This document discusses perioperative dysrhythmias. It begins by defining dysrhythmias and noting they represent an important cause of complications during surgery. While most are benign, some can be lethal or symptomatic. The document then discusses the incidence, which is seen in 70.2% of patients undergoing general anesthesia and varies depending on surgery type and monitoring. It provides details on the mechanisms, causes, and types of perioperative dysrhythmias, as well as their presentation, treatment, and contributing risk factors.

2.  Definition-
“Abnormality of cardiac rate, rhythm or conduction
which can be either lethal (sudden cardiac death), or
symptomatic (syncope, near syncope, dizziness, or
palpitations) or asymptomatic”.
 Dysrhythmias represent an important cause of
perioperative complications because during this
period there are several clinical situations that may
trigger changes in cardiac rhythm.
 Most perioperative dysrhythmias are benign, without
significant hemodynamic consequences.

3. Incidence-
 Seen in 70.2% of patients subjected to general
anaesthesia for various surgical procedures.
 Varies from patients undergoing cardiac or non-
cardiac surgery as well as on monitoring modality.
 Incidence varies from16.3 to 61.7%with intermittent
ECG monitoring & 89%with continuous holter
monitoring in patients undergoing non-cardiac
surgery,
 In patients undergoing cardiac surgery - reported
incidence of > 90%.

4.  Dysrhythmias are secondary to changes in cardiac ion
channels (sodium, calcium, and potassium channels)
and adrenergic receptors are the targets.
 Phase 0-initiates the conduction in the cardiac tissue.
In atria and ventricles the impulse originates in the
sodium current.
In the sinoatrial (SA) and atrioventricular (AV) nodes
phase 0 is produced by calcium current.
 Phases 1- represent repolarization,
 Phase 2- plateau (maintained by calcium current)
and
 Phase 3- is maintained by potassium current.
 During Phase 4- nodal cells undergo spontaneous
depolarization while atrial and ventricular tissues are
hyperpolarized.

6.  1. Injury or damage (pathology) to the cardiac
conduction systems.
 2. Re-entry: Reentry is a mechanism that may
precipitate a wide variety of supraventricular and
ventricular arrhythmias.
 3. Automaticity: Abnormal depolarization of atrial
or ventricular muscle cell during the periods of
action potential can lead to arrhythmias.
 4. Mutations in ion channels: Since these channels
are mainly responsible for depolarization, mutation
can lead to arrhythmias.
 5. Ectopic foci/ irritable foci

7.  Automaticity refers to abnormal atrial or ventricular
depolarization during the repolarization (phases 2 or 3)
or resting (phase 4) period of the action potential.
 Some molecular substrates, such as prolongation of
the QT interval and low potassium (K+) concentrations
can trigger automaticity.
 Mutations in ion channels responsible for
repolarization, and that can prolong it, make cardiac
cells more sensitive to dysrhythmias
 Factors that increase automaticity include increased
activity of the sympathetic nervous system,
hypokalemia, hypomagnesemia, catecholamines,
digoxin, hypoxemia, and atrial and ventricular dilation

8.  Three factors must be present for reentry to occur:
1) presence of two conduction pathways;
2) unidirectional blockade of one of the pathways
prevents progression of the impulse, but is allows
retrograde conduction; and
3) reduced impulse velocity in one of the
pathways giving time for the other pathway to
depolarize.
 Reentry is the mechanism of several
supraventricular and ventricular dysrhythmias
implying the presence of a pathologic circuit of
electrical impulse around a functional or anatomic
loop, which is seen in Wolff-Parkinson-White
syndrome (WPW).
 Ischemia also predisposes the development of
reentry tachycardia.

9. Unidirectio
nal
Block
Recovery
of
Excitabilit
y
Bidirectio
nal
Conductio
n
Mechanism of
Reentry

10.  Drugs that terminate reentry do this by two
mechanisms:
1.Suppression of the current responsible for phase 0
of the action potential that prolongs or blocks
conduction in the reentry pathway, interrupting the
dysrhythmia.
2. Drugs that prolong the action potential (with K+-
channel blocking properties) prolong cellular and
reentry circuit refractory period, blocking
propagation of impulses through the circuit.
 The main mechanism of monomorphic VT is also
reentry around the infarcted myocardium.

12.  Hypovolemia
 Hypoxia
 Hypo/Hyperkalemia
 Hypomagnesaemia /
Hypocalcaemia
 Hypoglycemia
 Hypothermia
 Acidosis
 Mechanical
Irritation (e.g. central
venous
lines, pulmonary art.
catheter,
chest tube)
 Cardiac ischaemia
 Light plane of
anaesthesia/pain
 Toxins/ Drugs
 Tamponade, Cardiac
 Tension pneumothorax
 Thrombosis (Coronary or
pulmonary)
 Trauma
 Surgical cause (Traction to
intestine, oculocardiac
reflex, neurosurgical
causes, cardiac
compression on beating
heart bypass surgery etc.)

13.  These factors can grossly be divided into following
categories:
1. Patient related factors
2. Anaesthesia related factors
3. Surgery related factors

14.  1. Patient related factors-
a. Preexisting cardiac disease
b. Central nervous system disease - Patients with
intracranial disease especially SAH may show ECG
abnormalities- changes in QT intervals, development of
Q waves, ST-segment changes, and occurrences of U
waves.
c. Old age - Postoperative atrial fibrillation (AF) is a
frequent complication in the elderly patients
undergoing thoracic surgery.Aging causes
degenerative change in atrial anatomy and is also
accompanied by relative changes in atrial pathology.

15.  2.Anaesthesia related factors-
a. Tracheal intubation – It is one of the most
commonest causes of arrhythmias during induction
as well as during the perioperative period, most
often associated with haemodynamic
disturbances.
b. General anaesthetics – The drugs used for
induction, maintenance as well as for reversal of
general anaesthesia are not primarily
arrhythmogenic, but arrhythmias can be produced
in the presence of a variety of triggering agents
and clinical situations generating high
catecholamines such as light plane of anaesthesia
with hypertension and tachycardia,hypoxaemia,
hypercarbia, exogenous epinephrine and
aminophylline.
 Halothane or enflurane produces arrhythmias,
probably by a reentrant mechanism.

16. c. Local anaesthesia –
Parasympathetic nervous system predominance →
bradyarrhythmias.
d. Electrolyte imbalance and abnormal arterial
bloodgases – hypercarbia, hypoxaemia or
electrolyte imbalance produce arrhythmias either
by producing reentrant mechanism or by altering
phase depolarization of conducting
fibers.Hypokalemia or hyperkalemia may also lead
to arrhythmias.
e. Central venous cannulation – Stimulation of
carotid sinus reflexes may occur due to pressure
from fingers during jugular vein cannulation as
excess insertion ofthe central venous catheter into
the right atrium during centralvenous cannulation
may also lead to arrhythmias.

17.  3. Surgery related factors-
a. Cardiac surgery – A spectrum of cardiac
arrhythmias can be observed during the
immediate period following the release of aortic
cross clamp when myocardium is recovering from
the ischaemic insult and regaining normal sinus
rhythm. Surgical manipulation such as retraction of
the heart during operation on beating heart,
venous cannulation or taking sutures over the
atrium can also precipitate arrhythmias.
b. Non-cardiac surgery –Vagal stimulation due to
traction on the peritoneum or direct pressure on
the vagus nerve during carotid artery surgery may
produce bradycardia or atrioventricular (AV)
blocks, or even asystole.

19. a.Sinus Bradycardia-
 HR ≤ 60 beats per minute.
 In patients on chronic beta-blocker therapy as in
(CAD)- heart rate ≤ 50 beats/min.
Causes-
 1. Drug effects: β blockers, digitalis and other anti-
arrhythmic drugs
 2. Acute myocardial ischaemia
 3. Hypothermia
 4. Underlying hypothyroidism, cholestatic jaundice
or raised intracranial pressure.
 5. Chronic degenerative change such as fibrosis of
the atrium and sinus node.

20. Treatment:
 Asymptomatic bradycardia -does not require
treatment.
 Symptomatic bradyarrhythmias -
 Atropine-
0.5 to 1.0 mg (IV bolus),
repeated every 3 to 5 minutes, if required (maximum
dose = 0.04 mg.kg-1).
 Should be used cautiously in patients with CAD, since
excessive increase in heart rate may worsen ischaemia
because of increased myocardial oxygen
consumption or reduced diastolic filling time.
 Still persists- Isoprenaline can be administered as an IV
bolus of 5 to 10 μg followed by an infusion of 2 to
10μg.min-1.
 Other alternative is dopamine infusion 5 to 20μg.min-1.
 While treating sinus bradycardia, various causes or
factors contributing should be searched and treatment
started.

21.  (AVHB) are broadly classified into three categories-
a) First degree heart block
b) Second degree heart block
c) Complete heart block
 May be transient or permanent.
 Transient AVHB can be produced by acute MI and
general anaesthetics such as enflurane or
halothane in patients using calcium channel
blocker drug (CCB) or amiodarone.
 Permanent AVHB-usually idiopathic, other causes
CAD and Lev’s or Lenegre disease, where fibrosis of
the conducting system occurs.

22. 1st Degree Heart Block-
 This is simple prolongation of the PR interval > 0.22 sec.
 Every atrial depolarization is followed by conduction to
the ventricle but with delay.
 The treatment is usually not necessary however, the
patients should be carefully observed for progression to
a higher degree of block, that requires prompt
treatment

23. 2nd Degree Heart Block-
 In "classic" Type I (Wenckebach) AV block the PR
interval gets longer (by shorter increments) until a
nonconducted P wave occurs.
 In Type II (Mobitz)AV block the PR intervals are
constant until a nonconducted P wave occurs.
There must be two consecutive constant PR
intervals to diagnose Type II AV block .

25. 3rd Degree Heart Block-
 Complete AV dissociation because the atria and
ventricles are each controlled by separate
pacemakers.
 Based on the QRS rhythm –Narrow/Wide QRS
rhythm
 Narrow complex: This is due to disease in the AV
node or the proximal bundle of His.
 The escape rhythm occurs with an adequate rate
(50-60 b.p.m.) and is relatively reliable.
 It occurs because of inferior wall MI and toxic
concentration of drugs such as digitalis, verapamil
or βblockers in perioperative period.

26.  Broad complex: Occurs because of disease in the
Purkinje system.
 The escape pacemaker arises from the distal
Purkinje network or the ventricular myocardium.
 Rhythm -slow (15-40 b.p.m) and relatively
insignificant or unharmful.
 In the elderly- usually caused by degenerative
fibrosis and calcification of the distal conduction
system (Lenegre’s disease) or the more proximal
conduction system (Lev’s disease).
 It may occur after closure of ventricular septal
defect (VSD) and sometimes following aortic valve
replacement (AVR).
 In younger patients, broad complex AV block may
be caused by perioperative myocardial
ischaemia.

28. Management -
 Treatment is not required in narrow complex 3°
block except for eradication of toxic causes.
 Occasionally, permanent pacing is advocated for
symptomatic, isolated AVblock.
 While in broad complex, pacing is indicated to
maintain the normal haemodynamics.

31. Definition-
 Supraventricular tachycardia can be defined as
sustained, non-sinus related, acceleration of the
cardiac rhythm, originating above the AV node.

32. a. Sinus tachycardia-
 HR > 100 beats/minute.
 Prolonged tachycardia for long duration can induce
ischaemia in CAD patients.
 Causes-
Anaemia because of blood loss
Pain
Inadequate anaesthesia
Hypovolaemia
Fever
Hypercarbia
Thyrotoxicosis/ thyroid crisis
Cardiac failure with compensatory sinus tachycardia
Catecholamines excess

33. Treatment:
 Precipitating factors must be identified and
corrected.
 Drug therapy -especially required in patients with
ischaemic heart disease who develop ST segment
changes to prevent further myocardial ischaemia.
 Beta-blockers -Esmolol is preferred drug .
It has half-life of 10min with bolus dose of 500
mcg.kg-1 over 1 min,
Followed by an infusion of 50-300mcg.kg-1.min-1.
If continuous use is required-longer lasting cardio
selective drugs such as Metoprolol in the dose of 5
to 10mg given slowly intravenously (IV) at 5min
interval to a total dose of 15 mg.
 Another drug - Propranolol 0.1 mg.kg-1.

34.  Recently, Landiolol has been introduced into clinical
practice in some countries.
 β-blocker whose cardioselective properties are
greater than the esmolol and has a shorter half-life (2
to 4 minutes), as it is rapidly hydrolyzed by plasma
esterases.
 Dexmedetomidine 0.3 mg.kg-1 used to treat persistent
sinus tachycardia resistant to treatment with esmolol
and suggested that this drug could be useful in
patients with bronchospasm and tachycardia

35. b.Atrial premature beat-
 Represents 10% of all intraoperative arrhythmias.
 ECG -appear as early and abnormal ‘P’ waves and
are usually but not always, followed by normal QRS
complexes.
 Duration of QRS wave- normal but wide QRS wave
may be present due to aberrant ventricular
conduction, which mimics premature ventricular
beat.
 Treatment-
Not normally required unless the ectopic beats
provoke more significant arrhythmias, where
βblockade may be effective.

37. c.Atrial tachycardia:
 Found in 6% of patients undergoing non cardiac
surgery.
 It is nonparoxysmal, narrow QRS rhythm with
retrograde or nonapparent P waves and a rate <70
beats/min
 If faster usually <130 beats/min, it is termed as
acceleratedAV junctional rhythm.
 Those arrhythmias can lead to fall in blood pressure
upto 15%in patients without cardiac disease and
upto 30%in diseased heart.

39. Treatment-
 Usually no treatment is required;
 Carotid sinus massage and verapamil are often
helpful in symptomatic patients.
 IV adenosine in 6 to 12 mg doses is another
alternative.
 Treatment with class Ia, Ic or III drugs is usually
successful e.g.disopyramide 2mg.kg-1 over 10min.

40. d.Atrial flutter-
 Usually associated with organic ischaemic heart
disease.
 Atrial rate varies between 280 and 350min-1 but is
usually around 300min-1.
 Most often every second flutter beat conducts giving
a ventricular rate of 150 min-1.
 Occasionally every beat conducts, producing a
heart rate of 300min-1.
 ECG: The ECG shows regular saw tooth-like atrial
flutter waves between QRST complexes.
 If they are not clearly visible,AV conduction may be
transiently impaired by carotid sinus massage or by
the administration of AV nodal blocking drugs such as
verapamil.

41. Treatment:
 Treatment of an acute paroxysm is electrical
cardioversion.
 Prophylaxis is achieved with class Ia, Ic or III drugs in
diseased heart patients.

42. e.Atrial fibrillation (AF)
 It accounts for > 90% of supraventricular tachycardia
(SVT) in the perioperative setting.
 Causes-
Raised atrial pressure, increased atrial muscle mass, atrial
fibrosis or inflammation and infiltration of the atrium.
Rheumatic disease often associated with cardiac causes
such as mitral valve disease, myocarditis and coronary
artery disease.
Systemic diseases include hyperthyroidism, pulmonary
embolism and electrolyte imbalance.
Can be seen in up to 60% of adult patients undergoing
myocardial revascularization, and it usually peaks on the
third postoperative day when inflammatory response is
greater.
 When caused by rheumatic mitral stenosis, the onset of
atrial fibrillation results in considerable worsening of
cardiac failure.

43.  Clinically the patient has a very irregular pulse, as
opposed to a basically regular pulse with an
occasional irregularity (extrasystoles) or recurring
irregular pattems.
 ECG -fine oscillations of the baseline (so called
fibrillation) and no clear P waves.
 QRS rhythm is usually 160-180min-1 but it slows with
treatment.
 ECG changes are more indicative in lead II .
 AF may be acute or recent onset (<48 hrs) and
chronic

45. Treatment-
 In the recent onset AF, initial treatment is directed
towards the control of ventricular response rate with
agents that slow AV node conduction.
 The precipitating or provoking agents should be
removed or treated first.
 Intravenous beta blockers or calcium channel
blockers produce rapid control of rate, regardless of
the level of sympathetic tone.
 However beta-blockers are preferred over calcium
channel blocker (CCB) during intraoperative period
due to shorter duration of action and lesser negative
inotropic effects.
 Amiodarone can also be effective after cardiac
surgeries
 Class Ic or III antiarhythmics can be used

46.  If haemodynamically unstable- DC cardioversion is
the most effective method of converting AF to sinus
rhythm.
 ChronicAF is often found in patients with rheumatic
heart disease undergoing cardiac surgery and may
have atrial thrombi, therefore, any attempt to restore
sinus rhythm by DC cardioversion may be associated
with increased risk of systemic or pulmonary
embolisation.
 Successful cardioversion is relatively rare in chronic
AF.
 The control of ventricular rate is the preferred
approach in these cases.

48.  The most useful drug for chronic AF is digoxin.
 The patients with chronic AF undergoing
noncardiac surgery should be evaluated for the
presence of atrial clot by echocardiogram prior to
surgery.
 In the presence of atrial clot, control of ventricular
response rate with appropriate medication is
instituted during perioperative period, if necessary.
 Statins have been tested in the preoperative
period to reduce the incidence of peri- and
postoperative AF

49.  When deciding for perioperative elective electrical
cardioversion that initially an attack dose of an
antiarhythmic agent should be administered to
minimize the recurrence of SVT after the shock.
 Adenosine is the drug of choice to treat SVTs
involving the SA or AV node (6 mg IV rapid flush,
which can be repeated as 12 mg bolus), important
especially in cases of node reentry, which is not the
main mechanisms of perioperative SVTs.

50. a.Ventricular premature beat (VPB)-
 VPB results from ectopic foci arising from below AV
node and give rise to wide (>0.12 sec) bizarre QRS
complex.
 More common in anaesthetized patients with pre
existing cardiac disease.
 New onset of VPB, may occur in the presence of
coronary artery insufficiency, myocardial infarction,
digitalis toxicity with hypokalemia and hypoxaemia.
 ECG -broad (>0.125) and bizarre QRS complex
because it arises from an abnormal (ectopic) site in
the ventricular myocardium.

53. Treatment:
 Underlying abnormalities in these patients should be
corrected immediately.
 No treatment is generally required for isolated VPB in
asymptomatic and healthy patients.
 However VPB which are multiple (>5 beats/min),
multifocal, or bigemminal or occur near the
vulnerable period of the preceding ventricular
repolarization (the so called R on T phenomenon),
associated with haemodynamic disturbance or
convert to worse arrhythmias require prompt
treatment.
 Lidocaine- initial bolus dose of 1.5mg.kg-1 followed by
infusion of 1 to 4 mg.min-1 can be given.
 Other drugs from class I, II or III are used to treat
these types of arrhythmias.

54. b.Ventricular tachycardia-
 Defined as three or more ventricular beats
occurring at a rate of 120 bpm or more lasting 30
seconds or less without hemodynamic compromise
 It may be potentially and life threatening.
 Can be divided according to their morphology
(monomorphic or polymorphic) and duration
(sustained or non-sustained).
 Main mechanism of monomorphic VT -formation of
a reentrant pathway around a tissue scar of a
healed myocardial infarction.
 In monomorphic VT the amplitude of the QRS
complex is constant,
 In polymorphic VT the morphology of the QRS
changes continuously.

55.  NSVT is a common perioperative occurrence and in
the absence of cardiac disease it does not require
treatment.
 In patients with cardiopathies this non-sustained
rhythm can predict malignant ventricular
dysrhythmias.
 The main strategy- prevention, instituting immediate
treatment when possible risk factors arise.
 A study of patients undergoing cardiac surgery
demonstrated that correction of magnesium after
ECC reduced the incidence of non-sustained VT.

56.  Examination reveals pulse rate of 120-220bpm.
 The ECG shows a rapid ventricular rhythm with
broad (often 0.14s or more), abnormal QRS
complexes.
 Dissociated P waves activity may be seen and
have no fixed relation to wide QRS complex.

59. Monomorphic
VT

60. V1
Polymorphic
VT

61. Treatment :
 May be urgent depending on the haemodynamic
situation.
 If the cardiac output and the 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-
100mg 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.

62.  Patients with recurrent episodes or unresponsive to
lidocaine,may require therapy with
 Procainamide (10-15 mg.kg-1 loading dose
followed by an infusion of 2 to 6 mg.min-1) or
 Bretylium (5 to 10 mg.min-1 over 2 to 5 min then
infusion of 1-2 mg.min-1) or
 Amiodarone in the dose of 150 mg IV over 10
minutes followed by an infusion of 1 mg.min-1 for 6
hours and 0.5 mg.min-1 thereafter.
 IV amiodarone has been shown to be as effective
as bretylium with added advantage of less
hypotension as compared to IV bretylium.

63. C.Ventricular fibrillation (VF)
 It is very rapid and irregular ventricular activation
with no mechanical effect.
 It is usually intiated from an ischaemic
myocardium or an aberrant foci (especially in
acute perioperative myocardial infarction),
ventricular tachycardia or torsades de pointes.
 On ECG, there are no defined QRS complexes,
shows shapeless rapid oscillations and on pulse
oximetry, there is acute fall in SpO2 because of low
or no cardiac output.
 Causes include myocardial ischaemia,
hypoxaemia, electrolyte imbalance and drug
effects.

65. Treatment:
 Cardiopulmonary resuscitationmust be performed
as rapidly as possible.
 Asynchronous external defibrillation should be
performed using 200-360J.
 A precordial thump is occasionally effective in
terminating VF, but should be attempted only if a
defibrillator is not available immediately.
 Intravenous bretyium5-10mg.kg-1 over 5 min can
be useful on some occasion.
 Supporting pharmacological therapy such as
lidocaine, amiodarone and procainamide are
used only to prevent recurrence of VF.

66. d. Torsades de pointes
 These arrhythmias are usually short in duration and
spontaneously revert to sinus rhythm.
 Occasionally it can change to VF.
 On ECG, it is characterized by rapid, irregular sharp
complexes that continuously change from an
upright to an inverted position.
 Between spells of tachycardia the ECG shows a
prolonged QT interval; the corrected QT is equal to
or greater than 0.44s.

67. Treatment:
1. Any electrolyte disturbance is corrected.
2. Causative drug and precipitating factors should
be stopped and removed.
3. Intravenous isoprenaline may be effective when
QT prolongation is acquired.
4. βBlockade is advised if the QT prologation is
congenital

75. Cla ss Action Exa mples Side Effects
1A Fast sodium chan nel blocker va ries
depolariza tion a nd a ction potential
dura tion
Q uinidine,
proca ina mide,
disop yra mide
Cla ss: nausea, vomiting
Q uinidine: hemolytic
a nemia, thrombo cytope nia ,
tinnitus
Procaina mide: lupus
1B Lido ca ine,
Mex iletine
Lido ca ine: dizziness,
confusion, se izures, coma
Mex iletine: tremor, a taxia,
ras h
1C Fleca inide,
Prop afen one
Fleca inide: pro-arrhythmia ,
na use a, dizzyness
2 beta-blockers SA nod e & AV node
conduction
Prop ra nolol,
metop rolol
Cla ss: CHF, b ronchospa sm,
bra dy cardia, hypo tension
3 Prolong action poten tia l by blocking
K+ cha nnels
Amioda rone,
sota lol
Amioda rone: hepa titis,
pulmonary fibrosis, thyroid
disorde rs, peripheral
neu ropa thy
So talol: bronchosp asm
4 calcium channel blockers AV node
conduction
Verapamil,
dilitiazem
Cla ss: AV block,
hypotension, bradycar dia,
constipa tion

77. Class I drugs-
 These are membrane-depressant drugs that reduce
the rate of entry of sodium into the cell.
 They may slow conduction, delay recovery or reduce
the spontaneous discharge rate of myocardial cells.
 Class Ia drugs (e.g. disopyramide) lengthen the
action potential, and
 Class Ic (flecainide, propafenone) do not affect the
duration of the action potential.
 Lidocaine- Loading dose 1mg.kg-1, repeat every
5min, continuous 30-50 μg.kg-1.min-1.
 Procainamide -20mg.min-1 IVinfusion (Max total dose
17mg.kg-1; infusion 1-4mg.min-1

78. Class II drugs-
 These antisympathetic drugs prevent the effects of
catecholamines on the action potential.
 Most are β-adrenergic antagonists. Cardioselective
β-blockers (β1) include metoprolol,atenolol, and
acebutalol.
 Propranolol -0.1mg.kg-1 by slow IV over 10min

79. 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 is also a β-blocker.
 Amiodarone -150mgIVover10min;360mg/IV over6hr
 Amiodarone also has class II (blocking adrenergic
receptors) and class IV (calcium blockers)
properties.
 Bretylium- 5mg.kg-1 IV push, repeat in 5 min at
10mg.kg-1, upto max dose of 35 mg.kg-1

80.  Class IV drugs
 The non-dihydropyridine calcium antagonists that
reduce the plateau phase of the action potential
are particularly effective at slowing conduction in
nodal tissue.
 Verapamil and diltiazem are the most important
drugs in this group

81. Adenosine-
 Adenosine is useful to classify SVTs because
tachycardia caused by atrial reentry such as AF or
flutter have transient response of decreased
frequency after adenosine, but it does not terminate
the dysrhythmia; on the other hand,
 SVTs due to reentry in the AV node ceases after
adenosine.
 Ventricular dysrhythmias do not respond to
adenosine because these dysrhythmias originate in
distal tissues of the conduction system.
 This also allows the use of adenosine to distinguish
between wide-complex SVT and VT, since adenosine
causes rapid AV block, with a half-life of 9 seconds,
and terminates most SVTs due to reentry;

82.  According to the 2005 guidelines of the American
Heart Association, it should not be used for
differential diagnosis between wide-complex SVT
and VT due to its vasodilator properties,
bronchospasm, paradoxal increase in conduction
in the accessory pathway, persistent bradycardia
or asystole, and degeneration to ventricular
fibrillation (VF).

83.  A term used to describe antiarhythmic drug-induced
dysrhythmia
 Class Ia drugs can also slow down conduction and
prolong repolarization, and may cause TdP.
 Class Ib drugs (lidocaine and mexiletine) are more
selective to abnormal or damaged myocytes and are
not associated with prodysrhythmia.
 Class Ic drugs should not be used in patients with
structural cardiomyopathies due to the high risk of
prodysrhythmia
 In patients after MI slow conduction due to class Ic
antiarhythmics leads to an increase in reentry allowing
the development of VT and, therefore, class Ic drugs
should not be used in patients with ischemia

84.  Beta blockers (class II) may be used to treat SVTs, as well
as calcium channel blockers (class IV), and they do not
have a great risk of prodysrhythmic phenomena.
 Class III agents (amiodarone, sotalol,and dofetilide)
block potassium channels prolonging repolarization,and
have the potential to induce TdP.
 Some antiarhythmic drugs such as verapamil and
amiodarone, Procainamide, sotalol, and bipyridyl can
occasionally lead to TdP, although amiodarone
prolongs the QT interval by more than 500 msecs.

85.  Drugs causing bradydysrhythmias -
βetablockers,calcium channel blockers, amiodarone,
clonidine,and dexmedetomidine.
 Inotropics -dobutamine and milrinone, may
precipitate arrhythmias and ventricular fibrillation.
 Dobutamine is directly dysrhythmogenic, causing
dose-dependent tachycardia;
 doses higher than 5 μg.kg-1.min-1 are prone to cause
dysrhythmias and generate little benefit in oxygen
transportation.
 Milrinone increases the inotropism without activating
adrenergic receptors, but it also has a dysrhythmic
potential.

86.  Digoxin increases intracellular calcium in cardiac
myocytes, slows AV node conduction, and can
increase automaticity, triggering any type of
dysrhythmia, the most common being premature
ventricular contraction, heart blocks of any degree
(although rarely Mobitz type II), paroxysmal atrial
tachycardia with heart block, accelerated junctional
rhythm, and bidirectional VT.
 Risk factors for digoxin intoxication include renal
dysfunction and electrolyte imbalance, such as
hypokalemia, hypomagnesemia, and
hypercalcemia.

87.  After the diagnosis of dysrhythmia the distinction
between benign dysrhythmia and those that carry the
risk of sudden death is fundamental.
 The choice of anesthetic agents is important to
minimize episodes of tachydysrhythmias.
 Prevention is as important as treating dysrhythmias.
 Recognition of risk factors, adequate selection of
drugs for each patient, and monitoring represent the
most important steps in prevention.
 Electrolytes should be monitored and corrected
whenever necessary.
 Supraventricular tachycardia responds to treatment
with adenosine, while AF does not, although in both
cases the frequency is controlled by beta-blockers or
calcium channel blockers

88.  Amiodarone and sotalol are class III drugs and they
prolong the action potential and repolarization, and
are currently among the most used antiarhythmics
drugs.
 Digoxin, magnesium,and adenosine have unique
antidysrhythmic properties.
 The management in perioperative dysrhythmias does
not always include the use of antiarhythmics agents,
although the use of antiarhythmic drugs should not be
delayed when indicated.