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Cardiac Arrhythmias: Diagnosis and
Management. The Bradycardias
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: Bradycardias are caused by a failure of the sinus node to generate normal
impulses or due to a defect in cardiac conduction that in turn causes a delay or failure of impulse propagation. During sleep, the heart rate may decrease to 30 beats per minute (bpm) with episodes of sinoatrial
block, junctional rhythms and first and second-degree atrioventricular block that occur often enough
(particularly in trained atheletes) to be considered normal variants. However, treatment is required if
symptoms of dizziness, confusion, fatigue, Stokes-Adams attacks or heart failure occur.
Sinus node dysfunction or ‘sick sinus syndrome’ is usually caused by intrinsic nodal disease and may
present with episodes of tachycardia and bradycardia (tachycardia-bradycardia syndrome). Treatment
usually requires a permanent pacemaker. Atrioventricular (AV) conduction disturbances are characterised
by a delay or failure of the atrial impulse to be conducted through the AV conducting system. If the escape
rhythm is unstable the patient also requires a pacemaker.
In the critically ill patient tachycardias are more often encountered than bradycardias. However, the
intensivist should be familiar and skilled in the management of complete heart block and asystole,
correcting the underlying defect (drug toxicity, hyperkalaemia, etc), while using catecholamines, atropine,
aminophylline or a temporary pacemaker for initial resuscitation.
Conclusions: Bradycardias are uncommon in the critically ill patient and often are caused by an
underlying disorder (e.g. hyperkalaemia, calcium channel blocker toxicity, beta-adrenergic receptor
blocker toxicity, etc). However, post cardiac bypass and acute myocardial infarction may cause cardiac
conduction defects that may require urgent resuscitation with a temporary pacemaker. (Critical Care and
Resuscitation 2002; 4: 54-60)
Key words: Critical illness, sinoatrial block, sinus bradycardia, sinus arrest, sick sinus syndrome syndrome,
atrioventricular block, complete heart block, idioventricular rhythm, asystole
Bradycardias are caused by a conduction block that
causes a delay or failure of impulse propagation. However, an asymptomatic bradycardia (even with sinoatrial
block, junctional rhythms, first-degree and seconddegree atrioventricular nodal block) can be considered a
normal variant of cardiac rhythm, although syncope,
weakness, fatigue, heart failure and an inability to
increase the rate in response to exercise (e.g. failure to
achieve a heart rate > 100 beats per minute) usually
indicate the need for treatment.1
Irrespective of the cause, most symptomatic conduction blocks are treated with a vagal inhibitor (e.g. intravenous atropine 0.6 - 2.4 mg), sympathomimetic agent
(e.g. intravenous isoprenaline 2 - 6 µg/min) or pacemaker. Theophylline (125 - 250 mg i.v.) has also been used
to treat bradycardias associated with acute myocardial
Correspondence to: Dr. D. Durham, Department of Critical Care Medicine, Flinders Medical Centre, Bedford Park, South
Australia 5042
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Critical Care and Resuscitation 2002; 4: 54-60
infarction2,3 and cardiac arrest,4 acting as a competitive
inhibitor of P1 receptors (i.e. adenosine A1 and A2 receptors) to inhibit the adenosine (released from ischaemic
cardiac cells) mediated reduction in cardiac conduction.
Table 1. Causes of bradycardia
Physiological
Convalescence from infections
Athletes
Sleep
Pathological
Excess vagal stimulation
Intraoperative stimulation (e.g. cervical
dilatation, eye, testicular and carotid surgery)
Orbital pressure
High intracranial pressure
Hypothermia
Obstructive jaundice
Myxoedema
Sleep apnoea syndrome
Infections
Typhoid fever, brucellosis
Chagas’ disease (trypanosomiasis)
Infiltrative or collagen diseases
Sarcoid, amyloid, haemochromatosis
Systemic lupus erythematosis, scleroderma
Rheumatoid arthritis
Myotonic dystrophy
Carotid sinus hypersensitivity
Drugs
Beta-blockers
Digoxin
Calcium-blockers (e.g. verapamil, nimodipine)
Tamoxifen
Antiarrhythmic agents
Hyperkalaemia, hypermagnesaemia
Sinoatrial node disorders
Sick sinus syndrome
Pericarditis
SA node trauma
Atrioventricular node disorders
Lev’s disease
Lenegre’s disease
Myocardial infarction or ischaemia
(usually inferior)
Acute rheumatic fever, infectious
mononucleosis, Lyme disease
Endocarditis, myocarditis
AV node trauma
D. DURHAM, ET AL
Sinus bradycardia. Sinus bradycardia is defined as a
sinus rhythm of less than 60 beats per minute (bpm). It
is associated with the physiological and pathological
conditions listed in Table 1. It rarely requires treat-ment.
Patients with acute myocardial infarction and sinus
bradycardia have a lower mortality compared with all
patients with myocardial infarction, which may be due to
the protective effect of sinus bradycardia on the
compromised myocardium.5
If the bradycardia is chronic and severe (e.g. less
than 40 beats per minute) and associated with hypotension and reduced cerebral and cardiac perfusion or
unstable escape rhythms (e.g. multifocal ectopics, ventricular tachycardia), a pacemaker is usually required
(although long term oral propantheline bromide 7.5 15.0 mg, 6- to 8-hourly, has also been used6).
Sinoatrial block. In sinoatrial (SA) block the sinus
impulse is blocked within the SA junction (i.e. the
junction between the SA node and the surrounding atrial
myocardium). First-degree SA exit block describes a
prolonged conduction time from the SA node to the
surrounding atrial tissue. It requires special techniques
for its diagnosis as it cannot be diagnosed from the
standard surface ECG.
Second-degree SA exit block is diagnosed in a
patient in sinus rhythm when there is an abrupt absence
of a P wave and QRS complex with the next P wave
occurring at double the normal PP interval. This disorder may be caused by excessive vagal stimulation, digoxin, quinidine, disease of the SA node (e.g. in association with pericarditis) and ‘sick sinus syndrome’.
Third-degree SA exit block is characterised by a lack
of atrial activity and cannot be distinguished from sinus
arrest on the surface ECG. An escape rhythm (usually
nodal rhythm) determines the heart rate.
Sinus arrest. In sinus arrest no impulse is generated
from the sinus node (Figure 1) and an escape rhythm
determines the rhythm of the heart. This disorder may be
caused by a severe increase in vagal tone.
Sinus node dysfunction
Sinus node dysfunction or ‘sick sinus syndrome’ can
be caused by intrinsic disease (fiberous tissue replacement of the SA node) or extrinsic causes (e.g. calcium
channel blockers, digoxin, beta-adrenergic receptor
blockers, hypothyroidism, excessive vagal tone, jaundice). Permanent injury from infarction (unlike the atrioventricular node) is an uncommon cause for SA node
dysfunction.7,8 The tachycardia-bradycardia syndrome is
a common manifestation of SA node dysfunction where
episodes of paroxysmal atrial fibrillation, flutter or
tachycardia are followed by severe sinus bradycardia
(Figure 2), sinoatrial block or sinus arrest, resulting in
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D. DURHAM, ET AL
Critical Care and Resuscitation 2002; 4: 54-60
Figure 1. Sinus rhythm at a rate of 75 bpm followed by sinus arrest.
Figure 2. Atrial fibrillation at a rate varying between 100 - 130 bpm followed by three supraventricular beats then sinus bradycardia at 46 bpm
(‘sick sinus syndrome’).
Figure 3. Sinus rhythm at a rate of 92 bpm with first-degree heart block (PR interval 0.24 s).
symptoms of low cardiac output (e.g. dizzness, confusion, fatigue, Stokes-Adams attacks, heart failure).9 The
diagnosis of the ‘sick sinus syndrome’ is made if there is
less than a 25% increase in heart rate with intra-venous
atropine (the normal response is an increase in heart rate
by 50 - 60%).
Treatment for this disorder, if symptomatic, usually
requires a pacemaker (an atrial pacemaker is preferred
as it reduces the incidence of atrial fibrillation, thromboembolism and pacemaker syndrome10), although
initial management with theophylline 200 - 400 mg/day
may be of benefit.11
56
Atrioventricular conduction disturbances
Atrioventricular block. This is characterised by a
delay or failure in conduction of the atrial impulse
through the AV conducting system. The conduction may
be inhibited in either the AV node or bundle of His;
inhibition of the impulse below the bifurication of the
bundle of His causes bundle branch or fascicular blocks
with AV conduction maintained unless all three fascicles
are affected simultaneously. There are three grades of
atrioventricular block:
Critical Care and Resuscitation 2002; 4: 54-60
D. DURHAM, ET AL
Figure 4. Second-degree atrioventricular block, Mobitz I (Wenckebach block).
Figure 5. Second-degree atrioventricular block, Mobitz II (2:1 block).
Figure 6. Third-degree atrioventricular block (complete heart block). A progressive reduction in the PR interval distinguishes it from a 2:1 block.
1. First-degree block. This is defined as a PR
interval greater than 0.20 s (Figure 3). The PR interval
represents the time taken for the impulse to travel from
the SA node to the AV node (usually 0.04 s) plus the
time taken for the impulse to travel through the AV
node, the bundle of His, the bundle branches and the
Purkinje system. Thus prolongation of the PR interval
may represent a delay in any stage along the conducting
pathway. However, if the duration of the QRS complex
is normal, a prolonged PR interval is almost always
caused by a delay within the AV node. If the QRS
duration is prolonged the delay may be present in any of
the levels previously mentioned. A delay within the His-
Purkinje system is always accompanied by a prolonged
QRS although it can occur with a normal PR interval.
2. Second-degree block. This is characterised by an
intermittent failure of AV conduction producing
intermittent absence of a QRS complex initiated from
the atrial impulse. The number of impulses which are
not conducted may be expressed as a conduction ratio;
for example, 2:1 block if every second atrial impulse is
not conducted (Figure 4) or 3:2 block if every third
impulse is not conducted. The His bundle electrocardiogram (where the His bundle ‘H’ deflection can be
identified) has enabled second-degree blocks to be
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D. DURHAM, ET AL
divided into prolongation of the AH interval (e.g. AV
nodal conduction is slowed) and prolongation of the HV
interval (i.e. infranodal block). There are two standard
ECG types of second-degree block:
a) Mobitz I (Wenckebach) block. This is characterised
by a progressive prolongation of the PR interval and
decrease in the RR interval (due to progressive
decrease in PR increments) until there is nonconduction of the P wave (Figure 5). The sinus rate
(i.e. PP interval) remains constant. The block results
in a rest period, which facilitates the recovery of the
conducting tissue, allowing the sequence to begin
again. The block is almost always associated with a
prolongation of the AH interval and a normal QRS
duration (in the absence of a bundle branch block),
and has been reported in 6% of asymptomatic
medical students without apparent heart disease.12 It
is often found as a transient abnormality in patients
with acute inferior myocardial infarction or with
drug toxicity (e.g. digoxin, beta-adrenergic receptor
blockers, calcium channel antagonists)
b) Mobitz II block. This is characterised by a constant
PR interval with a periodic nonconducted P wave
(Figure 4). It is usually associated with QRS widening and a likelihood of progressing to complete heart
block. The block is characteristically associated with
prolongation of the HV interval.
3. Third-degree block. This is characterised by a
complete block of the atrial conduction through the AV
conduction system (Figure 6). If the block is in the AV
node the escape rhythm is usually in the His bundle,
with a stable rate of 40 - 60 bpm, a QRS complex of
normal duration and is often haemodynamically stable.
The rhythm is usually under vagal influence (i.e. alters
with exercise and atropine). However, if the conduction
defect is either an intra- or infra- His block, the
ventricles are activated by a His-Purkinje system escape
pacemaker which has a lower intrinsic rate (i.e. 25 - 45
bpm, a wide QRS complex (idioventricular rhythm) and
is usually haemodynamically unstable (and therefore
requires a pacemaker) as it may lead to asystole.
The clinical features of complete heart block include
cannon ‘a’ waves, varying intensity of first heart sound,
and syncopal (i.e. Stokes-Adams) attacks. Third-degree
block may be caused by sclerodegenerative disease of
the cardiac conducting tissue (i.e. Lenegre’s disease),
fibro calcareous process of the cardiac skeleton (associated with aortic stenosis, and known as Lev’s disease),
intracardiac surgery, ischaemic heart disease, tumours,
digoxin toxicity, hyperkalaemia and congenital heart
disease. The ECG reveals AV dissociation and a QRS
complex which is often wide and bizarre.
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Bundle branch blocks. While left bundle branch
block (LBBB) is often observed in patients with cardiac
disease, both LBBB and right bundle branch block are
asymptomatic and almost always present as an
unexpected ECG finding.
AV dissociation. This describes the condition where
the atria and ventricles beat independently (i.e. the P
wave bears no relationship to the QRS) and characteristically occurs with complete heart block. However, it
can also occur in severe sinus bradycardia when the
escape and sinus rhythm are similar, where the P waves
occur just before, during or just after the QRS complex
(isorhythmic AV dissociation), or when a junctional or
ventricular pacemaker is enhanced and competes with
the normal sinus rhythm in ventricular tachycardia,
accelerated junctional or ventricular rhythms (interference AV dissociation).
Parasystole. Parasystole is defined as the simultaneous activity of two (rarely more) independent impulse
forming centres, one of which is protected from the
other by an entrance block. An extrasystole has a consistent coupling interval with the preceding beat, the
parasystolic beat has varying coupling intervals, a
constant shortest inter-ectopic interval (although it may
exhibit Wenckebach exit block and therefore vary by
0.04 - 0.12 s) and the frequent appearance of fusion
beats. Parasystole is usually associated with heart
disease (e.g. cardiomyopathy, ischaemic heart disease or
hypertensive heart disease), although the arrhythmia is
benign and usually does not require treatment.13
Ventricular parasystole usually has a rate of 30 - 40 bpm
(i.e. the inherent rate of the ventricle), whereas atrial
parasystole usually has a rate of 45 - 55 bpm. Atrial
parasystole occurs in cardiac transplant patients as both
the donor and the recipient SA nodes (the former has the
faster rate of the two as it is not under parasympathetic
control) generate independent P waves.
The treatment of a bradycardia depends upon the
severity of symptoms, the correlation between symptoms when bradycardia occurs and the presence of reversible causes.
For symptomatic patients management with a permanent pacemaker depends upon the correlation between
the bradycardia and symptoms and the presence (or
otherwise) of reversible causative factors. Patients who
have potentially reversible factors may be treated with a
temporary pacemaker during management of the underlying disorders.
If a patient is asymptomatic then the generally
acceptable indications for a permanent pacemaker are:14
a) a third-degree AV block with a documented asystolic period lasting 3 s or more, or an escape rhythm
less than 40 bpm while the patient is awake,
Critical Care and Resuscitation 2002; 4: 54-60
D. DURHAM, ET AL
b) a third-degree AV block or second-degree AV
Mobitz II block in patients with chronic bifascicular
and trifascicular block, and
c) a congenital third-degree AV block with a wide QRS
escape rhythm, ventricular dysfunction or
bradycardia inappropriate for age.
subcutaneously in the abdominal wall, chest wall or
axilla. Implantable pulse generators are sealed devices
weighing from 30 - 130 g. They are powered by a
lithium battery and, depending on the model, may last to
last 2 - 15 years and be transcutaneously (i.e.
noninvasively) programmable.15
CARDIAC PACING
Cardiac pacing involves the periodic delivery of low
electrical energies by a pulse generator, through bipolar
or unipolar pacing electrodes, to the heart to initiate and
maintain cardiac rhythm. Bipolar pacing electrodes
allow the electric current to travel down a wire to the
distal electrode, depolarise the myocardium and return
to the pacemaker via the proximal electrode. These
electrodes are commonly used for temporary pacing.
Unipolar pacing electrodes allow the electric current
to travel down a wire to the electrode, depolarise the
myocardium, and to return to the pacemaker via body
fluids. These electrodes are often used for permanent
pacing, although the skin electrode needed for the
returned current may cause muscle twitching, and
sensing of skeletal muscle potentials may lead to pacing
artifact.
Both the ventricular and atrial myocardium may be
sensed and paced by a pacing electrode, delivering the
impulse directly to the:15-17
a) endocardium via a pacing lead which is inserted
transvenously under fluoroscopic control, using a
rigid or balloon-tipped pacing catheter,
b) epicardium via a pacing lead which is fixed at the
time of cardiac surgery,
c) chest wall (i.e. transthoracic) via pads which are
applied to the chest wall providing temporary
cardiac pacing during an emergency, and
d) oesophagus (i.e. transoesophageal) via an oesophageal pacing lead providing temporary pacing.
Received: 20 December 2001
Accepted: 22 February 2002
Transvenous pacing
A semi-rigid or balloon-tipped pacing catheter may
be inserted percutaneously into the internal or external
jugular or subclavian vein and positioned into the right
ventricle under fluoroscopic control. When the electrode is correctly positioned, the stimulation threshold or
capture (i.e. minimum current required to consistently
pace the heart) is measured. This should ideally be less
than 1 mA, and certainly less than 2 mA with a pulse
duration of 0.5 ms. The pacemaker output is then
normally set at about 5 mA. The stability of the pacing
electrode is tested by asking the patient to breathe
deeply and cough.
If a temporary pacemaker is inserted, the generator
remains beside the patient. If a permanent pacemaker is
inserted, an implantable pulse generator is placed
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