), placing a magnet over the permanent pacemaker will usually result in a fixed-rate mode. Modern pacemakers may not be magnet-responsive, but they are also less likely to be affected by diathermy. Patients with temporary transvenous pacing can be switched to VOO or DOO mode. ICD devices should be switched off before diathermy is used. In contradistinction to pacemakers, placing a magnet over the ICD will deactivate the unit, although pacing functions will not be altered. After surgery the pacemaker or ICD should be tested and reprogrammed appropriately.

TECHNIQUE OF TEMPORARY TRANSVENOUS PACING

VENTRICULAR PACING

A sterile technique is mandatory. In emergencies, transcutaneous pacing (VVI) is used first while transvenous VVI pacing is being prepared. A bipolar lead introduced under fluoroscopic control is most commonly used.

Percutaneous insertion via the right internal jugular vein probably offers least complications with ease of manipulation and stability of the lead. The infraclavicular (subclavian vein) approach allows more freedom for patient arm movement. Antecubital veins are associated with lead instability and thrombophlebitis. The femoral vein is best avoided except in patients who have received thrombolytic agents, because of problems with sterility and increased risk of deep-vein thrombosis. The pacing lead is introduced using the Seldinger technique and manipulated under fluoroscopic control to the apex of the RV (Figure 19.10). After the lead has been manipulated to a satisfactory position, a chest X-ray should be obtained to exclude pneumothorax and to confirm adequate lead positioning. The lead should be sutured to the skin at two different sites: one where the lead exits the skin, and a second to a loop formed with the lead. Occasionally, transvenous RV pacing may not be feasible, owing to the presence of a prosthetic tricuspid valve or a congenital anomaly.

Figure 19.10 Characteristic appearance of temporary transvenous pacing leads ideally positioned in (a) the right atrium (right atrial appendage) and (b) apex of right ventricle.

DUAL-CHAMBER PACING

Modern external pacemakers are available (Figure 19.11) which will pace in all modes. These units are small, easy to use and can fit into a small pouch suitable for mobile patients.

Figure 19.11 External pacemakers. Medtronic, Inc. (i) Model 5388 (dual-chamber); (ii) model 5348 (single-chamber). Both are capable of rapid pacing for certain tachycardias (see text).

TESTING THE PACING LEADS

Pacing threshold and sensing should be tested adequately using the external pacemaker.

Pacing Threshold

The lead is attached to the external pulse generator with the distal electrode connected to the negative pacemaker terminal. The cardiac chamber is then paced at 5–10 beats/min faster than patient heart rate, while the pulse generator’s output is slowly decreased until consistent capture outside the myocardial refractory period is lost. Threshold testing is always performed at an identical pulse duration, usually 0.5–1.0 ms. Ideally, ventricular pacing threshold should be 1.0 mA and the atrial threshold 2.0 mA. Pacemaker output is usually set at 2–3 times pacing threshold and always > 3 mA to allow a reasonable safety margin. After acute myocardial infarction the amplitude must not be set higher than necessary, as inadvertent pacing during the vulnerable period of the cardiac cycle may result in VT or ventricular fibrillation (VF).

Sensing

A pacemaker senses the potential difference between the two pacing electrodes. The amplitude of the ventricular signal is commonly 5–15 mV and the atrial signal 2–5 mV. Modern external pacemakers can sense signals as small as 0.8 mV for the ventricle, and 0.4 mV for atrial depolarisation. Before testing the sensitivity, pacing output is set at zero, thereby avoiding potentially dangerous competition between the pacemaker and the spontaneous cardiac rhythm. Pacing rate is then set lower than the spontaneous rate of the tested cardiac chamber, and the pacemaker sensitivity is decreased until there is competition between paced and spontaneous cardiac rhythms. The pacemaker sensitivity is then set at twice that value. This involves reducing the numerical sensitivity value (e.g. changing sensitivity from 2.0 to 1.0 mV will double the sensitivity). Testing pacemaker sensing should not be attempted in pacemaker-dependent patients.

Assessment of sensing is important, particularly in inferior infarction with RV involvement, when the intracardiac ventricular signal may be very small and not sensed. This resultant competition between pacemaker and spontaneous cardiac rhythm can initiate VT (see Figure 19.6) or VF.

COMPLICATIONS OF TEMPORARY PACING²¹

Temporary transvenous pacemaker insertions should have a low complication rate. There are, however, problems when inexperienced and/or inadequately trained operators insert the pacing lead. Several studies from the UK report complications in a third to a half of all cases.^22,23 Temporary pacing involves two components: (1) obtaining central venous access; and (2) intracardiac placement of the pacing lead. Complications include:

FAILURE TO PACE

A life-threatening situation may arise if the pacemaker suddenly fails. The following is an ordered approach to such an emergency:

PACEMAKER PROGRAMMING

An external programmer emits signals capable of changing (‘programming’) various pacing parameters (Table 19.4). Virtually all modern permanent pacemakers are capable of programming rate, voltage, output, pulse width, sensitivity, mode and AV interval. Programmability is also helpful in assessing various pacemaker problems. The pacemaker format best suited to a particular patient’s needs may change with time, and programmability enables optimal pacemaker function to be achieved, i.e. ‘prescribed’. Pacing changes may be indicated under certain circumstances, for example, decreased pacing rate in a patient with angina or acute myocardial infarction to reduce myocardial oxygen consumption, or increased rate in a patient with haemorrhagic shock.

Table 19.4 Multiprogrammable permanent dual-chamber pacemakers

CARDIAC PACING IN TACHYARRHYTHMIAS

Certain tachyarrhythmias may be treated safely and effectively by rapid pacing and/or premature electrical stimulation. These include:

AVNRT and AVRT rarely require rapid atrial pacing as treatment with drugs such as adenosine or verapamil is usually successful. Atrial flutter, however, is often resistant to drug therapy, and rapid atrial pacing will usually convert it to sinus rhythm. When unifocal atrial tachycardia is associated with an atrial re-entry circuit, rapid atrial pacing will often revert this arrhythmia; conversely, when due to automatic focus discharging at a rapid rate, the arrhythmia is usually incessant and will respond only intermittently, if at all, to atrial pacing. Occasionally, dual-chamber pacing with a short AV interval can be used to prevent drug-resistant AVNRT or AVRT. Rapid continuous atrial pacing can be used to slow ventricular rate during resistant SVTs associated with a rapid ventricular response, by inducing AF and a high degree of AV block. Sustained VT is responsive to rapid ventricular pacing, but this should not be used for very rapid ventricular rates (e.g. > 300/min), or when severe haemodynamic compromise is present, as immediate DC cardioversion is indicated. Rapid cardiac pacing may at times have advantages over DC cardioversion (Table 19.5) and drug therapy (Table 19.6), but is of no value in sinus tachycardia, AF and VF (Table 19.7).

Table 19.5 Pacing versus cardioversion for the treatment of tachyarrhythmias

Table 19.6 Pacing versus drug therapy for the treatment of tachyarrhythmias

Table 19.7 Indications for rapid cardiac pacing in suitable arrhythmias

SUPRAVENTRICULAR TACHYARRHYTHMIAS

The pacing lead is manipulated to a suitable position in the RA. Atrial pacing is started at a slow rate (e.g. 60–80/min) and slowly increased to about 10–20% faster than the spontaneous atrial rate. Inadvertent ventricular pacing, especially at rapid rates, must be avoided. The atrium is paced for about 30 seconds and the pacemaker is then switched off. Normal sinus rhythm should ensue (Figure 19.12). If not, the pacing lead is manipulated to a different position and/or a faster pacing rate is tried. A more prolonged pacing period may be effective. If sinus rhythm still does not result, AF is deliberately precipitated by rapid atrial pacing at 400–800/min. This is an unstable rhythm which usually reverts spontaneously to normal sinus rhythm. AF persists occasionally, but the ventricular rate is usually slower and more responsive to drug therapy than with SVT.

Figure 19.12 Narrow-complex tachycardia. Rapid atrial pacing with atrial capture results in sinus rhythm on cessation of pacing.

VENTRICULAR TACHYCARDIA

Useful techniques to pace VT include the following:

1 Ventricular burst pacing (similar to rapid atrial pacing) is simple and effective. The ventricle is paced at a rate about 120% of the spontaneous VT rate for 5–10 beats. Normal sinus rhythm should ensue (Figure 19.13). Potential complications include entrainment (Figure 19.14), that is, speeding up of VT, and occasionally precipitation of VF. Trained personnel, a defibrillator and resuscitation facilities must be available.

2 Underdrive ventricular pacing at rates less than that of the tachycardia may occasionally be successful.

3 Overdrive atrial pacing may be useful if there is 1:1 AV conduction and the ventricular rate is relatively slow (e.g. 120–180/min).

Figure 19.13 Wide-complex tachycardia. Ventricular burst pacing with ventricular capture results in normal sinus rhythm on cessation of pacing.

Figure 19.14 Example of entrainment. Wide-complex tachycardia is followed by ventricular burst pacing. When pacing is discontinued, a wide-complex tachycardia of opposite polarity is precipitated.

IMPLANTABLE CARDIOVERTER/DEFIBRILLATOR²

This is an implantable device which can recognise and automatically terminate VT and VF. Guidelines¹³ have been published for ICD implantation; nevertheless, this is a rapidly evolving field with many trials in progress. ICDs are of proven survival benefit (class I) in patients who have had a cardiac arrest due to VF or VT, not due to transient or reversible cause. In other clinical situations ICD implantation may be a reasonable approach, for example, syncope with inducible VT at electrophysiology study which is poorly tolerated haemodynamically, and antiarrhythmic drugs are ineffective and/or contraindicated. A trial²⁴ in over 1200 patients with recent myocardial infarction (> 1 month) and low LV ejection fraction (30%) has demonstrated a decrease in mortality when prophylactic ICD implantation was compared to conventional treatment. ICDs are standard therapy to prevent sudden cardiac death in such high-risk patients.

Virtually all ICD systems are implanted transvenously and include antitachycardia pacing and back-up ventricular bradycardia pacing, dual-chamber pacing with rate-adaptive options. Single- or dual-chamber ICDs may be implanted. One trial²⁵ suggests that single-chamber ICDs may be superior to dual-chamber ICDs in patients who do not have an associated bradycardia. Current devices continuously monitor the patient’s heart rate and deliver therapy when the heart rate exceeds a predetermined limit. There is a graded response which is programmable:

COMPLICATIONS

Occasionally, multiple ICD discharges occur. This is a true clinical emergency. Shocks may be appropriate or inappropriate. Frequent malignant ventricular arrhythmias may result in multiple appropriate discharges. If DC shocks are unsuccessful, the device may need to be reprogrammed to deliver higher-energy shocks; conversely, if the multiple shocks are successful in defibrillating the patient during an arrhythmia ‘storm’, then the ICD device should probably be inactivated and external transthoracic defibrillation and antiarrhythmic drug therapy should be given as required. This will save battery power and allow the patient’s ICD system to be tested later. If inappropriate ICD shocks arise, the ICD device should be switched off at once. The most common reason for inappropriate shocks is AF or some other SVT. Reprogramming the device may solve the problem. Occasionally sensing of EMI may cause ICD discharge. Avoidance of EMI source and/or reprogramming may be necessary. Nerve stimulators have been sensed by an ICD.