PERIOPERATIVE CARDIAC DYSRYTHMIA.ppt 222t

Symptomatic sinus bradycardia
Symptomatic sinus arrest
Suppression of ventricular ectopy resulting from bradycardia
Atrial fibrillation

1. PERIOPERATIVE PERIOPERATIVE
DYSRYTHMIADYSRYTHMIA
MONALISA DATTAMONALISA DATTA

2. INTRODUCTIONINTRODUCTION
Abnormality of cardiac rate, rhythm Abnormality of cardiac rate, rhythm
or conduction, which can either be or conduction, which can either be
lethal (sudden cardiac death), or lethal (sudden cardiac death), or
symptomatic (syncope, near symptomatic (syncope, near
syncope, dizziness, palpitation) or syncope, dizziness, palpitation) or
asymptomaticasymptomatic
DYSRHYTHMIA

3. INCIDENCEINCIDENCE
INTRA-OPERATIVE DYSRHYTHMIA AS HIGH AS 84%INTRA-OPERATIVE DYSRHYTHMIA AS HIGH AS 84%

Higher in GA than Regional Higher in GA than Regional
(66% vs 42%)(66% vs 42%)

Higher in thoracic surgery than Higher in thoracic surgery than
peripheral surgery (93% vs peripheral surgery (93% vs
56%)56%)

Higher in intubated patients Higher in intubated patients
than in non-intubated patients than in non-intubated patients
(72% vs 44%)(72% vs 44%)

4. 
SA NodeSA Node

Inter-nodal andInter-nodal and
inter-atrial pathwaysinter-atrial pathways

A-V NodeA-V Node

Bundle of HisBundle of His

Perkinje FibersPerkinje Fibers
Conduction SystemConduction System

5. PhysiologyPhysiology

The Conduct SystemThe Conduct System
most rapid conduction
Control
ventricular
response to
increased supra
ventricular rates

6. Cardiac conductive tissuesCardiac conductive tissues
Sinoatrial node :
It sits high in lateral RT atrium just below
SVC.
It is the domonant site of impulse generation
that depolarises the whole heart.
SAN is richly innervated by adrenergic and
cholinergic receptors which alter the rate of
depolarisation and thus heart rate .

7. Atrioventricular node :
Situated in RA anterior to the opening of
coronary sinus an directly above the insertion
of septal leaflet of tricuspid valve. It is the only
electrical connection to the ventricle via the
Bundle of His. Like SAN it is also densely
innervated with autonomic fibers

8. His - Purkinjee system :
Originates from AVN to enter upper part of the
interventricular septum where it splits into RT
and LT branch. The RT bundle continues up to the apex of
RV and the base of the ant. Papillary muscle . The LT
divides further into ant. and post. fascicles . The terminal
Purkinjee fibers form interweaving network on the
endocardial surface so that a cardiac impulse is
transmitted almost simultaneously to the entire RT and LT
ventricles

9. Luo-Rudy Model of the Cardiac MyocyteLuo-Rudy Model of the Cardiac Myocyte

Cardiac ventricular myocytes are actually Cardiac ventricular myocytes are actually
composed of many different ion channels and composed of many different ion channels and
pumps whose expression varies in different pumps whose expression varies in different
regions of the heartregions of the heart

10. Physiology of cardiac action potentialPhysiology of cardiac action potential
The resting cardiac myocyte is electrically negative with
transmembrane voltage-80 to -95 mV
The negativity is maintained by the energy consuming Na/K
pump which transports three Na
+
ions out of the cell for two
K
+
ions inward.
When an impulse reaches cardiac myocyte the negativity is
decreased to -60 mV when an action potential is generated. It
has five parts.

12. Cardiac action potential Cardiac action potential (contd…)(contd…)

13. Cardiac action potential (contd…)
Automaticity: Automaticity:
ThThis is the ability of the cardiac is the ability of the cardiac cells to to
depolarise spontaneously. It is caused by depolarise spontaneously. It is caused by
the inward flow of the cations during diastole at the inward flow of the cations during diastole at
potentials more negative than -60mV. In SAN the potentials more negative than -60mV. In SAN the
slow influx of Caslow influx of Ca
++++
allows it to depolarise more allows it to depolarise more
rapidly and therefore it suppresses the automaticity rapidly and therefore it suppresses the automaticity
of other potential pace maker sites.of other potential pace maker sites.

14. Electrical Activity in the Normal Heart Electrical Activity in the Normal Heart (from Katzung)(from Katzung)

The different action potentials in different regions of the heart The different action potentials in different regions of the heart
reflect differential expression of ion channels, particularly Nareflect differential expression of ion channels, particularly Na
++

channelschannels

This leads to differential sensitivity to antiarrhythmic drugsThis leads to differential sensitivity to antiarrhythmic drugs

15. PhysiologyPhysiology

The Action PotentialThe Action Potential

16. PhysiologyPhysiology

The Action PotentialThe Action Potential

Spontaneous diastolic depolarizationSpontaneous diastolic depolarization

Resting potential not stable in conductive tissue cellResting potential not stable in conductive tissue cell

Slow spontaneous depolarization until the threshold Slow spontaneous depolarization until the threshold
potential is reachedpotential is reached
Slope is controlled by ANS

17. How to diagnose arrhythmia ?How to diagnose arrhythmia ?
11. . Is the rate slow (<60 bpm) or fast (>100 bpm)?Is the rate slow (<60 bpm) or fast (>100 bpm)?
Slow  Suggests sinus bradycardia, sinus arrest, or
conduction block
Fast  Suggests increased/abnormal automaticity or reentry
2. 2. Is the rhythm irregular?Is the rhythm irregular?
Irregular  Suggests atrial fibrillation, 2
nd
degree AV block,
multifocal atrial tachycardia, or atrial flutter with
variable AV block
3. Is the QRS complex narrow or wide?3. Is the QRS complex narrow or wide?
Narrow  Rhythm must originate from the AV node or
above
Wide  Rhythm may originate from anywhere

18. 4. Are there P waves?4. Are there P waves?
Absent P waves  Suggests atrial fibrillation, ventricular
tachycardia, or rhythms originating from the AV node

5. What is the relationship between the P waves and QRS 5. What is the relationship between the P waves and QRS
complexes?complexes?
More P waves than QRS complexes  Suggests 2
nd
or 3
rd

degree AV block
More QRS complexes than P waves  Suggests an
accelerated junctional or ventricular rhythm
6. Is the onset/termination of the rhythm abrupt or gradual?6. Is the onset/termination of the rhythm abrupt or gradual?
Abrupt  Suggests reentrant rhythm
Gradual  Suggests altered automaticity

19. Arrhythmogenic MechanismsArrhythmogenic Mechanisms

Enhanced automaticityEnhanced automaticity

Can occur in cells with spontaneous pacemaker activity Can occur in cells with spontaneous pacemaker activity
(diastolic depolarization) or cells that normally lack (diastolic depolarization) or cells that normally lack
pacemaker activity (ventricular cells)pacemaker activity (ventricular cells)

Afterdepolarizations and triggered automaticityAfterdepolarizations and triggered automaticity

Normal depolarizations can trigger automaticityNormal depolarizations can trigger automaticity

Delayed afterdepolarizations (DADs) are associated Delayed afterdepolarizations (DADs) are associated
with calcium overloadwith calcium overload

Early afterdepolarizations (EADs) are typically Early afterdepolarizations (EADs) are typically
associated with potassium channel block and can lead associated with potassium channel block and can lead
to torsades de pointesto torsades de pointes

ReentryReentry

The most common cause of arrhythmiasThe most common cause of arrhythmias

Can occur in any region of the heart where there is a Can occur in any region of the heart where there is a
region of non-conducting tissue and heterogeneous region of non-conducting tissue and heterogeneous
conduction around that regionconduction around that region

20. Automaticity: Mechanisms for Slowing Pacemaker RateAutomaticity: Mechanisms for Slowing Pacemaker Rate
-Adrenergic blockers
Na
+
and Ca
++
channel blockers
Adenosine and muscarinic
blockers
K
+
channel blockers
Drugs that Inhibit Automaticity

21. AFTERDEPOLARIZATIONS AND TRIGGERED AFTERDEPOLARIZATIONS AND TRIGGERED
AUTOMATICITYAUTOMATICITY

DADs arise from the resting potential and result from DADs arise from the resting potential and result from
calcium overloadcalcium overload

EADs arise from phase 3 (repolarization phase) and result EADs arise from phase 3 (repolarization phase) and result
from prolonging action potential duration (typically from from prolonging action potential duration (typically from
KK
++
channel block) channel block)

22. ReentryReentry

The most common cause of arrhythmiasThe most common cause of arrhythmias

Can occur in any region of the heart where there is a Can occur in any region of the heart where there is a
region of non-conducting tissue and heterogeneous region of non-conducting tissue and heterogeneous
conduction around that regionconduction around that region

Anatomically defined reentry refers to reentry that Anatomically defined reentry refers to reentry that
involves impulse propagation by more than one involves impulse propagation by more than one
anatomical pathway between two points in the heartanatomical pathway between two points in the heart

Wolff-Parkinson-White syndromeWolff-Parkinson-White syndrome

Atrial flutterAtrial flutter

Paroxysmal supraventricular tachycardiaParoxysmal supraventricular tachycardia

AV reentry and AV nodal reentryAV reentry and AV nodal reentry

Functionally defined reentry can occur in the absence of Functionally defined reentry can occur in the absence of
anatomically defined pathwaysanatomically defined pathways

Atrial and ventricular fibrillationAtrial and ventricular fibrillation

Torsades de pointesTorsades de pointes

23. Reentrant Mechanisms: AV Nodal ReentryReentrant Mechanisms: AV Nodal Reentry

In the Common Mode of AV Nodal In the Common Mode of AV Nodal
reentry, the anterograde impulse is slowed reentry, the anterograde impulse is slowed
as it passes through the AV nodeas it passes through the AV node

The retrograde pathway of the reentrant The retrograde pathway of the reentrant
circuit is fast.circuit is fast.

In the Uncommon Mode of AV Nodal In the Uncommon Mode of AV Nodal
reentry, the anterograde impulse is fast as it reentry, the anterograde impulse is fast as it
passes through the AV nodepasses through the AV node

The retrograde pathway of the reentrant The retrograde pathway of the reentrant
circuit is slowed.circuit is slowed.

24. CONTRIBUTARYCONTRIBUTARY
FACTORSFACTORS
Patient-related:
•Pre-existing
cardiac disease
•CNS disease
• Old age
Anaesthesia-related:
•Tracheal intubation
•GA
• LA
• Electrolyte
abnormality
• ABG abnormality
•Central venous
canulation
Surgery related:
•Cardiac surgery
•Non-cardiac surgery

25. CLASSIFICATION OF CLASSIFICATION OF
ARRHYTHMIASARRHYTHMIAS
BRADY-
ARRHYTHMIA
TACHY-
ARRHYTHMIA
i. Sinus Bradycardia
ii. Various forms of heart block
a. First degree
b. Second degree
c. Third degree
d. complete
i. Narrow QRS
complex (SVT)
tachycardias (QRS
<0.12 second)
ii. Wide QRS
complex
tachycardias (QRS >
0.12 second)
a. Sinus tachycardia
b. Atrial premature beat
c. Atrial tachycardia
d. Atrial flutter
e. Atrial fibrillation
a.VPB / Ventricular
extrasystole
b. VT
c. VF
d. Torsades de pointes

26. B
R
A
D
Y
D
Y
S
R
H
Y
T
H
M
I
A

27. Normal Sinus Rhythm:Normal Sinus Rhythm:
Implies normal sequence of conduction, originating in the sinus node and proceeding to
the ventricles via the AV node and His-Purkinje system.
Characteristics: Regular narrow-complex rhythm
Rate 60-100 bpm
Each QRS complex is proceeded by a P wave
P wave is upright in lead II & downgoing in lead
aVR

28. Sinus arrhythmia :
 Irregular spacing of normal complexes associated with
respiration
 Constant PR interval with beat to beat change in RR interval
 Normal finding in young people

29. Sinus tachycardia :
Rate >100 bpm with normal PQRST complexes
Causes :
Inadequate depth of anaesthesia, pain/surgical stimulation
Fever/sepsis, hypovolemia, anemia, heart failure, thyrotoxicosis
Drugs : atropine, ketamine, catecholamines
Rx : correct underlying causes,  blockers if tachycardia causes myocardial
ischemia( except in HF or bronchial asthma)

30. Sinus bradycardia :
Rate <60 bpm, in patients receiving  blocker <50 bpm
Causes :
Normal in athletes, may be due to vagal stimulation
Drugs :  blockers, digoxin, anticholinesterase, halothane,
suxamethonium, Ca channel blockers, clonidine, morphine
Myocardial Infarction, Sick Sinus Syndrome, HS carotid
Raised ICP, hypothyroidism, hypothermia, cholestatic jaundice

31. Sinus bradycardia :
(Management)
If hypotensive or
presyncopal :
Treatment of underlying
precipitating cause
Atropine
Isoprenaline
Temporary pacing
Long term treatment :
Permanent pacing if
not corrected after
removing underlying
cause. In episodic
bradycardia consider
Holter monitoring. If
R-R interval >2.5 sec
may require PPI

33. B
R
A
D
Y
D
Y
S
R
H
Y
T
H
M
I
A

34. Atrial ectopics:Atrial ectopics:
Common and benign. May occur normally. Other causes
Ischemia/ hypoxia
Light anaesthesia, sepsis, shock
Anaesthetic drugs, triggers (nicotin, caffiene, alcohol)
Valvular heart disease
Rx : Treatment of underlying cause, otherwise observe
for atrial tachycardia

35. 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
1.Normal sinus beat passing around and through scar
2.Ectopic beat passing around but blocked through scar
3.Re-entry circuit of tachycardia

36. Re-entry arrhythmias: contd…

The classical example of re entry arrhythmia is The classical example of re entry arrhythmia is Wolff- Parkinson- White Wolff- Parkinson- White
syndromesyndrome, where an accessory conduction pathway ( , where an accessory conduction pathway ( Kent fibersKent fibers) is ) is
present between atria and ventricles . 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 Other re-entry circuits occur with supraventricular tachycardia atrial
flutter, atrial fibrillation, venticular tachycardia.flutter, atrial fibrillation, venticular tachycardia.
Wolff- Parkinson- White Syndrome :

37. Re-entry arrhythmias: contd…
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
Junctional/AV Nodal/Supraventricular tachycardia

38. 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

39. Due to ectopic focus atria contracts> 150 bpm
Typical saw tooth pattern with no flat baseline between P waves
Varied degree of AV block e.g. 2:1,3:1 etc persists.
Risk of thromboembolism

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
Atrial flutter/ atrial tachycardia:

40. Uncoordinated atrial activity with 600-800 bpm atrial rate with irregularly irregular
ventricular rate dependent on AV node transmission , commonly 120-180 bpm.
Presence of “fibrillatory” wave, absence of P wave.
Causes: Hypertension, myocardial ischemia
Pericarditis, mediastinitis, thoracic surgery
Mitral valve disease
Electrolyte disturbances
Sepsis, thyrotoxicosis, binge drinking of alcohol


Atrial fibrillation:

41. Side effects : 1. : 1. Reduction in ventricular filling and cardiac output
2. 2. Ischemia due to high ventricular rate and diastolic
shortening
3. 3. Risk of thromboembolism. The risk is higher if there is a
return to sinus rhythm >48 hrs after AF .

Management : Management : Correction of precipitating cause especially sepsis,
electrolyte disturbance
Onset <48 hrs
Synchronised DC cardioversionat 200 then 360j
Flecainide is best for converting to sinus rhythm in absence of LV dysfunction
and ventricular arrhythmia
Atrial fibrillation: contd....

42. 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

Atrial fibrillation: contd…

43. T
A
C
H
Y
D
Y
S
R
H
Y
T
H
M
I
A

45. Classification:Classification: contd…
Broad complex arrhythmias :
Ventricular ectopics
Ventricular tachycardia
SVT with aberrant conduction
Ventricular fibrillation

46. Ventricular ectopics:
Paired PVCs/ couplets
Multiform PVCs
Potentially dangerous ventricular ectopics

47. Ventricular ectopics: contd…
Ventricular bigeminy
R on T phenomenon

48. Ventricular ectopics: contd…
In absence of structural heart disease usually benign
May be provoked by hypokalemia, dental procedures, anal stretch
In combination with halothane, raised EtCO
2 , light plane of anaesthesia
Potentially dangerous variety of PVCs herald onset of ventricular tachycardia or
fibrillation.
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.

49. Ventricular tachycardia:
Focus in the ventricular muscle depolarises at high frequencies resultingin
tachycardia with wide QRS which may vary in shape.
Serious, potentially life threatening arrhythmia .
Caused by reentry, commonly triggered by M I, myocardial ischemia,
hypoxia, hypotension, fluid overload, electrolyte imbalance ( low K
+
,
Mg
++
), injection of adrenaline or other catecholamines.

50. Ventricular tachycardia: contd…

Polymorphic wide QRS ventricular tachycardia with a phasic variation in electrical Polymorphic wide QRS ventricular tachycardia with a phasic variation in electrical
polarity.polarity.

Associated with electrolte imbalance( hypokalemia, hypocalcemia, hypomagnesimia)Associated with electrolte imbalance( hypokalemia, hypocalcemia, hypomagnesimia)
Torsades de pointes

51. Ventricular tachycardia: contd…
For pulseless VT immediate defibrillation
For unstable patient withpulse 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
Correction of electrolyte imbalances
Implantable Cardioverter Defibrillator (ICD)
Management:

52. SVT with aberrant conduction:

Though supraventricular in origin may have wide QRS due to aberrant Though supraventricular in origin may have wide QRS due to aberrant
conduction between atria and ventricles or bundle branch block.conduction between atria and ventricles or bundle branch block.
Adenosine may be used diagnostically to slow AV conduction to reveal
underlying rhythm which is converted to sinus rhythm in this case
Unless proved otherwise all broad complex tachyarrhythmias should
be treated as VT.

53. Ventricular fibrillation :
Coarse
Fine
 Chaotic, disorganized contraction of ventricular muscle and no QRS complexes
can be identified on ECG
 Immediate defibrillation as per resuscitation protocol (200-200-360 j)

54. Antiarrhythmic drugs :
Drugs IndicationIndication Special considerations
Class IA
Disopyramide
Procainamide
Quinidine
AF
VT
A flutter
PAT
Check apical pulse, if noted
extremes---- withhold
 with caution in reactive airway ds
Monitor widening QRS, prolonged
QT
Class IB
Lidocaine
Mexlitine
Tocainide
VT
VF
Potentiates effects of other
antiarrhythmics
Class IC
Flecainide
Moricizine
Propafenone
VT
VF
SVT
Correct electrolyte imbalance
Monitor QRS widening, prolonged
QT

55. Drugs
Indication
Special considerations
Class II
Beta blockers
AF
A flutter
PAT
MonitorHR and BP
Abrupt stoppage exacerbate angina
and precipitate MI
Monitor PR
Cautious in reactive airway ds
May mask features of shock and
hypoglycemia
Class III
Amiodarone
Dofetilide
Ibutilide
Sotalol
Life
threateningar
rhythmias
resistant to
other drug
BP, HR, rhythm
Amiodarone increases digoxine
toxicity
Signs of pulmonary toxicities
Prolonged QT with sotalol,
dofetilide, ibutilide
Class IV
Diltiazem
Verapamil
SVT
Monitor HR, rhythm, BP when
initiating and increasing
Calcium supplements reduce
effectiveness

56. Drugs
Indication
Special considerations
Class V
Adenosine
PSVT
Short acting
Saline flush following i.v. use
Record rhythm strip
Atropine Symptomatic
SB
AV block
Asystole
PEA
Monitor HR ,rhythm
Cautious in IHD
Paradoxical slowering in dose
<0.5mg
Epinephrine
Pulseless
VT,VF
Asystole
PEA
Monitor HR ,rhythm
Cautious in IHD
I.V. in large vein
Vasopressin
VF unresponsive
to defib
•Monitor HR ,rhythm
•Cautious in IHD
•Hypersensitivity reaction

57. ANTI-ARRHYTHMIC AGENTSANTI-ARRHYTHMIC AGENTS

58. Heart block:Heart block:
Prolongation of the PR interval, which is constant. All P waves are
conducted
1st Degree AV Block

59. Heart block: Heart block: contd…contd…
Progressive prolongation of the PR
interval until a P wave is not
conducted.
As the PR interval prolongs, the RR
interval actually shortens
Constant PR interval with
intermittent failure to conduct
2nd Degree AV Block
Type 1 (Wenckebach)
Type 2

60. Heart block: Heart block: contd…contd…
No relationship between P waves and QRS complexes
Relatively constant PP intervals and RR intervals
Greater number of P waves than QRS complexes
3rd Degree (Complete) AV Block

61. Bundle Branch Block :Bundle Branch Block :
RV depolarization is delayed
giving RSR pattern in V1 and
prominent S in lead1 and V6
Normal variant,ASD, PE,Cor
Pulmonale
RBBB

62. Bundle branch block cont.Bundle branch block cont.
LV depolalarization delayed
giving notched R in lead1 and
V6 and M pattern in V1
Blocks confined to ant. or post.
fascicles gives LAD or RAD
respectively
LBBB

63. Bundle Branch Block Cont. Bundle Branch Block Cont.
Bifasicular Block=RBBB+LAHB(LAD)
=RBBB+LPHB(RAD)
=LBBB
Trifasicular block =Bifasicularblock +
1
st
degree AV Block

64. SUMMARYSUMMARY
Therapeutic decisions in patients with cardiac dysrhythmias are based
on an assessment of the haemodynamic impact of the rhythm
disturbance, the patient’s underlying cardiac function, contributing
factors and the correct diagnosis of the arrhythmia.
 Symptomatic bradyarrhythmia can be treated initially with atropine;
pacing, either external or transvenous, is the definitive therapy of
choice.
Adenosine is the drug of first choice in treating patients with PSVT
(AV-nodal reentry)
In non-reentrant SVT, 12-lead ECG should first be searched to
define the mechanismof the arrhythmia. Other pharmacologic
options diltiazem and verapamil, β-blocking drugs, and amiodarone
and digoxin.
Cardioversion should be considered if drug use is contraindicated or
if the arrhythmia is not controlled with drug therapy

65. SUMMARYSUMMARY
Ventricular tachycardia can be monomorphic or polymorphic.
When PVT is accompanied by prolonged repolarization,
manifested as QT-interval lengthening on the ECG before or
after episodes of tachycardia, the tachycardia is torsades de
pointes, and its presence mandates specific diagnostic and
therapeutic considerations.
If the origin of a wide-QRS tachycardia cannot be confirmed
clinically or electrocardiographically, amiodarone or
procainamide, should be used. In all situations, emergency
cardioversion takes precedence if haemodynamic compromise is
present or develops during drug therapy
Pulseless VT and VF are forms of ventricular tachyarrhythmia
that require cardiac arrest therapy with defibrillation and drug :
smost importantly epinephrine, for maintenance of myocardial
and cerebral blood flow during external chest compression or
open-chest cardiac massage.

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67. THANK YOU…...