Abnormal Automaticity

The action potential of sinus and atrioventricular conducting tissue differs from that of the myocardium in that phase 4 of their action potentials are less stable and possess the property of spontaneous automaticity and consequent depolarisation. This is an important property that allows these tissues to assume the role of electrophysiological pacemaker dominance. However, in some circumstances, such as myocardial ischaemia or cardiostimulatory influences, regional levels of spontaneous automaticity can be abnormally accelerated, stimulating subsidiary pacing cells (such as those within the AV junction and ventricular Purkinje fibres) to override the normal sinus rate.^3,4

Triggered Activity

Arrhythmias may occur through the occurrence of abnormal oscillations within the early and late repolarisation stages of the cardiac action potential that lead to the propagation of aberrant ‘triggered’ arrhythmic events. Such oscillations are classified as either ‘early after depolarisations’ that occur during phases 2 and 3 of the action potential or late after depolarisations, which occur during phase 4. Digitalis toxicity, ischaemia, hypokalaemia, hypomagnesaemia and elevated catecholamine levels are the more common causes of triggered activity.⁵ Excessive prolongation of the action potential duration enhances the risk of such triggered activity and as such these mechanisms are implicated in the development of certain subtypes of ventricular tachyarrhythmias, in particular torsade de pointes (refer to description later in this chapter).

Reentry

The most common cause of tachyarrhythmias is reentry, in which current can continue to circulate through the heart because of different rates of conduction and repolarisation in different areas of the heart (temporal dispersion). Slow conduction through a region of the heart may allow enough time for other tissues which have already been depolarised to recover, and then to be re-excited by the arrival of the slowly-conducting wavefront. Once this pattern of out-of-phase conduction and repolarisation is established, a current may continue to circulate back and forth between adjacent areas, or around a re-entry circuit. Each ‘lap’ of the circuit gives rise to another depolarisation (P wave or QRS complex).^4,6 The ultimate rate of the tachycardia depends on the size of the circuit (micro versus macro reentry) and the conduction velocity around the circuit.

Sinus Tachycardia

In adults, a sinus rate of greater than 100/min is termed sinus tachycardia and may occur with normal exertion^7,8 (see Figure 11.2). When sinus tachycardia occurs in the patient at rest, reasons other than exertion must be sought and include compensatory responses to stress, hypotension, hypoxaemia, hypoglycaemia or pain, in which there is increased neurohormonal drive. Many drugs such as inotropes and sympathomimetics also accelerate the sinus rate. Sinus tachycardia should therefore be regarded as a response to a physiological stimulus rather than an arrhythmia arising from sinus node dysfunction. Treatment is directed at the trigger for the tachycardia, not the tachycardia itself. As sinus tachycardia may point to covert events such as internal bleeding or pulmonary embolism, there should be thorough investigation for unexplained, persistent sinus tachycardia.

FIGURE 11.2 Sinus tachycardia. The rhythm is slightly irregular and varies between 105/min and 115/min.

Sinus Bradycardia

A sinus rate of less than 60 beats/min is termed sinus bradycardia^7,8 (see Figure 11.3). In general terms the slower the rate, the more likely it is to produce symptoms related to low cardiac output. Slowing of the rate to less than 50/min is commonplace during sleep, especially in the athletic heart, but is otherwise uncommon. Bradycardia may accompany myocardial ischaemia (especially when due to right coronary artery disease), conduction system disease, hypoxaemia, and vagal stimulation (e.g. nausea, vomiting, or painful procedures). It also accompanies beta-blocker, antiarrhythmic or calcium channel blocker treatment.⁹ Treatment of sinus bradycardia reflects the treatment of AV block and is covered below under the management of atrioventricular block.

FIGURE 11.3 Sinus bradycardia. The rhythm is regular and at a rate of 50/min. Borderline first-degree AV block: the P-R interval is 0.20 sec.

Sinus Arrhythmia

When the rhythm is clearly sinus in origin but is irregular, then the term sinus arrhythmia may be used (see Figure 11.4). Generally, a gradual rise and fall in rate can be appreciated in synchrony with respiration. The gradual rise and fall in rate is important: it distinguishes sinus arrhythmia from the abrupt prematurity with which atrial ectopic beats make their appearance, or the abrupt slowing of the sinus rate seen in sinus pause and sinus arrest. Sinus arrhythmia may accompany sinus node dysfunction but is seen also in the normal heart. Of itself, sinus arrhythmia does not require treatment.

FIGURE 11.4 Sinus arrhythmia with marked rate variation in synchrony with respiration. The rhythm is clearly sinus but is irregular, accelerating from 75 to 120/min before slowing back to 75/min by the end of the strip.

Sinus Pause and Sinus Arrest

Abrupt interruption to the sinus discharge rate has spawned a variety of descriptive terms, based partly on physiology and partly on severity. Sinus pause is self-descriptive: during a period of sinus rhythm, there is a sudden pause during which the sinus node does not fire.⁹ The heart rate abruptly drops, during which time there may be bradycardic symptoms. Sinus arrest tends to be used as a descriptor when the sinus pause is longer rather than shorter (usually above 3 seconds) (see Figure 11.5). The longer the period of sinus arrest, the greater the likelihood of symptoms, and syncope is possible.⁹ Sinus pause may be indistinguishable from sinus exit block (in which there is sinus discharge that fails to excite the atria), as both result in missing P waves. The distinction is academic, however, as both arrhythmias arise from the same groups of causes, and are significant only when they cause symptomatic bradycardia. Pauses in which the P–P intervals spanning the pause are multiples of the pre-pause P-P interval favour the diagnosis of exit block (Figure 11.6).⁵ Recurrent syncopal pauses may require acute responses for symptomatic bradyarrhythmias (see AV block treatment below). If episodes continue, consideration should be given to permanent pacemaker implantation.

FIGURE 11.5 Sinus pause and sinus arrest. Sinus rhythm at 60/min followed by an abrupt rate drop. Using 3 sec as a cut off between sinus pause and sinus arrest, the first long interval of 2.5 sec would qualify as sinus pause whereas the next interval (3.2 sec) would be classified as sinus arrest.

FIGURE 11.6 Sinus exit block. An abrupt rate drop follows the first three sinus beats. As the P-P interval spanning the pause is exactly twice the P-P interval of the preceding beats, the pause here could be due to sinus exit block. It could equally simply be a sinus pause.

Atrial Ectopy

Impulses arising from atrial sites away from the sinus node (atrial foci) conduct through the atria in different patterns to sinus beats, and so give rise to P waves of different morphologies. These altered P waves define atrial ectopy, and their prematurity, or faster discharge rate, sees them more completely described as premature atrial beats. A characteristic P wave morphology cannot be provided, as ectopy may arise anywhere within the atria, causing upright, inverted or biphasic P waves. Ectopic P waves are often so premature that they become hidden within the preceding T wave. At such times evidence of their presence can be concluded only because they deform the T wave, and because premature QRS complexes of normal morphology follow, suggesting a supraventricular origin of those beats. Premature atrial beats most commonly conduct normally, although they may conduct aberrantly, or not at all, depending on their degree of prematurity and the state of AV nodal and intraventricular conduction (see Figure 11.7).

FIGURE 11.7 Sinus rhythm with frequent atrial ectopics. The notched P waves at a rate of 75–80/min are the Ps of the dominant sinus rhythm, while the more rapidly firing P waves with peaked configurations are the atrial ectopic beats. Note that the ectopic P waves have some variability in their shapes and firing rate. They should therefore be described as multifocal atrial ectopics.

Atrial Tachycardia

A rapidly firing atrial focus or (more commonly) the presence of an atrial reentry circuit may give rise to a rapid rate, which is termed atrial tachycardia. Rates range from 140–230 beats/min and the rhythm is typically very regular.⁵ P waves may be difficult to identify, as they become hidden in T waves. At such times, the presence of narrow QRS complexes, confirming supraventricular conduction, aid diagnosis and discrimination from ventricular tachycardia. Distinction from other supraventricular arrhythmias may rely on the absence of characteristic features of other SVTs (e.g. the sawtooth baseline of flutter, the irregularity of fibrillation, or the pseudo-R waves and onset pattern of atrioventricular nodal reentry tachycardia). When the atrial rate exceeds the conduction capability of the AV node, varying degrees of AV block occur. Atrial tachycardia may be paroxysmal, sustained or incessant (see Figure 11.8). Symptoms vary and are partly dependent on the rate of the arrhythmia, and the presence or absence of myocardial dysfunction.

FIGURE 11.8 Atrial tachycardia. In this narrow complex tachycardia the rhythm is very regular and the rate close to 210/min. It is not possible to clearly identify P waves within the T waves.

Multifocal Atrial Tachycardia

When multiple atrial sites participate in generating atrial ectopic beats at a rapid rate, the term multifocal atrial tachycardia is used (see Figure 11.9). The different foci produce P waves of varying morphology, and typically the strict regularity seen during atrial tachycardia is lost.⁹ Multifocal atrial tachycardia in particular complicates chronic obstructive pulmonary disease (COPD), as well as other pulmonary diseases as part of the cor pulmonale spectrum.¹¹

FIGURE 11.9 Multifocal atrial tachycardia. After 3 beats of sinus rhythm, the rate abruptly rises during a paroxysm of multifocal atrial tachycardia, which spontaneously reverts. The resultant tachycardia is irregular, and P waves of varying shapes can sometimes be clearly seen while others can be gleaned only by the deformity of T waves.

AV Conduction During Supraventricular Tachyarrhythmias

The rapid atrial rates associated with some atrial arrhythmias exceed the conduction capability of the AV node, with the result that not all of the atrial impulses can be conducted (see Figures 11.10 and 11.11). This usually occurs when the atrial rate exceeds 200/min. Thus during atrial flutter, or rapid atrial tachycardia, it is common to see 2 : 1 block or greater. During atrial fibrillation the ventricular response rate rarely exceeds 170/min.

FIGURE 11.10 Atrial tachycardia with high-degree block (many consecutive P waves do not conduct). The atrial rate is around 190/min, but because there is variable AV block (3 : 1 to 4 : 1) the resultant ventricular rate is between 50 and 60/min. This patient had digitalis toxicity.

FIGURE 11.11 Atrial flutter with variable block. Note the sawtooth baseline, which characterises atrial flutter. The atrial rate is regular and is a little faster than 300/min, while the ventricular rate is irregular because of the variable block. At times the ventricular rate is close to 150/min (when there is 2 : 1 block) and at other times close to 100/min (when there is 3 : 1 block).

Atrial Flutter

Atrial flutter is a rapid, organised atrial tachyarrhythmia (see Figure 11.11). The atrial rate may be anywhere between 240 and 430/min, but most commonly the rate is close to 300/min.⁹ At these rates the atrial depolarisation waves (flutter waves) run together to produce the characteristic ECG feature of this arrhythmia: the so-called ‘sawtooth’ baseline, because of its resemblance to the teeth of a saw. This sawtooth baseline is generally best shown in the inferior leads. By contrast, in lead V1 the flutter waves usually appear more like discrete P waves, whilst in leads I and aVL, it may appear more like fibrillatory waves. The atrial rate of close to 300/min rarely conducts on a 1 : 1 basis to the ventricles. Rather 2 : 1, 3 : 1, 4 : 1 or variable levels of AV block intervene to limit the ventricular response rate, often to between 75 and 150/min.⁹ When the AV block is variable, beats at 3 : 1, 4 : 1 or other ratios are seen together in a single strip. When there is 2 : 1 block, the flutter waves are often concealed within the QRS and/or T wave, and so definite identification may be difficult (see Figure 11.12). At such times, the presence of a narrow QRS tachycardia at a fixed rate close to 150/min is particularly suggestive of atrial flutter with 2 : 1 block. The tendency for flutter waves to appear as discrete P waves in lead V1 may also be useful, as they may be more easily visualised in this lead. Vagal manoeuvres, or adenosine administration, may increase the degree of block and so reveal the flutter waves (Figure 11.12).^7,8

FIGURE 11.12 A narrow complex tachycardia at a rate of 150/min in the top strip could be any number of supraventricular rhythms, among them atrial flutter with 2 : 1 block. Administration of IV adenosine produces momentary high-degree AV block (middle ⅔ of the lower strip), during which flutter waves at a rate of 300/min become apparent. Carotid sinus massage or other vagal manoeuvres may produce the same diagnostic impact via transient AV block.

Atrial Fibrillation

Atrial fibrillation is a chaotic atrial rhythm in which multiple separate foci either discharge rapidly or participate in reentry circuits, resulting in rapid and irregular depolarisations that are not able to gain complete control of the atria.^7,9 Discrete P waves (representing the coordinated depolarisation of the atria) are therefore not seen; rather there is a continuous undulation of the ECG baseline (fibrillatory waves at a rate between 300 and 500/min), reflecting the continuous erratic electrical activity within the atria. This erratic, uncoordinated electrical activity results in uncoordinated contraction, and the atria can be seen not so much to contract but to quiver continuously. It is this quivering (fibrillatory) motion that gives atrial fibrillation its name.

The irregularity of the atrial rate results in an irregular arrival of impulses at the AV node and, as a result, conduction to the ventricles at irregular intervals.⁷ Thus, a hallmark of atrial fibrillation is the marked irregularity of the ventricular rhythm. The ventricular response rate to the rapid atrial rate is determined by the state of AV nodal conduction, and in patients with normal AV conduction is often in the range of 140–180/min (rapid or uncontrolled atrial fibrillation) (see Figure 11.13). Alternatively, when AV conduction is impaired, or limited by drug effect, slower ventricular rates are seen. When atrial fibrillation is accompanied by a ventricular rate less than 100/min, it may be termed slow (or controlled) atrial fibrillation. Atrial fibrillation is a common significant arrhythmia¹² and, while not usually immediately life-threatening, it contributes significantly to morbidity, especially in patients with existing cardiac failure. The loss of organised atrial contraction (atrial kick) as well as rapid rates deprive the ventricles of adequate filling, and so hypotension and low cardiac output may result. Consequent pooling of blood in the atria enhances the risk of emboli formation and stroke. In addition, the incomplete atrial emptying results in congestion of first the atria and then the pulmonary circulation, and contributes to dyspnoea, increased work of breathing, and hypoxaemia. Patients with left ventricular failure rely more heavily on atrial kick, and so symptoms and the severity of their heart failure typically worsen during atrial fibrillation. At times, atrial fibrillation is debilitating in this group, and shock and/or acute pulmonary oedema may develop.

FIGURE 11.13 Atrial fibrillation with a rapid (uncontrolled) ventricular response. The rate is around 170/min and the rhythm clearly irregular. Because of the rapid rate there is little opportunity to identify the fibrillatory baseline, but enough can be seen for confirmation.

Antiarrhythmic therapy aims at reverting atrial fibrillation, or to limiting the ventricular rate (rate control) even if fibrillation is persistent.¹² For patients with chronic atrial fibrillation in whom adequate rate control cannot be achieved pharmacologically, it is sometimes necessary to perform radiofrequency ablation of the AV node itself. Permanent pacemaker implantation is therefore also necessary.

Atrioventricular Nodal Reentry Tachycardia

Atrioventricular Nodal Reentry Tachycardia (AVNRT) is the most common type of paroxysmal supraventricular tachycardia (PSVT), accounting for greater than 50% of cases of PSVT.⁵ (Note that PSVT as used here does not include atrial flutter or fibrillation). AVNRT is more common in women (75% of cases), more often in younger than older patients, and in some individuals there is an identifiable link to stress, anxiety or stimulants. As the name suggests the arrhythmia arises because of reentry involving the AV node. Normally, atrial impulses reach the AV node via both slow and fast AV nodal pathways which link the atria to the AV node proper. The resultant PR interval is <0.20 sec. In AVNRT, the trigger mechanism is a premature atrial ectopic which is blocked by the fast pathway because of refractoriness. Conduction into the AV node and to the ventricles is still possible by the slow AV nodal pathway, but the resultant PR interval will be quite long (AV delay plus slow conduction into the AV node). Following this atrial ectopic with its long PR interval is the onset of the tachycardia.¹³

The tachycardia develops because the initiating impulse, the atrial ectopic, is delayed in reaching the AV node. Once it does reach the AV node it conducts to the ventricles, but also now finds the previously refractory fast pathway recovered and able to conduct retrogradely back to the atria. There is now a functional circuit for reentry between the atria and the AV node. Impulses conduct slowly into the AV node, lengthening the PR interval, but on reaching the AV node conduct just as quickly to atria as to the ventricles. As a result, the P waves appear at much the same time as the QRS.¹³ In some instances of AVNRT it is not possible to identify P waves at all because they are hidden within the QRS. Often, however, the P waves can be seen distorting the final part of the QRS complex, appearing as small R waves in V1 and small S waves in lead II. Because they are P waves rather than part of the QRS, the ECG appearance has been dubbed ‘pseudo R waves’ in V1 and ‘pseudo-S waves’ in lead II¹³ (Figure 11.14). AVNRT is typically regular, and most commonly at rates between 170 and 240/min but may be slower. The QRS is narrow unless there is concommitant bundle branch block. AVNRTs sometimes respond well to vagal manoeuvres, including coughing, bearing down, and carotid sinus massage. Adenosine may interrupt the arrhythmia, and other AV blocking drugs or antiarrhythmics may be necessary to prevent recurrence. Elective cardioversion is sometimes necessary, and if the arrhythmia is chronically troublesome, slow pathway ablation may be undertaken.^5,13

FIGURE 11.14 Atrioventricular Nodal Reentry Tachycardia. Lead V1. There is sinus rhythm initially. A premature atrial ectopic (arrow) conducts with a long PR interval (0.36 sec), initiating onset of AVNRT at a rate of 140/min. Note the P waves during the tachycardia can be seen distorting the end of the QRS (the ‘pseudo R wave in V1’ of AVNRT) which is not present before the tachycardia. Note also the monitor designations above each beat: N = normal, S = supraventricular.

Nursing Management of Atrial Arrhythmias

General symptoms of atrial tachyarrhythmias include: palpitations, dyspnoea/tachypnoea, fullness in the throat/neck, fatigue, lightheadedness, syncope, chest pain and angina symptoms and nausea and/or vomiting. Management of atrial tachyarrhythmias includes: (a) searching for and correction of the cause; (b) rate control limiting the ventricular response, even if the arrhythmias cannot be suppressed;^14,15 (c) reversion of the arrhythmias by vagal manoeuvres, medication, cardioversion or overdrive pacing; (d) ablation;¹⁶ (e) prophylactic anticoagulation; and (f) prevention of recurrence using cardiac resynchronisation therapies such as biventricular pacing.¹⁷

Bradycardic Influences

Conduction system depression may occur with abnormal autonomic balance (increased vagal or decreased sympathetic tone), decreased endocrine stimulation (reduced catecholamine or thyroid hormone secretion), or from pathological influences such as conduction system disease, or congestive, ischaemic, valvular or cardiomyopathic heart diseases. Many biochemical and pharmacological factors cause conduction system depression with resultant bradycardia.¹⁸ The causes of bradycardia and AV block include:¹⁸

In the absence of stimulation by the SA node, other tissues within the conduction system and myocardium can generate cardiac rhythms at rates slower than the normal sinus rate. Thus sinus node failure need not severely compromise the patient, as the inherent automaticity of the AV node can generate a (nodal) rhythm at a rate of 40–60 beats/min. Similarly, should the AV node fail and the ventricles receive no stimuli, there is an additional layer of protection, as the ventricles themselves can generate (ventricular) rhythms at rates of 20–40 beats/min.⁷

Junctional Escape Rhythms

This term describes the AV node response to bradycardia. When sinus bradycardia falls to a rate slower than the inherent automatic rate of the AV node, then the junctional tissues fire.^7,9 Typical rates are 40–60/min but may be slower, as the cause of the primary bradycardia may also suppress the firing of escape foci. Intraventricular conduction usually follows the same pattern as had been present before junctional rhythm and so the QRS is unchanged from how it was previously, although occasionally aberrant ventricular conduction may occur, widening the QRS complex. P waves may or may not be evident and are often inverted because of retrograde conduction, as atrial activation spreads from the AV node and upwards through the atria. These P waves may at times be seen in advance of the QRS (at shorter than normal P–R intervals), within the ST segment, or may be hidden within the QRS complexes (see Figure 11.15).

FIGURE 11.15 Sinus bradycardia followed by onset of junctional escape rhythm. Note that the sinus rate is initially around 37/min. It then slows into the escape rate range of the AV node, which then discharges at 35/min. The junctional beats are not preceded by P waves: the more slowly discharging sinus node probably has its P waves hidden first in the QRS of the second-last beat and then distorts the ST segment of the last beat.

Ventricular Escape Rhythms

When either the sinus or AV node fails, and stimulation of the ventricles does not occur, the ventricles can autoexcite themselves, usually at a rate of 20–40 beats/min (Figure 11.16). Symptoms of bradycardia commonly accompany these idioventricular rates, and acute rate restoration may be necessary. However, true cardiac arrest requiring cardiopulmonary resuscitation is less common, with the escape rhythm providing sufficient cardiac output to sustain vital functions in the short term. ECG features of idioventricular escape beats include:

FIGURE 11.16 Ventricular escape rhythm (idioventricular rhythm). Note that after the first sinus beat, the slow rate allows the ventricular escape rhythm to emerge. The resultant rhythm is at a rate of 35/min, with wide QRS complexes and absent P waves.

When these beats occur at a rate of 20–40/min the rhythm is termed ventricular escape, or idioventricular rhythm. Under excitatory influences the ventricular pacemaker cells may increase their firing rate to between 60 and 100/min (accelerated idioventricular rhythm) or to faster than 100/min (ventricular tachycardia).²⁰

Accelerated Idioventricular Rhythm

Accelerated idioventricular rhythm (AIVR) has assumed a special place in cardiology because of its relatively common appearance during postinfarction reperfusion, thus often indicating successful revascularisation following PCI or thrombolytic therapy.^20,21 It may therefore imply therapeutic success rather than mishap, and usually needs no treatment. The arrhythmia is commonly due to increased automaticity and as with other automaticity arrhythmias may show a ‘warm-up’ in rate, i.e. it may commence and then gradually accelerate and settle at a faster rate. This behaviour can be useful in differentiating arrhythmias from reentry which typically have an abrupt change in rate as their onset. When it occurs outside of the context of reperfusion, AIVR should be regarded as inappropriate ventricular excitation (Figure 11.17).

FIGURE 11.17 Accelerated Idioventricular Rhythm (AIVR) following reperfusion in myocardial infarction. An accelerated ventricular focus emerges at 65/min, taking over from the slower sinus rate of 60/min. It then accelerates gradually until settling at a rate of 85/min by the end of the second strip. This display of rate ‘warm-up’ at onset is a characteristic of arrhythmias due to increased automaticity. The distortion of the ST segment from the third beat of AIVR onwards is due to retrograde conduction to the atria, and explains the absence of the sinus P waves.

Atrioventricular Conduction Disturbances

Atrioventricular conduction disturbances make their appearance as delayed or blocked conduction from atria to ventricles, and thus appear as altered P–QRS (or P–R) relationships. The conventional classifications for AV block are based purely on the patterns of conduction. The classification as first-, second- and third-degree partially represents the severity of AV node or His-bundle dysfunction.^7,9 AV block may complicate heart disease but is also seen commonly with drug therapy (e.g. digitalis, calcium channel blockers, beta-blockers and other antiarrhythmics).²⁰ It may occur abruptly following vagal stimulation. When accompanying myocardial infarction, it is more likely to be transient following inferior infarction; whereas its appearance following anterior infarction is more likely to be permanent.

Degrees of Atrioventricular Block

First-degree AV block

All atrial impulses are conducted to the ventricles but conduction occurs slowly, with a P-R-interval >0.20 sec. 1 : 1 AV conduction is maintained (see Figure 11.18).

FIGURE 11.18 Sinus rhythm with first-degree AV block. Rhythm is regular, rate 100/min, 1 : 1 AV conduction, with a P-R interval of 0.24 sec.

Second-degree AV block

This is an intermediate level of block in which some P waves conduct to the ventricles while others do not. Thus there are periodic non-conducted P waves, or ‘dropped’ beats. A further distinction is usually made into either type I or type II second-degree AV block, as follows:

• Second-degree AV block type I (Wenckebach): A cyclical pattern of AV conduction is seen in which the conducted P waves show a progressive lengthening of the P–R interval until one fails altogether to be conducted (blocked, or dropped, P waves). Cycles begin with a normal or (often) prolonged P–R interval, which then extends over succeeding beats until there is a dropped beat. After the dropped beat the cycle recurs, commencing with a P–R interval equivalent to that commencing previous cycles⁶³ (Figure 11.19). The frequency of dropped beats partially represents the severity of AV block. When, for example, every fifth P wave is not conducted, 5 : 4 conduction is said to be present. If AV conduction deteriorates further, more frequent P waves fail to be conducted (4 : 3, 3 : 2 conduction).

• Second-degree AV block Mobitz type II: Dropped beats (non-conducted P waves) are also present, but the conducted beats show a uniform P–R interval rather than any progressive lengthening⁹ (Figure 11.20). The dropping of beats may be regular, e.g. every fourth P wave (termed 4 : 1 block), progressing to 3 : 1, or even 2 : 1 block as AV nodal, or more commonly, His-Bundle conduction, worsens. Alternatively, the dropping of beats may be more irregular (variable block), with combinations of 2 : 1, 3 : 1, 4 : 1 or other levels of block evident in a given strip. The more frequent the dropped beats, the slower the ventricular rate and the greater the likelihood of symptoms. Second-degree Type II AV block is often associated with intraventricular conduction delay, with corresponding widening of QRS complexes. When this is seen it represents conduction impairment not just of the AV node but of intraventricular conduction as well. Progression to complete AV block is more common.⁹

FIGURE 11.19 Sinus rhythm with second-degree AV block type I. Every third P wave is not conducted (3 : 2 conduction). The P–R interval can be seen to lengthen before the dropped beats(*). After the dropped beats the cycle starts with a P–R interval of 0.18 sec. It then extends to 0.25 sec before again dropping a beat.

FIGURE 11.20 Second degree AV block type II. A non conducted beat confirms the second degree block. There is no progressive prolongation of the P–R interval before the dropped beat (*), rather, the uniformity of all P–R intervals distinguishes this as type II.

A final form of second-degree block is ‘high-degree’ AV block, in which conducted P waves show a uniform P–R interval but, rather than single periodic dropped beats, multiple consecutive non-conducted P waves can be seen (Figure 11.21).

FIGURE 11.21 Sinus rhythm with high degree AV Block. At the beginning and end of the strip there is second degree block (2 : 1). Alternate P waves fail to conduct, qualifying as at least second degree AV block. The appearance of consecutive non-conducted P waves in the middle of the strip (5 in a row), however, escalates the classification to ‘high degree’ block.

Third-degree (complete) AV block

None of the atrial impulses are conducted to the ventricles, resulting in a loss of any relationship between P waves and QRS complexes (AV dissociation). Usually a lower pacemaker assumes control of the ventricular rate, and this focus may be either junctional (narrow QRS, at a rate of 40–60/min) or ventricular (wide QRS, at a rate of 20–40/min) (Figure 11.22).⁹

FIGURE 11.22 Sinus rhythm with third-degree AV block. Note the P waves (asterisks) at a rate of 90–100/min and the ventricular rate of 40/min. The P waves bear no relationship to the QRS complexes – they are dissociated. (The seventh asterisked P wave is premature and different in morphology from the others, and is therefore possibly an atrial ectopic P wave).

Nursing Management During AV Block

AV block may be progressive in nature, and may worsen with advancing heart disease or after introduction, or dose modification of drugs that depress AV conduction.^23,24 Thus monitoring should include P–R interval measurement, and where the P–R interval becomes prolonged there should be an increase in vigilance directed towards further prolongation or the development of dropped beats, to signify advancing AV block. Treatment of AV block and bradycardia includes immediate assessment of cardiovascular status or other symptoms, including chest pain, dyspnoea, conscious state and nausea. The cause should be identified and treated where possible. Patients need to be on rest in bed, provided with reassurance and oxygen by mask or nasal prongs. If the patient is hypotensive, IV fluids should be administered and the patient laid flat. Standardised protocols for bradycardia should be applied if the patient is symptomatic, and these usually include:¹⁸

If the patient is pulseless or unconscious, standard advanced life support should be administered (see Chapter 24). Persistent or recurrent symptomatic bradycardia or AV block may require permanent pacemaker implantation.^18,19

Patterns of Ectopy

Some patterns of ectopic frequency and morphology may warn of increasing risk for the development of serious arrhythmias such as ventricular tachycardia or fibrillation, and therefore earn a particular mention in monitoring. Historically, ectopic patterns have been graded according to their pre-emptive risk of serious arrhythmia development or 2-year mortality.²⁹ Studies undertaken in 2003 and 2005 did however call into question the predictive status of certain ‘high risk’ ectopic patterns (such as ‘R on T’ ectopy), instead postulating that other factors such as a patient’s underlying left ventricular function and level of autonomic responsiveness may play a more significant role in the generation of life threatening ventricular tachyarrhythmias, independent of the prior presence or pattern of ectopy present.^30,31 However, in the critical care context it is reasonable to respond to certain patterns (as shown in Box 11.1) by investigating and managing potential contributing causes. If the patient can be seen to be advancing through stages of increased arrhythmic complexity consideration for antiarrhythmic therapy should be given.

Ventricular Tachycardia

Ventricular tachycardia (VT) is described as a ‘run’ of three or more consecutive ventricular ectopic beats, at a rate greater than 100/min (Figure 11.24).¹² The arrhythmia varies in its clinical impact, but when sustained is typically symptomatic with some degree of haemodynamic compromise. Ventricular tachycardia often presents as cardiac arrest, with the patient pulseless and unconscious, and is one of the major mechanisms of sudden cardiac death. The severity of symptoms depends partly on the rate (which may be 100–250/min), the duration of the arrhythmia, the presence of cardiac disease (ischaemic, congestive, hypertrophic, cardiomyopathic), and the presence of co-morbidities.^9,32 When it develops, VT may be categorised as self-limiting (terminating without treatment), sustained for some period of time (minutes or longer), incessant (persisting until or despite treatment) or intermittent. Additional defining terminology includes monomorphic (all beats of the same morphology) or polymorphic (in which the rhythm conforms to the other features of VT but there is variability in the QRS shapes). ECG features of ventricular tachycardia:^14,32,33

FIGURE 11.24 Sinus rhythm at 65/min before onset of ventricular tachycardia. Note a ventricular ectopic emerges from the T wave of the third sinus beat (R-on-T ventricular ectopic), precipitating ventricular tachycardia (VT). The VT is then sustained at a regular rate of 220/min, with the characteristic wide QRS and ST/T in opposite direction to the QRS.

If VT is not self-limiting, treatment depends on the severity of the symptoms. If the patient becomes pulseless and unconscious, advanced life support is initiated (see Chapter 24). If the patient is conscious and has a pulse, therapy can be undertaken more cautiously. Occasionally, robust coughing may revert VT in the cooperative patient. Antiarrhythmic therapy (at slower administration rates than during cardiac arrest) is usually undertaken first, along with biochemical normalisation. If unsuccessful, sedation and elective cardioversion may be necessary. Consideration for internal cardioverter defibrillator (ICD) implantation should be given to patients surviving ventricular tachycardia or fibrillation.^34,35

Ventricular Flutter

This uncommon arrhythmia is most likely just a subset of ventricular tachycardia, but because of its rapid rate (at times up to 300/min or more) and the appearance of QRS complexes that are largely indistinguishable from the T waves, ventricular flutter has earned its own classification.³² An example is shown in Figure 11.25. The diagnostic separation from other types of VT is clinically unimportant, and treatment should follow normal guidelines for VT.

FIGURE 11.25 Probable ventricular flutter. The complexes are broad, regular and monomorphic (one shape), but it is difficult to know which is the QRS deflection and which is the T wave. This feature plus the very fast rate of 300/min or more are the typical defining characteristics of this uncommon but serious arrhythmia, recorded during recovery from tricyclic antidepressant overdose in a 16-year-old female.

Ventricular Fibrillation

During ventricular fibrillation there is no recognisable QRS complex. Instead, there is an irregular and wholly disorganised undulation about the baseline.^5,9 There are deflections, which at times approach rates of 300–500/min, but these are typically of low amplitude and none convincingly resemble QRS complexes (Figure 11.26). In the absence of organised QRS complexes the patient becomes immediately pulseless, and unconsciousness follows within seconds. Immediate defibrillation is required. If VF persists treatment occurs according to standing basic and advanced life support guidelines.

FIGURE 11.26 Ventricular fibrillation. Rapid, irregular and wholly disorganised deflections from the baseline are present, and produce nothing resembling QRS complexes.

Polymorphic Ventricular Tachycardias

These forms of VT do not have a single QRS morphology. Rather, the QRS complexes during the rhythm vary from one shape to another, either alternating on a beat-to-beat basis or switching between groups of beats, with first one morphology and then another (bidirectional VT).^9,32 The more common form of polymorphic VT is Torsades de Pointes (TdP), in which the QRS undergoes a gradual transition from one QRS pattern to another. The descriptive French term, literally ‘twisting of the points’, refers to the appearance of the ‘points’ (QRS direction), which is first positive and then negative, usually with an ill-defined transition between the two (Figure 11.27).^28,36,37

FIGURE 11.27 Torsades de pointes polymorphic ventricular tachycardia. After 3 beats of sinus rhythm a ventricular ectopic beat emerges from the T wave and precipitates onset of a rapid and sustained polymorphic ventricular rhythm. The characteristic sinusoidal twisting around the baseline and changing direction of the QRS is clearly apparent, and along with the rate of 300/min defines this as torsades de pointes.

ECG features of Torsades de Pointes are:^28,36,37

Because of the very rapid rate, syncope and cardiac arrest are common, and advanced life support practices required. A thorough search for possible causes of Q–T prolongation should be undertaken. Causes include: class Ia (procainamide, quinidine, disopyramide) or class III (amiodarone, sotalol) antiarrhythmics,^5,9 erythromycin, antidepressants, hypocalcaemia, hypokalaemia and hypomagnesaemia.³² Congenital long Q–T syndromes also exist.³⁶ Apart from the general ventricular arrhythmia management principles listed below, the treatment of TdP includes cessation of Q–T prolonging agents, a greater emphasis on IV magnesium, and the use of isoprenaline and/or pacing to shorten the Q–T interval and prevent bradycardia.³⁸

Bradycardia in patients with long QT requires special mention as Torsades de Pointes is so often bradycardia, or pause, dependent. Pauses prolong the QT and favour ectopy which more easily find the T wave, triggering TdP. The role of pacing and isoprenaline are to both prevent pauses, and to shorten the QT interval.^36,39

Management of Ventricular Arrhythmias

The emergency management algorithm for life-threatening ventricular arrhythmias is described in the chapter on resuscitation. In general terms, the management of ventricular arrhythmias should include the following:³⁸

Capture

A ventricular pacing stimulus that successfully generates a QRS complex is said to have ‘captured’ the ventricles. The same applies when an atrial pacing stimulus ‘captures’ the atrium. It is important to verify that all of the stimuli cause capture. If pacing stimuli are not followed by a P wave or a QRS complex, ‘failure to capture’ is said to be occurring and requires immediate corrective action (see Figure 11.28).

FIGURE 11.28 Ventricular pacing at 86/min. There is capture on the first five beats but none of the remaining pacing spikes are followed by the expected wide QRS of capture. Note: while there is capture, the patient’s own rhythm is suppressed. When capture is lost, the patient’s slower rate emerges. Consistent capture needs to be re-established, by either increasing the pacemaker output or correcting factors that depress myocardial responsiveness.

Output and Threshold

The strength of the pacing stimulus applied is termed the pacing ‘output’, which is adjustable by the operator. On initiation of pacing, output is typically increased gradually until 100% capture is achieved. The minimum output required to achieve capture is termed the output threshold. Threshold may vary significantly with changes in biochemistry, arterial pH, myocardial perfusion, drugs and other factors.^53,57–59 To accommodate potential threshold changes, output settings on the pulse generator are set with a ‘safety margin’, i.e. at least double the threshold value.⁵⁸

Demand versus Asynchronous Pacing

Pacing can be configured in either demand (sensing), or asynchronous (non-sensing) modes.

Demand pacing

The most common approach to pacing are the so-called ‘demand’ modes. In these modes, pacing is provided only on demand: that is, when the heart rate falls below a nominated level (demand rate) (Figure 11.29). Demand pacing requires pacemaker detection of the patient’s intrinsic cardiac rhythm. If intrinsic rhythm is sensed, it ‘inhibits’ the pacemaker from delivering a pacing stimulus. The demand modes ensure that pacing is provided only when needed, and also protect against pacing during arrhythmically vulnerable moments in the cardiac cycle. Ventricular pacing delivered at the time of the T wave may induce ventricular tachyarrhythmias (Figure 11.30), whilst atrial pacing during atrial repolarisation (shortly after the P wave) may precipitate atrial tachyarrhythmias.⁶⁰

FIGURE 11.29 Demand ventricular pacing at a rate of 60/min. The patient’s rate increases after the first two paced beats and inhibits the pacemaker. It then slows to below 60/min and the pacemaker recommences ‘on demand’.

FIGURE 11.30 Intermittent asynchronous pacing due to incomplete sensing. Set pacing rate 66/min. The 1st, 3rd and 4th beats are sensed and appropriately inhibit pacing. However, a pacing spike can be seen at the apex of the T wave of the 2nd beat, which does not cause arrhythmia. The next pacing spike, just after the apex of the T wave of the 5th beat, arrives during the period of increased excitability in the action potential and precipitates ventricular tachycardia.

Ventricular Pacing

Stimulation of just the ventricles results in the generation of a ventricular ectopic rhythm. Functionally this will be no different from an intrinsic ventricular rhythm. There will be loss of atrioventricular synchrony, and the loss of effective atrial kick may cause low cardiac output and hypotension. To offset the loss of atrial kick, ventricular pacing is sometimes undertaken at slightly higher rates than normally seen in the resting patient (e.g. 70–80/min, rather than 50–60/min).

The delivered pacing stimulus should be followed immediately by a QRS complex which is wide (>0.12 sec) and often notched. Pacing from near the apex will produce an ECG which closely resembles left bundle branch block morphology, with left axis deviation. Repolarisation abnormalities are also seen, with ST segments and T waves displaced in the opposite direction to the major QRS direction in each lead.⁵⁷

Ventricular pacing provides protection against bradycardia or AV block by stimulating the ventricles at a set (programmable) rate (Figure 11.31). Temporary, emergency, ventricular pacing may also be undertaken to prevent bradycardia-dependant tachyarrhythmias such as TdP.⁶³ Pacing provides protection by both reducing the QT interval, as well as preventing pauses which give rise to ectopy and onset of TdP.⁶³

FIGURE 11.31 Onset of ventricular pacing. At the start of the strip the patient’s heart rate is around 70/min. The pacemaker is then turned on with the rate set at 80/min. Capture is achieved immediately, and because the pacing rate is faster there is suppression of the patient’s own rhythm. Note the wide QRS and ST elevation during pacing. This is the expected appearance.

Atrial Pacing and AV Block

Any degree of AV block is possible during atrial pacing and is rate dependent.^64,65 Thus the severity of AV block may be worsened, not only by AV node dysfunction but also by changes in the atrial pacing rate. A patient with first-degree block may develop second-degree block if the atrial pacing rate is increased, without this implying worsening AV node function. Conversely, AV block developing during atrial pacing may be lessened or overcome by reducing the atrial pacing rate. An example of such rate-dependent AV block behaviour is demonstrated in Figures 11.33 to 11.35 which are sequential strips from the same patient.

FIGURE 11.33 Atrial pacing at 70/min with first-degree AV block. Note the long P–R interval, at almost 0.4 sec; particular caution is warranted in increasing the rate, as, although AV conduction is 1 : 1, it is already very slow. See the next 2 figures for worsening of AV block as the atrial rate is increased.

FIGURE 11.34 Second-degree AV block type I with 3 : 2 conduction. The same patient as above, with worsening AV block after increasing the atrial pacing rate to 80/min. Note: the 1 : 1 conduction has been lost and there are dropped beats. After each of the dropped beats the P–R is 0.30 sec, which extends to 0.46 sec on the next beat, before dropping of the 3rd beat of each cycle.

FIGURE 11.35 The same patient again, now with the atrial pacing at 86/min. At the faster atrial rate, AV conduction has worsened further. There is now a 2 : 1 block yielding a ventricular rate of 43/min.

DDD Pacing: The ‘Universal’ Pacing Mode

The introduction of the DDD mode of pacing added an important new dimension to dual-chamber pacing, that is, the ability to synchronise ventricular pacing to spontaneous atrial activity in patients with AV block.⁶² In addition to the normal bradycardia and AV block protection, the DDD mode features a ‘triggered’ function. If the pacemaker detects a P wave but a QRS does not follow within the preset AV interval (AV block), the pacemaker will be triggered to provide ventricular pacing at the end of the programmed AV interval. This means that the ventricular rate can be brought back under control of the sinus node, even though there is AV block. Consequently, in a DDD pacemaker it is common to see ventricular pacing at a range of different rates as it responds to sinus activity. This triggered behaviour of the DDD device is sometimes called ‘P-synchronous ventricular pacing’, although ‘atrial tracking’ is a more practical term as the ventricular pacing ‘tracks’ the atrial rate.

Atrial tracking allows the pacemaker to pace the ventricles in response to the atrial rate sensed by the pacemaker. This is desirable when the atrial rate is controlled by the sinus node, but is inappropriate during atrial arrhythmias. Atrial tracking at a 1 : 1 rate during atrial flutter would produce an intolerable ventricular rate of 300/min, and during atrial fibrillation the tracking rate could be even higher. For this reason, an ‘upper rate’ for atrial tracking is programmed in the DDD pacemaker. The upper rate controls the maximal rate at which ventricular pacing can be provided, (how fast it may track the atria at a 1 : 1 ratio). This is typically set to around 120–130 per minute. In younger patients it may be set higher, e.g. 140–150/min.

This triggering of ventricular pacing in response to sensed P waves is intended to mimic the behaviour of the AV node. It ensures that a QRS follows each P wave and brings the ventricular rate back under the control of the sinus node (see Figures 11.38 and 11.39). Pacing will be seen at a wide range of rates, as the ventricular pacing follows the normal speeding and slowing of the sinus rate in response to such conditions as pain, fever and activity. If the atrial rate exceeds the upper rate for tracking, then it is no longer possible for all of the atrial beats to be tracked. DDD pacemakers will start ‘dropping’ beats in a manner analagous to the behaviour of the AV node.

FIGURE 11.38 ECG excerpt from a patient with sinus rhythm and 2 : 1 AV block. The non-conducted P waves are partially concealed but can be seen distorting the T waves (arrows). Although the sinus node can generate a rate of 75/min, the patient is rendered bradycardic by the AV block.

FIGURE 11.39 The same patient as above, 2 hours later. A DDD pacemaker has been inserted, and although some of the pacing spikes are difficult to see, all QRSs are paced beats. The sinus rate is again close to 75/min, and atrial tracking ensures that a paced QRS follows each P wave. The ventricular rate has been brought back under control of the sinus node. Note: although set to a backup rate of 60/min, the pacemaker is pacing much faster than this because of the triggered behaviour of DDD.

External (’Transcuataneous’) Pacing

Emergency pacing may be undertaken noninvasively via external pacing electrodes, and is termed ‘external’, ‘transthoracic’, or ‘transcutaneous’ pacing. Standard, self-adhesive defibrillation pads are applied in either the antero-posterior (preferred), or standard right parasternal-apical positions as per defibrillation. These are connected to a defibrillator with additional pacing capability. Pacing stimuli of large current (10–200 mA) are necessary to achieve myocardial capture, and frequently also cause uncomfortable or painful skeletal muscle stimulation. Its use is therefore usually reserved for highly symptomatic/life-threatening bradyarrhythmias, and only as a short-term bridge to invasive pacing. Sedation is typically required in the conscious patient.

External cardiac pacing provides ventricular pacing only, and the patient should be assessed not only for reliable capture, but also for an adequate pulse and blood pressure during pacing. Pacing may be in either demand or asynchronous mode, usually at rates of 40–80 beats per minute.

Failure to capture

The event in which pacing spikes do not successfully stimulate the heart is termed ‘failure to capture’. Pacing spikes are evident on the ECG but are not followed by either QRS complexes (in ventricular pacing) or P waves (in atrial pacing) (see Figures 11.40 and 11.41). Failure to capture may occur when the myocardial responsiveness (threshold) worsens, or when impulses do not reach responsive myocardium. Note that dislodgement of a lead from the myocardium will still show pacing spikes on the ECG as long as the lead is in contact with body fluids or tissue. Repositioning of leads must therefore be included in considerations during management.

FIGURE 11.40 Intermittent failure to capture. The 1st, 2nd, 6th and 7th spikes gain ventricular capture but the rest do not. Note the significant pause during failure to capture, in which there is atrial but not ventricular activity. Symptoms during failure to capture depend on the rate of any underlying rhythm.

FIGURE 11.41 Atrial pacing with intermittent failure to capture (output set at 14 mA). Note: capture is evident following the 1st, 3rd, 5th, 7th and 8th pacing spikes, but not the others. Fortunately, here the patient has an underlying sinus rhythm, so that the impact of failure to capture is of no great consequence.

Failure to capture may present as a clinical emergency and requires immediate attention. With failure to capture, patients are left to generate their own rhythm, which may be unacceptably slow. Failure to capture may be complete (all spikes not capturing) or intermittent (with only some spikes achieving capture). Even if there are only occasional spikes that fail to capture, immediate attention is required, as complete failure to capture may ensue (see Case Study at the end of this Chapter). Causes and management of failure to capture^{51,58,59,68,69} are listed in Table 11.5.

TABLE 11.5 Failure to capture: causes and management

Pacemaker testing in the unstable pacemaker-dependent patient

Greater caution must be applied in the testing of pacemaker functions if the patient has marked haemodynamic instability or has little or no underlying rhythm. It is common for pacemaker testing to be avoided altogether in such circumstances although this may be misguided. Routine testing of pacemaker function as described in Figure 11.46 may not be suitable, but testing for underlying rhythm, and some level of testing of capture threshold so as to be confident of safety margins is beneficial. For the patient with haemodynamic instability and/or inotrope use, testing for underlying rhythm becomes of even greater important as pacing may either prevent or conceal the return of sinus rhythm capability, and cardiac output may be as much as 50% greater with the atrial kick of sinus rhythm than during pacing (see Figure 11.47). It may take several seconds for the sinus node to ‘warm up’ and express itself, so decrease the rate gradually and only to reasonable levels (sinus rates of less than 50 are unlikely to be beneficial). Be sure to gain agreement from the multi-disciplinary team before undertaking testing in this context.

FIGURE 11.47 Unveiling haemodynamically superior underlying rhythm (strips are continuous). Initially there is ventricular pacing at a rate of 68/min. No atrial activity can be seen and the blood pressure is 85/50 mmHg with noradrenaline support at 8 mcg/min. Across the top strip the paced rate is reduced, allowing P waves to emerge at a rate of 60/min (arrow) and then accelerate to around 70/min across the lower strip. Note the impressive BP increase to 125/65 mmHg allowing discontinuation of noradrenaline infusion. (Note also: cardiac index recorded during V pace 1.7 L/min/m², during sinus rhythm 2.3 L/min/m²). Importantly, there was no suggestion of sinus capability until the pacing rate was reduced.

Threshold testing in the pacemaker-dependent patient is also contentious as loss of capture during testing may be poorly tolerated. If the capture threshold is not measured, however, a rising threshold and loss of safety margins cannot be identified, and may only become apparent upon development of acute failure to capture, possibly with outputs already set to maximum and therefore no scope for recovering capture. An alternative approach to testing thresholds in this context is useful. Rather than formally measuring threshold by creating loss of capture, the output may be decreased to a value which confirms safety margins are still possible, but without having lost capture at any point, e.g. decreasing output to 10 mA on a device with an output capability of 20 mA. If there is still capture at 10 mA then further reductions can be avoided because a 10 mA safety margin has been demonstrated.

Tachyarrhythmia Detection and Classification

ICDs are configured to classify and treat arrhythmias first on the basis of rate. Defibrillation algorithms using high-energy settings (30–40 J) are followed when the rate is very fast (e.g. >200/min), as syncope is likely even if the rhythm is not ventricular fibrillation (e.g. very fast VT). At slower rates, other antitachycardia options may first be attempted as described above. Additionally, at slower rates of tachycardia, attempts are made to discriminate between ventricular and supraventricular (including sinus) tachycardias (SVTs) using a variety of criteria, as shown in Figure 11.51. SVT discrimination by a device is similar to criteria a clinician would use when deciding between VT and SVT and includes regularity or irregularity of the rhythm, sudden or gradual onset, similar or different morphology to the previous sinus rhythm and atrioventricular relationships. If these discriminators indicate that a tachyarrhythmia is supraventricular, then therapy can be withheld, avoiding inappropriate therapy. The major device capabilities and programming options of an ICD are shown in Figure 11.51.

FIGURE 11.51 Implantable cardioverter defibrillator (ICD) programmed parameter summary report from St Jude Medical ICD Atlas^TM DR Model V-240 (Courtesy St Jude Medical, St Paul, MN): box 1, detection criteria. Arrhythmias are classified first on the basis of ventricular rate as detected by sensing circuitry. Defining rates for each rhythm classification are programmable. In the example shown above a rate of >182/min or greater is the cut-off for ‘Fib Detection’, which then initiates treatment following the steps for fibrillation (Fib/MTF) (box 3). ‘Tach Detection’ is classified when the rate is between 160 and 182, then further information can be sought to differentiate between supraventricular and ventricular arrhythmias and initiate appropriate treatment (box 2); box 2, SVT criteria. When rhythms fall into the ‘Tach Detection’ rate (here 160–182/min), treatment is momentarily suspended to allow classification as SVT. If ventricular rate >atrial rate, then the rhythm is classified as VT and therapy applied according to ‘Tach’ (box 3). When ventricular rate <atrial rate (V<A in box 2), the rhythm could be either SVT or VT and an assessment of interval stability is made (with marked irregularity supporting AF and the withholding of treatment). ECG morphology distinction can also be enabled (although here is OFF) that compares morphology prior to and during tachycardia. If the ventricular and atrial rates are the same (V=A), again the rhythm could be either VT or SVT and further discrimination is made on morphology and on whether onset was sudden or gradual. This process of rhythm detection is extremely rapid and does not unnecessarily delay therapy. Additionally, even when SVT criteria are met, they are usually subordinate to sustained rate in the ‘Tach Detection’ algorithm; thus, if the tachycardia persists for a set qualifying period, therapy is initiated according to the ‘Tach’ algorithm in box 3; box 3, tachyarrhythmia therapy. Usually two treatment arms, each with six steps, are prescribed and are independently programmable. Tachyarrhythmias in the ‘Fib’ range are managed more aggressively than those in the ‘Tach’ range. Escalating energy settings for defibrillation may be described, but here all six attempts at defibrillation are at maximum (36 J). Treatment in the ‘Tach’ range usually commences with one or more attempts at antitachycardia pacing (ATP), progressing to cardioversion; box 4, tach ATP. This describes the parameter setting during antitachycardia pacing. In this example 7.5 V is delivered to the ventricles at a basic cycle length (BCL), which is 85% of the cycle length of the tachycardia (pacing is delivered slightly faster than the tachycardia). It will provide up to three ‘bursts’ of pacing, each of 10 beats or ‘stimuli’. Ramping is turned off in this case, but if ON it permits the pacing rate to increase progressively after each unsuccessful attempt at overdrive.

Patients receiving ICDs require particular education and support, as the experience of shocks can be painful and disturbing and the anticipation of shocks is a cause of anxiety and/or depression.^70,103 This is especially true of shocks delivered to the conscious patient. Inappropriate therapy delivery remains a significant problem, and as many as 25% of ICD therapies have been reported as inappropriate, delivered due either to supraventricular arrhythmias or oversensing of electromagnetic interference.^103,104 The avoidance of strong electrical fields (welding, magnetic resonance imaging, generators) should be stressed, as well as direct contact with devices such as TENS machines or electrocautery devices.⁷⁰ If surgery requiring diathermy becomes necessary, antitachycardia therapies are usually programmed to OFF to avoid inappropriate detection and treatment.

Patients should be encouraged to rest after any therapy delivery, and where multiple or inappropriate discharges occur they should report to a healthcare facility for assessment.¹⁰⁵ If repeated inappropriate therapy continues, it may be suspended by the placement of a ring magnet over the device.⁷⁰ This suspends the antitachycardia features of the device while the magnet is in place – no therapy will be delivered by the device. Removal of the magnet will immediately reactivate antitachycardia therapies. Back-up (antibradycardia) pacing functions remain active and unaffected during magnet application.

In the event of unsuccessful reversion of a ventricular arrhythmia by ICD therapy, standard advanced life support protocols should be applied. External defibrillation can be undertaken with paddles in normal positions, taking care to avoid positioning paddles over the ICD.¹⁰⁵ External chest compressions can safely be undertaken by rescuers, including during device therapy.⁷⁰

Terminal Care and Mechanisms of Death in the Patient with an ICD

ICDs often create uncertainty amongst health care workers as to how death may occur. In the palliative patient, where active resuscitation for cardiac death is not to be pursued, the decision to disable antitachycardia therapies is often taken. This can be achieved by reprogramming the ICD, and there is often sufficient time to incorporate this step into palliative planning. Alternatively, when active treatment is being withdrawn as a patient progresses more rapidly towards an unexpected (acute) death, there may be a need to disable therapy before the availability of personnel to reprogram the device. In this context it may be appropriate to secure a ring magnet over the ICD (tape it in place). This will disable tachycardia therapies so that if the terminal rhythm is VT or VF, therapies will not be delivered.

Other than by disabling therapy, cardiac death may occur by normal mechanisms. Cardiac arrest in the acute context, as well as when it occurs as the endpoint of terminal illness, ultimately occurs when cardiac metabolism fails or systemic factors cause cardiac depression or arrhythmic irritability. The same remains true of the patient with an ICD. However, cardiac depressive factors will not cause bradycardia or asystole because of the pacemaker function. What would otherwise be a bradyarrhythmic death will instead become eventual failure to capture by the pacemaker. Similarly, if the cardiac impact of acute or terminal illness produce tachyarrhythmias, then these same influences will increase the defibrillation threshold and antitachycardia therapies will become unsuccessful. Devices offer no protection against pulseless electrical activity.