Clinical practice review Cardiac Arrhythmias: Diagnosis and Management. The Tachycardias D. DURHAM, L. I. G. WORTHLEY Department of Critical Care Medicine, Flinders Medical Centre, Adelaide, SOUTH AUSTRALIA ABSTRACT Objective: To review the diagnosis and management of cardiac arrhythmias in a two-part presentation. Data sources: Articles and published peer-review abstracts on tachycardias and bradycardias. Summary of review: Normal cardiac rhythm originates from impulses generated within the sinus node. These impulses are conducted to the atrioventricular node where they are delayed before they are distributed to the ventricular myocardium via the His-Purkinje system. Abnormalities in cardiac rhythm are caused by disorders of impulse generation, conduction or a combination of the two and may be life- threatening due to a reduction in cardiac output or myocardial oxygenation. Cardiac arrhythmias are commonly classified as tachycardias (supraventricular or ventricular) or bradycardias. The differentiation between supraventricular and ventricular tachycardias usually requires an assessment of atrial and ventricular rhythms and their relationship to each other. In the critically ill patient the commonest tachycardia is sinus tachycardia and treatment generally consists of management of the underlying disorder. Other supraventricular tachycardias (SVTs) include, atrial flutter, atrial fibrillation and paroxysmal supraventricular tachycardia (PSVT) all of which may require cardioversion, although to maintain sinus rhythm, antiarrhythmic therapy is often needed. Adenosine is useful in the management and treatment of many SVTs although its use in PSVT with Wolff- Parkinson-White syndrome is hazardous. Multifocal atrial tachycardia is a characteristic supraventricular tachycardia found in the critically ill patient. While it usually responds to intravenous magnesium sulphate, its management also requires removal of various precipitating factors. Ventricular tachycardia (VT) and ventricular fibrillation (VF) require urgent cardioversion and defibrillation respectively. Torsade de pointes should be differentiated from these ventricular arrhythmias as antiarrhythmic therapy may be contraindicated. Conclusions: Supraventricular and ventricular tachycardias in the critically ill patient often have underlying disorders that precipitate their development (e.g. hypokalaemia, hypomagnesaemia, anti- arrhythmic proarrhythmia, myocardial ischaemia, etc). While antiarrhythmic therapy and cardioversion or defibrillation may be required to achieve sinus rhythm, correction of the associated abnormalities is also required. (Critical Care and Resuscitation 2002; 4: 35-53) Key words: Critical illness, atrial flutter, atrial fibrillation, paroxysmal supraventricular tachycardia, Wolff- Parkinson White syndrome, torsade de pointes, multifocal atrial tachycardia, ventricular tachycardia, ventricular fibrillation Correspondence to: Dr. D. Durham, Department of Critical Care Medicine, Flinders Medical Centre, Bedford Park, South Australia 5042 35 D. DURHAM, ET AL Critical Care and Resuscitation 2002; 4: 35-53 NORMAL CARDIAC RHYTHM relationship to be determined.8 In unusual circumstan- The rhythm of a normal resting adult heart is initiat- ces, a trace of up to 60 seconds may be required. ed from impulses generated from the sinoatrial (SA) However, leads II and V are not ideal for the recog- 1 node with a rate varying between 60 - 100 beats per nition of myocardial ischaemia, although V , which 5 minute (bpm). During sleep the rate may decrease to 30 shows approximately 90% of all ST segment changes - 50 bpm,1,2 with episodes of sinus pauses up to 3 secon- due to anterior, inferior or posterior ischaemia, is.9 A ds, sinoatrial block, junctional rhythms, first degree and modification of both leads II and V , where the right 5 second degree atrioventricular nodal block occurring arm lead is mounted on the manubrium sterni, the left often enough (particularly in trained athletes) to be arm lead is mounted on the xiphisternum and left leg considered normal variants.3 lead is placed in V position, facilitates the diagnosis of 5 The impulses generated from the SA node spread via both rhythm and ischaemic changes. Using this lead, the specialised internodal atrial conducting pathways to the setting of lead I results in maximal P wave amplitude atrioventricular (AV) node, where they are delayed and the setting of lead II offers optimal ischaemic before they are finally distributed to the ventricular detection, with the added advantages of reducing inter- myocardium via the His-Purkinje system. Normally, ference and electrical artifact.10 with exercise the heart rate increases to at least 85% of To perform the cardiac ECG ‘rhythm trace’ the pat- the age predicted maximum of 220 - age in years, with ient should be in a warm environment to reduce ‘shiver- failure to do so being termed ‘chronotropic incompete- ing’ artifact, and the recording should not be performed nce’. Sinus arrhythmia is defined as sinus rhythm with during body movement, as muscle or limb movement P-P variations of more than 10%. It is due to cyclical artifact can simulate ventricular tachycardia.11 variations in vagal tone commonly related to respiration (the rate is faster with inspiration and slower with Description of an arrhythmia expiration), and is often seen in individuals with sinus Arrhythmias may be described from their following bradycardia.4 It disappears with exercise, breath holding characteristics:12 and atropine and is more likely to be seen in individuals 1. Rate (e.g. tachycardia or bradycardia) who do not have cardiac disease. a. tachycardia is defined as three or more Frequent multifocal ventricular ectopic beats have consecutive impulses from the same pacemaker been noted in up to 12% of normal adults during a 24 hr at a rate exceeding 100 bpm in adults (i.e. > 8 period, indicating that, in the absence of underlying years of age). cardiovascular disease, ventricular ectopic beats are not b. bradycardia is defined as three or more a prelude to something more sinister.1,5-7 consecutive impulses from the same pacemaker at a rate less than 60 bpm. CARDIAC ARRHYTHMIAS 2. Rhythm (e.g. regular or irregular) An arrhythmia is defined as any cardiac rhythm other 3. Origin of impulse (i.e. supraventricular, ventricular, than regular sinus rhythm. It is caused by a disorder of or artificial pacemaker) impulse generation, impulse conduction or a 4. Impulse conduction (i.e. atrioventricular, ventriculo- combination of the two, and may be life-threatening due atrial or block) to a reduction in cardiac output, reduction in myocardial 5. Ventricular rate blood flow or precipitation of a more serious arrhyth- 6. Special phenomena (e.g. pre-excitation) mia. While the term ‘dysrhythmia’ would appear to be better suited as a label for an abnormal cardiac rhythm Management of an arrhythmia (as the term arrhythmia suggests an absence of rhythm), In general, the management of an arrhythmia focuses the term ‘arrhythmia’ will be used in this review as it has on: now become the accepted medical term. - correcting precipitating causes (e.g. hypokalaemia, Diagnosis of an arrhythmia hypomagnesaemia, hypercapnia, hypocapnia, hypo- The assessment of an arrhythmia requires the xia, metabolic alkalosis, drug poisoning or toxicity), determination of the site of the conduction disturbance, - restoring sinus rhythm or providing a the atrial and ventricular rhythms present and the relati- supraventricular rhythm with an acceptable onship between the atrial and ventricular impulses. ventricular rate, and When using the standard ECG leads, the cardiac rhythm - preventing a relapse. is often best considered from leads II or V as they 1 provide the maximum P and QRS wave amplitudes to The specific management of an arrhythmia depends allow the supraventricular and ventricular impulse upon whether it is an ectopic impulse, a sustained arrhy- 36 Critical Care and Resuscitation 2002; 4: 35-53 D. DURHAM, ET AL thmia (supraventricular or ventricular tachycardia, or Ventricular ectopics bradycardia) or a special phenomenon. Ventricular ectopics are of little clinical significance in normal individuals.14 They assume significance when ECTOPIC IMPULSES they are associated with clinical evidence of heart An ectopic impulse is one that arises from any site disease, as an indicator of cardiac disease rather than a other than the SA node. An escape impulse is one which disorder that needs to be treated, as treatment to arises from a different pacemaker from the underlying suppress them may be associated with an increase rather pacemaker due to a delay in the arrival of the expected than a decrease in mortality.15,16 impulse of the prevailing rhythm. An extrasystole is a Ventricular ectopic beats are characterised by a wide premature impulse (i.e. arises earlier than one would QRS complex that is not preceded by a P wave. It often anticipate by observing the prevailing rhythm) and usu- bears a relatively fixed relationship to the preceding ally shows a fixed, and probably causal, relationship to sinus complex. If fixed coupling does not exist but the the preceding activation of the same cardiac chamber.13 intervals between the ventricular ectopic beats are An increase in both atrial and ventricular ectopics regular, then the ectopic beat has an entry block and may be associated with: ventricular parasystole is said to be present. - physiological conditions (e.g. cold, emotion, fatigue, If every sinus beat is followed by a ventricular pregnancy) ectopic, then ventricular bigeminy is said to be present. - drugs (e.g. alcohol, tea, coffee, tobacco, aminophy- If every second sinus beat is followed by a ventricular lline, tricyclics, digoxin, quinidine, sympathomime- ectopic, then ventricular trigeminy is said to be present, tics) etc. If every sinus beat is followed by two ventricular - disease (e.g. ischaemic heart disease, cardio- ectopic beats then this is described as ventricular myopathies, pulmonary embolism, COPD, systemic couplets (if a sinus beat is followed by three ectopics disease, fever, renal colic, hypokalaemia and biliary then ventricular tachycardia is present if the ventricular tract disease). rate is greater than 100 beats per minute). The ventricular ectopic impulse is often not conduc- Atrial ectopics ted retrogradely and therefore, while it usually blocks Atrial ectopics commonly occur in early cardiac the sinus beat, it usually does not alter the sinus rate. failure and often herald the onset of atrial fibrillation or Post-extrasystolic T wave changes (i.e. alteration in the atrial flutter, particularly when they are associated with T wave vector, amplitude or contour compared with the acute myocardial infarction, post operative thoraco- preceding sinus beat T wave) occur in 68% of normal tomy, rheumatic fever or thyrotoxicosis. They can also individuals and 81% of patients with coronary heart initiate paroxysmal supraventricular tachycardias in disease, and are not indicative of heart disease.17 susceptible patients. The premature atrial complex may Warning ventricular ectopic beats preceding ventric- arise from any location in the atria and are recognised as ular tachycardia (VT) or ventricular fibrillation (VF) an early P wave with a morphology that differs from the have been described as, greater than 1 in 10 beats, two sinus P wave. There are three different effects that the or more beats in succession, multifocal (i.e. have atrial ectopic may produce on the rhythm of the heart: differing contours in any one lead and differing coupling 1. It may discharge the SA node, so that the pause times to the preceding impulse of the prevailing following it is the same as normal, rhythm), R on T phenomenon (i.e. refers to an ectopic 2. It may not discharge the SA node, so that there is a impulse which is superimposed on the T wave of a compensatory pause before the next sinus beat, or preceding impulse), and arising from the left ventricle 3. It may be partially or completely blocked in the AV (i.e. show a RBBB pattern). However, these ‘warning node, to prolong the PR interval or exhibit a P wave arrhythmias’ have been detected in up to 60% of with no ventricular response. patients who do not develop VF,18,19 and episodes of VF not preceded by these ‘warning arrhythmias’, have been Junctional ectopics observed in up to 40% of patients with acute myocardial As the AV node in vitro does not have the property infarction.20-24 of automaticity, it is believed that junctional ectopics The R on T ventricular ectopic as a predictor of VF arise from the bundle of His. The impulses are conduc- in patients with acute myocardial infarction is neither a ted retrogradely to the atria and antegradely to the specific nor sensitive phenomenon,25,26 and it may have ventricles with the P wave being hidden by the QRS or been confused with the vulnerable phase for fibrillating appearing just before, or after, the QRS wave and an animal ventricle by stimulation techniques not analo- inverted in leads II, III and aVF. gous to ectopic beats.27 37 D. DURHAM, ET AL Critical Care and Resuscitation 2002; 4: 35-53 SUSTAINED ARRHYTHMIAS expiration.4 The carotid sinus on one side is stimulated The sustained arrhythmias are classified as either first. If there is no effect, after a delay of 1 minute, the tachycardias or tachyarrhythmias (if there are three or opposite carotid sinus is stimulated. A pause of greater more complexes with a rate of greater than 100 beats per than 3 s or a decrease in systolic blood pressure of more minute) or bradycardias or bradyarrhythmias (if the rate than 50 mmHg is abnormal, and indicative of carotid of the complexes are less than 60 beats per minute). The sinus hypersensitivity.32 This manoeuvre is contraindic- tachycardias may be caused by disorders of impulse ated in patients who have AV block, or known conduction (i.e. re-entry) or impulse generation (i.e. cerebrovascular disease. enhanced automaticity or triggered activity). The brady- Valsalva manoeuvre. This is performed by asking cardias may be caused by a decrease in impulse format- the patient not to take a deep breath before blowing into ion or conduction. an aneroid manometer up to 40 mmHg for 10 - 15 s. The vagal response occurs during the period of termin-ation Tachycardias of the manoeuvre. Uncontrolled tachycardias can induce cardiac failure Facial immersion. This is performed by asking the (even a reversible cardiomyopathy28), cardiac ischaemia patient to hold his/her breath on inspiration while a and may degenerate into ventricular fibrillation. In the towel with cold water is placed over the jaw.33 This management of a patient with tachycardia, the clinician produces a profound vagal response with peripheral is required to assess whether the origin of the rhythm is vasoconstriction, unlike a vasovagal attack which is supraventricular (e.g. atrial) or ventricular. However, the associated with vasodilation. relationship between an atrial and ventricular rhythm Other physical methods. These include, ocular may be extremely difficult to define and may require pressure (Aschner-Dagnini manoeuvre), vomiting and methods to reduce the ventricular rate (e.g. increase the squatting. In one study of 35 patients with induced and AV block by vagal stimulation; Figure 1), enhance the sustained junctional tachycardia, the Valsalva manoeu- atrial ECG complexes (e.g. intra-atrial or oesophageal vre in the supine position was successful in terminating leads) or observe aortic and mitral valve movement the arrhythmia in 54%, right carotid sinus massage in during echocardiography29 to clarify the relationship. 17%, left carotid sinus massage in 5% and facial immersion in 17% of cases.30 Vagal stimulation This is often used to diagnose and treat supra- Drugs ventricular tachycardias by slowing the atrial rate and Ephedrine, phenylephrine, edrophonium and neosti- increasing the AV block. The standard responses to gmine have all been used to either directly or indirectly vagal stimulation are reduction of sinus rate (even stimulate the vagus. These agents are now rarely used. transient second- or third-degree block), slowing of the ventricular response in atrial fibrillation, transient Atrial tachycardias increase in the AV block in atrial flutter (Figure 1), conversion of 50 - 60% of junctional tachycardias (i.e. Sinus tachycardia paroxysmal supraventricular, idio-nodal, and multifocal In sinus tachycardia the rate is usually between 100 - atrial tachycardia) to sinus rhythm and no effect in VT.30 160 bpm but may increase to 220 bpm particularly with In latent digoxin toxicity, bigeminal or multifocal severe sympathetic stimulation or drug effect. The ventricular ectopics may occur. causes include anxiety, tetanus, delirium, phaeochromo- Vagal stimulation may be performed by physical cytoma, thyrotoxicosis, fever (with an increase of 8 bpm methods (e.g. carotid sinus massage, Valsalva manoe- for every 1ºC increase in temperature, if the fever is due uvre, facial immersion, etc) or drugs. to an infection),34 pain, shock, drug withdrawal and sympathomimetic agents. Treatment should be directed Physical methods at the underlying cause (e.g. pain, hypoxia, etc.). Beta- Carotid sinus massage (Czermak’s manoeuvre). blockers may be required if the tachycardia has been Carotid sinus massage is performed with ECG monitor- generated by an inappropriate sympathetic hyper- ing, the patient supine and the head turned to the oppos- activity, for example in patients with tetanus, drug with- ite side. The carotid bifurcation is localised by palpating drawal, delirium tremens, thyrotoxic crisis or phaeochr- the carotid impulse at the angle of the jaw. While omocytoma. observing the ECG trace, pressure or massage is applied for no longer than 3 s at the bifurcation of the carotid Atrial flutter artery.31 To increase the vagal effect, the manoeuvre Atrial flutter in its common form has an atrial rate should be performed at the end of inspiration or during that varies between 250 - 350 bpm (usually it is almost 38 Critical Care and Resuscitation 2002; 4: 35-53 D. DURHAM, ET AL exactly 300 bpm), and is often caused by a single re- To maintain sinus rhythm, class Ia, III or IV anti- entrant circuit in the right atrium35 (Figure 1). In type 1 arrhythmic drugs (Table 1) may be required following atrial flutter, the circuit runs anticlockwise around the the cardioversion (e.g. procainamide, amiodarone or right atrium, in type 2 atrial flutter it runs clockwise. verapamil). Verapamil, digoxin, or amiodarone may also Unlike atrial fibrillation, there is a discrete atrial be used instead of cardioversion to slow the ventricular mechanical systole after each electrical flutter wave, rate or convert the arrhythmia to sinus rhythm. explaining why arterial embolism is rare with atrial Verapamil will convert the rhythm to sinus in 10 - 30% flutter.36 of cases. If class Ia or III drugs are used to convert the Atrioventricular regurgitation does not occur in atrial arrhythmia (which have conversion rates varying flutter, whereas it always occurs with atrial fibrillation. between 30% - 50%), these drugs may, in rare instances, Classically, the ECG trace shows a sawtooth pattern in increase the AV conduction before the rhythm reverts, leads II and III, characterised by a regular atrial rhythm causing a 1:1 ventricular response and dangerous and, in the untreated patient, a 2:1 AV block with a tachycardia that may proceed to VF. To reduce this ventricular rate around 150 bpm. There is no isoelectric hazard, digoxin is often used first to increase the AV line between the P waves, which appear inverted in II, block and control the ventricular rate before class Ia or III and aVF in 70% (typical pattern or type 1) and type III agents are used. upright in 30% (atypical pattern or type 2). A variant is Recently, pure class III drugs (e.g. dofetilide 8 µg/kg flutter/fibrillation, where the atrial activity alternates or ibutilide 0.01- 0.025 mg/kg i.v. over 10 minutes) have between both rhythms, and in this condition arterial been reported to convert atrial flutter to sinus rhythm in embolism can occur. Atrial flutter is commonly caused up to 60 - 75% of patients.43 by those disorders which also cause atrial fibrillation. In prolonged and resistant cases of atrial flutter, The treatment of choice is cardioversion with low- radiofrequency ablation between the tricuspid valve and voltage direct current shock (e.g. 50 J). While prior the inferior vena cava has been successful in up to 90% anticoagulation was not initially recommended37,38 of cases, although 25% of patients developed atrial unless the patient varied between atrial flutter and fibrillation after 1 year.44 fibrillation, recent reports of embolic events following cardioversion for atrial flutter without anticoagulation, Atrial fibrillation have prompted many to recommend otherwise.39-41 This may be caused by mitral valve disease (the Higher energies (100 J) may be required if the flutter incidence is 41% in mitral stenosis and 75% in mitral has been prolonged. However, in one study of 330 regurgitation),45 cardiomyopathy, ischaemic heart disea- patients with atrial flutter a higher conversion rate was se, thyrotoxicosis, myxoedema, pneumonia, systemic reported using 100 J when compared with 50 J (85% c.f. infection, alcohol intoxication and withdrawal, hypoth- 70%), irrespective of the duration of the arrhyth-mia.42 ermia, thoracotomy, post cardiac surgery, lung and If a right atrial pacing wire is present then 15 s of rapid mediastinal malignancy, rheumatic fever, pre-excitation atrial pacing (with a pacing cycle length 10 ms less than syndromes, pulmonary embolism, constrictive pericard- the atrial rate and progressively decreased to 150 ms or itis, COPD, ‘sick’ sinus syndrome, hypovolaemia and 400 per minute for 15 - 30 seconds) will also convert the idiopathic (i.e. lone atrial fibrillation).46 The arrhythmo- arrhythmia.35 Figure 1. Atrial flutter with 2:1 block and ventricular rate of 150 bpm. The flutter waves are shown when carotid sinus pressure is performed. 39 D. DURHAM, ET AL Critical Care and Resuscitation 2002; 4: 35-53 Table 1 Classification of antiarrhythmic drugs Class Action Antiarrhythmic drug Ia Block inward sodium current Quinidine, procainamide, disopyramide Ib Lignocaine, tocainide, mexiletine, phenytoin Ic Flecainide, encainide, lorcainide II Beta adrenergic receptor blockers Propranolol, metoprolol, atenolol, sotalol III Prolong the action potential Amiodarone, bretylium, sotalol, ibutilide, dofetilide IV Calcium channel blockers Verapamil, diltiazem, tiapamil Agents not classified (Digoxin, Adenosine) Figure 2. Atrial fibrillation with a ventricular rate varying between 190 - 200 bpm genic atrial premature beats that appear to trigger atrial control (e.g. reversion to sinus rhythm with antiarrhyth- fibrillation arise predominantly from the pulmonary mic agents to maintain sinus rhythm) compared with veins.47 those who have rate control (e.g. negative chronotropic The clinical features include palpitations, irregular agents and anticoagulation), although exercise tolerance pulse, variable intensity of the second heart sound, is better (yet hospital admission is more frequent) when fatigue, cardiac failure and embolic phenomena (there is rhythm control is compared with rate control.51 a six-fold increase in strokes in patients with chronic The agent most often used to slow the ventricular atrial fibrillation).48 The ECG reveals a variable R-R response is digoxin (unless atrial fibrillation is present in interval and fibrillatory (f) waves particularly in lead II a patient who has Wolff-Parkinson-White syndrome and V (Figure 2). The f waves may be coarse (i.e. where intravenous procainamide is recommended),52 1 waves greater than 0.5 mm from trough to peak) particularly in patients who have left ventricular systolic particularly if the atrial fibrillation is of recent onset), or dysfunction. Digoxin does not alter the incidence of fine, particularly if the atrial fibrillation is chronic, or spontaneous reversion of acute atrial fibrillation to sinus caused by ischaemic heart disease or congestive cardio- rhythm, which occurs within 24 hr in 60 - 80% of acute myopathy. All patients with atrial fibrillation should cases.53 Amiodarone has also been used which reduces have an ECG, chest X-ray, serum electrolytes, echo- the ventricular rate (and does not increase the risk of cardiogram and thyroid function studies.35 death in patients with chronic heart failure)54 increases Treatment is aimed at correction of any underlying the incidence of spontaneous reversion to sinus rhythm55 causes or precipitating factors and control of rapid (although this was not found in another study56) and ventricular response (to a resting heart rate of < 110, to maintains more than 50% of patients in sinus rhythm for increase coronary perfusion, reduce cardiac work and one year following cardioversion.57 reduce left atrial pressure). This will be achieved by Calcium channel blockers (e.g. verapamil, diltiazem) either restoration of sinus rhythm and prevention of and beta-adrenergic receptor blockers (e.g. sotalol), recurrence of atrial fibrillation or slowing ventricular have also been used to reduce ventricular rate, although rate with AV blocking drugs and anticoagulation to their negative inotropic effects make them not as useful prevent thromboembolic complications.49,50 as digoxin in patients with left ventricular systolic Symptomatic improvement in patients with atrial dysfunction.49 Recently, pure class III agents have been fibrillation will be similar in those who have rhythm used to pharmacologically convert atrial fibrillation (e.g. 40 Critical Care and Resuscitation 2002; 4: 35-53 D. DURHAM, ET AL either intravenous dofetilide 8 µg/kg or ibutilide 0.025 recurrence commonly occurs unless the underlying mg/kg, converting approximately 30% to sinus rhythm), disorder has been corrected. although polymorphic ventricular tachycardia may If atrial fibrillation has been present for more than 48 develop in 4 - 8% of patients.43 Oral dofetilide in hr then warfarin is given for 3 weeks prior to the patients monitored in hospital for the first three days cardioversion and continued for 4 weeks after the (250 µg daily or twice daily, depending on the creatinine cardioversion to reduce the incidence of post cardio- clearance - patients with prolongation of QTc, version stroke,37,38,69 which occurs from 6 hr to 6 days bradycardia, hypokalaemia or severe renal failure were after the cardioversion as atrial mechanical function may excluded) was associated with an increase in the not be normal for up to several weeks after the return of spontaneous conversion rate to sinus rhythm (12% cf sinus rhythm.70 One large multicentre, rand-omised, 1% after 1 month) in patients with atrial fibrillation and controlled trial in patients with atrial fibrillation chronic heart failure with no effect on mortality demonstrated that patients who had no transoesophageal (although 3% patients developed torsade de pointes, echocardiographic evidence of left atrial thrombus did usually within the first three days).58 not require a three week period of anticoagulation Class I agents (e.g. quinidine, procainamide, diso- before cardioversion but could be anticoagulated with pyramide, flecainide) tend not to be used particularly warfarin then cardioverted (with anticoagulation when left ventricular dysfunction coexists as they are continuing for a further 4 weeks) without increasing the often associated with an adverse prognosis.59 incidence of an embolic stroke.71 This study prompted In a prospective, multicentre and randomised trial of the suggestion that this approach be recommended in patients with atrial fibrillation of less than 6 months patients who have an increased risk of haemorrhage with duration, amiodarone (200 mg daily) was more effec- warfarin or in those who have atrial fibrillation of less tive compared with sotalol (80 - 160 mg 12-hourly) and than 3 weeks duration.72 propafenone (150 mg 8 to 12-hourly) in maintaining However, while transoesophageal echocardiography sinus rhythm following cardioversion.60 may detect patients with atrial fibrillation who have In the presence of pyrexia or shock due to pulmonary atrial thrombosis (and therefore select those who require embolism or hypovolaemia, the ventricular rate is often anticoagulation prior to cardioversion),73 it may still rapid and controllable only by correcting the underlying miss small atrial thrombi and thereby incorrectly simul- condition (e.g. fluid administration for hypovolaemia).61 ate safe conditions for cardioversion,70 (e.g. cerebral Anticoagulation should be considered for all patients embolism after cardioversion without anticoagulation in who have chronic or intermittent atrial fibrillation (with a patient with negative findings on transoesophageal the exception of ‘lone’ atrial fibrillation before the age echocardiography, has been reported).74 of 60 years, in the absence of cardiopulmonary disease If the f waves in V are greater than 2 mm, cardio- 1 and hypertension) to reduce the incidence of stroke.62-64 version using 100 J may be chosen first; if the f waves in In five independent randomised trials, embolic compli- V are less than 2 mm then 200 J is commonly used.75 1 cations associated with chronic nonrheumatic atrial Quinidine has been considered the mainstay of fibrillation occurred in approximately 6% of patients, therapeutic agents to prevent recurrence of atrial and was reduced by two-thirds or more (e.g. to 1.5%) by fibrillation following cardioversion. However, in most warfarin (to keep the INR between 2.0 and 3.0; although trials 20 - 50% of patients treated with quinidine, the optimal value may be closer to 3.0).65 The incidence compared with 10 - 25% of patients given placebo, have of intracranial bleeding was less than 0.5% and about remained in sinus rhythm for 1 year after electrical 100 patients needed to be treated to prevent 2 - 3 serious conversion of atrial fibrillation.76 Quinidine therapy may strokes.66 While aspirin did not consistently reduce the also be at a cost of an increase in long term embolic complications in patients with atrial mortality.77,78 Other class Ia agents, (e.g. procainamide, fibrillation,66 it is recommended in those patients with disopyramide) are no more successful or any better atrial fibrillation in whom warfarin is contraindicated.67 tolerated.76 While the class III agents of amiodarone and Minidose warfarin (i.e. 1.25 mg daily) does not reduce sotalol provide alternatives, the side-effects of the the incidence of embolic stroke.68 former and the reduction in cardiac function with the Cardioversion may be considered if atrial fibrillation latter make them less than ideal, although currently they is acute (i.e. less than 7 days) or associated with shock, are the agents of choice.52 Low dose amiodarone (e.g. < hypertrophic cardiomyopathy or Wolff-Parkinson-White 400 mg/day) appears to have a lower 5 year mortality (WPW) syndrome. It is usually not considered if atrial when compared to quinidine when used to maintain fibrillation has been present for longer than 6 months or sinus rhythm after cardioversion.79 Flecainide has also the left atrium is dilated (greater than 4.5 cm), because been used to maintain sinus rhythm.49 41 D. DURHAM, ET AL Critical Care and Resuscitation 2002; 4: 35-53 Recently, surgical procedures to provide an retrograde conduction it is termed a concealed bypass electrically isolated corridor of tissue from the sinus tract. In the latter case the QRS complex during sinus node to the atrioventricular node (e.g. ‘atrial corridor rhythm is normal. procedure’, although atrial transport function is usually not restored and thus atrial thrombus remains a risk; 1. Atrioventricular nodal rentrant tachycardia furthermore sinus node dysfunction is common and (AVNRT) permanent pacing may be required),80 or multiple atrial AV nodal re-entrant tachycardia has a rate that varies incisions to disrupt the atrial re-entrant pathways (e.g. between 160 and 220 bpm, a regular R-R interval and a ‘maze procedure’, which usually maintains atrial retrograde P wave (which is often difficult to distinguish transport function, although return of atrial fibrillation, in the standard ECG trace) that is buried, precedes or atrial atrial flutter or complete heart block may occur)80 proceeds the narrow QRS complex. While patients who have been used to maintain sinus rhythm in patients who have a left bundle branch block (LBBB) or right bundle have had disabling atrial fibrillation uncontrolled by branch block (RBBB) may also have PSVT (LBBB or pharmacological therapy.49,80 Radiofrequency ablat-ion RBBB patterns are not uncommonly associat-ed with has also been used successfully in patients in whom PSVT), if the PSVT produces aberrant conduction and a atrial fibrillation originated from ectopic beats in the widened QRS, the pattern is RBBB in 85%, RBBB with pulmonary veins.47 LAD in 10% and LBBB in 5%, of cases. The heart performs more efficiently with the return The re-entrant pathway is permitted by a fast and of sinus rhythm by responding appropriately to stress slow pathway that exists within the AV node. The fast and restoring the AV valve competence, and an acute (anterior) pathway exhibits rapid conduction and a long decrease in heart rate and increase in stroke volume are refractory period while the slow (posterior) pathway usually observed.81 However, an acute change in cardiac exhibits slow conduction and a short refractory period. output following conversion is not consistently observ- As only the fast pathway conducts during sinus rhythm, ed and may be due to a delay in the return of the atrial the PR interval during sinus rhythm is normal. Howe- contraction.70,81 ver, an appropriately timed atrial ectopic dissociates conduction between two pathways and permits the Supraventricular tachycardias establishment of circulating electrical activity that spreads to both the atrial and ventricular myocardium Paroxysmal supraventricular tachycardia (PSVT) or causing the tachyarrhythmia. In up to 90% of cases the paroxysmal atrial tachycardia (PAT) antegrade conduction proceeds via the slow pathway This is caused by re-entry in 96% of cases (Figure and the retrograde conduction via the fast pathway.83 3). The re-entry path is at the AV junction in 70%, sinus node in 1 - 2%, atria in 1 - 2%, and is an AV nodal 2. Atrioventricular re-entrant tachycardia (AVRT) bypass tract in 15% of cases. The remaining 4% or so of Atrioventricular re-entrant tachycardia incorporates a cases are due to an ectopic focus.82 concealed AV bypass tract as part of the re-entrant Reentry involving an AV bypass tract usually travels circuit. The AV bypass tract allows retrograde antegradely through the AV node and retrogradely conduction only. through the bypass tract. If the bypass tract also conducts antegradely then pre-excitation exists (i.e. 3. Sinus node and intraatrial re-entrant tachycardias WPW syndrome); if the bypass tract only manifests The sinus node and intraatrial re-entry tachycardias Figure 3. Paroxysmal supraventricular tachycardia with a ventricular rate of 198 bpm 42 Critical Care and Resuscitation 2002; 4: 35-53 D. DURHAM, ET AL incorporate a re-entrant pathway within the sinus node cardiac failure, or when beta-blockers have or within the atrium, respectively. These arrhythmias are been used. less common than AVNRT and AVRT. iii. Longer acting intravenous drugs are often used for converting and stabilising the rhythm. For Clinical features example: While the rapid ventricular rate may be tolerated for - Propranolol (5 - 10 mg/70 kg) 1 - 3 days or longer, cardiac failure, hypotension, shock - Procainamide (500 - 1000 mg/70 kg) and pulmonary oedema may develop if the rate is - Digoxin (1 - 1.5 mg/70 kg) to increase allowed to continue unabated. PSVT may occur in the vagal tone and AV block absence of heart disease or may be associated with - Neostigmine (2 - 5 mg/70 kg) to increase hypokalaemia, WPW syndrome, ischaemic heart vagal tone disease, rheumatic heart disease, thyrotoxicosis, phaeo- c. Cardioversion 50 - 100 J (or rapid atrial pacing) chromocytoma, cardiomyopathy, mitral valve prolapse d. Surgical ablation or cryo or radiofrequency cathet- or tetanus. In 50% of patients without underlying heart er ablation to interrupt the re-entrant pathway. disease, the attack is associated with polyuria caused by These techniques should be considered if the an inhibition of vasopressin and release of a natriuretic episodes of PSVT are numerous and debilitat- peptide.84 This occurs 20 - 30 minutes after the onset of ing.90-92 the attack, with micturition occurring every 30 - 90 min up to 8 hr later. 4. Atrioventricular pre-excitation (Wolff-Parkinson- White or WPW syndrome) Treatment Pre-excitation exists if the whole or some part of the The treatments for AVNRT, AVRT and sinus node ventricular muscle is activated earlier than normally by and intra-atrial re-entrant tachycardias are similar and the impulse that originates from the atrium passing includes a chronological sequence of: through accessory AV conducting fibres rather than a. Vagal stimulation through the normal AV conduction system. The connec- b. Drugs tions may occur anywhere around the cardioskeletal i. Short acting intravenous drugs (i.e. an action ring.93 The atrial vector is normal (i.e. the P wave is which is terminated within 1 - 2 min): upright in II), differentiating pre-excitation from nodal - Adenosine (3 - 15 mg/70 kg, which has now impulses or ventricular impulses with retrograde atrial taken the place of verapamil as the activation. treatment of choice, except in asthmat- The characteristics of WPW syndrome are episodic ics).85-87 supraventricular tachycardia in patients who have speci- - Esmolol (35 mg/70 kg)88 fic ECG abnormalities that consist of:94,95 - Edrophonium (5 - 20 mg/70 kg) ii. Intermediate acting drugs - a PR interval which does not exceed 0.12 s - Verapamil 5 - 10 mg intravenously (0.075 - - a delta wave (a slurred thickened proximal portion of 0.15 mg/kg) infused over 1 - 3 min the QRS complex). A negative delta wave in V is 1 (terminates 80% of cases).89 This is the diagnostic of a right-sided bypass tract (Figure 4). treatment of choice in asthmatic patients - a QRS which equals or exceeds 0.12 s. A Q wave in with PSVT, or if the PSVT recurs after the III and aVF often mimics an inferior myocardial effect of adenosine has worn off. However, infarct. verapamil, should not be used as a second line drug if adenosine has failed, as The classical ECG changes of WPW syndrome verapamil is unlikely to succeed and it will occur in 1 - 2 per 1000 of the general population and only compound the negative inotropic effect tachycardias occur in 40 - 80% of these patients, 75% of of both agents, causing severe hypotension. which are re-entrant supraventricular tachycardias (95% If the PSVT recurs following the first due to retrograde conduction through the bypass tract dose of verapamil, then an intravenous dose causing an orthodromic tachycardia with a normal QRS of 5 - 10 mg may be repeated every 30 min complex and 5% due to antegrade conduction through or infused at 0.005 mg/kg/min, or an oral the bypass tract causing an antidromic tachycardia with dose of 240 - 480 mg/day (e.g. 80 - 160 mg a wide QRS complex) and 20% atrial fibrillation 8-hourly) may be used. Verapamil often (usually wide complex and rapid ventricular rate); atrial causes troublesome constipation, it is also flutter is rare.96,97 contraindicated in patients who have overt The WPW syndrome may be associated with mitral 43 D. DURHAM, ET AL Critical Care and Resuscitation 2002; 4: 35-53 Figure 4. A 12 lead ECG of a patient with Wolff-Parkinson-White syndrome showing a short PR interval a delta wave and Q wave in III and aVF. valve prolapse, ischaemic heart disease, hypertrophic bundle ECG and atrial pacing to facilitate operative subaortic stenosis, cardiomyopathy, ‘sick’ sinus syndro- identification and surgical ablation of the anomalous me, rheumatic fever, Ebstein’s anomaly, bicuspid aortic pathway, have been used. Currently, however, radio- or pulmonary valves, coarctation of the aorta, ventricu- frequency intracardiac ablation is being offered in spec- lar septal defect and atrial septal defect. False-positive ialised centres as a safe alternative to medical treatment exercise tests may also occur with WPW syndrome. in patients who have only minor symptoms.92,106 Patients The treatment of PSVT associated with WPW inclu- with pre-excitation who are asymptomatic have a benign des increasing vagal tone, adenosine, lignocaine, procai- clinical course and only warrant careful follow-up.107 namide, amiodarone, propranolol and cardioversion.98 Sotalol has also been recommended as the drug of first 5. Nonparoxysmal junctional tachycardia choice in patients with acute PSVT and for long-term This rhythm usually results from conditions that management.99 The treatment of atrial fibrillation with enhance automaticity (e.g. theophylline, catecholamine WPW includes cardioversion, or drugs which act on toxicity) or triggered activity (e.g. digoxin toxicity) in both the atrial and accessory pathways (i.e. class Ia, Ic the AV junction. The rate usually varies between 70 and or III). Beta-blockers or lignocaine are ineffective, and 130 bpm, the QRS complex is identical to that observed digoxin, verapamil and adenosine are contraindicated as with sinus rhythm and the rate may be influenced by they may increase the ventricular rate leading to VT and vagotonic and vagolytic agents. Treatment is directed VF by blocking antegrade AV conduction, shortening towards eliminating the underlying factors. atrial refractoriness (facilitating the induction of AF) and enhancing the conduction through the anomalous 6. Multifocal atrial tachycardia (MAT) pathway97,100-103(digoxin-facilitated ventricular rate in This is a non-reentrant atrial tachycardia that causes WPW syndrome may be reversed by using 8 mmol of supraventricular tachycardia in 1 - 2% of cases. The rate magnesium sulphate, intravenously).104 By prolonging varies from 100 to 220 bpm and is characterised by an the refractory period of the AV and His-Purkinje system absence of one predominant atrial focus with three or as well as the accessory pathway, one study found that more P waves of different morphologies in a single ECG ibutalide terminated AF in 95% of patients with pre- lead, an isoelectric baseline between the P waves, and a excitation.105 variation in PR, PP and RR intervals (Figure 5).108,109 It Ablation of the anomalous pathway. In patients in differs from the condition of ‘wandering pacemaker’, whom the episodes of supraventricular tachycardia are which usually refers to multifocal supra-ventricular numerous, debilitating and not controlled by long-term escape complexes in the presence of sinus antiarrhythmic treatment, epicardial mapping, His bradycardia.110 44