Management of cardiac arrhythmias

Chapter 18 Management of cardiac arrhythmias




CARDIAC ELECTROPHYSIOLOGY


The electrophysiological properties of cardiac cells are important in understanding cardiac arrhythmias and their management. Cardiac cells undergo cyclical depolarisation and repolarisation to form an action potential. The shape and duration of each action potential are determined by the activity of ion channel protein complexes on the myocyte surface. These highly selective ion channels determine the rate of ion flux which in turn determines the magnitude and rate of change of myocyte membrane potential. Many of these ion channels are the molecular targets for antiarrhythmic drugs.


Ion channel function can be affected by:








The spectrum of cardiac action potentials varies from fast-response cells – conducting and contractile myocytes (Figure 18.1a) – to slow-response cells of pacemaker myocytes – sinoatrial (SA) and atrioventricular (AV) nodes (Figure 18.1b). Fast myocytes lose their characteristic action potential and behave more like slow myocytes when ischaemic. The action potential is divided into five phases, as follows.




PHASE 0


In fast myocytes (Figure 18.1a) rapid depolarisation occurs due to activation of voltage-dependent Na+ channels. Activation is initiated in an all-or-none response once the threshold is reached. The Na+ channels are inactivated as membrane potential rises to +30 mV and remain inactivated until repolarisation occurs. Rapidity of depolarisation determines speed of conduction. In slow-response myocytes depolarisation does not involve Na+ channels and the slower rate of depolarisation is due to a slow inward Ca2+ current via L- and T-type voltage-dependent Ca2+ channels.






PHASE 4


This is a stable electrical state in fast non-pacemaker myocytes. In slow pacemaker myocytes the resting membrane potential (RMP) slowly depolarises until the action potential threshold is reached (Figure 18.1b). This inward or pacemaker current is due to If K+ channels.


Fast-response and slow-response myocytes also have important differences in properties of refractoriness. In fast myocytes, Na+ channels are progressively reactivated during phase 3 repolarisation as the membrane potential becomes more negative. When an extra stimulus occurs during phase 3, the magnitude of the resulting inward Na+ current and likelihood of impulse propagation depend on the number of reactivated Na+ channels. Refractoriness is therefore determined by the voltage-dependent recovery of Na+ channels. The absolute refractory period (Figure 18.1) is that minimum time needed for recovery of sufficient Na+ channels for a stimulus to result in impulse propagation. However, once propagation in fast myocytes occurs, conduction velocity is normal. In contrast, slow-response or Ca2+ channel-dependent myocytes exhibit time-dependent refractoriness. Even after full repolarisation further time is needed before all Ca2+ channels are reactivated. Stimuli during this period produce reduced Ca2+ current and the propagation velocity of any resulting impulse is reduced. The conduction velocity independence of premature action potentials with fast-response myocytes is lost in the setting of Na+ channel-blocking drugs or ischaemia because they behave increasingly like slow-response myocytes with resulting slowed impulse conduction.



GENETIC BASIS TO ARRHYTHMIA1


In the absence of structural abnormalities of the heart, primary electrical disease is associated with mutations in ion channel genes. The long-QT syndrome (LQTS), short-QT syndrome, Brugada syndrome (idiopathic ventricular fibrillation (VF)) and catecholaminergic polymorphic ventricular tachycardia (VT: causes of sudden cardiac death (SCD) in the young) are examples of primary electrical disease where genetic mutations encoding for ion channel proteins have been characterised. The ion channel basis of congenital LQTS has been verified with the discovery of disease-causing mutations in the KCNQ1, KCNH2 and SCN5A genes that encode for the cardiac delayed rectifier K+ (IKs, IKr) and sodium (INa) channels respectively. Single-gene mutations can also give rise to more than one distinct syndrome with mutation of the SCN5A gene producing both LQTS and Brugada syndromes. This phenotype complexity is presumably the result of interactions between gene expression and environmental factors or the effect of other modifier genes.


Genetic mutations can result in increased or decreased ion channel function. Mutations to the gene KCNQ1 encoding for IKs K+ channel can result in:




Inheritable forms of structural ventricular disease are associated with atrial arrhythmias and SCD. Examples include hypertrophic and dilated cardiomyopathies and arrhythmogenic right ventricular dysplasia which are linked to mutations in sarcomeric, cytoskeletal and intercellular junction proteins, respectively.


The risk of cardiac arrhythmias and SCD in the setting of acquired structural heart disease such as ischaemic heart disease is in part genetically determined. Studies demonstrate an increased risk of SCD in patients who have a parental history of cardiac arrest.



MOLECULAR BASIS TO ARRHYTHMIA1


Structural and electrical remodelling in response to myocardial injury, altered haemodynamic loads and changes in neurohumoral signalling lead to alterations in:






All of these factors lead to heterogeneous slowing of conduction velocity and prolonged refractoriness.


Tachycardic remodelling of the atrium is associated with:



Heart failure is associated with:





Intercellular ion channels or connexins at gap junctions are decreased and redistributed from the intercalated disc to lateral cell borders, slowing conduction velocity and uncoupling myocytes.


Myocardial infarction scar produces:





ARRHYTHMOGENIC MECHANISMS24


Many factors in isolation or combination give rise to the substrate of arrhythmogenesis (Figure 18.2). Arrhythmia may arise from abnormalities of impulse generation or conduction. Table 18.1 demonstrates the relationship between mechanism and type of arrhythmia, and desired antiarrhythmic effect.





ABNORMAL IMPULSE GENERATION (Table 18.2)






ABNORMAL IMPULSE CONDUCTION5


Abnormal impulse conduction may cause an arrhythmia by the phenomena of re-entry. Re-entry describes the re-excitation of an area or entire heart by a circulating impulse. Although the classic ‘bifurcating Purkinje fibre’ model of Schmitt and Erlanger has given way to a much more complex picture, the essential electrophysiological requirements for re-entrant excitation remain. Requirements for re-entry are (Figure 18.3):






When these properties are present, the chance of a circulating impulse producing re-entrant excitation depends on pathway geometry, the electrical properties and length of the depressed area and conduction velocity within each component. The segment of the re-entry pathway that is initially refractory and therefore blocks conduction down one limb and recovers in time to conduct the return impulse is termed the ‘excitable gap’. Therefore, the generation and subsequent maintenance of a circuit depend on this excitable gap of non-refractory tissue circulating between the advancing depolarising wave front and the repolarising tail. The resulting re-entrant impulse can be self-terminating, causing ectopic beats, or lead to atrial or ventricular tachyarrhythmias.


Risk of re-entry can be further modelled and quantified. Cardiac wavelength (λ) is the physical distance an electrical impulse travels in one refractory period. λ equals conduction velocity × refractory period (or action potential duration). Re-entry is critically dependent on the λ being shorter than the potential reentrant pathway. If λ exceeds the path length then the advancing impulse encroaches on the refractory tail and re-entry is terminated. Reducing λ (decreasing conduction velocity or refractory period) promotes re-entry circuits.


Re-entry may be terminated by:





Ordered re-entry occurs along anatomical pathways which are ‘macroscopic’ loops (macro-re-entry), as in Wolff–Parkinson–White (WPW) syndrome. Functional circuits can be created following myocardial infarction, resulting in VT. ‘Microscopic’ loops (micro-re-entry) occur at the level of single fibres where antegrade and retrograde impulse propagation occurs in parallel fibres. Random re-entry refers to the generation of a circulating impulse, not from a fixed circuit but from constantly changing electrophysiologically distinct fibres or pathways created by the circulating impulse, resulting in atrial fibrillation (AF) or VF.


The cellular properties that lead to impaired conduction include:






ELECTROLYTE ABNORMALITIES AND ARRHYTHMIA6





AUTONOMIC NERVOUS SYSTEM AND VENTRICULAR ARRHYTHMIA10


The autonomic nervous system, particularly vagal tone, has a significant effect on the occurrence of post myocardial infarction VF, as seen by the following:







Vagal tone can be measured by variability in the heart rate (RR interval) or blood pressure rise induced by the pressor agent phenylephrine. Heart rate variability is considered a measure of tonic vagal activity whereas the phenylephrine method is considered a measure of magnitude of the vagal reflex in response to stimulus. A reduced vagal tone has been found postinfarction in humans, which returns to normal over a 3–6-month period. There is no relationship between vagal tone and ejection fraction and the origin of reduced vagal tone postinfarction appears to be due to afferent stimulation in response to necrotic tissue and impaired cardiac contractile geometry. This reduced vagal tone has also been shown to be predictive of mortality and inductility of arrhythmia at electrophysiological study (EPS).



PROARRHYTHMIC EFFECTS OF ANTIARRHYTHMIC DRUGS11,12


Concomitant proarrhythmia with the use of antiarrhythmic drugs is increasingly recognised. The ‘quinidine syncope’ due to VF and polymorphic VT at therapeutic concentrations was also seen with disopyramide. The Cardiac Arrhythmia Suppression Trial (CAST) clearly defined the magnitude of this deleterious side-effect in drugs that were previously perceived to be of benefit.13 This study, which involved flecainide, encainide and morizicine (a class IA drug), was terminated early because of adverse outcome in the flecainide and encainide groups (relative risk of arrhythmic death or non-fatal cardiac arrest of 3.6, 95% confidence interval (CI) 1.7–8.5). Proarrhythmia is reported between 5.9% and 15.8% depending on agent, clinical setting and definition of proarrhythmia, and now considered ubiquitous with all antiarrhythmic drugs.


Proarrhythmia has been defined as an increase in frequency of ventricular ectopic beat (VEB) or aggravation of the target arrhythmia on Holter monitor or exercise test. Manifestations of proarrhythmia not only include VEB, monomorphic and polymorphic VT and VF, but also bradyarrhythmias and Afl with 1:1 AV conduction. Most proarrhythmic events occur soon after starting the drug, but late arrhythmias are also a significant problem.


Proarrhythmia appears to be correlated with the degree of drug-induced QT prolongation or characteristics of sodium channel blockade. Sodium channel blocking agents with a long time constant for recovery of the sodium channel blockade cause more pronounced blockade, even at slow heart rates, slow conduction to a greater extent and are mostly proarrhythmic. Agents with a short time constant of sodium channel blockade, where sodium channel blockade is more pronounced at fast heart rates (e.g. class IB: lidocaine and mexiletine) are less proarrhythmic than drugs with long time constants (e.g. class IC: flecainide and propafenone). Class III drugs and quinidine proarrhythmia correlate with degree of QT prolongation.


The mechanism of drug proarrhythmia is probably via both slowing of conduction and abnormal automaticity. Paradoxically slowing conduction, which may block a re-entry circuit, may also create the very substrate needed for re-entry, unidirectional block and an excitable gap. The existence of a re-entrant circuit requires the circulating wave front of the impulse not to catch up with the refractory tissue behind the tail. Re-entry is more likely to occur with a shorter refractory period and reduced conduction velocity (Figure 18.4).11



Increasing conduction velocity is an ideal antiarrhythmic property but there are no antiarrhythmic drugs that accelerate conduction. However antiarrhythmic drugs readily slow conduction and the degree of conduction slowing and therefore proarrhythmic tendency correlates with the potency of antiarrhythmic properties.


Prolonging the refractory period is also an ideal antiarrhythmic property, which increases the likelihood of abolishing any excitable gap by ensuring the wave front of a re-entrant circuit meets refractory tissue. The potency of class IA and III antiarrhythmic agents is dependent on the prolongation of the refractory period. This property is also protective against proarrhythmia due to re-entry mechanism. The effect of class IB agents on shortening the refractory period will contribute to proarrhythmia by this mechanism in this class.


Surface mapping of the heart has been used to quantify proarrhythmic effect. The scale of potency of proarrhythmia has been found to be:




image



Amiodarone was not included in this study but presumably its proarrhythmic potential is similar to other class III agents and less than the class I agents.


Antiarrhythmic drugs are effective at suppressing abnormal automaticity, with the exception of triggered automaticity due to EAD. Class IA, class III and many non-antiarrhythmic drugs can produce proarrhythmia via EAD. These drugs increase not only the frequency of EAD, but also the likelihood of them leading to triggered tachyarrhythmias. Slowing repolarisation, which leads to QT prolongation and slower heart rate, is central to this increased frequency and sensitivity to EAD. EAD manifests as prominent and bizarre T-U waves on the ECG and, if triggered activity results, VEB and ventricular tachyarrhythmias may occur. Torsade de pointes is the classical resulting arrhythmia, although less classical polymorphic VT and VF result. Risk of proarrhythmia via this mechanism correlates with the degree of QT prolongation.


All antiarrhythmic drugs are capable of producing bradyarrhythmias via decreasing normal automaticity and slowing conduction. Digoxin can be proarrhythmic via the production of triggered activity due to DAD.


Antiarrhythmic drug proarrhythmia is facilitated by several factors, which are frequently found in patients on antiarrhythmic drugs or with heart disease (Table 18.4).


Table 18.4 Factors facilitating antiarrhythmic drug proarrhythmia

















Toxic blood levels due to excessive dose or reduced clearance from old age, heart failure, renal disease or hepatic disease
Severe left ventricular dysfunction. Ejection fraction less than 35%
Pre-existing arrhythmia or arrhythmia substrate
Digoxin therapy
Hypokalaemia or hypomagnesaemia
Bradycardia
Combinations of antiarrhythmic drugs and concomitant drugs with similar toxicity

(Adapted from Campbell TJ. Proarrhythmic actions of antiarrhythmic drugs: a review. Aust NZ J Med 1990; 20: 275–82, with permission.)



MANAGEMENT OF THE PATIENT WITH A CARDIAC ARRHYTHMIA






MANAGEMENT OF SPECIFIC ARRHYTHMIAS


Treatment has two aspects: acute termination of the arrhythmia and long-term prophylaxis. The decision whether to treat depends on the rhythm diagnosis, haemodynamic consequences, aetiology of the arrhythmia and the prognosis (e.g. risks of sudden death or long-term complications).




PREMATURE VENTRICULAR ECTOPIC BEATS


These are also known as ventricular premature beats and ventricular premature complexes. The ventricle is not normally activated via the rapidly conducting bundle branches, and a wide QRS complex results from slow ventricular conduction.






SUPRAVENTRICULAR TACHYCARDIAS22,23 (Table 18.5)


Supraventricular tachycardias (SVT) are any tachycardias that require atrial or AV nodal tissue for their initiation and maintenance.





Table 18.5 Classification of supraventricular tachycardias























Atrioventricular (AV) node-dependent
AV nodal re-entry tachycardia: re-entry within the AV node
AV re-entry tachycardia: re-entry includes accessory pathway between atria and ventricles
Accelerated idionodal rhythm: increased automaticity of AV nodea
AV node-independent
Atrial flutter: re-entry confined to atria
Atrial fibrillation: multiple re-entry circuits confined to atria
Unifocal atrial tachycardia: usually due to increased automaticity
Multifocal atrial tachycardia: increased automaticity or triggered activity
Others: sinus node re-entry tachycardia

A clinically useful classification divides SVT into AV node-dependent and AV node-independent.


Distinguishing between AV node-dependent and independent SVTs can be difficult. Vagal manoeuvres or drugs that prolong AV nodal refractoriness (e.g. adenosine) may assist in diagnosis:







AV NODAL RE-ENTRY TACHYCARDIA (AVNRT)(Figure 18.9)


Re-entry tachycardia is confined to the AV node. Antegrade conduction to the ventricles usually occurs over the slow pathway and retrograde conduction over the fast pathway.








AV RE-ENTRY TACHYCARDIA (SEE Figure 18.9)


The re-entry pathway consists of the AV node and an accessory pathway, which bypasses the AV node. The accessory pathway may be evident during sinus rhythm, with the ECG showing pre-excitation: short PR interval, delta wave and widening of the QRS (see WPW, below, under pre-excitation syndrome). However, in 25% of cases, the accessory pathway conducts only retrogradely from ventricle to atria and the ECG pre-excitation will be concealed in sinus rhythm. Orthodromic AVRT, with antegrade nodal and retrograde accessory pathway circuit, is the most common regular SVT in patients with accessory pathway.








UNIFOCAL ATRIAL TACHYCARDIA


This is sometimes called ectopic atrial tachycardia to distinguish it from the atrial tachycardias (referring collectively to unifocal atrial tachycardia, Afl and AF). However, it is inappropriate to call atrial tachycardia paroxysmal atrial tachycardia. Paroxysmal, by definition, indicates an abrupt onset and termination, which applies less commonly to unifocal atrial tachycardia. Vagal manoeuvres will not terminate this arrhythmia, but AV block may be induced, or increased if already present.






MULTIFOCAL ATRIAL TACHYCARDIA28


Multifocal atrial tachycardia (MAT) is defined as an atrial rhythm, with a rate greater than 100 beats/min, with organised, discrete non-sinus P-waves having at least three different forms in the same ECG trace. The baseline between P-waves is isoelectric, and the PP, PR and RR intervals are irregular. This is an uncommon arrhythmia, also known as chaotic or mixed atrial tachycardia.





TREATMENT


Treatment should correct the underlying cause (e.g. treatment of cardiorespiratory failure, electrolyte and acid–base abnormalities and theophylline toxicity). Spontaneous reversion is common, and few patients require antiarrhythmic therapy. Magnesium is the drug of choice for acute control.29 β-Blockers are probably more effective than diltiazem, but because of the common association of MAT with obstructive lung disease have limited utility.30 Digoxin and cardioversion are ineffective, which highlights the need to differentiate MAT from AF. Longer-term control is best achieved with diltiazem in patients with good left ventricular (LV) function and amiodarone in those without.



ATRIAL FLUTTER31


Atrial rate during classical Afl is 250–350 beats/min, and in most cases, close to 300 beats/min. Afl is due to a single re-entry circuit lying within the right atrium and the wave of depolarisation in most patients is anticlockwise. If the right atrium is significantly enlarged the rate may be considerably slower. Studies in patients who had recently undergone cardiac surgery subdivided Afl into type I and II on the basis of rate and typical responses to atrial pacing.


Type I flutter was slower – rate 240–320 beats/min – and was readily entrained with overdrive pacing. Type II flutter was faster than type I, with rates of 340–430 beats/min. Type II flutter could not be entrained or terminated by pacing. Type II is thought to arise from a circus pathway with a very short excitable gap.



ECG


Afl waves (characteristic sawtooth appearance with no isoelectric baseline) are best seen in V1 (Figure 18.17) or aVF, but leads II and III may also be useful. The flutter waves are usually negative in aVF. Rapid QRS waves may obscure typical flutter waves, and vagal manoeuvres may unmask them (see Figure 18.5). AV conduction block (usually 2:1) is usually present, so that alternate flutter waves are conducted to the ventricles, with a ventricular rate close to 150 beats/min. Frequently flutter waves are not obvious and a ventricular rate of 150 beats/min leads to the presumption of Afl (Figure 18.18). Type II Afl results in greater atrial and ventricular rates (Figure 18.19). Treatment with drugs that affect AV node conduction may lead to higher degrees of AV block (Figure 18.20) and/or variable AV block with irregular QRS duration. Rarely, Afl with 1:1 conduction occurs. This is usually associated with sympathetic overactivity or class I antiarrhythmic drugs (which slow atrial discharge rate to 200 beats/min, thereby allowing each atrial impulse to be conducted) (Figure 18.21). QRS complexes are usually narrow, as conduction through the bundle branches is normal.











ATRIAL FIBRILLATION32


AF is the most common arrhythmia requiring treatment and/or hospital admission. The incidence increases with age: 5% of individuals over 70 years have this arrhythmia. There is also an age-independent increase in frequency due to increase in obesity and obstructive sleep apnoea. LV dyfunction increases risk of AF (4.5-fold in men and 5.9 in women) with atrial stretch and fibrosis causing electrical and atrial ionic channel remodelling.


AF is common in:





Idiopathic or lone AF (i.e. with no structural heart disease or precipitating factor) in someone aged under 60 years has an excellent prognosis; however, AF developing after cardiac surgery, for instance, is associated with increased stroke, life-threatening arrhythmias and longer hospital stays.





TREATMENT25,34,35


The goals of treatment include ventricular rate control, anticoagulation where appropriate and conversion to sinus rhythm. There is increasing evidence available on the ‘rate versus rhythm’ control debate. Results from several recent major studies have challenged the previous belief that achievement of sinus rhythm is important in the long term (Table 18.6). When comparing control of ventricular rate versus reversion to sinus rhythm no clear survival benefit is apparent. However composite end-points of death, stroke and recurrent hospilisation favour rate control only.3639



The possible reasons why rhythm control has not been shown to be superior include:








However rhythm control (if possible) appears superior in patients with LV dysfunction, with both amiodarone and dofetilide reducing mortality when sinus rhythm is achieved.40,41 The paucity of data in younger patients (less than 60 years) favours initial attempts at rhythm control, particularly in those with structurally normal hearts, in the hope that progressive atrial electrical and anatomical remodelling is prevented.



RECENT ONSET OR PAROXYSMAL AF







ANTIARRHYTHMIC DRUGS


The drugs used for ventricular rate control – digoxin, diltiazem and β-adrenergic blockers – are unlikely to result in pharmacological cardioversion.


Antiarrhythmic drugs that may cardiovert are unfortunately relatively ineffective and may possibly be dangerous. They are more effective at retaining sinus rhythm. About 50% will remain in sinus rhythm 1 year after cardioversion with drugs and 25% without drugs.


Quinidine is more effective than placebo, but increases mortality through proarrhythmia (generally class IA and IC antiarrhythmic drugs are contraindicated). Ibutilide and dofetilide are newer antiarrhythmic drugs with particular success at pharmacological cardioversion. Pretreatment with ibutilide increased DC shock cardioversion from 72% for placebo to 100%. In placebo failures, cross-over to ibutilide resulted in a 100% success rate with subsequent cardioversion. Ibutilide also resulted in reduction in DC shock energy required from 228 ± 93 J to 166 ± 80 J. However, ibutilide was associated with a 3% incidence of sustained polymorphous VT.45 Dofetilide appears to cardiovert AF and Afl pharmacologically in about a third of patients (intravenous (IV) better than oral, recent onset better than prolonged and Afl may be more responsive than AF). Dofetilide is far superior to placebo and sotalol, with similar recurrence rates to amiodarone.46


Other drugs currently used to promote onset of sinus rhythm and prevent AF relapse include amiodarone, sotalol, procainamide, flecainide and propafenone. Amiodarone was found to be superior in preventing AF recurrence with a recurrence rate of 35% compared to a recurrence rate of 63% for sotalol and propafenone.47


The factors dictating choice are:





When using amiodarone for prevention of AF recurrence there was an 18% incidence of adverse effects versus 11% for sotalol and propafenone.47



ATRIAL FIBRILLATION ABLATION THERAPY


Ablation techniques for AF have been continuously refined since the original Maze III surgical procedure which involved numerous atrial incisions to form a maze-like pattern of scarring, blocking propagation of arrhythmia. The ultility of this procedure was limited because it was surgical, with longer bypass times, postoperative bleeding and impaired atrial contractility. The magnitude of this original procedure was based on the belief that the entire atrium was involved in the initiation and maintenance of the fibrillatory conduction. This may be true for long-standing AF but paroxysmal AF appears to originate primarily at the junction of the left atrium and pulmonary veins. AF in 94% of patients is initiated by rapid discharges from one or more foci at or near the pulmonary vein orifices.48 Atrial tissue in this area has heterogeneous electrophysiological properties and there is also clustering of vagal inputs, which creates substrate for rapid discharges that initiate microre-entrant circuits or ‘rotors’. These high-frquency periodic rotors send spiral wave fronts of activation into surrounding atria. Localised ablation of a single dominant foci and rotor is inadequate as there are usually multiple foci.


There is renewed interest in surgical AF ablation therapy in conjunction with cardiac surgery. Complications have been reduced with energy (cryotherapy, radiofrequency) rather than incisions and the extent of lesions reduced. The minimum lesion set is now considered to be encirclement of pulmonary veins, linear lesion from the inferior pulmonary vein to mitral annulus and from the coronary sinus to the inferior vena cava.


Left atrial catheter (transatrial septum) AF ablation isolating all four pulmonary veins using radiofrquency is being heralded as the possible AF cure. Results are improving as all pulmonary veins are now isolated and the encircling lesion is clear of the pulmonary vein antrum (reducing pulmonary vein stenosis). Success rates of 81% (75–88%) free of AF and off drugs are reported. Success appears long-term as recurrence occurs early. A further 10–20% may become responsive to antiarrhythmic drugs which were previously ineffective. Repeating the procedure can increase success to > 90% with failure only in patients found to have extensive atrial scarring (predicting and excluding patients with this extensive atrial scarring is a major future challenge). Although not yet the universal cure the results are two- to threefold better than antiarrhythmic drugs alone.


Complication rates are also falling associated with:





Transient ischaemic attacks, strokes, tamponade/perforation and symptomatic pulmonary vein stenosis are all well below 1% respectively. Proarrhythmia resulting from re-entrant tachycardias from incomplete ablative lesions is more common. Some are advocating ablation as first-line treatment whereas most are selecting younger patients (less than 70 years) with paroxysmal AF for whom antiarrhythmic therapy has failed, left atrial diameter is less than 5 cm and ejection fraction is greater than 40%.26 Head-to-head studies comparing ablation and antiarrhythmic drugs are appearing with suggested survival benefit, improved quality of life, reduced adverse effects and cost-effectiveness after approximately 3 years with catheter AF ablation therapy.49,50





ANTICOAGULATION FOR CHRONIC ATRIAL FIBRILLATION


Consider for all patients, especially those with risk factors (Table 18.7).


Table 18.7 Prognostic factors for ischaemic stroke and systemic embolism in patients with atrial fibrillation
































High Previous stroke, transient ischaemic attack, systemic embolism
Mitral stenosis
Prosthetic heart valve
Moderate Age > 75 years
Left atrial size > 45 mm
Hypertension
Congestive cardiac failure
Diabetes mellitus
Left ventricular ejection fraction < 35%
Low Female
Age 65–74 years
Coronary artery disease
Thyrotoxicosis


< div class='tao-gold-member'>

Jul 7, 2016 | Posted by in CRITICAL CARE | Comments Off on Management of cardiac arrhythmias

Full access? Get Clinical Tree

Get Clinical Tree app for offline access