• Threshold (Fig. 25.2) – the minimum stimulus needed to capture the heart. It is given as current (amperes) or voltage (volts) over a time period (pulse width, ms).

• Unipolar/bipolar – refers to the arrangement (Fig. 25.3) of the negatively charged cathode and the positively charged anode. In the bipolar circuit, the cathode and the anode are separated by a short distance at the pacing lead tip. The circuit is localized to the immediate myocardium. In the unipolar circuit, the cathode is at the pacing lead tip with the anode at a distance; in the permanent pacing system it is found in the pacing box. The unipolar pacing circuit is larger and, therefore, produces a larger pacing artefact on the ECG. While there is little difference between the pacing characteristics of these two conformations, bipolar sensing is less susceptible to external noise.

• Impedance – this represents the total resistance to current flow in the pacing circuit. This resistance occurs in the leads, at the lead–myocardial interface for endocardial leads and in the tissue between the cathode and the anode. Fractures in the leads increase impedance, while insulation breaks reduce it.

Figure 25.2 A printout from a VVI pacemaker is shown. A standard ECG lead is seen at the top. The pacemaker marker channel is seen beneath, VP indicating ventricular pacing. The bottom line shows the electrogram seen by the bipolar lead. Loss of capture is seen at 1.1V.

Figure 25.3 Bipolar (A) and unipolar (B) pace/sense circuits are shown. Representative ECGs are shown beneath; note the larger pacing artefact on the unipolar ECG due to the larger pacing circuit.

Temporary pacing

Temporary pacing is used in emergency situations of life-threatening bradycardia or where a bradyarrhythmia could occur temporarily.

Transvenous pacing

This is the usual method for temporary pacing. A thin, semi-flexible, shaped, bipolar pacing lead is normally used. The central circulation is accessed via the internal jugular, subclavian or femoral veins, the first of these being preferable as there is a lower risk of complication (e.g. pneumothorax with the subclavian route, infection and deep vein thrombosis with the femoral). Furthermore, with the internal jugular approach, the veins used for permanent pacing are not directly punctured. The lead is manipulated into position at the right ventricular apex under X-ray guidance. Some leads may have a central shapeable stylet to allow more accurate positioning. Others have a tip-mounted flotation balloon to allow non-radiographic positioning. Active fixation (screw tipped) leads are also available to prevent lead displacement. In most cases one ventricular lead is used. Atrial pacing and dual chamber pacing are also possible. For temporary transvenous pacing, due consideration must be given to the possible need for permanent pacemaker insertion and the impact thereon of infection and local complications at vascular access. It is hence advisable to avoid the subclavian route and to use ultrasound guidance for vascular puncture. Various guidelines are listed in the bibliography section at the end of this chapter.

The pacing lead is connected to an external box which allows various programming options:

1. Mode: usually VVI (’demand’) or VOO (‘asynchronous’ or ‘fixed rate’)

2. Output: either the output voltage or current is programmable, the pulse width being fixed. Maximum outputs are higher than with permanent systems as battery size is unrestricted and the threshold is more unstable

3. Sensitivity: the threshold above which electrical activity will be detected as cardiac. This is usually measured in millivolts, a higher value indicating lower sensitivity

4. Rate: usually 30–150 or even higher for the overdrive pacing of tachyarrhythmias.

Transoesophageal and transgastric pacing

An electrode (on a device similar to an oesophageal stethoscope or nasogastric tube),¹ placed in the oesophagus, can capture the left atrium, while in the stomach ventricular pacing may be possible. Transoesophageal atrial pacing (TAP) is a simple and safe method for temporary treatment of bradyarrhythmias and is particularly applicable to use during anaesthesia.² Because voltages of up to 20V or more may be required to achieve capture (Fig. 25.2), a signal amplifier is needed if using an ordinary external (transvenous) pacing box (signal generator). TAP, like transgastric pacing, is rarely used because of unfamiliarity with the technique and scarcity of equipment.

Transcutaneous pacing

In the peri-arrest situation it may be difficult to position a transvenous temporary wire. It is possible to capture the ventricle by passing a large enough current through the chest using specially designed electrodes (Fig. 25.4). These electrodes may also be used for monitoring and defibrillation.

Figure 25.4 The suggested positioning for transcutaneous pacing electrodes is shown, antero-posterior (A.) and antero-lateral (B.). There is no significant difference in pacing thresholds between the two conformations.

There is significantly greater impedance in the transcutaneous pacing circuit than with endocardial stimulation, due to the additional significant impedances of the electrode–skin interface, the lung and the pericardium. High currents are required, usually 50–90 mA, at pulse widths of 10–20 ms. Pacing thresholds may be further increased by poor electrode–skin contact, metabolic disturbance (hypoxia, acidosis) and pericardial effusion. Unpleasant cutaneous nerve and skeletal muscle stimulation occur at currents as low as 10 mA making this method of pacing, without sedation, short-lived by necessity. Pulse widths of the order of 10 ms produce optimal pacing thresholds and reduce patient discomfort. Significant pacing artefacts occur on the ECG, making myocardial capture difficult to assess without pulse or blood pressure monitoring.

Another form of transcutaneous pacing is also used by cardiothoracic surgeons. One or more wires are implanted directly into the atrial and/or ventricular myocardium at the time of operation and brought out through the skin. Two wires can be used per chamber to allow bipolar pacing, or a second wire may be stitched into the praecordial skin as and when pacing is actually required. These can be connected to a temporary pacing box. Similar to temporary wires they are prone to infection and thresholds can rise without warning. They are usually used to await recovery of the normal conducting system. Atrial pacing may also reduce the incidence of postoperative atrial fibrillation.

Permanent pacing

The principles of permanent pacing remain the same as temporary pacing; the indications continue to expand and have been recently updated. Following significant improvements in battery and lead technology, devices are now small enough to be placed subcutaneously in the pre-pectoral region, the leads passed via the subclavian or cephalic veins. Other routes including the femoral veins and epicardial systems may also be used where subclavian access is impossible or due to previous pacemaker infection.

Hardware

The pacemaker box consists of:

1. The battery. This forms a major part of the volume of the pacemaker. It has a number of important requirements including:

a. small size

b. the ability to produce small amounts of current reliably and consistently over long periods

c. a low self-discharge rate so that it does not wear out without use

d. a predictable discharge rate so that replacement can be planned in advance

e. lack of gas production to allow hermetic sealing

f. significant longevity to allow infrequent box changes. It is not unusual for batteries to require replacement only once a decade.

A number of different power sources have been used, including nuclear devices. However, the lithium-iodine battery is currently the industry standard.

2. Voltage/output circuits. Various circuits are required to allow the battery voltage (usually 2.8 V at implant) to be altered to produce a range of programmable outputs, according to the threshold, to prolong battery life.

3. Telemetry circuits. These allow an external computer to communicate and programme the pacemaker using radiofrequency signals.

4. Pacing circuits. These control all aspects of pacemaker function including the timing circuits, diagnostics and the rate response circuitry.

5. Sensing circuits. These allow sensing of intrinsic cardiac activity with filtering allowing exclusion of external electromagnetic noise.

6. Memory. Modern pacemakers are able to store significant quantities of data, for example on arrhythmias and heart rate variability.

7. Reed switch. This is activated by the magnet, completing a circuit allowing a particular predefined programme to start.

In contrast to temporary leads, permanent pacing leads are expensive, highly engineered multi-component devices, required to be in situ for several decades, without failing or producing significant local damage. Their components include:

1. Electrode. Most newly implanted leads are bipolar with a cathodal tip and a larger anode further back. The cathode is surprisingly complex – it is small, producing: a high charge-density, thus improving myocardial capture; and a high pacing impedance which reduces battery drain. Platinum, titanium or activated carbon is used for their good conducting properties and durability. A small reservoir of steroid is also found in the lead tip to reduce the inflammatory reaction at the lead–myocardial interface, maintaining lower stimulation thresholds.

2. Fixation mechanism. It is necessary to secure the lead in the myocardium thus maintaining capture. Passive fixation is achieved with small flexible protrusions from the lead tip, tines, which hook into the trabeculated muscle. For less stable positions active fixation mechanisms are available, often a small retractable screw (Fig. 25.5D).

3. Lead conductor. This is the wire, often made of a complex alloy, which transmits the electrical current. Bipolar leads require two, one each for the cathode and the anode. Coiling the wires produces great lead flexibility, the anodal conductor being wound inside the cathode, separated by an insulator (coaxial wire). A recent advance involves coating each individual conductor with insulation (coated wire technology), which allows the anodal and cathodal conductors to run together producing leads with even smaller diameters.

4. Lead insulation. Silicon was used initially; polyurethane is used today; it allows flexibility, resistance to damage, biocompatibility and good handling characteristics.

5. Lead connector. The metal connectors which link the conductor to the pacemaker. There is now an industry standard, IS-1.

6. Central lumen. A central lumen runs the length of the lead allowing the passage of a stylet that can be shaped to allow accurate positioning. A number of leads are also shaped to allow positioning in certain positions, e.g. the coronary sinus or the right atrial appendage.

Figure 25.5 A chest radiograph of a biventricular ICD is shown. A number of the components are visible: the box (A), the screw tip of the active-fixation ventricular lead (B), the distal shocking coil (C), the atrial lead (D) and the coronary sinus left ventricular pacing lead (E).

Software

Pacemakers are becoming increasingly complex with multiple programmable parameters and functions, including:

1. Mode (see The NASPE/BPEG code, above)

2. Base rate – the minimum paced rate

3. Hysteresis rate – it is possible to allow the intrinsic heart rate to drop to a lower value, say 40, before pacing is initiated at a higher rate, say 60

4. Maximum paced rate – the maximum rate above which pacing will not occur, either driven by the patient’s atrial rate or by the rate sensor

5. AV delay – the paced equivalent of the PR interval

6. Rate response functions. An increase in heart rate is a prime mechanism through which cardiac output is increased during both physical and mental activity. To allow a more physiological heart rate response in paced patients with abnormal sinus node function, many pacemakers sense this requirement; motion sensors, changes in transthoracic impedance as a marker of respiratory rate and QT interval are used. The pacing response can then be tailored to each patient

7. Sensitivity. The signal amplitude above which electrical activity will be ‘seen’

8. Mode switch. Pacemakers should not track atrial tachycardias. Modern pacemakers can detect these arrhythmias and change mode accordingly.

The evolving complexity of the programmable parameters (the most important of which are summarized above) has made it increasingly difficult to diagnose pacemaker malfunction from the surface ECG without knowledge of the pacemaker set-up. In general terms, ‘pacemaker malfunction’ due to software or hardware failure is a rare event.

Future directions

Pacemaker therapy for traditional bradycardic indications is currently underused in the UK; implant rates are likely to increase. Furthermore, pacemaker indications are expanding beyond bradyarrhythmias, for example:

1. pacing to improve symptoms and prognosis in heart failure. Many patients with heart failure have conducting system abnormalities, e.g. left bundle branch block which produces dyssynchonous contraction of the right and left ventricles. Biventricular pacing (Fig. 25.5), in which both the right and left ventricle, via the coronary sinus, are paced, can restore co-ordinated ventricular activation and has been shown to improve symptoms and reduce mortality

2. pacing to prevent atrial tachyarrhythmia

3. pacing to prevent ventricular tachyarrhythmia in long QT syndrome

4. pacing to alleviate symptoms in vasovagal syncope

5. pacing to reduce the outflow gradient in hypertrophic cardiomyopathy.

In addition, we now have the ability to monitor pacemaker function remotely via wireless technology which will become increasingly important in years to come. Device-treated patients in the future are likely, therefore, to be part of an expanding, increasingly heterogeneous group requiring highly individualized care.

Vagal nerve stimulators

Another application of pacemaker technology that is becoming increasingly prevalent is the implantable vagal nerve stimulator (VNS). This is currently approved as adjunctive therapy for medically refractive epilepsy and major depression. Possible indications in the future may eventually include obesity, chronic pain syndromes and various neuropsychiatric disorders, such as obsessive compulsive and panic disorders.

The system consists of a constant current pulse generator placed subcutaneously, as with cardiac pacemakers, in the pectoral region and connected onto the left vagus with a tunnelled lead culminating in spiral platinum electrodes embedded in silicone rubber (Fig. 25.6). The left nerve is used as the right vagus nerve carries a higher proportion of cardiac efferents. Again, as with cardiac pacemakers, subsequent programming is via an external computer with radiofrequency signals. Stimulation patterns are episodic (e.g. up to 90 s on and 5–10 min off) and patients carry a magnet whose transient application results in an additional pre-programmed burst of stimulation which may abate or prevent a seizure. The magnet can be held or fixed over the signal generator to pause stimulation, in order to limit some of the problems below.

Figure 25.6 VNS system positioning.

Patients usually also carry a copy of the manufacturer’s instructions for reference.

In addition to the usual issues regarding electromagnetic interference (see later), there are a number of specific problems that are noteworthy for anaesthetists. They are mostly related to ‘on time’ of the device, when stimulation is taking place:

• Effects on heart rate and automaticity. Bradycardia appears commonplace; complete heart block and asystole are reported under anaesthesia and particularly at device insertion/activation.

• Vocal cord and laryngeal apparatus dysfunction, resulting in cough, voice alteration, swallowing difficulties and aspiration.³

• In addition to the above, effects on respiratory control (central and/or peripheral) are noted which can manifest as induced or worsened obstructive sleep apnoea.

Defibrillators

Introduction

To understand defibrillator design and function and why defibrillation may fail requires some understanding of the pathophysiology of fibrillation and defibrillation.

Ventricular fibrillation (VF) is a complex arrhythmia consisting of random, disorganized, three-dimensional waves of depolarization, thus producing the loss of cardiac output and allowing arrhythmia persistence.

The mechanisms through which a shock of sufficient strength allows the return of spontaneous, co-ordinated electrical activity remain incompletely understood. A shock can have three effects depending on its timing in the action potential. Early on, during the absolute refractory period, no effect occurs. Later on, action potential prolongation is seen. Later still, a new action potential is induced. It is hypothesized that a shock of sufficient strength and appropriate timing will extend the refractory period in enough of the myocardium to allow the waves of depolarization to die out. Subsequently, cardiac automaticity allows the return of normal electrical activity, depending upon the underlying cardiac condition.

The amount of current required to produce defibrillation is known as the defibrillation threshold (DFT). For historical reasons, this is given in terms of energy (joules). Its determinants explain the success or failure of a shock. As with the pacing threshold, there is a minimum current below which defibrillation will not occur. Above a certain level, detrimental effects may occur, reducing the likelihood of success. Between these values success is most likely. However, as the waves of depolarization in VF are entirely random, an element of chance exists that the shock is delivered at the optimal time to defibrillate a critical mass of myocardium. This concept is known as the probabilistic nature of DFTs.

Factors affecting DFTs include:

1. Charge characteristics. A monophasic shock is one where the polarity of the shock remains constant throughout its delivery (Fig. 25.7A). In biphasic shocks (Fig. 25.7B) the polarity is reversed during delivery. In general terms, DFTs are lower and there is less post-shock myocardial depression with biphasic shocks. The shape and time-course of the shock can also be varied to produce optimal effects.

2. Electrode position. In implantable systems shocks can occur in a number of configurations that may affect the DFT (see Hardware, below). Altering the position of the endocardial coils can also have some effect. External paddle positions may also have an effect.

3. Shock polarity. Which electrode is used as the anode and which the cathode can affect DFTs, particularly with monophasic shocks.

4. Underlying cardiac condition. The more severe the cardiac condition, as assessed using heart size, ejection fraction, QRS width or heart failure symptoms, the higher the DFT. Furthermore, the time spent in VF prior to defibrillation adversely affects DFTs.

5. Metabolic disturbance. DFTs are higher in hypoxic and acidotic patients.

6. Medication. DFTs can be affected by numerous medications. Of note, intravenous amiodarone reduces DFTs, whereas its chronic administration increases them. Fentanyl reduces DFTs. Common inhalational anaesthetic agents do not appear to have significant effects.

7. Shock impedance. Shock impedance affects current delivery to the myocardium. The transthoracic impedance for external defibrillation is dependent on lung volume, skin contact and tissue thickness.