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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
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D. DURHAM, ET AL Critical Care and Resuscitation 2002; 4: 35-53
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Critical Care and Resuscitation 2002; 4: 35-53 D. DURHAM, ET AL
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D. DURHAM, ET AL Critical Care and Resuscitation 2002; 4: 35-53
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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 g/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.
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D. DURHAM, ET AL Critical Care and Resuscitation 2002; 4: 35-53
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 V1 (Figure 2). The f waves may be coarse (i.e. where intravenous procainamide is recommended),52
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.
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Critical Care and Resuscitation 2002; 4: 35-53 D. DURHAM, ET AL
either intravenous dofetilide 8 g/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 g 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 V1 are greater than 2 mm, cardio-
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- V1 are less than 2 mm then 200 J is commonly used.75
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
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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 V1 is
(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
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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, Ebsteins 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
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Critical Care and Resuscitation 2002; 4: 35-53 D. DURHAM, ET AL
Multifocal atrial tachycardia is required to be differ- used, and in one study was more effective than
entiated from atrial fibrillation because digoxin is often verapamil in reducing ventricular rate and converting
used in the latter but is not effective for the former.111 MAT to sinus rhythm.118 However, as many of these
The tachycardia usually occurs in the critically ill patients are elderly with COPD, metoprolol may be
elderly (i.e. 70 years or more) male patient,109 is often associated with adverse side effects (e.g. severe bronc-
associated with COPD, cardiac failure or ischaemic hospasm, hypotension). Treatment with digoxin, quinid-
heart disease, and is usually precipitated by hypoxia, ine, procainamide, lignocaine, phenytoin or cardiovers-
hypercapnia, sepsis, electrolyte disorders, sympatho- ion is usually ineffective.109,111
mimetics, digoxin or methylxanthines.112,113 While the
mortality due to the arrhythmia may be low, patients Wide complex tachycardias
who develop this arrhythmia have an in-hospital The main question that arises in the management of
mortality of about 45%.111 Treatment consists of efforts a patient with a tachycardia is is it supraventricular or is
to correct drug toxicity (e.g. sympathomimetic, digoxin it ventricular? If the QRS complex is wide (Figure 6),
or theophylline toxicity) and correct electrolyte the bedside diagnosis of the tachycardia is difficult. The
abnormalities (i.e. hypokalaemia, hypomagnesaemia or features that help distinguish supraventricular from
alkalosis). If the ventricular rate is deemed too rapid ventricular tachycardias are given in Table 2.119-124
then therapy of choice is intravenous magnesium If there is doubt about the origin of the impulse then
sulphate, 10 mmol in 2 - 3 min (which may be followed the patient should be cardioverted, particularly if there is
by an infusion of 20 - 40 mmol of magnesium sulphate cardiac failure or hypotension.125 If the patient is not
in 4 - 6 hr114,115) or intravenous verapamil 5 - 10 mg.116 haemodynamically compromised, intravenous ligno-
If verapamil is used then pretreatment with 1 g of caine (1.5 mg/kg as an intravenous bolus which may be
intravenous calcium gluconate before administering repeated after 10 min) followed, if required, by
verapamil has been used to prevent any hypotensive adenosine (6 mg as an intravenous bolus, which is follo
effect, without preventing its anti-arrhythmic effect.117 wed 2 min later, if required, by 12 mg as an intravenous
Metoprolol (10 mg i.v. over 5 minutes) has also been bolus) is currently recommended.126 Adenosine is used
Figure 6. A wide complex tachycardia (in this case ventricular tachycardia) with a ventricular rate of 190 bpm
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D. DURHAM, ET AL Critical Care and Resuscitation 2002; 4: 35-53
Clinical features
Hypotension Rare Not uncommon
Pulse rate (beats/min) 160-220 130-180
JVP cannon A waves Rare Common
Beat-to-beat variation in blood pressure Rare Common
Varying intensity of S1 Rare Common
Reversion with vagal stimulation Common Rare
Echocardiograph
atrioventricular dissociation Rare Common
ECG features
RR irregularity Rare Not uncommon
Atrioventricular relationship
a. Relationship between the QRS
and the preceding P wave Common Rare
b. Fusion beats Never Not uncommon
c. Capture Never Not uncommon
d. Retrograde atrial activation Rare Common
(inverted P in II upright P in aVR)
e. A 2:1 or 3:1 ventriculoatrial
conduction with vagal stimulation Never Common
QRS duration
a. A narrow QRS complex Common Rare
b. If broad complex (> 0.14 s)
LBBB pattern Not uncommon Rare
RBBB pattern Not uncommon Rare
Precordial QRS mainly:
Positive Uncommon Common
Negative Uncommon Common
Biphasic Uncommon Common
QRS axis Normal Abnormal
as it has a rapid offset of action, will terminate any ventricular tachycardia,128,129 it is contraindicated in
arrhythmia that has an obligatory participation of the patients with wide complex tachycardia of unknown
AV node, and will not cause haemodynamic compro- origin as the majority are of ventricular origin and
mise or change the tachycardia to a life threatening verapamil is ineffective and potentially hazardous in
arrhythmia (although it may do so in patients who have most of these patients.119,130,131
WPW with atrial fibrillation).102,103
In patients with wide complex tachycardias there is Ventricular tachycardias
little difference between bolus doses of adenosine and
adenosine triphosphate in relation to the minimal effect- Ventricular tachycardia. This is defined as three or
ive dose and incidence of side effects.87,127 Amiodarone more consecutive ectopic ventricular impulses having
or procainamide may also be tried as these agents may approximately the same contour and separated by a
terminate both ventricular or supraventricular arrhythm- fixed interval. It is sustained if either its duration is
ias. While verapamil may on rare occasions terminate greater than 30 s or if it has to be terminated by
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Critical Care and Resuscitation 2002; 4: 35-53 D. DURHAM, ET AL
cardioversion or pacing in less than 30 s because of converted 69% to sinus rhythm) was more effective than
severe hypotension. lignocaine (100 mg i.v. over 5 minutes converted 20%
The rate usually ranges from 130 - 180 bpm (if it is to sinus rhythm) in terminating VT, and the incidence of
greater than 180 bpm it is often considered as a form of adverse effects was similar for both drugs.133
ventricular flutter), the R-R interval may be slightly Accelerated idioventricular rhythm. This is also
irregular (i.e. 0.01 - 0.02 s variations) or regular (Figure known as slow ventricular tachycardia and has a rate
6). Characteristically there is AV dissociation, although which ranges from 60 - 120 bpm (Figure 7). It usually
rarely retrograde conduction may occur and give rise to occurs in patients with acute myocardial infarction,
a P wave following, or less than 0.12 s before, the QRS cardiomyopathy, or digoxin intoxication and is often
complex. Fusion beats or capture are pathognomonic transient, resistant to antiarrhythmic therapy, but rarely
of ventricular rhythm (Figure 7). The QRS complex causes significant haemodynamic disturbance. Apart
during VT is usually uniform (mono-morphic); if it from correction of drug toxicities and electrolyte abnor-
varies from beat to beat it is said to be polymorphic. malities, specific treatment for accelerated idioventric-
Bidirectional VT is due to either two ventricular foci or ular rhythm is rarely necessary.
one focus with aberration of the conducting impulses
(e.g. alternating bundle-branch block). Torsade de pointes
The causes of VT include ischaemic heart disease, This is a ventricular arrhythmia which has
ventricular aneurysm, prolonged QTc syndrome, WPW characteristics of both VT and VF. Some believe that it
syndrome, rheumatic fever, cardiomyopathy, drug tox- is an atypical VT,134 whereas others consider it an early
icity (e.g. tricyclic antidepressants, digoxin, quinidine), phase of VF.135 However it is commonly considered to
hypokalaemia and hypomagnesaemia. be a polymorphic VT which is preceded by QT
The clinical features of hypotension, shock, angina prolongation (Figure 8) and is characterised by:135,136
or cardiac failure are not pathognomonic of VT and may
be associated with the disorder due to the underly-ing - a ventricular rate exceeding 200 bpm
myocardial disease. - a widened QRS deflection which shows a continual
Treatment of VT involves cardioversion, if the change in amplitude giving the appearance of a
patient is haemodynamically compromised, followed by modulated sine wave, or spindle
class I or III agents, (e.g. amiodarone, sotalol, ligno- - a complete reversal of the QRS and T wave
caine, procainamide, bretylium). If the patient is not in deflections as they appear to twist around the
cardiac failure or is not hypotensive, class I or III agents isoelectric line (hence the name)
without cardioversion are often used. - atrioventricular dissociation
In a multicentred study of patients with ventricular
tachycardia, sotalol was found to be more effective than The arrhythmia is associated with disorders listed in
imipramine, mexiletine, procainamide or quinidine in Table 3.136
preventing death and recurrences of ventricular tachy- The attacks are often short lived and self-limiting,
arrhythmias.132 In a double blind study of patients with and the patient often does not lose consciousness as a
acute sustained VT, sotalol (100 mg i.v. over 5 minutes mean arterial pressure ranging from 20 - 40 mmHg is
Figure 7. Accelerated ventricular rhythm showing a ventricular rate of 80 bpm, two fusion beats, capture and sinus rhythm at a rate of 82 bpm.
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D. DURHAM, ET AL Critical Care and Resuscitation 2002; 4: 35-53
Figure 8. Sinus rhythm at 88 bpm with a prolonged QTc interval, two ventricular ectopic beats, another sinus beat then torsade de pointes.
usually present. However, the episodes may recur and or VF, and correction of the underlying disorder (i.e.
become prolonged, particularly when hypokalaemia, hypokalaemia, hypomagnesaemia and drug toxicity).
hypomagnesaemia and an underlying bradycardia coex- Otherwise, intravenous magnesium sulphate (bolus 5 -
ist,137 and may deteriorate into VF with clinical signs of 10 mmol) is the agent of choice. Other treatments
cardiac arrest.138 include potassium supplements to keep the plasma
potassium at 4 mmol/L or greater,139,140 or (if the patient
Table 3 Disorders associated with torsade de pointes has an underlying bradycardia), producing a ventricular
rate of 100 beats/min or greater using intravenous
Complete atrioventricular or sinoatrial block atropine (0.6 - 2.4 mg), an infusion of isoprenaline (2 to
Prolonged QT syndromes 6 g/ min) or a pacemaker.141,142 Class Ia drugs are to be
Hypokalaemia, hypomagnesaemia avoided as they tend to sustain the arrhythmia.
Mitral valve prolapse Phenytoin and lignocaine are generally ineffective,
Ischaemic heart disease although bretylium (which now is no longer available)
Myocarditis has been useful.142
Central nervous system disorders
Liquid-protein diets Ventricular fibrillation
Drugs This is characterised by a loss of an orderly sequence
quinidine, procainamide, disopyramide, cisapride of ventricular myocardial contraction caused by a
phenothiazines (particularly thioridazine), random and chaotic spread of electrical activity. The
antihistamines, tricyclic antidepressants, ECG reveals completely irregular, chaotic and deformed
chloral hydrate, deflections of varying height, width and shape.143
erythromycin, azithromycin, fluconazole (Figure 9). Death results from loss of cardiac output and
absence of cerebral perfusion, unless direct current
defibrillation successfully restores sinus rhythm.
Treatment of the arrhythmia includes resuscitation Diseases associated with ventricular fibrillation include,
and defibrillation if it is prolonged or degenerates to VT ischaemic heart disease, cardiomyopathies, electrocut-
ion, disorders associated with prolonged QTc syndrome
48
Critical Care and Resuscitation 2002; 4: 35-53 D. DURHAM, ET AL
and drugs (i.e. phenothiazines, antihistamines and pro- 17. Engel TR, Meister SG, Frankl WS. Postextrasystolic T
arrhythmic effect of quinidine, disopyramide, etc.).143,144 wave changes and angiographic coronary heart disease.
The treatment involves external cardiac massage and Br Heart J 1977;39:371-376.
18. El-Sherif N, Myerburg RJ, Scherlag BJ, et al.
defibrillation at the earliest opportunity and correction
Electrocardiographic anticedents of primary ventricular
of any underlying disorder. fibrillation: value of the R on T phenomenon in
myocardial infarction. Br Heart J 1976;38:415-422.
Received: 20 December 2001
19. Lie KI, Wellens HJ, Downar E, Durrer D. Observations
Accepted: 22 Febuary 2002
on patients with primary ventricular fibrillation
complicating acute myocardial infarction. Circulation
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