Cardiac Arrhythmias: Diagnosis and Management. The Tachycardias

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 lifethreatening 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 WolffParkinson-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, antiarrhythmic 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, WolffParkinson 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
NORMAL CARDIAC RHYTHM
The rhythm of a normal resting adult heart is initiated from impulses generated from the sinoatrial (SA)
node with a rate varying between 60 - 100 beats per
minute (bpm). During sleep the rate may decrease to 30
- 50 bpm,1,2 with episodes of sinus pauses up to 3 seconds, sinoatrial block, junctional rhythms, first degree and
second degree atrioventricular nodal block occurring
often enough (particularly in trained athletes) to be
considered normal variants.3
The impulses generated from the SA node spread via
specialised internodal atrial conducting pathways to the
atrioventricular (AV) node, where they are delayed
before they are finally distributed to the ventricular
myocardium via the His-Purkinje system. Normally,
with exercise the heart rate increases to at least 85% of
the age predicted maximum of 220 - age in years, with
failure to do so being termed ‘chronotropic incompetence’. Sinus arrhythmia is defined as sinus rhythm with
P-P variations of more than 10%. It is due to cyclical
variations in vagal tone commonly related to respiration
(the rate is faster with inspiration and slower with
expiration), and is often seen in individuals with sinus
bradycardia.4 It disappears with exercise, breath holding
and atropine and is more likely to be seen in individuals
who do not have cardiac disease.
Frequent multifocal ventricular ectopic beats have
been noted in up to 12% of normal adults during a 24 hr
period, indicating that, in the absence of underlying
cardiovascular disease, ventricular ectopic beats are not
a prelude to something more sinister.1,5-7
CARDIAC ARRHYTHMIAS
An arrhythmia is defined as any cardiac rhythm other
than regular sinus rhythm. It is caused by a disorder of
impulse generation, impulse conduction or a
combination of the two, and may be life-threatening due
to a reduction in cardiac output, reduction in myocardial
blood flow or precipitation of a more serious arrhythmia. While the term ‘dysrhythmia’ would appear to be
better suited as a label for an abnormal cardiac rhythm
(as the term arrhythmia suggests an absence of rhythm),
the term ‘arrhythmia’ will be used in this review as it has
now become the accepted medical term.
Critical Care and Resuscitation 2002; 4: 35-53
relationship to be determined.8 In unusual circumstances, a trace of up to 60 seconds may be required.
However, leads II and V1 are not ideal for the recognition of myocardial ischaemia, although V5, which
shows approximately 90% of all ST segment changes
due to anterior, inferior or posterior ischaemia, is.9 A
modification of both leads II and V5, where the right
arm lead is mounted on the manubrium sterni, the left
arm lead is mounted on the xiphisternum and left leg
lead is placed in V5 position, facilitates the diagnosis of
both rhythm and ischaemic changes. Using this lead, the
setting of lead I results in maximal P wave amplitude
and the setting of lead II offers optimal ischaemic
detection, with the added advantages of reducing interference and electrical artifact.10
To perform the cardiac ECG ‘rhythm trace’ the patient should be in a warm environment to reduce ‘shivering’ artifact, and the recording should not be performed
during body movement, as muscle or limb movement
artifact can simulate ventricular tachycardia.11
Description of an arrhythmia
Arrhythmias may be described from their following
characteristics:12
1. Rate (e.g. tachycardia or bradycardia)
a. tachycardia is defined as three or more
consecutive impulses from the same pacemaker
at a rate exceeding 100 bpm in adults (i.e. > 8
years of age).
b. bradycardia is defined as three or more
consecutive impulses from the same pacemaker
at a rate less than 60 bpm.
2. Rhythm (e.g. regular or irregular)
3. Origin of impulse (i.e. supraventricular, ventricular,
or artificial pacemaker)
4. Impulse conduction (i.e. atrioventricular, ventriculoatrial or block)
5. Ventricular rate
6. Special phenomena (e.g. pre-excitation)
Management of an arrhythmia
In general, the management of an arrhythmia focuses
on:
-
Diagnosis of an arrhythmia
The assessment of an arrhythmia requires the
determination of the site of the conduction disturbance,
the atrial and ventricular rhythms present and the relationship between the atrial and ventricular impulses.
When using the standard ECG leads, the cardiac rhythm
is often best considered from leads II or V1 as they
provide the maximum P and QRS wave amplitudes to
allow the supraventricular and ventricular impulse
36
-
correcting precipitating causes (e.g. hypokalaemia,
hypomagnesaemia, hypercapnia, hypocapnia, hypoxia, metabolic alkalosis, drug poisoning or toxicity),
restoring
sinus
rhythm
or
providing
a
supraventricular rhythm with an acceptable
ventricular rate, and
preventing a relapse.
The specific management of an arrhythmia depends
upon whether it is an ectopic impulse, a sustained arrhy-
Critical Care and Resuscitation 2002; 4: 35-53
thmia (supraventricular or ventricular tachycardia, or
bradycardia) or a special phenomenon.
ECTOPIC IMPULSES
An ectopic impulse is one that arises from any site
other than the SA node. An escape impulse is one which
arises from a different pacemaker from the underlying
pacemaker due to a delay in the arrival of the expected
impulse of the prevailing rhythm. An extrasystole is a
premature impulse (i.e. arises earlier than one would
anticipate by observing the prevailing rhythm) and usually shows a fixed, and probably causal, relationship to
the preceding activation of the same cardiac chamber.13
An increase in both atrial and ventricular ectopics
may be associated with:
- physiological conditions (e.g. cold, emotion, fatigue,
pregnancy)
- drugs (e.g. alcohol, tea, coffee, tobacco, aminophylline, tricyclics, digoxin, quinidine, sympathomimetics)
- disease (e.g. ischaemic heart disease, cardiomyopathies, pulmonary embolism, COPD, systemic
disease, fever, renal colic, hypokalaemia and biliary
tract disease).
Atrial ectopics
Atrial ectopics commonly occur in early cardiac
failure and often herald the onset of atrial fibrillation or
atrial flutter, particularly when they are associated with
acute myocardial infarction, post operative thoracotomy, rheumatic fever or thyrotoxicosis. They can also
initiate paroxysmal supraventricular tachycardias in
susceptible patients. The premature atrial complex may
arise from any location in the atria and are recognised as
an early P wave with a morphology that differs from the
sinus P wave. There are three different effects that the
atrial ectopic may produce on the rhythm of the heart:
1. It may discharge the SA node, so that the pause
following it is the same as normal,
2. It may not discharge the SA node, so that there is a
compensatory pause before the next sinus beat, or
3. It may be partially or completely blocked in the AV
node, to prolong the PR interval or exhibit a P wave
with no ventricular response.
Junctional ectopics
As the AV node in vitro does not have the property
of automaticity, it is believed that junctional ectopics
arise from the bundle of His. The impulses are conducted retrogradely to the atria and antegradely to the
ventricles with the P wave being hidden by the QRS or
appearing just before, or after, the QRS wave and
inverted in leads II, III and aVF.
D. DURHAM, ET AL
Ventricular ectopics
Ventricular ectopics are of little clinical significance
in normal individuals.14 They assume significance when
they are associated with clinical evidence of heart
disease, as an indicator of cardiac disease rather than a
disorder that needs to be treated, as treatment to
suppress them may be associated with an increase rather
than a decrease in mortality.15,16
Ventricular ectopic beats are characterised by a wide
QRS complex that is not preceded by a P wave. It often
bears a relatively fixed relationship to the preceding
sinus complex. If fixed coupling does not exist but the
intervals between the ventricular ectopic beats are
regular, then the ectopic beat has an entry block and
ventricular parasystole is said to be present.
If every sinus beat is followed by a ventricular
ectopic, then ventricular bigeminy is said to be present.
If every second sinus beat is followed by a ventricular
ectopic, then ventricular trigeminy is said to be present,
etc. If every sinus beat is followed by two ventricular
ectopic beats then this is described as ventricular
couplets (if a sinus beat is followed by three ectopics
then ventricular tachycardia is present if the ventricular
rate is greater than 100 beats per minute).
The ventricular ectopic impulse is often not conducted retrogradely and therefore, while it usually blocks
the sinus beat, it usually does not alter the sinus rate.
Post-extrasystolic T wave changes (i.e. alteration in the
T wave vector, amplitude or contour compared with the
preceding sinus beat T wave) occur in 68% of normal
individuals and 81% of patients with coronary heart
disease, and are not indicative of heart disease.17
Warning ventricular ectopic beats preceding ventricular tachycardia (VT) or ventricular fibrillation (VF)
have been described as, greater than 1 in 10 beats, two
or more beats in succession, multifocal (i.e. have
differing contours in any one lead and differing coupling
times to the preceding impulse of the prevailing
rhythm), R on T phenomenon (i.e. refers to an ectopic
impulse which is superimposed on the T wave of a
preceding impulse), and arising from the left ventricle
(i.e. show a RBBB pattern). However, these ‘warning
arrhythmias’ have been detected in up to 60% of
patients who do not develop VF,18,19 and episodes of VF
not preceded by these ‘warning arrhythmias’, have been
observed in up to 40% of patients with acute myocardial
infarction.20-24
The R on T ventricular ectopic as a predictor of VF
in patients with acute myocardial infarction is neither a
specific nor sensitive phenomenon,25,26 and it may have
been confused with the vulnerable phase for fibrillating
an animal ventricle by stimulation techniques not analogous to ectopic beats.27
37
D. DURHAM, ET AL
SUSTAINED ARRHYTHMIAS
The sustained arrhythmias are classified as either
tachycardias or tachyarrhythmias (if there are three or
more complexes with a rate of greater than 100 beats per
minute) or bradycardias or bradyarrhythmias (if the rate
of the complexes are less than 60 beats per minute). The
tachycardias may be caused by disorders of impulse
conduction (i.e. re-entry) or impulse generation (i.e.
enhanced automaticity or triggered activity). The bradycardias may be caused by a decrease in impulse formation or conduction.
Tachycardias
Uncontrolled tachycardias can induce cardiac failure
(even a reversible cardiomyopathy28), cardiac ischaemia
and may degenerate into ventricular fibrillation. In the
management of a patient with tachycardia, the clinician
is required to assess whether the origin of the rhythm is
supraventricular (e.g. atrial) or ventricular. However, the
relationship between an atrial and ventricular rhythm
may be extremely difficult to define and may require
methods to reduce the ventricular rate (e.g. increase the
AV block by vagal stimulation; Figure 1), enhance the
atrial ECG complexes (e.g. intra-atrial or oesophageal
leads) or observe aortic and mitral valve movement
during echocardiography29 to clarify the relationship.
Vagal stimulation
This is often used to diagnose and treat supraventricular tachycardias by slowing the atrial rate and
increasing the AV block. The standard responses to
vagal stimulation are reduction of sinus rate (even
transient second- or third-degree block), slowing of the
ventricular response in atrial fibrillation, transient
increase in the AV block in atrial flutter (Figure 1),
conversion of 50 - 60% of junctional tachycardias (i.e.
paroxysmal supraventricular, idio-nodal, and multifocal
atrial tachycardia) to sinus rhythm and no effect in VT.30
In latent digoxin toxicity, bigeminal or multifocal
ventricular ectopics may occur.
Vagal stimulation may be performed by physical
methods (e.g. carotid sinus massage, Valsalva manoeuvre, facial immersion, etc) or drugs.
Physical methods
Carotid sinus massage (Czermak’s manoeuvre).
Carotid sinus massage is performed with ECG monitoring, the patient supine and the head turned to the opposite side. The carotid bifurcation is localised by palpating
the carotid impulse at the angle of the jaw. While
observing the ECG trace, pressure or massage is applied
for no longer than 3 s at the bifurcation of the carotid
artery.31 To increase the vagal effect, the manoeuvre
should be performed at the end of inspiration or during
38
Critical Care and Resuscitation 2002; 4: 35-53
expiration.4 The carotid sinus on one side is stimulated
first. If there is no effect, after a delay of 1 minute, the
opposite carotid sinus is stimulated. A pause of greater
than 3 s or a decrease in systolic blood pressure of more
than 50 mmHg is abnormal, and indicative of carotid
sinus hypersensitivity.32 This manoeuvre is contraindicated in patients who have AV block, or known
cerebrovascular disease.
Valsalva manoeuvre. This is performed by asking
the patient not to take a deep breath before blowing into
an aneroid manometer up to 40 mmHg for 10 - 15 s. The
vagal response occurs during the period of termin-ation
of the manoeuvre.
Facial immersion. This is performed by asking the
patient to hold his/her breath on inspiration while a
towel with cold water is placed over the jaw.33 This
produces a profound vagal response with peripheral
vasoconstriction, unlike a vasovagal attack which is
associated with vasodilation.
Other physical methods. These include, ocular
pressure (Aschner-Dagnini manoeuvre), vomiting and
squatting. In one study of 35 patients with induced and
sustained junctional tachycardia, the Valsalva manoeuvre in the supine position was successful in terminating
the arrhythmia in 54%, right carotid sinus massage in
17%, left carotid sinus massage in 5% and facial
immersion in 17% of cases.30
Drugs
Ephedrine, phenylephrine, edrophonium and neostigmine have all been used to either directly or indirectly
stimulate the vagus. These agents are now rarely used.
Atrial tachycardias
Sinus tachycardia
In sinus tachycardia the rate is usually between 100 160 bpm but may increase to 220 bpm particularly with
severe sympathetic stimulation or drug effect. The
causes include anxiety, tetanus, delirium, phaeochromocytoma, thyrotoxicosis, fever (with an increase of 8 bpm
for every 1ºC increase in temperature, if the fever is due
to an infection),34 pain, shock, drug withdrawal and
sympathomimetic agents. Treatment should be directed
at the underlying cause (e.g. pain, hypoxia, etc.). Betablockers may be required if the tachycardia has been
generated by an inappropriate sympathetic hyperactivity, for example in patients with tetanus, drug withdrawal, delirium tremens, thyrotoxic crisis or phaeochromocytoma.
Atrial flutter
Atrial flutter in its common form has an atrial rate
that varies between 250 - 350 bpm (usually it is almost
Critical Care and Resuscitation 2002; 4: 35-53
exactly 300 bpm), and is often caused by a single reentrant circuit in the right atrium35 (Figure 1). In type 1
atrial flutter, the circuit runs anticlockwise around the
right atrium, in type 2 atrial flutter it runs clockwise.
Unlike atrial fibrillation, there is a discrete atrial
mechanical systole after each electrical flutter wave,
explaining why arterial embolism is rare with atrial
flutter.36
Atrioventricular regurgitation does not occur in atrial
flutter, whereas it always occurs with atrial fibrillation.
Classically, the ECG trace shows a sawtooth pattern in
leads II and III, characterised by a regular atrial rhythm
and, in the untreated patient, a 2:1 AV block with a
ventricular rate around 150 bpm. There is no isoelectric
line between the P waves, which appear inverted in II,
III and aVF in 70% (typical pattern or type 1) and
upright in 30% (atypical pattern or type 2). A variant is
flutter/fibrillation, where the atrial activity alternates
between both rhythms, and in this condition arterial
embolism can occur. Atrial flutter is commonly caused
by those disorders which also cause atrial fibrillation.
The treatment of choice is cardioversion with lowvoltage direct current shock (e.g. 50 J). While prior
anticoagulation was not initially recommended37,38
unless the patient varied between atrial flutter and
fibrillation, recent reports of embolic events following
cardioversion for atrial flutter without anticoagulation,
have prompted many to recommend otherwise.39-41
Higher energies (100 J) may be required if the flutter
has been prolonged. However, in one study of 330
patients with atrial flutter a higher conversion rate was
reported using 100 J when compared with 50 J (85% c.f.
70%), irrespective of the duration of the arrhyth-mia.42
If a right atrial pacing wire is present then 15 s of rapid
atrial pacing (with a pacing cycle length 10 ms less than
the atrial rate and progressively decreased to 150 ms or
400 per minute for 15 - 30 seconds) will also convert the
arrhythmia.35
D. DURHAM, ET AL
To maintain sinus rhythm, class Ia, III or IV antiarrhythmic drugs (Table 1) may be required following
the cardioversion (e.g. procainamide, amiodarone or
verapamil). Verapamil, digoxin, or amiodarone may also
be used instead of cardioversion to slow the ventricular
rate or convert the arrhythmia to sinus rhythm.
Verapamil will convert the rhythm to sinus in 10 - 30%
of cases. If class Ia or III drugs are used to convert the
arrhythmia (which have conversion rates varying
between 30% - 50%), these drugs may, in rare instances,
increase the AV conduction before the rhythm reverts,
causing a 1:1 ventricular response and dangerous
tachycardia that may proceed to VF. To reduce this
hazard, digoxin is often used first to increase the AV
block and control the ventricular rate before class Ia or
type III agents are used.
Recently, pure class III drugs (e.g. dofetilide 8 µg/kg
or ibutilide 0.01- 0.025 mg/kg i.v. over 10 minutes) have
been reported to convert atrial flutter to sinus rhythm in
up to 60 - 75% of patients.43
In prolonged and resistant cases of atrial flutter,
radiofrequency ablation between the tricuspid valve and
the inferior vena cava has been successful in up to 90%
of cases, although 25% of patients developed atrial
fibrillation after 1 year.44
Atrial fibrillation
This may be caused by mitral valve disease (the
incidence is 41% in mitral stenosis and 75% in mitral
regurgitation),45 cardiomyopathy, ischaemic heart disease, thyrotoxicosis, myxoedema, pneumonia, systemic
infection, alcohol intoxication and withdrawal, hypothermia, thoracotomy, post cardiac surgery, lung and
mediastinal malignancy, rheumatic fever, pre-excitation
syndromes, pulmonary embolism, constrictive pericarditis, COPD, ‘sick’ sinus syndrome, hypovolaemia and
idiopathic (i.e. lone atrial fibrillation).46 The arrhythmo-
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
Ib
Ic
II
III
IV
Block inward sodium current
Quinidine, procainamide, disopyramide
Lignocaine, tocainide, mexiletine, phenytoin
Flecainide, encainide, lorcainide
Beta adrenergic receptor blockers Propranolol, metoprolol, atenolol, sotalol
Prolong the action potential
Amiodarone, bretylium, sotalol, ibutilide, dofetilide
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
fibrillation arise predominantly from the pulmonary
veins.47
The clinical features include palpitations, irregular
pulse, variable intensity of the second heart sound,
fatigue, cardiac failure and embolic phenomena (there is
a six-fold increase in strokes in patients with chronic
atrial fibrillation).48 The ECG reveals a variable R-R
interval and fibrillatory (f) waves particularly in lead II
and V1 (Figure 2). The f waves may be coarse (i.e.
waves greater than 0.5 mm from trough to peak)
particularly if the atrial fibrillation is of recent onset), or
fine, particularly if the atrial fibrillation is chronic, or
caused by ischaemic heart disease or congestive cardiomyopathy. All patients with atrial fibrillation should
have an ECG, chest X-ray, serum electrolytes, echocardiogram and thyroid function studies.35
Treatment is aimed at correction of any underlying
causes or precipitating factors and control of rapid
ventricular response (to a resting heart rate of < 110, to
increase coronary perfusion, reduce cardiac work and
reduce left atrial pressure). This will be achieved by
either restoration of sinus rhythm and prevention of
recurrence of atrial fibrillation or slowing ventricular
rate with AV blocking drugs and anticoagulation to
prevent thromboembolic complications.49,50
Symptomatic improvement in patients with atrial
fibrillation will be similar in those who have rhythm
40
control (e.g. reversion to sinus rhythm with antiarrhythmic agents to maintain sinus rhythm) compared with
those who have rate control (e.g. negative chronotropic
agents and anticoagulation), although exercise tolerance
is better (yet hospital admission is more frequent) when
rhythm control is compared with rate control.51
The agent most often used to slow the ventricular
response is digoxin (unless atrial fibrillation is present in
a patient who has Wolff-Parkinson-White syndrome
where intravenous procainamide is recommended),52
particularly in patients who have left ventricular systolic
dysfunction. Digoxin does not alter the incidence of
spontaneous reversion of acute atrial fibrillation to sinus
rhythm, which occurs within 24 hr in 60 - 80% of acute
cases.53 Amiodarone has also been used which reduces
the ventricular rate (and does not increase the risk of
death in patients with chronic heart failure)54 increases
the incidence of spontaneous reversion to sinus rhythm55
(although this was not found in another study56) and
maintains more than 50% of patients in sinus rhythm for
one year following cardioversion.57
Calcium channel blockers (e.g. verapamil, diltiazem)
and beta-adrenergic receptor blockers (e.g. sotalol),
have also been used to reduce ventricular rate, although
their negative inotropic effects make them not as useful
as digoxin in patients with left ventricular systolic
dysfunction.49 Recently, pure class III agents have been
used to pharmacologically convert atrial fibrillation (e.g.
Critical Care and Resuscitation 2002; 4: 35-53
either intravenous dofetilide 8 µg/kg or ibutilide 0.025
mg/kg, converting approximately 30% to sinus rhythm),
although polymorphic ventricular tachycardia may
develop in 4 - 8% of patients.43 Oral dofetilide in
patients monitored in hospital for the first three days
(250 µg daily or twice daily, depending on the creatinine
clearance - patients with prolongation of QTc,
bradycardia, hypokalaemia or severe renal failure were
excluded) was associated with an increase in the
spontaneous conversion rate to sinus rhythm (12% cf
1% after 1 month) in patients with atrial fibrillation and
chronic heart failure with no effect on mortality
(although 3% patients developed torsade de pointes,
usually within the first three days).58
Class I agents (e.g. quinidine, procainamide, disopyramide, flecainide) tend not to be used particularly
when left ventricular dysfunction coexists as they are
often associated with an adverse prognosis.59
In a prospective, multicentre and randomised trial of
patients with atrial fibrillation of less than 6 months
duration, amiodarone (200 mg daily) was more effective compared with sotalol (80 - 160 mg 12-hourly) and
propafenone (150 mg 8 to 12-hourly) in maintaining
sinus rhythm following cardioversion.60
In the presence of pyrexia or shock due to pulmonary
embolism or hypovolaemia, the ventricular rate is often
rapid and controllable only by correcting the underlying
condition (e.g. fluid administration for hypovolaemia).61
Anticoagulation should be considered for all patients
who have chronic or intermittent atrial fibrillation (with
the exception of ‘lone’ atrial fibrillation before the age
of 60 years, in the absence of cardiopulmonary disease
and hypertension) to reduce the incidence of stroke.62-64
In five independent randomised trials, embolic complications associated with chronic nonrheumatic atrial
fibrillation occurred in approximately 6% of patients,
and was reduced by two-thirds or more (e.g. to 1.5%) by
warfarin (to keep the INR between 2.0 and 3.0; although
the optimal value may be closer to 3.0).65 The incidence
of intracranial bleeding was less than 0.5% and about
100 patients needed to be treated to prevent 2 - 3 serious
strokes.66 While aspirin did not consistently reduce the
embolic complications in patients with atrial
fibrillation,66 it is recommended in those patients with
atrial fibrillation in whom warfarin is contraindicated.67
Minidose warfarin (i.e. 1.25 mg daily) does not reduce
the incidence of embolic stroke.68
Cardioversion may be considered if atrial fibrillation
is acute (i.e. less than 7 days) or associated with shock,
hypertrophic cardiomyopathy or Wolff-Parkinson-White
(WPW) syndrome. It is usually not considered if atrial
fibrillation has been present for longer than 6 months or
the left atrium is dilated (greater than 4.5 cm), because
D. DURHAM, ET AL
recurrence commonly occurs unless the underlying
disorder has been corrected.
If atrial fibrillation has been present for more than 48
hr then warfarin is given for 3 weeks prior to the
cardioversion and continued for 4 weeks after the
cardioversion to reduce the incidence of post cardioversion stroke,37,38,69 which occurs from 6 hr to 6 days
after the cardioversion as atrial mechanical function may
not be normal for up to several weeks after the return of
sinus rhythm.70 One large multicentre, rand-omised,
controlled trial in patients with atrial fibrillation
demonstrated that patients who had no transoesophageal
echocardiographic evidence of left atrial thrombus did
not require a three week period of anticoagulation
before cardioversion but could be anticoagulated with
warfarin then cardioverted (with anticoagulation
continuing for a further 4 weeks) without increasing the
incidence of an embolic stroke.71 This study prompted
the suggestion that this approach be recommended in
patients who have an increased risk of haemorrhage with
warfarin or in those who have atrial fibrillation of less
than 3 weeks duration.72
However, while transoesophageal echocardiography
may detect patients with atrial fibrillation who have
atrial thrombosis (and therefore select those who require
anticoagulation prior to cardioversion),73 it may still
miss small atrial thrombi and thereby incorrectly simulate safe conditions for cardioversion,70 (e.g. cerebral
embolism after cardioversion without anticoagulation in
a patient with negative findings on transoesophageal
echocardiography, has been reported).74
If the f waves in V1 are greater than 2 mm, cardioversion using 100 J may be chosen first; if the f waves in
V1 are less than 2 mm then 200 J is commonly used.75
Quinidine has been considered the mainstay of
therapeutic agents to prevent recurrence of atrial
fibrillation following cardioversion. However, in most
trials 20 - 50% of patients treated with quinidine,
compared with 10 - 25% of patients given placebo, have
remained in sinus rhythm for 1 year after electrical
conversion of atrial fibrillation.76 Quinidine therapy may
also be at a cost of an increase in long term
mortality.77,78 Other class Ia agents, (e.g. procainamide,
disopyramide) are no more successful or any better
tolerated.76 While the class III agents of amiodarone and
sotalol provide alternatives, the side-effects of the
former and the reduction in cardiac function with the
latter make them less than ideal, although currently they
are the agents of choice.52 Low dose amiodarone (e.g. <
400 mg/day) appears to have a lower 5 year mortality
when compared to quinidine when used to maintain
sinus rhythm after cardioversion.79 Flecainide has also
been used to maintain sinus rhythm.49
41
D. DURHAM, ET AL
Recently, surgical procedures to provide an
electrically isolated corridor of tissue from the sinus
node to the atrioventricular node (e.g. ‘atrial corridor
procedure’, although atrial transport function is usually
not restored and thus atrial thrombus remains a risk;
furthermore sinus node dysfunction is common and
permanent pacing may be required),80 or multiple atrial
incisions to disrupt the atrial re-entrant pathways (e.g.
‘maze procedure’, which usually maintains atrial
transport function, although return of atrial fibrillation,
atrial atrial flutter or complete heart block may occur)80
have been used to maintain sinus rhythm in patients who
have had disabling atrial fibrillation uncontrolled by
pharmacological therapy.49,80 Radiofrequency ablat-ion
has also been used successfully in patients in whom
atrial fibrillation originated from ectopic beats in the
pulmonary veins.47
The heart performs more efficiently with the return
of sinus rhythm by responding appropriately to stress
and restoring the AV valve competence, and an acute
decrease in heart rate and increase in stroke volume are
usually observed.81 However, an acute change in cardiac
output following conversion is not consistently observed and may be due to a delay in the return of the atrial
contraction.70,81
Supraventricular tachycardias
Paroxysmal supraventricular tachycardia (PSVT) or
paroxysmal atrial tachycardia (PAT)
This is caused by re-entry in 96% of cases (Figure
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
bypass tract in 15% of cases. The remaining 4% or so of
cases are due to an ectopic focus.82
Reentry involving an AV bypass tract usually travels
antegradely through the AV node and retrogradely
through the bypass tract. If the bypass tract also
conducts antegradely then pre-excitation exists (i.e.
WPW syndrome); if the bypass tract only manifests
Critical Care and Resuscitation 2002; 4: 35-53
retrograde conduction it is termed a concealed bypass
tract. In the latter case the QRS complex during sinus
rhythm is normal.
1. Atrioventricular nodal rentrant tachycardia
(AVNRT)
AV nodal re-entrant tachycardia has a rate that varies
between 160 and 220 bpm, a regular R-R interval and a
retrograde P wave (which is often difficult to distinguish
in the standard ECG trace) that is buried, precedes or
proceeds the narrow QRS complex. While patients who
have a left bundle branch block (LBBB) or right bundle
branch block (RBBB) may also have PSVT (LBBB or
RBBB patterns are not uncommonly associat-ed with
PSVT), if the PSVT produces aberrant conduction and a
widened QRS, the pattern is RBBB in 85%, RBBB with
LAD in 10% and LBBB in 5%, of cases.
The re-entrant pathway is permitted by a fast and
slow pathway that exists within the AV node. The fast
(anterior) pathway exhibits rapid conduction and a long
refractory period while the slow (posterior) pathway
exhibits slow conduction and a short refractory period.
As only the fast pathway conducts during sinus rhythm,
the PR interval during sinus rhythm is normal. However, an appropriately timed atrial ectopic dissociates
conduction between two pathways and permits the
establishment of circulating electrical activity that
spreads to both the atrial and ventricular myocardium
causing the tachyarrhythmia. In up to 90% of cases the
antegrade conduction proceeds via the slow pathway
and the retrograde conduction via the fast pathway.83
2. Atrioventricular re-entrant tachycardia (AVRT)
Atrioventricular re-entrant tachycardia incorporates a
concealed AV bypass tract as part of the re-entrant
circuit. The AV bypass tract allows retrograde
conduction only.
3. Sinus node and intraatrial re-entrant tachycardias
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
or within the atrium, respectively. These arrhythmias are
less common than AVNRT and AVRT.
Clinical features
While the rapid ventricular rate may be tolerated for
1 - 3 days or longer, cardiac failure, hypotension, shock
and pulmonary oedema may develop if the rate is
allowed to continue unabated. PSVT may occur in the
absence of heart disease or may be associated with
hypokalaemia, WPW syndrome, ischaemic heart
disease, rheumatic heart disease, thyrotoxicosis, phaeochromocytoma, cardiomyopathy, mitral valve prolapse
or tetanus. In 50% of patients without underlying heart
disease, the attack is associated with polyuria caused by
an inhibition of vasopressin and release of a natriuretic
peptide.84 This occurs 20 - 30 minutes after the onset of
the attack, with micturition occurring every 30 - 90 min
up to 8 hr later.
Treatment
The treatments for AVNRT, AVRT and sinus node
and intra-atrial re-entrant tachycardias are similar and
includes a chronological sequence of:
a. Vagal stimulation
b. Drugs
i. Short acting intravenous drugs (i.e. an action
which is terminated within 1 - 2 min):
- Adenosine (3 - 15 mg/70 kg, which has now
taken the place of verapamil as the
treatment of choice, except in asthmatics).85-87
- Esmolol (35 mg/70 kg)88
- Edrophonium (5 - 20 mg/70 kg)
ii. Intermediate acting drugs
- Verapamil 5 - 10 mg intravenously (0.075 0.15 mg/kg) infused over 1 - 3 min
(terminates 80% of cases).89 This is the
treatment of choice in asthmatic patients
with PSVT, or if the PSVT recurs after the
effect of adenosine has worn off. However,
verapamil, should not be used as a second
line drug if adenosine has failed, as
verapamil is unlikely to succeed and it will
only compound the negative inotropic effect
of both agents, causing severe hypotension.
If the PSVT recurs following the first
dose of verapamil, then an intravenous dose
of 5 - 10 mg may be repeated every 30 min
or infused at 0.005 mg/kg/min, or an oral
dose of 240 - 480 mg/day (e.g. 80 - 160 mg
8-hourly) may be used. Verapamil often
causes troublesome constipation, it is also
contraindicated in patients who have overt
c.
d.
cardiac failure, or when beta-blockers have
been used.
iii. Longer acting intravenous drugs are often used
for converting and stabilising the rhythm. For
example:
- Propranolol (5 - 10 mg/70 kg)
- Procainamide (500 - 1000 mg/70 kg)
- Digoxin (1 - 1.5 mg/70 kg) to increase
vagal tone and AV block
- Neostigmine (2 - 5 mg/70 kg) to increase
vagal tone
Cardioversion 50 - 100 J (or rapid atrial pacing)
Surgical ablation or cryo or radiofrequency catheter ablation to interrupt the re-entrant pathway.
These techniques should be considered if the
episodes of PSVT are numerous and debilitating.90-92
4. Atrioventricular pre-excitation (Wolff-ParkinsonWhite or WPW syndrome)
Pre-excitation exists if the whole or some part of the
ventricular muscle is activated earlier than normally by
the impulse that originates from the atrium passing
through accessory AV conducting fibres rather than
through the normal AV conduction system. The connections may occur anywhere around the cardioskeletal
ring.93 The atrial vector is normal (i.e. the P wave is
upright in II), differentiating pre-excitation from nodal
impulses or ventricular impulses with retrograde atrial
activation.
The characteristics of WPW syndrome are episodic
supraventricular tachycardia in patients who have specific ECG abnormalities that consist of:94,95
-
a PR interval which does not exceed 0.12 s
a delta wave (a slurred thickened proximal portion of
the QRS complex). A negative delta wave in V1 is
diagnostic of a right-sided bypass tract (Figure 4).
a QRS which equals or exceeds 0.12 s. A Q wave in
III and aVF often mimics an inferior myocardial
infarct.
The classical ECG changes of WPW syndrome
occur in 1 - 2 per 1000 of the general population and
tachycardias occur in 40 - 80% of these patients, 75% of
which are re-entrant supraventricular tachycardias (95%
due to retrograde conduction through the bypass tract
causing an orthodromic tachycardia with a normal QRS
complex and 5% due to antegrade conduction through
the bypass tract causing an antidromic tachycardia with
a wide QRS complex) and 20% atrial fibrillation
(usually wide complex and rapid ventricular rate); atrial
flutter is rare.96,97
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
subaortic stenosis, cardiomyopathy, ‘sick’ sinus syndrome, rheumatic fever, Ebstein’s anomaly, bicuspid aortic
or pulmonary valves, coarctation of the aorta, ventricular septal defect and atrial septal defect. False-positive
exercise tests may also occur with WPW syndrome.
The treatment of PSVT associated with WPW includes increasing vagal tone, adenosine, lignocaine, procainamide, amiodarone, propranolol and cardioversion.98
Sotalol has also been recommended as the drug of first
choice in patients with acute PSVT and for long-term
management.99 The treatment of atrial fibrillation with
WPW includes cardioversion, or drugs which act on
both the atrial and accessory pathways (i.e. class Ia, Ic
or III). Beta-blockers or lignocaine are ineffective, and
digoxin, verapamil and adenosine are contraindicated as
they may increase the ventricular rate leading to VT and
VF by blocking antegrade AV conduction, shortening
atrial refractoriness (facilitating the induction of AF)
and enhancing the conduction through the anomalous
pathway97,100-103(digoxin-facilitated ventricular rate in
WPW syndrome may be reversed by using 8 mmol of
magnesium sulphate, intravenously).104 By prolonging
the refractory period of the AV and His-Purkinje system
as well as the accessory pathway, one study found that
ibutalide terminated AF in 95% of patients with preexcitation.105
Ablation of the anomalous pathway. In patients in
whom the episodes of supraventricular tachycardia are
numerous, debilitating and not controlled by long-term
antiarrhythmic treatment, epicardial mapping, His
44
bundle ECG and atrial pacing to facilitate operative
identification and surgical ablation of the anomalous
pathway, have been used. Currently, however, radiofrequency intracardiac ablation is being offered in specialised centres as a safe alternative to medical treatment
in patients who have only minor symptoms.92,106 Patients
with pre-excitation who are asymptomatic have a benign
clinical course and only warrant careful follow-up.107
5. Nonparoxysmal junctional tachycardia
This rhythm usually results from conditions that
enhance automaticity (e.g. theophylline, catecholamine
toxicity) or triggered activity (e.g. digoxin toxicity) in
the AV junction. The rate usually varies between 70 and
130 bpm, the QRS complex is identical to that observed
with sinus rhythm and the rate may be influenced by
vagotonic and vagolytic agents. Treatment is directed
towards eliminating the underlying factors.
6. Multifocal atrial tachycardia (MAT)
This is a non-reentrant atrial tachycardia that causes
supraventricular tachycardia in 1 - 2% of cases. The rate
varies from 100 to 220 bpm and is characterised by an
absence of one predominant atrial focus with three or
more P waves of different morphologies in a single ECG
lead, an isoelectric baseline between the P waves, and a
variation in PR, PP and RR intervals (Figure 5).108,109 It
differs from the condition of ‘wandering pacemaker’,
which usually refers to multifocal supra-ventricular
escape complexes in the presence of sinus
bradycardia.110
Critical Care and Resuscitation 2002; 4: 35-53
D. DURHAM, ET AL
Figure 5. Multifocal atrial tachycardia with a ventricular rate of 173 bpm
Multifocal atrial tachycardia is required to be differentiated from atrial fibrillation because digoxin is often
used in the latter but is not effective for the former.111
The tachycardia usually occurs in the critically ill
elderly (i.e. 70 years or more) male patient,109 is often
associated with COPD, cardiac failure or ischaemic
heart disease, and is usually precipitated by hypoxia,
hypercapnia, sepsis, electrolyte disorders, sympathomimetics, digoxin or methylxanthines.112,113 While the
mortality due to the arrhythmia may be low, patients
who develop this arrhythmia have an in-hospital
mortality of about 45%.111 Treatment consists of efforts
to correct drug toxicity (e.g. sympathomimetic, digoxin
or theophylline toxicity) and correct electrolyte
abnormalities (i.e. hypokalaemia, hypomagnesaemia or
alkalosis). If the ventricular rate is deemed too rapid
then therapy of choice is intravenous magnesium
sulphate, 10 mmol in 2 - 3 min (which may be followed
by an infusion of 20 - 40 mmol of magnesium sulphate
in 4 - 6 hr114,115) or intravenous verapamil 5 - 10 mg.116
If verapamil is used then pretreatment with 1 g of
intravenous calcium gluconate before administering
verapamil has been used to prevent any hypotensive
effect, without preventing its anti-arrhythmic effect.117
Metoprolol (10 mg i.v. over 5 minutes) has also been
used, and in one study was more effective than
verapamil in reducing ventricular rate and converting
MAT to sinus rhythm.118 However, as many of these
patients are elderly with COPD, metoprolol may be
associated with adverse side effects (e.g. severe bronchospasm, hypotension). Treatment with digoxin, quinidine, procainamide, lignocaine, phenytoin or cardioversion is usually ineffective.109,111
Wide complex tachycardias
The main question that arises in the management of
a patient with a tachycardia is ‘is it supraventricular or is
it ventricular?’ If the QRS complex is wide (Figure 6),
the bedside diagnosis of the tachycardia is difficult. The
features that help distinguish supraventricular from
ventricular tachycardias are given in Table 2.119-124
If there is doubt about the origin of the impulse then
the patient should be cardioverted, particularly if there is
cardiac failure or hypotension.125 If the patient is not
haemodynamically compromised, intravenous lignocaine (1.5 mg/kg as an intravenous bolus which may be
repeated after 10 min) followed, if required, by
adenosine (6 mg as an intravenous bolus, which is follo
wed 2 min later, if required, by 12 mg as an intravenous
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
45
D. DURHAM, ET AL
Critical Care and Resuscitation 2002; 4: 35-53
Table 2. Differentiation between supraventricular (SVT) and ventricular tachycardia (VT)
SVT
VT
Clinical features
Hypotension
Pulse rate (beats/min)
JVP cannon A waves
Beat-to-beat variation in blood pressure
Varying intensity of S1
Reversion with vagal stimulation
Rare
160-220
Rare
Rare
Rare
Common
Pressure trace recordings
Right atrial pressure: cannon A waves Rare
Blood pressure: beat-by-beat variation
Rare
Common
Common
Echocardiograph
atrioventricular dissociation
Rare
Common
Rare
Not uncommon
Common
Never
Never
Rare
Rare
Not uncommon
Not uncommon
Common
ECG features
RR irregularity
Atrioventricular relationship
a. Relationship between the QRS
and the preceding P wave
b. Fusion beats
c. Capture
d. Retrograde atrial activation
(inverted P in II upright P in aVR)
e. A 2:1 or 3:1 ventriculoatrial
conduction with vagal stimulation Never
QRS duration
a. A narrow QRS complex
b. If broad complex (> 0.14 s)
LBBB pattern
RBBB pattern
Precordial QRS mainly:
Positive
Negative
Biphasic
QRS axis
as it has a rapid offset of action, will terminate any
arrhythmia that has an obligatory participation of the
AV node, and will not cause haemodynamic compromise or change the tachycardia to a life threatening
arrhythmia (although it may do so in patients who have
WPW with atrial fibrillation).102,103
In patients with wide complex tachycardias there is
little difference between bolus doses of adenosine and
adenosine triphosphate in relation to the minimal effective dose and incidence of side effects.87,127 Amiodarone
or procainamide may also be tried as these agents may
terminate both ventricular or supraventricular arrhythmias. While verapamil may on rare occasions terminate
46
Not uncommon
130-180
Common
Common
Common
Rare
Common
Common
Rare
Not uncommon
Not uncommon
Rare
Rare
Uncommon
Uncommon
Uncommon
Normal
Common
Common
Common
Abnormal
ventricular tachycardia,128,129 it is contraindicated in
patients with wide complex tachycardia of unknown
origin as the majority are of ventricular origin and
verapamil is ineffective and potentially hazardous in
most of these patients.119,130,131
Ventricular tachycardias
Ventricular tachycardia. This is defined as three or
more consecutive ectopic ventricular impulses having
approximately the same contour and separated by a
fixed interval. It is sustained if either its duration is
greater than 30 s or if it has to be terminated by
Critical Care and Resuscitation 2002; 4: 35-53
cardioversion or pacing in less than 30 s because of
severe hypotension.
The rate usually ranges from 130 - 180 bpm (if it is
greater than 180 bpm it is often considered as a form of
ventricular flutter), the R-R interval may be slightly
irregular (i.e. 0.01 - 0.02 s variations) or regular (Figure
6). Characteristically there is AV dissociation, although
rarely retrograde conduction may occur and give rise to
a P wave following, or less than 0.12 s before, the QRS
complex. Fusion beats or ‘capture’ are pathognomonic
of ventricular rhythm (Figure 7). The QRS complex
during VT is usually uniform (mono-morphic); if it
varies from beat to beat it is said to be polymorphic.
Bidirectional VT is due to either two ventricular foci or
one focus with aberration of the conducting impulses
(e.g. alternating bundle-branch block).
The causes of VT include ischaemic heart disease,
ventricular aneurysm, prolonged QTc syndrome, WPW
syndrome, rheumatic fever, cardiomyopathy, drug toxicity (e.g. tricyclic antidepressants, digoxin, quinidine),
hypokalaemia and hypomagnesaemia.
The clinical features of hypotension, shock, angina
or cardiac failure are not pathognomonic of VT and may
be associated with the disorder due to the underly-ing
myocardial disease.
Treatment of VT involves cardioversion, if the
patient is haemodynamically compromised, followed by
class I or III agents, (e.g. amiodarone, sotalol, lignocaine, procainamide, bretylium). If the patient is not in
cardiac failure or is not hypotensive, class I or III agents
without cardioversion are often used.
In a multicentred study of patients with ventricular
tachycardia, sotalol was found to be more effective than
imipramine, mexiletine, procainamide or quinidine in
preventing death and recurrences of ventricular tachyarrhythmias.132 In a double blind study of patients with
acute sustained VT, sotalol (100 mg i.v. over 5 minutes
D. DURHAM, ET AL
converted 69% to sinus rhythm) was more effective than
lignocaine (100 mg i.v. over 5 minutes converted 20%
to sinus rhythm) in terminating VT, and the incidence of
adverse effects was similar for both drugs.133
Accelerated idioventricular rhythm. This is also
known as slow ventricular tachycardia and has a rate
which ranges from 60 - 120 bpm (Figure 7). It usually
occurs in patients with acute myocardial infarction,
cardiomyopathy, or digoxin intoxication and is often
transient, resistant to antiarrhythmic therapy, but rarely
causes significant haemodynamic disturbance. Apart
from correction of drug toxicities and electrolyte abnormalities, specific treatment for accelerated idioventricular rhythm is rarely necessary.
Torsade de pointes
This is a ventricular arrhythmia which has
characteristics of both VT and VF. Some believe that it
is an atypical VT,134 whereas others consider it an early
phase of VF.135 However it is commonly considered to
be a polymorphic VT which is preceded by QT
prolongation (Figure 8) and is characterised by:135,136
-
a ventricular rate exceeding 200 bpm
a widened QRS deflection which shows a continual
change in amplitude giving the appearance of a
modulated sine wave, or spindle
a complete reversal of the QRS and T wave
deflections as they appear to twist around the
isoelectric line (hence the name)
atrioventricular dissociation
The arrhythmia is associated with disorders listed in
Table 3.136
The attacks are often short lived and self-limiting,
and the patient often does not lose consciousness as a
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.
47
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.
Figure 9. Ventricular fibrillation
usually present. However, the episodes may recur and
become prolonged, particularly when hypokalaemia,
hypomagnesaemia and an underlying bradycardia coexist,137 and may deteriorate into VF with clinical signs of
cardiac arrest.138
Table 3 Disorders associated with torsade de pointes
Complete atrioventricular or sinoatrial block
Prolonged QT syndromes
Hypokalaemia, hypomagnesaemia
Mitral valve prolapse
Ischaemic heart disease
Myocarditis
Central nervous system disorders
Liquid-protein diets
Drugs
quinidine, procainamide, disopyramide, cisapride
phenothiazines (particularly thioridazine),
antihistamines, tricyclic antidepressants,
chloral hydrate,
erythromycin, azithromycin, fluconazole
Treatment of the arrhythmia includes resuscitation
and defibrillation if it is prolonged or degenerates to VT
48
or VF, and correction of the underlying disorder (i.e.
hypokalaemia, hypomagnesaemia and drug toxicity).
Otherwise, intravenous magnesium sulphate (bolus 5 10 mmol) is the agent of choice. Other treatments
include potassium supplements to keep the plasma
potassium at 4 mmol/L or greater,139,140 or (if the patient
has an underlying bradycardia), producing a ventricular
rate of 100 beats/min or greater using intravenous
atropine (0.6 - 2.4 mg), an infusion of isoprenaline (2 to
6 µg/ min) or a pacemaker.141,142 Class Ia drugs are to be
avoided as they tend to sustain the arrhythmia.
Phenytoin and lignocaine are generally ineffective,
although bretylium (which now is no longer available)
has been useful.142
Ventricular fibrillation
This is characterised by a loss of an orderly sequence
of ventricular myocardial contraction caused by a
random and chaotic spread of electrical activity. The
ECG reveals completely irregular, chaotic and deformed
deflections of varying height, width and shape.143
(Figure 9). Death results from loss of cardiac output and
absence of cerebral perfusion, unless direct current
defibrillation successfully restores sinus rhythm.
Diseases associated with ventricular fibrillation include,
ischaemic heart disease, cardiomyopathies, electrocution, disorders associated with prolonged QTc syndrome
Critical Care and Resuscitation 2002; 4: 35-53
and drugs (i.e. phenothiazines, antihistamines and proarrhythmic effect of quinidine, disopyramide, etc.).143,144
The treatment involves external cardiac massage and
defibrillation at the earliest opportunity and correction
of any underlying disorder.
Received: 20 December 2001
Accepted: 22 Febuary 2002
D. DURHAM, ET AL
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