Indian Journal of Anaesthesia 2007; 51 (4) : 310-323 Indian Journal of Anaesthesia, August 2007

Management of Perioperative Arrhythmias

N. Dua1 , V.P. Kumra2
Key words Perioperative, Arrhythmias

Definition Pathogenesis
Arrhythmia is defined as “Abnormality of cardiac 1. Injury or damage (pathology) to the cardiac con-
rate, rhythm or conduction which can be either lethal (sud- duction systems.
den cardiac death), or symptomatic (syncope, near syn- 2. Re-entry: Reentry is a mechanism that may pre-
cope, dizziness, or palpitations) or asymptomatic”. Imme- cipitate a wide variety of supraventricular and ven-
diate diagnosis and intervention with appropriate therapy tricular arrhythmias.
often will prevent degeneration of an arrhythmia into a
life-threatening event. 3. Automaticity: Abnormal depolarization of atrial or
ventricular muscle cell during the periods of action
Cardiac arrhythmias are the most frequent
potential can lead to arrhythmias.
perioperative cardiovascular abnormalities in patients un-
dergoing both cardiac and non-cardiac surgery. The oc- 4. Mutations in ion channels: Since these channels
currence of arrhythmias have been reported in 70.2% of are mainly responsible for depolarization, mutation
patients subjected to general anaesthesia for various sur- can lead to arrhythmias.
gical procedures. 1,2 The incidence of arrhythmias varies 5. Ectopic foci/ irritable foci
from patients undergoing cardiac or non-cardiac surgery
The mechanism of arrthythmogenesis has been il-
as well as on monitoring modality. The incidence has been
lustrated 6 in Fig. 1
reported to vary from 16.3 to 61.7% with intermittent ECG
monitoring 3 and 89% with continuous holter monitoring 4
in patients undergoing non-cardiac surgery, while patients
undergoing cardiac surgery are more prone to develop
arrhythmia with reported incidence of more than 90%. 5
Regardless of the terminology (arrhythmia or dys-
rhythmia), cardiac rhythm disturbance represents one of
the most misunderstood, frustrating and potentially dev-
astating problems faced by the general or cardiac
anaesthesiologist. The first basic principle of anti-arrhyth-
mic therapy is to identify and correct possible precipitat-
ing factors related to the administration of anaesthesia.
Arrhythmias in the presence of cardiovascular disease
are more dangerous and at times may be life threatening
unlike those occurring in healthy patients which are usu-
ally of little clinical consequence. Pacemakers and im-
plantable cardioverter - defibrillators (ICD) are being used
in the treatment of tachyarrhythmias and bradyarrhythmias
nowadays very frequently. The basic understanding of
their perioperative function and management needs to be
highlighted. This text will provide a simpler way to diag-
Fig 1. Mechanism of arrthythmogenesis
nose and manage arrhythmias in the perioperative period.

1. M.D., Consultant, 2. M.D., D.A., D.Ac., M.Ac.F.I., Emeritus Consultant, Department of Anaesthesiology, Pain & Perioperative Medicine,
Sir Ganga Ram Hospital, Sir Ganga Ram Hospital Marg, New Delhi - 110 060, INDIA. Correspondence to : Naresh Dua, Department of
Anaesthesiology, Pain and Perioperative Medicine, Sir Ganga Ram Hospital, Sir Ganga Ram Hospital Marg, New Delhi - 110 060, INDIA.
E mail: ndua14@yahoo.com

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N. Dua et al. Perioperative arrhythmias

a) Increased automaticity due to reduced threshold po- b. Central nervous system disease - Patients with in-
tential or an increased slope of phase 4 depolariza- tracranial disease especially sub-arachnoid
tion haemorrhage may show ECG abnormalities such as
b) Triggered activity due to ‘after’depolarizations reach- changes in QT intervals, development of Q waves,
ing threshold potential ST-segment changes, and occurrences of U waves.
c) Mechanism of circus movement or reentry. In panel c. Old age - Postoperative atrial fibrillation (AF) is a fre-
(1) the impulse passes down both limbs of the poten- quent complication in the elderly patients 3
undergoing
tial tachycardia circuit. In panel (2) the impulse is thoracic surgery. Aging causes degenerative change in
blocked in the pathway but proceeds slowly down atrial anatomy and is also accompanied by relative
the pathway and returns along the pathway. In changes in atrial pathology.The injury to sympathovagal
panel (3) the impulse travels so slowly along the  fibers of cardiac plexus during surgery and preexisting
pathway that when it returns along the pathway to atrial electrical changes in these patients predispose them
its starting point it is able to travel again down the  to postoperative atrial fibrillation
pathway, producing a circus movement tachycardia. 2. Anaesthesia related factors
Factors and causes- There are several contribut- a. Tracheal intubation – It is one of the most com-
ing factors. The causes mainly responsible for arrhythmias monest causes of arrhythmias during induction as well
are listed in Table 1. as during the perioperative period, most often asso-
Table 1. Contributing factors and causes ciated with haemodynamic disturbances.
 Hypovolemia  Cardiac ischaemia b. General anaesthetics – The drugs used for induc-
 Light plane of anaesthesia/pain
tion, maintenance as well as for reversal of general
 Hypoxia
anaesthesia are not primarily arrhythmogenic, but
 Hypo/Hyperkalemia  Toxins/ Drugs
arrhythmias can be produced in the presence of a
 Hypomagnesaemia /  Tamponade, Cardiac
variety of triggering agents and clinical situations
Hypocalcaemia  Tension pneumothorax generating high catecholamines such as light plane
 Hypoglycemia  Thrombosis (Coronary or pul- of anaesthesia with hypertension and tachycardia,
 Hypothermia monary) hypoxaemia, hypercarbia, exogenous epinephrine and
 Acidosis  Trauma aminophylline. Halothane or enflurane produces
 Mechanical
 Surgical cause (Traction to intes- arrhythmias, probably by a reentrant mechanism.3
Irritation (e.g. central venous tine, oculocardiac reflex, neuro- c. Local anaesthesia – Regional anaesthesia (epidu-
lines, pulmonary art. catheter, surgical causes, cardiac compres- ral anaesthesia) followed by central neuraxial block-
sion on beating heart bypass sur-
chest tube) ade may be associated with pharmacological sym-
gery etc.)
pathectomy leading to parasympathetic nervous sys-
These factors can grossly be divided into following tem predominance causing bradyarrhythmias. It may
categories: be mild to very severe in nature. 7
1. Patient related factors d. Electrolyte imbalance and abnormal arterial blood
2. Anaesthesia related factors gases – Abnormal blood gases such as hypercarbia,
hypoxaemia or electrolyte imbalance produce
3. Surgery related factors arrhythmias either by producing reentrant mechanism
1. Patient related factors or by altering phase depolarization of conducting fi-
bers. Hypokalemia or hyperkalemia may also lead to
a. Preexisting cardiac disease - The patients with arrhythmias.
known cardiac disease (e.g. myocardial ischaemia -
MI) have much higher incidence of arrhythmias dur- e. Central venous cannulation – Stimulation of carotid
ing anaesthesia than patients without known cardiac sinus reflexes may occur due to pressure from fingers
disease1 .The arrhythmias are more fatal in patients during jugular vein cannulation as excess insertion of
with associated cardiac pathology. the central venous catheter into the right atrium during
central venous cannulation mayalsolead toarrhythmias.7
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3. Surgery related factors raised intracranial pressure

a. Cardiac surgery – A spectrum of cardiac 5. Chronic degenerative change such as fibrosis of the
arrhythmias can be observed during the immediate atrium and sinus node
period following the release of aortic cross clamp Treatment:
when myocardium is recovering from the ischaemic
insult and regaining normal sinus rhythm. Surgical Asymptomatic bradycardia usually does not require
manipulation such as retraction of the heart during treatment. Symptomatic bradyarrhythmias should be di-
agnosed and immediate therapy should follow. In patients
operation on beating heart, venous cannulation or tak-
who manifest haemodynamic compromise such as hy-
ing sutures over the atrium can also precipitate
arrhythmias. potension, atropine is the first line of treatment. It can be
used in the dose of 0.5 to 1.0 mg (IV bolus), repeated
b. Non-cardiac surgery – Vagal stimulation due to trac- every 3 to 5 minutes, if required (maximum dose = 0.04
tion on the peritoneum or direct pressure on the va- mg.kg-1 ). However, it should be used cautiously in pa-
gus nerve during carotid artery surgery may produce tients with CAD, since excessive increase in heart rate
bradycardia or atrioventricular (AV) blocks, or even may worsen ischaemia because of increased myocardial
asystole. Dental surgery causes profound stimula- oxygen consumption or reduced diastolic filling time. If
tion of both sympathetic and parasympathetic ner- bradycardia still persists despite treatment, isoprenaline
vous stimuli. can be administered as an IV bolus of 5 to 10 g followed
Arrhythmias are broadly classified as by an infusion of 2 to 10g.min-1. Other alternative is
dopamine infusion 5 to 20g.min-1.
Table 2 : Classification of arrhythmias
While treating sinus bradycardia, various causes or
1. Bradyarrhythmia 2. Tachyarrhythmia
factors contributing should be searched and treatment
i. Sinus Bradycardia i. Narrow QRS ii. Wide QRS
complex (SVT) complex started. Be ready for percutaneous and transvenous pac-
ii. Various forms of
heart block tachycardias (QRS tachycardias (QRS > ing.8 (Flow Chart 1)
<0.12 second) 0.12 second)
a. First degree Expert cardiologist opinion must be sought for fur-
a. Sinus tachycardia
b. Second degree a. Ventricular prema- ther management.
b. Atrial premature
c. complete beat ture beat (VPB) / Ven- ii. Various forms of heart block: Heart blocks
tricular extrasystole
c. Atrial tachycardia (AVHB) are broadly classified into three categories
b. Ventricular tachy-
d. Atrial flutter cardia (VT) a) First degree heart block
e. Atrial fibrillation c. Ventilation fibrilla- b) Second degree heart block
tion c) Complete heart block
d. Torsades de pointes
Anatomical or functional abnormalities underlie atrio-
1. Bradyarrhythmia ventricular heart block (AVHB). These may be transient
i. Sinus bradycardia – bradycardia is generally de- or permanent. Transient AVHB can be produced by acute
fined as a heart rate of less than 60 beats per minute. MI and general anaesthetics such as enflurane or hal-
In patients on chronic beta-blocker therapy such as othane in patients using calcium channel blocker drug
those suffering from coronary artery disease (CAD), (CCB) or amiodarone. Permanent AVHB, on the other
it is defined as a heart rate of less than 50 beats/min. hand is usually idiopathic, other causes include CAD and
Lev’s or Lenegre disease, where fibrosis of the conduct-
Causes ing system occurs.
The causes of sinus bradycardia are as follows: a) First degree heart block: This is simple prolonga-
1. Drug effects: blockers, digitalis and other anti-ar- tion of the PR interval to more than 0.22 sec. Every
rhythmic drugs atrial depolarization is followed by conduction to the
ventricle but with delay. The treatment is usually not
2. Acute myocardial ischaemia
necessary however, the patients should be carefully
3. Hypothermia observed for progression to a higher degree of block,
4. Underlying hypothyroidism, cholestatic jaundice or that requires prompt treatment. (Fig.2) 9
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 Flow C hart 1

gation of PR interval untila ‘P’wave fails to conduct.

The PR intervalbefore the blocked Pwave ismuch longer
than thePR intervalafter theblocked P wave. Treatment
isusually not necessary exceptin slowventricular rate,
where atropine or isoprenaline can be used. (Fig.3) 9
Mobitz Type II Block: There is no progressive
lengthening of thePR interval, but occasionally there is
an atrialcontraction withouta subsequentventricular con-
traction.This iscalled the“Mobitz TypeII” phenomenon.
a) Second degree heart block: This occurs when It mayprogress suddenly and unpredictivelyto complete
some P waves conduct electrical activationand oth- heart block. Itis clear indication forthe placement of a
ers do not. There are several forms of second de- temporary pacemaker.(Fig.4)9
gree AV block
Mobitz Type I Block(Wenckebach’s phenom-
enon): Inthis type of AVHB, there isprogressive prolon-

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Note Note
 Progressive lengthening of PR interval  Regular P waves (normal atrial depolarization)
 One non-conducted P wave  P wave rate 145/min
 Next conducted beat has a shorter PR interval than the preceding  QRS complexes highly abnormal because of abnormal conduction
through ventricular muscle
Fig 3. Second degree heart block (Wenckebach type)
 QRS (ventricular escape) rate 15/min
 No relationship between P waves and QRS complexes
Fig 6. Complete heart block

 Broad complex: This occurs because of disease in

the Purkinje system. The escape pacemaker arises
from the distal Purkinje network or the ventricular
Note
myocardium. The resulting rhythm is slow (15-40
 PR interval of the conducted beats is constant b.p.m) and relatively insignificant or unharmful. In
 One P wave is not followed by a QRS complex and here second the elderly, it is usually caused by degenerative fibro-
degree block is occurring sis and calcification of the distal conduction system
Fig 4. Second degree heart block (Mobitz type 2) (Lenegre’s disease) or the more proximal conduc-
tion system (Lev’s disease). It may occur after clo-
either broad ( > 0.15) or narrow (< 0.15) QRS com- sure of ventricular septal defect (VSD) and some-
9
plexes. (Fig. 5 & 6) times following aortic valve replacement (AVR). In
younger patients, broad complex AV block may be
caused by perioperative myocardial ischaemia.
Management: Treatment is not required in narrow
complex 3° block except for eradication of toxic causes.
Occasionally, permanent pacing is advocated for symp-
tomatic, isolated AV block. While in broad complex, pac-
ing is indicated to maintain the normal haemodynamics.
Note
 P wave rate 90/min 2. Tachyarrhythmia
 QRS complex rate 36/min The tachycardia can be classified based on the ap-
 No relationship between P waves and QRS complex pearance of the QRS complex as tachycardia, narrow
 Abnormally-shaped QRS complexes because of abnormal spread of complex supraventricular tachycardia (SVT), and wide
depolarization from a ventricular focus
complex tachycardia. Most wide complex (broad com-
Fig 5. Third degree block plex) tachycardias are ventricular in origin. Symptomatic
tachy-arrhythmias should be monitored and immediate
 Narrow complex: This is due to disease in the AV therapy should be done. 8 (Flow Chart 2)
node or the proximal bundle of His. The escape Tachyarrhythmias are classified in two categories depend-
rhythm occurs with an adequate rate (50-60 b.p.m.) ing upon the QRS complexes.
and is relatively reliable. It occurs because of infe-
i. Narrow QRS complex (QRS<0.12): In these
rior wall MI and toxic concentration of drugs such as
type of arrhythmias the QRS complex is less than 0.12
digitalis, verapamil or blockers in perioperative pe-
sec.
riod.
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N. Dua et al. Perioperative arrhythmias

Flow Chart 2

Flow Chart 3

diltiazem - blockers

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 Indian Journal of Anaesthesia, August 2007
N. Dua et al. Perioperative arrhythmias
a. Sinus tachycardia: it is defined as an increase
in the sinus rate of more than 100 beats/minute. Prolonged
tachycardia for long duration can induce ischaemia in coro-
nary artery diseased patients.
Causes: It includes Note
 Anaemia because of blood loss  After one sinus beat the SA node fails to depolarize. After a delay,
 Pain an abnormal P wave is seen because excitation of the atrium has
begun somewhere away from the SA node. The abnormal P wave is
 Inadequate anaesthesia followed by a normal QRS complex, because excitation has spread
normally down the His bundle. The remaining beats show a return
 Hypovolaemia to sinus arrhythmia.
 Fever Fig 7. Arial premature beat

 Hypercarbia
 Thyrotoxicosis/ thyroid crisis
 Cardiac failure with compensatory sinus tachy-
cardia
 Catecholamines excess Note :
Treatment: Before instituting pharmacological  After three sinus beats, atrial tachycardia develops at a rate of 150/
treatment for sinus tachycardia, precipitating factors must min. P waves can be seen superimposed on the T waves of the
preceding beats. The QRS complexes have the same as those of the
be identified and corrected. Drug therapy is especially sinus beats.
required in patients with ischaemic heart disease who Fig 8. Atrial tachycardia
develop ST segment changes to prevent further myocar-
dial ischaemia. Tachyarrhythmia should be managed ac- faster usually less than 130 beats/min, it is termed as accel-
cording to Flow Chart 2. Beta-blockers such as esmolol erated AV junctional rhythm. Those arrhythmias can lead
is preferred drug for managing it. It has half-life of 10 min to fall in blood pressure upto 15% in patients without car-
with bolus dose of 500 mcg.kg-1 over 1 min, followed by diac disease and upto 30% in diseased heart.11 Usually no
an infusion of 50-300 mcg.kg-1 .min-1 . If continuous use is treatment is required; carotid sinus massage and verapamil
required, it may be replaced by longer lasting cardio se- are often helpful in symptomatic patients. Intravenous ad-
lective drugs such as metoprolol in the dose of 5 to 10 mg enosine in 6 to 12 mg doses is another alternative. Treat-
given slowly intravenously (IV) at 5 min interval to a total ment with class Ia, Ic or III drugs is usually successful e.g.
dose of 15 mg. 10 Another drug can be used is propranolol disopyramide 2 mg.kg-1 over 10 min. (Fig.8)9
0.1 mg.kg -1.
d.Atrial flutter
b. Atrial premature beat: It represents 10% of all
intraoperative arrhythmias. On the ECG they appear as This is a rhythm disturbance that is usually associated
early and abnormal ‘P’ waves and are usually but not with organic ischaemic heart disease. The atrial rate varies
always, followed by normal QRS complexes. The dura- between 280 and 350 min-1 but is usually around 300 min -1.
tion of QRS wave is normal but wide QRS wave may be Most often every second flutter beat conducts giving a
present due to aberrant ventricular conduction, which ventricular rate of 150 min-1. Occasionally every beat con-
mimics premature ventricular beat. Treatment is not nor- ducts, producing a heart rate of 300 min-1. More often, espe-
mally required unless the ectopic beats provoke more sig- cially when patients are receiving treatment,AV conduction
nificant arrhythmias, where blockade may be effective. block reduces the heart rate to approximately 75 min-1.
(Fig.7) 9 ECG: The ECG shows regular saw tooth-like atrial
c. Atrial tachycardia: These arrhythmias are found flutter waves between QRST complexes. If they are not
in 6% of patients undergoing non cardiac surgery. 2 It is clearly visible, AV conduction may be transiently impaired
nonparoxysmal, narrow QRS rhythm with retrograde or by carotid sinus massage or by the administration of AV
nonapparent P waves and a rate less than 70 beats/min. if nodal blocking drugs such as verapamil. (Fig.9) 9

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N. Dua et al. Perioperative arrhythmias

nary embolisation. Successful cardioversion is relatively

rare in chronic AF. The control of ventricular rate is the
preferred approach in these cases. The most useful drug
for this purpose is digoxin. The patients with chronic AF
Note undergoing noncardiac surgery should be evaluated for

-1
P waves can be seen at a rate of 300 min , giving a saw-toothed the presence of atrial clot by echocardiogram prior to sur-
appearance. There are four P waves per QRS complex,
-1
and ven- gery. In the presence of atrial clot, control of ventricular
tricular activation is perfectly regular at 75min .
response rate with appropriate medication is instituted
Fig 9. Atrial flutter
during perioperative period, if necessary.
Treatment: Treatment of an acute paroxysm is
ii. Wide QRS complex (QRS>0.12): In these
electrical cardioversion. Prophylaxis is achieved with class
types of arrhythmias the QRS complex is usually more
Ia, Ic or III drugs in diseased heart patients.
than 0.12 sec.
e. Atrial fibrillation (AF)
It accounts for more than 90% of supraventricular ta-
chycardia (SVT) in the perioperative setting. It is caused by
a raised atrial pressure, increased atrial muscle mass, atrial
fibrosis or inflammation and infiltration of the atrium. Rheu-
matic disease is often associated with cardiac causes such
Note
as mitral valve disease, myocarditis and coronary artery dis-
 No P waves – irregular baseline
ease. Systemic diseases include hyperthyroidism, pulmonary
 Irregular QRS complexes
embolism and electrolyte imbalance. When caused by rheu-
 Normally shaped QRS complexes
matic mitral stenosis, the onset of atrial fibrillation results in
 In lead V 1 waves can be seen with some resemblance to those seen in
considerable worsening of cardiac failure. atrial flutter this is common in atrial fibrillation
Clinically the patient has a very irregular pulse, as Fig 10. Atrial fibrillation
opposed to a basically regular pulse with an occasional
a. Ventricular premature beat (VPB) / Ventricular
irregularity (extrasystoles) or recurring irregular pattems.
extrasystole
The ECG shows fine oscillations of the baseline (so called
fibrillation) and no clear P waves. The QRS rhythm is VPB results from ectopic foci arising from below
usually 160-180min-1 but it slows with treatment. ECG AV node and give rise to wide (>0.12 sec) bizarre QRS
changes are more indicative in lead II (Fig.10) 9. AF may complex. They account for 15% of the observed
be acute or recent onset (<48 hrs) and chronic. In the arrhythmias, more common in anaesthetized patients with
recent onset AF, initial treatment is directed towards the pre existing cardiac disease. New onset of VPB, may
control of ventricular response rate with agents that slow occur in the presence of coronary artery insufficiency,
AV node conduction. The precipitating or provoking agents myocardial infarction, digitalis toxicity with hypokalemia
should be removed or treated first. Intravenous beta- and hypoxaemia. On the ECG, the premature beat has a
blockers or calcium channel blockers produce rapid con- broad (>0.125) and bizarre QRS complex because it arises
trol of rate, regardless of the level of sympathetic tone. from an abnormal (ectopic) site in the ventricular myo-
However beta-blockers are preferred over calcium chan- cardium. Following the premature beat there is usually a
nel blocker (CCB) during intraoperative period due to complete compensatory pause because the timing of sinus
shorter duration of action and lesser negative inotropic rhythm is not induced by the premature beat. (Fig.11 & 12) 9
effects. 10,12 In haemodynamically-compromised patients, Treatment: Underlying abnormalities in these pa-
DC cardioversion is the most effective method of con- tients should be corrected immediately. No treatment is
verting AF to sinus rhythm. Chronic AF is often found in generally required for isolated VPB in asymptomatic and
patients with rheumatic heart disease undergoing cardiac
healthy patients. However VPB which are multiple (>5
surgery and may have atrial thrombi, therefore, any at-
beats/min), multifocal, or bigemminal or occur near the
tempt to restore sinus rhythm by DC cardioversion may
be associated with increased risk of systemic or pulmo- vulnerable period of the preceding ventricular repolariza-

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 Indian Journal of Anaesthesia, August 2007

blood pressure are very depressed, emergency DC-

cardioversion must be considered. On the other hand, if
the blood pressure and cardiac output are well maintained,
intravenous therapy with class I drugs is usually advised.
First-line drug treatment consists of lidocaine (50-100 mg
i.v. over 5 min) followed by a lidocaine infusion (2-4
mg.min-1 i.v.). DC-cardioversion may be necessary if
medical therapy is unsuccessful. The administration of
multiple antiarrhythmic drugs should be avoided.
Patients with recurrent episodes or unresponsive to
lidocaine, may require therapy with procainamide (10-15
Note mg.kg-1 loading dose followed by an infusion of 2 to 6
 The upper trace shows five sinus beats, then an early beat with a mg.min -1) or bretylium (5 to 10 mg.min-1 over 2 to 5 min
wide QRS complex and an abnormal T wave: this is a ventricular
extrasystole. In the lower trace, the ventricular extrasystole occur then infusion of 1-2 mg.min-1) or amiodarone in the dose
(arrows) at the peak of the T waves of the preceding sinus beats: of 150 mg IV over 10 minutes followed by an infusion of
this is the ‘R on T’ phenomenon. 1 mg.min-1 for 6 hours and 0.5 mg.min-1 thereafter. IV
Fig 11. Ventricular extrasystole amiodarone has been shown to be as effective as bretylium
with added advantage of less hypotension as compared
to IV bretylium. (Fig.13) 9

Note
 Three sinus beats are followed by a ventricular extrasystole. No P
wave is seen after this beat, but the next P wave arrives on time.
Fig 12. Ventricular extrasystole
Note
tion (the so called R on T phenomenon), associated with  After two sinus beats, the rate increases to 150/min. The QRS
complexes become broad, and the T waves are difficult to identify.
haemodynamic disturbance or convert to worse The final beat shows a return to sinus rhythm.
arrhythmias require prompt treatment. Lidocaine with an Fig 13. Ventricular tachycardia
initial bolus dose of 1.5 mg.kg-1 followed by infusion of 1
C. Ventricular fibrillation (VF)
to 4 mg.min-1 can be given. Other drugs from class I, II or
III are used to treat these types of arrhythmias. It is very rapid and irregular ventricular activation with
no mechanical effect. It is usually intiated from an ischaemic
b. Ventricular tachycardia myocardium or an aberrant foci (especially in acute
This is defined as three or more ventricular beats perioperative myocardial infarction), ventricular tachycar-
occurring at a rate of 120 bpm or more. It may be poten- dia or torsades de pointes. On ECG, there are no defined
tially life threatening. Examination reveals pulse rate of QRS complexes, shows shapeless rapid oscillations and on
120-220bpm. Usually there are clinical signs of atrioven- pulse oximetry, there is acute fall in SpO 2 because of low
tricular dissociation i.e. intermittent cannon 'a' waves and or no cardiac output. Causes include myocardial ischaemia,
variable intensity of the first heart sound. The ECG shows hypoxaemia, electrolyte imbalance and drug effects.
a rapid ventricular rhythm with broad (often 0.14s or Treatment: Cardiopulmonary resuscitation must be
more), abnormal QRS complexes. Dissociated P waves performed as rapidly as possible. Asynchronous external
activity may be seen and have no fixed relation to wide defibrillation should be performed using 200-360J. A pre-
QRS complex. cordial thump is occasionally effective in terminating VF,
but should be attempted only if a defibrillator is not avail-
Treatment may be urgent depending on the
able immediately. Intravenous bretyium 5-10 mg.kg-1 over
haemodynamic situation. If the cardiac output and the 5 min can be useful on some occasion. Supporting phar-
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N. Dua et al. Perioperative arrhythmias

macological therapy such as lidocaine, amiodarone and positive electrode on the cardiac chamber being paced.
procainamide are used only to prevent recurrence of VF. The combination of wires allows atrial, ventricular, or atrial
d. Torsades de pointes ventricular sequential pacing when used in combination
with a dual output (atrial and ventricular) sequential ex-
These arrhythmias are usually short in duration and
spontaneously revert to sinus rhythm. Occasionally it can ternal pacemaker. 13
change to VF. On ECG, it is characterized by rapid, ir- Prophylactic transvenous pacing is recommended
regular sharp complexes that continuously change from in patients who are considered at high risk for developing
an upright to an inverted position. Between spells of ta- haemodynamically significant bradycardia due to AV heart
chycardia the ECG shows a prolonged QT interval; the block or sinus node dysfunction. Whereas, direct cardiac
corrected QT is equal to or greater than 0.44s.
pacing methods are preferred for the patients having car-
Treatment: diac surgery, especially in the postbypass period. In these
The arrhythmia is treated as follows patients, current output of the pacemaker is slowly in-
1. Any electrolyte disturbance is corrected. creased until desired cardiac chamber contraction is cap-
tured (usually 5-10 milliamperes), then current output is
2. Causative drug and precipitating factors should be
stopped and removed. further increased by 5 more milliamperes to assure con-
tinued capture. When atrial ventricular sequential pacing
3. Intravenous isoprenaline may be effective when QT
is required, the optimal PR interval will need to be deter-
prolongation is acquired.
mined. It is generally 150 msec but can vary between 120
4. Blockade is advised if the QT prologation is con-
to 200 msec so as to optimize ventricular filling and car-
genital.
diac output. If extensive electrocautery is being used dur-
Collapse rhythm- There is no ECG rhythm in the
ing the operation, pacemaker may have to be put on asyn-
case of cardiac arrest or asystole. Immediate manage-
chronous mode to prevent inhibition of the pacemaker by
ment should be done according to Flow Chart 3.
electrocautery radiofrequency current. (Fig.14) 9
Pacemaker
New or worse cardiac arrhythmias in the
perioperative period are usually temporary occurrences,
often due to the result of transient physiologic or pharma-
cologic imbalance. Antiarrhythmic drugs have the poten-
Note
tial to further aggravate this imbalance. Therefore, early
 Occasional P waves are visible, but are not related to the QRS com-
use of temporary pacemaker during perioperative period plexes. The QRS complexes are preceded by a brief spike, represent-
is preferred nowadays. More than 90% of pacemakers ing the pacemaker stimulus. The QRS complexes are broad. Because
pacemakers stimulate the right ventricle and cause ‘ventricular’ beats.
are inserted for the treatment of bradyarrhythmias oc- Fig 14. Pacemaker
curring either after tachycardia (bradytachy syndrome) Anaesthetic considerations
or AV conduction disorders or by themselves (sick sinus
All patients undergoing anaesthesia and surgery
syndrome).
should have ECG monitoring. Lead II and V5 are supe-
Temporary pacemaker may be invasive (epicardial rior for arrhythmia detection and diagnosis before the ap-
and endocardial) or non-invasive (transcutaneous and pearance of physical signs e.g. changes in BP, heart rate
transesophageal). The pacing may also be unipolar or bi- or heart sounds. After establishing from ECG that ar-
polar. Unipolar pacing describes the placement of the rhythmia is present, it is crucial to evaluate patient’s re-
negative (stimulation) electrode in the atrium or ventricle sponse to altered rhythm in rate and type of treatment
required. Correction of contributing cause and final line
and the positive (ground) electrode distant from the heart.
of treatment follows thereafter. Routine measures for all
Bipolar pacing describes placement of the negative and
intraoperative arrhythmias are as follows (Table 3 & 4)
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 Indian Journal of Anaesthesia, August 2007

Flow Chart 3


g/kg/min

g/min

Table 3 Routine measures for all intraoperative Table 4. Management of arrhythmias

arrhythmias Ai ms
Routine measures for all intraoperative arrhythmias Cure
- Assure adequate oxygenation and ventilation Prevention (suppression)
- Alteration in depth of anaesthesia Termination
- Assure optimum PaO , PaCO , acid base, electrolyte and Reduction of ventricular rate
2 2
temperature
Techniques available
- Reevaluate cardiac history/pathology
Vagotonic methods
Get ready for
DC cardioversion
- Anti-arrhythmic drugs
Antiarrhythmic drugs
- Anti-ischaemic drugs
Pacemakers and other electronic devices
- Pacing and DC shock
Surgery and other ablation methods

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N. Dua et al. Perioperative arrhythmias

Antiarrhythmic drugs
Drugs that modify the rhythm and conduction of the
heart are used to prevent cardiac arrhythmias. All such
drugs may aggravate or produce arrhythmias and they
may also depress ventricular contractility and must, there-
fore, be used with caution. There are more than 30 anti-
arrhythmic drugs. They are classified according to their
effect on the action potential (Vaughan Williams’ classifi-
cation.) (Fig 15 & Table 5)
Class I drugs
Fig.15. Vaughan Williams’ classification, the dotted line indi-
These are membrane-depressant drugs that reduce cate the effects of antiarrhythmic drugs
the rate of entry of sodium into the cell. They may slow
Class IV drugs
conduction, delay recovery or reduce the spontaneous dis-
charge rate of myocardial cells. Class Ia drugs (e.g. The non-dihydropyridine calcium antagonists that re-
disopyramide) lengthen the action potential, and Class Ic duce the plateau phase of the action potential are particu-
(flecainide, propafenone) do not affect the duration of the larly effective at slowing conduction in nodal tissue.
action potential. Verapamil and diltiazem are the most important drugs in
this group.
Table 5. Vaughan Williams’ classification of antiar-
rhythmic drugs Another clinical classification 6 is based on the part
of the heart that is affected by the antiarrhythmic drug.
Class I
The features of the major antiarrhythmic drugs are given
Ia Quinidine, procainamide, disopyramide in Fig.16.
Ib Lidocaine, mexiletine, tocainide
Ic Flecainide, propafenone
Class II -adrenergic blocking drugs
Class III Amiodarone, sotalol, bretylium
Class IV Verapamil, diltiazem
(Other drugs Adenosine, digoxin)
Class II drugs
These antisympathetic drugs prevent the effects of
catecholamines on the action potential. Most are -adr-
energic antagonists. Cardioselective -blockers (1) in-
clude metoprolol, atenolol, and acebutalol.
Class III drugs
These prolong the action potential and do not affect
sodium transport through the membrane. There are two
major drugs in this class; amiodarone and sotalol. Sotalol
Fig.16. Drugs affecting different parts of the heart
is also a -blocker.
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 Indian Journal of Anaesthesia, August 2007
N. Dua et al. Perioperative arrhythmias
The main drugs useful for arrhythmia management Adenosine is the drug of first choice in treating pa-
with dosage are as follows tients with PSVT. It is therapeutic in over 90% of pa-
Antidysrhythmic drugs useful for ventricular dys- tients with this tachyarrhythmias, in which AV-nodal re-
rhythmia entry is the most common mechanism. In non-reentrant
SVT, such as automatic (ectopic) atrial tachycardia or
Lidocaine Loading dose 1mg.kg-1, repeat every
multifocal atrial tachycardia, adenosine may be useful in
5min, continuous 30-50 g.kg-1.min-1
unmasking the underlying arrhythmia mechanism, but the
Phenytoin 50-100mg slowly every 5 min (Max 12-lead ECG should first be searched to define the mecha-
1gm) nism of the arrhythmia. Other pharmacologic options in-
Procainamide 20mg.min-1 IV infusion (Max total dose clude diltiazem and verapamil, -blocking drugs, and
17mg.kg-1 ; infusion 1-4mg.min-1 amiodarone and digoxin. Cardioversion should be consid-
ered if drug use is contraindicated or if the arrhythmia is
Propranolol 0.1mg.kg-1 by slow IV over 10min
not controlled with drug therapy.
Amiodarone 150mgIV over 10min; 360mg/IV over 6hr
Ventricular tachycardia can be monomorphic or
Flecainide 2mg.kg at 10mg.min (slowly)
-1 -1
polymorphic. When PVT is accompanied by prolonged
Verapamil 2.5 to 5mg IV bolus over 2 min; 2nd dose repolarization, manifested as QT-interval lengthening on
5-10mg in 15-30min the ECG before or after episodes of tachycardia, the ta-
chycardia is torsades de pointes, and its presence man-
Bretylium 5mg.kg-1 IV push, repeat in 5 min at
dates specific diagnostic and therapeutic considerations.
10mg.kg-1, upto max dose of 35 mg.kg -1
If the origin of a wide-QRS tachycardia cannot be con-
Mexiletine 400mg bolus dose followed by 200 mg firmed clinically or electrocardiographically, amiodarone
po q 8hrly or procainamide, should be used. In all situations, emer-
Tocainide 1200-1800mg PO in divided doses q8- gency cardioversion takes precedence if haemodynamic
12hr compromise is present or develops during drug therapy.

Digoxin 0.5mg IV single loading dose then 1.0- Pulseless VT and VF are forms of ventricular
1.5mg in divided doses over 8-24hrs tachyarrhythmia that require cardiac arrest therapy with
defibrillation and drugs; most importantly epinephrine, for
Key points maintenance of myocardial and cerebral blood flow dur-
Therapeutic decisions in patients with cardiac ing external chest compression or open-chest cardiac
arrhythmias are based on an assessment of the massage.
haemodynamic impact of the rhythm disturbance, the
patient’s underlying cardiac function, contributing factors Conclusion
and the correct diagnosis of the arrhythmia. Both clinical Acute-onset cardiac arrhythmia carries the poten-
examination and the ECG should be considered in making tial of haemodynamic instability, including cardiovascular
the diagnosis. Incorrect diagnosis can lead, not only to
ineffective therapy but also to potentially dangerous therapy, collapse. Knowledge of both electric and pharmacologic
especially when wide-QRS tachyarrhythmias are present. options and an understanding of the therapeutic interven-
tion is mandatory. Precipitating factors or causes should
Symptomatic bradyarrhythmia can be treated initially
with atropine; in many forms of bradycardia, however, pac- be treated or removed immediately. In many situations,
ing, either external or transvenous, is the definitive therapy cardioversion or defibrillation is the initial intervention of
of choice. In some situations, including Mobitz type II sec- choice, with drug therapy as follow-up in an attempt to
ond-degree block and in wide-QRS, new-onset complete prevent recurrence of the arrhythmia. In other more
heart block, external pacing can be used temporarily to haemodynamically stable situations, drug therapy is used
bridge the patient over to transvenous pacing. initially.
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N. Dua et al. Perioperative arrhythmias

th
References: 7. Sokolow M and Mcllroy B (1986) Clinical radiology, 4 eds.
New York. Lange. 116-7.
1. Forrest J, Cahalan M, Rehder K, et al. Multicenter Study of
General Anesthesia II. Results. Anesthesiology 1990; 72:262- 8. The American Heart Association, in collaboration with the Inter-
68. national Liason Committee on Resuscitation Guidelines 2000
for Cardiopulmonary Resuscitation and Emergency Cardiovas-
2. Forrest J, Rehder K, Cahalan M, Goldsmith C. Multicenter
cular Care. Part 6: advanced cardiovascular life support 7D: the
Study of General Anesthesia III. Predictors of severe
tachycardia algorithms. Circulation 2000; 102:1158-65.
perioperative adverse outcomes. Anesthesiology 1992; 76:3-15.
rd
9. Hampton JR (1986). The ECG made easy, 3 eds. Edinburgh:
3. Katz RL, Bigger JT Jr. Cardiac arrhythmias during anaesthesia
Churchill Livingstone. 31-34, 59,61,65-68, 79,85.
and operation. Anesthesiology 1970; 33:193-213.
10. Oxorn D, Knox JW, Hill J. Bolus doses of esmolol for the pre-
4. Bertrand CA, Steiner NJ, Jameson AG, et al. Disturbances of
vention of perioperative hypertension and tachycardia. Can J
cardiac rhythm during anesthesia and surgery. JAMA 1971;
Anaesth 1990; 37:206-209.
216:1615-17.
11. Atlee J, Bosnjak Z. Mechanisms for cardiac dysrhythmias dur-
5. Fisher DM. Preoperative cardiac dysrhythmias; Diagnosis and
ing anesthesia. Anesthesiology 1992; 76: 3-15.
Management. Anesthesiology 1997; 86:1397-424.
rd 12. Das G, Ferris J. Esmolol in the treatment of supraventricular
6. Kumar P Clark M. Clinical Medicine. 3 eds. Cardiac arrhythmias
tachyarrhythmias. Can J Cardiol 1988; 4:177-80.
1994. ELBS 554-555, 566-568.
13. Salukhe TV. Dob D, Sutton R. Pacemakers and defibrillators:
anaesthetic implication. Br J Anaesth 2004; 93; 95-104.

MEDICO LEGAL QUERY?

Dear Members,
Of late, cases under CPA, against anaesthesiologists, are increasing throughout the country. Though most of
the cases are dismissed ultimately by the court of law, they are causing lot of tension and worry for the
anaesthesiologists and their families. The following members of ISA, are qualified in ‘Law’ and are well versed in
medico-legal aspects. They have kindly volunteered to answer any of the medico legal queries related to our
profession raised by any of the members of ISA. Please contact any of them, in case of necessity.
Dr. D.N. Upasani Dr. S.C.Parakh Dr. Mahesh S. Kapadia
E-mail : drupasani@rediffmail.com E-mail : scparakh@yahoo.co.in E-mail : pamskapadia@yahoo.com

SHORT TERM COURSE

Department of Anaesthesiology announces short term (3 Months) course in Intraoperative
transesophageal echocardiography for post MDAnaesthesiologists working in private or government institu-
tion setup starting from 1st March 2008.
For detail:
Dr.R.C.Rathod
Prof. & Head of Anaesthesia
Sree Chitra Tirunal Institute for Medical Sciences and Technology
Trivandrum-695011 (Kerala)
Ph: 0471-2524643, Fax: (91) 471-2446433
Email: rcrathod@sctimst.ac.in , rcrathod@gmail.com

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Indian Journal of Anaesthesia 2007; 51 (4) : 324-333 Indian Journal of Anaesthesia, August 2007

Transesophageal Echocardiography and Anaesthesiologist

Thomas Koshy1, Bhupesh Kumar2, Prabhat Kumar Sinha 3
Key words Transesophageal echocardiography, Anaesthesia
Introduction
Echocardiography – the use of ultrasound to exam- yrs. Also the cardiovascular physiology of anaesthetized
ine the heart- is a safe, powerful, non-invasive and pain- patients is not similar to physiology of awake patients and
less technique. The introduction of transesophageal anaesthesiologists with knowledge and understanding of
echocardiography (TEE) has provided a new acoustic this altered physiology is in better position to interpret the
window to the heart and mediastinum. Superior quality information obtained from intraoperative TEE. In current
images of most cardiovascular structures can be obtained practice in the UK, 90 % of the TEEs are performed not
readily with an ultrasound probe in the esophagus. TEE by cardiologist but, by cardiac anaesthesiologist. 4 As we
has revolutionized cardiac anaesthesia and has also be- view the field of echocardiography in the 2000s, it is almost
come increasingly popular in the management of patients impossible to conceive of a state-of-the-art cardiac OR
in the intensive care unit (ICU) and during certain non- without TEE machines.
cardiac surgical procedures as well. Several authors have described the usefulness of
Although clinical application of TEE is recent, TEE on cardiac surgical practice. 5,6 Kneeshaw and co-
transesophageal application of ultrasonography to assess workers had showed that in a group of 309 patients who
cardiac function was first reported by Side and Gosling in underwent intraoperative TEE, management changed in
1971.1 The early transesophageal probes did not attract 26% patients. 7 In 6% of patients the changes were in
clinicians because of the problems associated with swal- inotrope use and fluid management. However, in 20% of
lowing of the probe in conscious patients and also due to patients, TEE resulted in a change in the procedure car-
the logistical difficulties of introducing a rigid endoscope. ried out. Among noncardiac surgical procedures it has
Transducers were subsequently mounted on flexible
been found to be useful in management of neurosurgical
endoscopes, and DiMagno et al first reported the use of a patients for detection of air embolism and other major
linear phased array flexible endoscope in 1980.2 In 1982,
surgical areas where haemodynamic instability may oc-
Souquet and co-workers, first produced a clinically usable
cur. The role of TEE in ICU is also steadily increasing. It
flexible endoscope with a sector phased array two-dimen-
sional echocardiographic transducer having a frequency of was found to be of particular value in managing
2.25 MHz – a frequency equal to that of the standard pre- haemodynamic instability in post cardiopulmonary bypass
cordial transducer.3 This represented the definitive break- (CPB) period. Now it is being also used as rapid imaging
through for the transesophageal approach. Application of modality in the general ICU as an adjunct to other moni-
these probes took different directions in the United States toring modality to provide data in haemodynamically un-
and Europe. The cardiologists in Europe began using TEE stable patients. To summarize, the usefulness of TEE in-
to supplement the diagnosis of different cardiac patholo- cludes, augmentation of preoperative cardiac evaluation,
gies. In the United States on the other hand, increasing planning of surgery, evaluation of surgical results and dif-
number of anaesthesiologists started using TEE probes for ferential diagnosis of haemodynamic instability. TEE is
monitoring patients in the operating rooms (OR). As the associated with a long learning curve, because the com-
practice expanded it became clear that very few cardiolo- plexities of transducer positioning, imaging sector align-
gists were able to spend long period in the OR since cardi- ment and three dimensional cardiac anatomies are not
ology has become much more invasive speciality in last 20 familiar to most beginners.

1. MD, PDCC, Additional Professor, 2.MD, DM Cardiac Anaesthesia Resident, 3. MD, Associate Professor Department of Anaesthesiology,
Sree Chitra Tirunal Institute for Medical Sciences and Technology, Trivandrum, Kerala. Correspondence to: Thomas Koshy, Sree Chitra
Tirunal Institute for Medical Sciences & Technology, Trivandrum-695011, Kerala, India. Email : koshy61@rediffmail.com

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