Cardiac Rhythm Assessment and Management

11 Cardiac Rhythm Assessment and Management







The Cardiac Conduction System


The normal heartbeat sequence occurs through rhythmic stimulation of the heart via its specialised conduction system. The sinoatrial node, located superiorly in the right atrium, spontaneously generates an activation current that conducts across preferential right and left atrial pathways (producing a P wave on the surface ECG) and then to the atrioventricular node at the lower interatrial septum. After a brief physiological slowing of the current (to allow the ventricles to be optimally ‘pre-loaded’), the impulse travels to the Bundle of His in the upper interventricular septum before spreading down through the ventricles via the right and left bundle branches. These terminate distally as branching Purkinje fibres which penetrate and activate the ventricles. This ventricular activation (or depolarisation) sequence produces a QRS complex on the surface ECG and subsequent repolarisation gives rise to an electrocardiographic T wave. Pathophysiological processes may disrupt this sequence, giving rise to arrhythmia production.1,2



Arrhythmogenic Mechanisms


Arrhythmias result from three primary electrophysiological mechanisms; abnormal automaticity, triggered activity and reentry, each of which is described below.






Arrhythmias and Arrhythmia Management


Arrhythmias may arise from myocardial or conduction system tissue, and may represent inappropriate excitation or depression of automaticity, altered refractoriness resulting in micro-reentry arrhythmias, or may involve reentry on a larger scale, as between the atria, AV node and/or ventricles.3


The clinical impact of tachyarrhythmias is highly variable and is influenced by the rate and duration of the arrhythmia, the site of origin (ventricular vs supraventricular), and the presence or absence of underlying cardiac disease. As a result, arrhythmias may require no treatment, at least in the short term, or at worst may present as cardiac arrest and require treatment according to advanced life support algorithms (as described in Chapter 24).


Bradyarrhythmias may be due to failure of sinus node discharge (sinus bradycardia, pause, arrest, or exit block) or to failure of AV conduction (second- or third-degree AV block). In any of these contexts, junctional or ventricular escape rhythms may make their appearance. Failure of escape foci may result in asystole or ventricular standstill.



Arrhythmias of the Sinoatrial Node and Atria


In health, the sinus node controls the heart rate according to metabolic demand, responding to autonomic, adrenal and other inputs, which vary according to exertion or other stressors. In response to needs, the sinus node discharge rate typically varies from as low as 50 beats/min to as high as 160 beats/min. In the conditioned heart (e.g. in athletes), this range extends perhaps down to as low as 40 beats/min, and to as high as 180 beats/min. Peak activity in the elite athlete may even achieve sinus rates of 200/min, though this represents the extreme end of the sinus rate. Sinus rhythm is illustrated in Figure 11.1.




Sinus Tachycardia


In adults, a sinus rate of greater than 100/min is termed sinus tachycardia and may occur with normal exertion7,8 (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.




Sinus Bradycardia


A sinus rate of less than 60 beats/min is termed sinus bradycardia7,8 (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.




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.




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.





Arrhythmias of the Atria and Atrioventricular Node


The term supraventricular tachycardia (SVT) is often used to group the tachyarrhythmias which arise from tissues above the ventricles. In its more common usage, SVT is thus an umbrella term, to include any of the tachyarrhythmias arising from the sinus node, the atrial tissue or the atrioventricular node.10 However, when a specific arrhythmia can be classified, the specific term is used rather than the more general term SVT. On occasion the electrocardiographic distinction between atrial flutter, atrial tachycardia and atrioventricular nodal reentry tachycardia may be difficult to make, and it may be useful in that context to use the more general term SVT. Supraventricular arrhythmias may occur as single-beat ectopics arising from atrial or junctional tissue, or runs of consecutive premature beats, and thus be termed supraventricular tachycardias. SVTs may be self-limiting (paroxysmal) or sustained (until treatment), recurrent or incessant (sustained despite treatment).




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.






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




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.



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





Bradyarrhythmias and Atrioventricular Block


Bradycardia, a slowing of the ventricular rate to less than 60 beats/min, may occur in the form of slowing of the sinus node rate or failure of conduction at the level of the AV node. As the rate slows, escape rhythms should intervene, limiting the severity of the bradycardia. However, these may also fail, rendering the patient asystolic or with catastrophic bradycardia.18,19



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).






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




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




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).





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



Ventricular Arrhythmias


Ventricular ectopic rhythms may either occur as a response to slowing of the dominant cardiac rhythm (escape beats or escape rhythms) or may emerge at faster rates than the dominant rhythm (as premature ectopic beats, couplets, or ‘runs’ of ventricular tachycardia).9 Escape rhythms (occurring after a pause) should be regarded as physiological, as they protect against otherwise severe bradycardia (see Figure 11.16), whereas premature beats and rapid ventricular ectopic rhythms (occurring in advance of the dominant rhythm) occur when pathology gives rise to increased automaticity or reentry behaviour (Figure 11.23).7,9 Single ectopic beats may be benign occurrences, often seen in the absence of heart disease. However, their new appearance accompanying cardiac or systemic disease may precede the development of more serious arrhythmias, such as ventricular tachycardia or fibrillation, and thus warrant close monitoring. Ectopic beats, whether premature or late (escape), show characteristic features as follows:




Ectopic beats may occur as single or coupled beats, or in runs of consecutive beats. Ventricular tachycardia is defined as greater than 3 consecutive ventricular beats occurring at a rate greater than 100/min.5


Causes of ventricular tachyarrhythmias include:3,8,28




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




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 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.




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



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



a search for and correction of causes, including










immediate CPR and cardioversion/defibrillation for pulseless, unconscious ventricular arrhythmias (cardiac arrest).38 In conscious patients, initial treatment is usually pharmacological, and, if necessary, cardioversion is applied under the influence of short-acting anaesthetics (e.g. propofol)


antiarrhythmic therapy




heart failure management, which needs to be aggressive if contributory


electrophysiological (EP) testing, which should be performed for serious arrhythmias to identify foci or pathways and confirm effectiveness of treatment41


pacing strategies




implantable cardioverter defibrillator therapy, which should be considered for all survivors of sudden cardiac death,34,35 especially those with low ejection fraction and recurrent sustained ventricular arrhythmias41


where a myocardial scar can be confirmed as the arrhythmic focus, surgical resection may sometimes be undertaken.



Antiarrhythmic Medications


Antiarrhythmic drugs are classified partly on the basis of beta-receptor or membrane channel activity, and partly by their physiological effects on the cardiac action potential. This is well represented by the Vaughan Williams classification system (see Table 11.1).39 However, as action potential abnormalities cannot be expediently identified at the bedside, matching antiarrhythmic agents to cellular physiology cannot realistically be undertaken. Instead, antiarrhythmics are chosen partly on the basis of their known efficacy, by their suitablity to atrial or ventricular arrhythmias, and after consideration of side effects and contraindications to known comorbidities in a given patient.41,42


TABLE 11.1 Antiarrhythmic classifications43































Class Action Drugs
IA Sodium channel blockers: action potential prolongation quinidine
procainamide
disopyramide
IB Sodium channel blockers: accelerate repolarisation; shorten action potential duration lignocaine
mexiletine
IC Potent sodium channel blockers: little effect on repolarisation flecainide
II Beta-blockers: depress automaticity (prolong phase 4); indirect prolongation phase 2 metoprolol
propanolol
esmolol
III Potassium (outward) channel blockers: prolong duration of action potential (prolonged repolarisation) amiodarone
sotalol (beta-blocker with class II actions)
IV Calcium channel blockers verapamil
diltiazem

Table 11.2 depicts the classification of the major acute antiarrhythmics in use in Australia and New Zealand, along with doses, arrhythmic indications, precautions and side effects. Class I agents all slow phase 1 (depolarisation) and so may slow down conduction and prolong the QRS. The subgroups of class I agents denote strength (A = weakest, C = strongest) and affect repolarisation, with class IA (prolonging), IB (shortening) and IC (not affecting) repolarisation duration. The class II agents (beta-blockers) depress automaticity, slowing the heart rate and prolonging the action potential. The class III agents notably prolong repolarisation, action potential duration and the Q–T interval. Class IV agents slow inward calcium channel flux, decreasing automaticity and prolonging the action potential.37


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Jul 11, 2016 | Posted by in NURSING | Comments Off on Cardiac Rhythm Assessment and Management

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