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.

PACEMAKER MODES

The North American Society of Pacing and Electrophysiology (NASPE) and the British Pacing and Electrophysiology Group (BPEG) developed the NBG code⁴ for pacing. It is a generic code used to identify modes of pacing (Table 19.1). The code was updated in 2002 to include multisite pacing therapy (position V).⁵

• Position I: refers to the chamber(s) paced: A = atrium; V = ventricle; and D = dual chambers, i.e. both A and V.

• Position II: refers to chamber(s) in which sensing occurs: A = atrium; V = ventricle; and D = dual chambers, i.e. both A and V.

• Position III: refers to the pacemaker’s response to a sensed event. This may be:

• (a) I (inhibition) – a pacemaker’s discharge is inhibited (switched off) by a sensed signal, for example, VVI, where ventricular pacing is inhibited by spontaneous ventricular activity.

• (b) T (triggering) – a pacemaker’s discharge is triggered by a sensed signal.

• (c) D (dual) – both T and I responses can occur. This designation is reserved for dual-chamber systems. A depolarisation sensed in the atrium inhibits the atrial output but triggers ventricular pacing. There is, however, a delay (the AV interval) between the sensed atrial depolarisation and the triggered ventricular pacing which mimics the normal P-R interval. If a spontaneous ventricular depolarisation is sensed, ventricular pacing is inhibited.

• Position IV: refers to R or rate modulation. An R indicates that the pacemaker incorporates a sensor to vary the pacemaker independently of intrinsic cardiac activity. A sensor,⁶ in effect an artificial sinoatrial (SA) node, increases or decreases the heart rate according to the body’s metabolic needs. Two different sensors are widely used:

1 Activity sensors with vibration detectors (accelerometer or piezoelectric crystal) have the disadvantage that they may respond to non-physiological stimuli, for example, pacing rate increase may occur when the patient is using an electrical drill. On occasions this response can be used to good effect, for example, an inappropriate bradycardia in a shocked patient with a rate-adaptive (activity sensor) permanent pacemaker can usually be speeded up by tapping the skin over the unit.

2 Minute ventilation sensors (respiratory rate times tidal volume, which is estimated by measuring impedance differences between the pacing electrode and the pacemaker unit) rely on minute volume changes to alter the pacing rate. This sensor may occasionally inappropriately accelerate the pacing rate, for example, in a mechanically ventilated patient requiring a large minute volume. Changing the ‘upper rate’ limit of the pacemaker or switching the rate-adaptive function ‘off’ will usually solve the problem.

Table 19.1 The North American and British Group (NBG) pacemaker code

Other sensors, such as ventricular paced Q-T interval systems, have also been successfully used in clinical practice. Recently, rate-adaptive systems with dual sensors, where one sensor cross-checks the other and only responds if both sensors are receiving consistent data, have become available.

All modern permanent pacemakers are programmable, i.e. multiple pacing parameters, such as current output, rate and mode, can be changed by an external device (programmer).

• Position V: is now used to indicate whether multisite pacing is present: O = none of the cardiac chambers; A = one or both atria; V = one or both ventricles; or D = any combination of atria and ventricles, e.g. the code for a patient with dual-chamber, rate-adaptive pacing (DDDR) and biventricular pacing is DDDRV.

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.

Table 19.2 Examples of pacemaker modes

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.