Management of

Perioperative
Arrhythmias
Dr. Abhishek V.Lonikar,Fellow
Dept. of Anaesthesiology
Tata Medical Centre,Kolkata.
ARRHYTHMIA - Definition
Abnormality of cardiac rate, rhythm or
conduction, which can either be lethal (sudden
cardiac death), or symptomatic (syncope, near
syncope, dizziness, palpitation), or
asymptomatic.
Incidence
• Intra-operative arrhythmias- As high as 84%
• GA 66% v/s regional 42%

• Thoracic surgery 93% v/s peripheral surgery 56%

• Intubated patients 72% v/s non-intubated patients 44%

• Age-atrial arrhythmias following surgery has been an age of 60
years or older.(A.Clinics).
Factors causing arrhythmias in
the perioperative period
1. General Anaesthetics-
• Volatile anaesthetics( halothane or enflurane) produce arrhythmias(re-
entrant mechanism).

• Halothane sensitizes myocardium to catecholamines.

• Sevoflurane severe bradycardia and nodal rhythm in high

concentrations during induction in infants.

• Desflurane may prolong the QTc within the 1st minute of anaesthesia in
patients with a normal heart.

• Cocaine and ketamine block reuptake of norepinephrine

development of epinephrine-induced arrhythmias.
2. Local Anaesthetics-
• Central neuraxial blocks especially when extending to very high
thoracic levels mild to very severe bradyarrhythmias.
• Inadvertent IV injection of large dose of local anaesthetics
asystole and cardiac arrest.

3. Abnormal blood gases and electrolyte imbalance-

• Hypoxia
• Hypercarbia
• Acidosis
• Hypo/Hyper- kalemia
4. Endotracheal intubation- Most common cause of arrhythmias
during surgery.

5. Autonomic reflexes-
Vagal stimulation  Sinus bradycardia allows ventricular escape
mechanisms, AV block, asystole.

This may occur during-

• Peritoneal traction
• Direct pressure on vagus nerve during carotid surgery
• Carotid sinus stimulation due to palpation of neck during IJV
cannulation
• Occulocardiac reflex etc.
6. CNS stimulation- CNS diseases esp. SAH  ST-T wave changes
mimicking myocardial ischemia/infarction.
Mechanism- Changes in ANS tone.
7. Pre-existing cardiac disease- Most common background for
arrhythmia during anaesthesia and surgery.
In response to perioperative stress or acute withdrawal of oral
antiarrhythmic drugs esp. beta blockers.
8. Central venous cannulation.
9. Surgical manipulation of cardiac structures- self limited. Cease at
end of manipulation.
10. Location of surgery- Dental surgery, ocular surgery esp. strabismus
surgery.
Significance of Perioperative
Arrhythmias
• In healthy adults  wide variations in heart rate can be
tolerated because normal compensatory mechanisms
maintain cardiac output & blood pressure.

• In patients with cardiac disease dysrhythmias & conduction

disturbances can overwhelm normal compensatory
processes hemodynamic instability.
 Cardiac Action potential
Pharmacology of Anti-Arrhythmic drugs :-
-Anti-arrhythmic drugs can be classified into 4 class broadly
1.Class I-Na channel blcoking drugs.
2.Class II-Beta blockers.
3.Class III-Potassium channel blocking.
4.Class IV-calcium channel blockers,miscellaneous.
1.Class I-membrane-depressant drugs
that reduce
the rate of entry of sodium into the cell
2.Class II-antisympathetic drugs
prevent the effects of
catecholamines on the action potential
3.Class III-prolong the action potential
and do not affect
sodium transport through the
membrane(Bretyllium).
4.Class IV-The non-dihydropyridine
calcium antagonists that reduce
the plateau phase of the action
potential are particularly
effective at slowing conduction in
nodal tissue.
Mechanism of arrhythmia
• Mainly 2 types-
Disorders of impulse formation:
1. Enhanced automaticity
2. Triggered activity or after depolarization
Disorders of impulse conduction:
1.Re-entry
2. Conduction block
A. Mechanism of tachyarrhythmias
i. Increased automaticity in normal conduction tissue or in an
ectopic focus.
ii. Re-entry of electrical potentials through abnormal pathways.
iii. Triggering of abnormal cardiac potentials due to after
depolarizations.
B.Mechanism of Bradyarrhythmia

1.Slowing or stoppage of spontaneous depolarization of SA

node- due to drugs, electrolyte abnormalities, hypothyroidism,
intrinsic disease Role of pacemaker taken up by AV node(
junctional rhythm) or ventricles( ventricular rhythm). Known as
‘escape mechanism’

2.Conduction block: SA nodal, AV nodal(1⁰,2⁰,3⁰), ventricular.

 CLASSIFICATION OF
ARRHYTHMIAS

TACHY- ARRHYTHMIA
BRADY- ARRHYTHMIA
>100 bpm
<60 bpm
(Approach as per QRS morphology)

i. Sinus Bradycardia
ii. Various forms of heart 1.. Narrow QRS complex 2.. Wide QRS
blocks: tachycardias (QRS complex
<0.12 second) tachycardias (QRS >
a. SA block/arrest 0.12 second)
(Supraventricular)
b. First degree AV block
c. Second degree AV block
d. Third degree AV block

a. Sinus tachycardia a. Ventricular extra systole

b. Atrial premature beat b. VT
c. Atrial tachycardia c. VF
d. SVT with aberrant conduction
d. Atrial flutter
e. Atrial fibrillation
Supraventricular Tachycardias- Ventricular Tachycardias:
 Ventricular tachycardia
Atrial tachycardias and
tachyarrhythmias: Torsades de pointes ( a special
 Sinus tachycardia type of VT)
 Atrial tachycardia Ventricular fibrillation
 Multifocal Atrial Tachycardia
(MAT)
 Atrial flutter
 Atrial fibrillation

Tachyarrhythmias involving the AV

node:
 Junctional tachycardia
 AV nodal reentrant tachycardia
(AVNRT)
 AV reentrant tachycardia (AVRT)
Bradyarrhythmias
• A bradyarrhythmia is any abnormal rhythm that results in a
heart rate of < 60 bpm.

• They include:
 Sinus bradycardia
Junctional rhythms or ventricular escape rhythms
 Heart block ( first, second and third degree)
How to diagnose
arrhythmias?
Look at the ECG strip and ask the following six questions:
1. Heart rate? Tachy- or brady- arrhythmia?
2. Rhythm regular or irregular?
3. QRS complex narrow or wide?
4. P waves absent or present?
5. What is the relationship between P waves and QRS
complexes?
6. Is the onset and termination abrupt or gradual?
Diagnosing
Tachyarrhythmias
• Follow three simple steps:
• Determine whether the QRS complexes are narrow or wide.
• Determine whether the QRS complexes are occuring at regular or
irregular intervals.
• Determine if there is any evidence of P waves or atrial activity present.
• Based on these tachyarrhythmias fall into one of three categories:
• Narrow complex regular tachycardias.
• Narrow complex irregular tachycardias.
• Wide complex tachycardias.
• Narrow complex regular tachycardias include:
• Sinus tachycardia  Normal P waves before each
QRS complex
• Atrial tachycardia Abnormal/inverted P waves
before each QRS complex
• Atrial flutter Flutter waves
• Junctional tachycardia No P waves/ retrograde P waves after QRS
complex. Rate usually 101-120 bpm
• Narrow complex irregular tachycardias:

• Multifocal Atrial Tachycardia Multiple P waves

of different
morphology before
each QRS complex

• Atrial flutter with variable conduction Flutter

waves

• Atrial fibrillation No P waves or organised atrial

activity
• Wide complex tachycardias:

• Any supraventricular tachycardia with bundle branch block QRS

morphologies and RR intervals are all perfectly same. P or flutter waves
may be present.

• Ventricular tachycardia There is slight or more variation in the QRS

morphologies and the RR intervals . There is P wave dissociation.
Diagnosing
Bradyarrhythmias
• Normal P wave, normal PR interval, P:QRS=1:1 Sinus
bradycardia
• No/inverted P waves before each QRS, QRS narrow, rate 40-
60bpm Junctional rhythm
• Some P waves followed by QRS, not all 2⁰ heart block. 2
types:
• Mobitz type I (Wenkebach)
• Mobitz type II
• P waves ‘marching through’ QRS complexes 3⁰ or complete
heart block
Management Of Arrhythmias
 Types of Arrhythmias:-
A. Bradyarrhythmias:-
i. Sinus bradycardia – bradycardia is generally defined as a
heart rate of less than 60 beats per minute.
-on chronic beta-blocker therapy such as those suffering from
coronary artery disease (CAD), it is defined as a heart rate of
less than 50 beats/min.
ii. Various forms of heart block- are broadly classified into three
categories
a) First degree heart block
b) Second degree heart block
c) Complete heart block
a)First degree heart block: This is simple prolongation of the PR
interval to more than 0.22 sec. Every atrial depolarization is followed
by conduction to the ventricle but with delay.
-No specific investigation or treatment in absence of symptoms
b)Second degree heart block:-
-two types:Mobitz type1 and Mobitz type 2.
-Mobitz Type 1
-Mobitz type II:-
Rx May require pacing
c)Third degree heart block or complete heart block:-
 Heart block
Management of intraoperative heart block :
• Atropine
• If profound hypotension isoprenaline infusion
• Transcutaneous pacing
• Oesophageal pacing
• Transvenous pacing
Pre operative pacing indicated in :
1. Symptomatic 1st, second degree blocks
2. Complete heart block
3. Symptomatic/Asymptomatic bi or trifascicular blocks.
4. Slow rates unresponsive to drugs
B. Tachyarrhythmia:-
Narrow QRS complex :-
i. Sinus tachycardia: it is defined as an increase in the sinus rate
ofmore than 100 beats/minute. Prolonged tachycardia for long
duration can induce ischaemia in coronary artery diseased
patients.
ii. Atrial premature beat: It represents 10% of all intraoperative
arrhythmias.
-The duration of QRS wave is normal but wide QRS wave may be
present due to aberrant ventricular conduction, which mimics
premature ventricular beat.
-Common and benign. May occur normally.
-Other causes
a.Ischemia/ hypoxia
b.Light anaesthesia, sepsis, shock
c.Anaesthetic drugs, triggers (nicotin, caffiene, alcohol)
d.Valvular heart disease
Rx : Treatment of underlying cause, otherwise observe for atrial
tachycardia.
iii. Atrial tachycardia : These arrhythmias are found in 6%
of patients undergoing non cardiac surgery.
-Rx : 1. Sensitive to DC cardioversion- nearly 100%
conversion. In anaesthetised patient it is first line of
treatment .
2. Carotid sinus massage and adenosine will slow AV
conduction and reveal underline rhythm . Other drugs like
AF
-multifocal atrial tachycardia(MAT) rapid, irregular atrial
rhythm arising from multiple ectopic foci within the atria.
-typically a transitional rhythm between frequent premature
atrial complexes (PACs) and atrial flutter / fibrillation.
-AKA “Chaotic atrial tachycardia”.
iv.Atrial Flutter :-
v.Atrial Fibrillation :-
-Irregularly irregular rhythm.
-No P waves.
-Absence of an isoelectric baseline.
-Variable ventricular rate.
-QRS complexes usually < 120 ms unless pre-existing bundle
branch block, accessory pathway, or rate related aberrant
conduction.
Management : Correction of precipitating cause especially
sepsis,electrolyte disturbance
 Onset <48 hrs
Synchronised DC cardioversion at 200 then 360 J
Flecainide is best for converting to sinus rhythm in absence
of LV dysfunction and ventricular arrhythmia
 Onset >48 hrs
DC cardioversion is associated with risk of arterial
thromboembolism unless patient is anticoagulated (at
least 3 wks)
• Digitalisation and maintenance to reduce ventricular rate and
further episodes of paroxysmal AF (if K + is normal)

• Beta blockers( esmolol, sotalol, metoprolol) slow ventricular rate,

but to be cautious in impaired myocardium, with Ca channel
blockers

• Amiodarone slows rate and sustains normal rhythm. Well tolerated

in LV impairment. Long-term side effects like pulmonary fibrosis .

• Verapamil i.v.to slow ventricular rate when patient is unable to

tolerate beta blocker
 Re-entry arrhythmias:
- Reentry arrhythmias occur where there is an anatomical branching
and re-joining of conduction pathways. Two distinct pathways
must exist around an area of conduction block, so that a
perpetually propagating wave form can constantly meet an
excitable myocardium
 Re-entry arrhythmias:
contd…
Wolff- Parkinson- White Syndrome :

 The classical example of re entry arrhythmia is Wolff- Parkinson- White syndrome,

where an accessory conduction pathway ( Kent fibers) is present between atria and
ventricles .
 Characterised by short PR interval with slurred QRS upslope called Delta wave.
 Other re-entry circuits occur with supraventricular tachycardia, atrial flutter, atrial
fibrillation, venticular tachycardia.
Junctional/AV Nodal/Supraventricular tachycardia

 Abrupt onset and termination

 ECG shows narrow complex tachycardia with rate 150-200
bpm.
 The first P wave is different from others( if at all seen)
 A broad complex pattern may occur in presence of accessory
pathway or bundle branch block.
 May cause severe circulatory disturbance
Rx : 1. If hypotensive :First line treatment synchronised DC
cardioversion with 200 then 360 J
2. Carotid sinus massage :Differentiates from atrial
flutter and fast AF
3. Adenosine :Useful for terminating re-entry SVT
4. Beta blockers : Esmolol infusion or metoprolol i.v.
5. Verapamil ,Amiodarone when first line drugs have failed.
6. Digoxin should be avoided as it facilitates conduction
through AV accessory pathways in WPW and worsens tachycardia
 Broad QRS complex :-
i. Ventricular premature beat (VPB) /Ventricular
Extrasystole :-results from ectopic foci arising from below AV
node and give rise to wide (>0.12 sec) bizarre QRS complex.
-15% of the observed arrhythmias,more common in anaesthetized
patients with pre existing cardiac disease.
Rx : 1. Correction of contributing causes -----adequate
oxygenation,normocarbia,analgesia.
2. If ventricular rate is <50 bpm, ectopics may be
ventricular escape beats. Atropine or glycopyrrolate may
be helpful.
 Ventricular tachycardia:

 Focus in the ventricular muscle depolarizes at high frequencies resulting in

tachycardia with wide QRS which may vary in shape.
 Serious, potentially life threatening arrhythmia .
 Caused by reentry, commonly triggered by MI, myocardial ischemia,
hypoxia, hypotension, fluid overload, electrolyte imbalance ( low K+, Mg++),
injection of adrenaline or other catecholamines.
 Management:
 For pulseless VT- immediate defibrillation

 For unstable patient with pulse- immediate synchronised

cardioversion(200-360 j)

 For stable patients with monomorphic or polymorphic VT and

normal cardiac function: procainamide, sotalol, amiodarone or
lidocaine

 For stable patients with monomorphic or polymorphic VT but poor

EF- amiodarone or lidocaine i.v. followed by DC cardioversion.
ii. Ventricular fibrillation (VF) :-
iii.Torsade de pointes :-
-specific form of polymorphic ventricular tachycardia
occurring in the context of QT prolongation.
-it has a characteristic morphology in which the QRS
complexes “twist” around the isoelectric line.
-often short lived and self terminating, however can be
associated with hemodynamic instability.
References
• Management of Perioperative Arrhythmias.N.Dua,V.P.Kumra-Indian
Journal Of Anaesthesia-2007.

• Intraoperative management of critical arrhythmia.Chang Kwon-

Seong-Hyop Kim - Korean Journal of Anesthesiology - 2017
• Perioperative cardiac arrhythmias.A. Thompson-J.r. Balser - British
Journal of Anaesthesia – 2004

• Prevention and Management of Perioperative Arrhythmias in the

Thoracic Surgical Population.David Amar - Anesthesiology Clinics –
2008.
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