ACLS Arrhythmias & Defibrillation

7/27/2019 ACLS Arrhythmias & Defibrillation

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SARAWAK GENERAL HOSPITAL


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Conduction System

SA Node

AV node

His bundle

Right bundle branch

Left bundle branch

Anterior fascicle

Posterior fascicle

Purkinje fibers


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1

2

3

4

5

5

6


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Physiology of Action Potential An electrical impulse precedes each

heartbeat (mechanical contraction). Each heart muscle cell is stimulated to

contract by electrical process called actionpotential. (composed of five phases) The ECG records the summation of action

potential of the muscle cells in the atria

and ventricles. i.e records only theelectrical event Echocardiogram records the mechanical

contraction from the electrical event


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Action Potential

Electrical Activity

Mechanical Activity

Muscle Cells

ECG Tracing

Cardiac Muscle


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Causes Three mechanisms:

(1) Disturbances in AUTOMATICITY

speeding up (tachycardia),

slowing down (bradycardia), abnormal depolarization (ectopic or escape beat)

May involve

SA node atrium

AV node

ventricles


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Causes

(2) Disturbances in CONDUCTION

Either too rapid (WPW syndrome) or

Too slow ( AV heart block)

(3) Combination of altered

automaticity and conduction


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Normal Pacemaker Rate

SA NODE

RATE 60-100AV JUNCTION

RATE 40-60

VENTRICLES

RATE 15-40


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NORMAL SINUSRHYTHM

Pacemaker impulses are

initiated in the sinoatrial (SA) node,

through atrial pathways,

delayed at atrioventricular (AV) node.

down the bundle branches to Purkinje

fibers in the ventricles

Atrial depolarization P wave.

Ventricular depolarization QRS


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Normal Sinus Rhythm

Sinus Arrhythmias

Sinus Tachycardia

Sinus Bradycardia

Sinus Rhythm & its variants


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NORMAL SINUSRHYTHM

CHARACTERISTICS

The P wave is usually upright in leads II, III, aVF,

and V1. Its morphology remains constant at all times.

P-P and R-R intervals are equal and regular.

Atrial and ventricular rates are identical range between 60 and 100 bpm.

There is no ectopic activity.


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SINUS ARRHYTHMIA

(SINUSDYSRHYTHMIA)

a sinus rhythm with a rate that varies with

respiration (respiratory sinus arrhythmia)

characterized by alternate speeding up andslowing down of the heart rate

usually benign

Rarely non respiratory sinus arrhythmia


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SINUS ARRHYTHMIA

(SINUSDYSRHYTHMIA)

In respiratory sinus arrhythmia,

the rate increases with inspiration &

decreases with expiration.

In non respiratory sinus arrhythmia,

the irregularity of the rhythm, not

correlated with the respiratory cycle.


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SINUS ARRHYTHMIA (SINUS

DYSRHYTHMIA)ETIOLOGY

Respiratory sinus arrhythmia

Normal in children and young adults.

Non respiratory sinus arrhythmia may be

with cardiac disease and

MI esp with sinus bradycardia,digoxin therapy

enhanced vagal tone.


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ExpirationInspiration


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SINUS TACHYCARDIAsinus rhythm at a rate 100 bpm.

ETIOLOGY

1. increased physiologic demand for oxygen

(stress, exercise, pain, excessive caffeine)2. Hyperthyroidism, heart failure, myocardial

infarction, pulmonary embolism, medications(e.g., atropine, epinephrine, isoproterenol), fever,anemia, hypoxia, and shock

3. Physiologic ST commonly observed in neonates(HR may btw 100 - 160 bpm)


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SINUS TACHYCARDIA

CHARACTERISTICS

same characteristics as NSR

except the ventricular rate 100 bpm

gradual acceleration of sinus node discharge


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Sinus Bradycardia

Characteristics

same as for NSR,except the ventricular rate 60bpm


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Sinus BradycardiaEtiology

1. physiologic causes (athletes, sleep)

2. Vagal stimulation

3. Sick sinus syndrome4. hypothyroidism, hypothermia, electrolyte

imbalances (e.g., hyperkalemia), Inferiormyocardial infarction

5. medications (e.g., blk, ca2+ channel blk,digoxin)


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Atrial Premature Complexes

Atrial Tachycardia

Multifoci Atrial Tachycardia Paroxymal Supraventriculat Tachycardia

Atrial Flutter

Atrial Fibrillation Junctional Premature Complexes

Supraventricular Arrhythmias


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ATRIAL PREMATURE COMPLEXES

(APC)DEFINITION

results from apremature supraventrictilar

impulse that originates somewhere in theatria outside of sinoatrial (SA) node.

also called atrial ectopic complexes


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ATRIAL PREMATURE

COMPLEXESCHARACTERISTICS

1. R-R interval is irregular. The premature complexdisturbs the regularity of the underlying rhythm

2. The morphology of the ectopic/premature Pwave is different from the sinus P wave.

3. The premature P wave is followed by a QRS

complex if the impulse conducted into theventricles.


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ATRIAL PREMATURE

COMPLEXES1. QRS complex is narrow if conduction in the

ventricles is disturbed.

2. If the AV node conducts a premature impulseinto the ventricle when they have not fully

repolarized, the resulting QRS complex may

appear wide and abnormally shaped.

3. This is known as an APC conducted withaberration and must be differentiated from a

ventricular premature complex


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Clinical tips

The best leads for assessment of atrial

rhythm disturbances are

II, III, aVF, and V1,

P waves are usually most prominent in these

leads.


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WANDERING ATRIAL

PACEMAKERDEFINITION

a supraventricular rhythm in which

pacemaker impulses originate from 2

sites in the SA node, atria, or AV junction

discharge at a rate of 60 to 100 beats per

minute


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WANDERING ATRIAL

PACEMAKERCHARACTERISTICS1. P wave morphologies vary because impulses

originate from different sites.

2. P-P intervals (and subsequent R-R intervals) mayalso vary because each impulse travels throughthe atria via a slightly different route.

3. One P wave for every QRS complex.

4. Overall atrial and ventrictilar rates remain

between 60 and 100 bpm.5. QRS complexes are usually unchanged. They are

narrow as long as ventricular depolarization isundisturbed.


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MULTIFOCAL ATRIALTACHYCARDIA

DEFINITION

Multifocal atrial tachycardia (MAT) is an

ectopic supraventricular tachycardia originates from three or more atrial foci

rate of 100 to 250 bpm.


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MULTIFOCAL ATRIALTACHYCARDIA

CHARACTERISTICS

1. Three or more P wave morphologies

(multiple foci)

2. One P wave for every QRS complex

(1: 1 conduction)3. Irregular rhythm; varying P-P and R-R intervals

4. PR intervals varying slightly from beat to beat

5. QRS complexes possibly identical to each otheror slightly widened secondary to aberrantintraventricular conduction

6. Rate than 100 bpm


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ATRIAL TACHYCARDIA

DEFINITION

a supraventrictilar rhythm originating

outside of the SA node

rate between 120 and 250 bpm.

frequently a result of digitalis toxicity.


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ATRIAL TACHYCARDIA

CHARACTERISTICS

rhythm is regular(R-R intervals are equal)

atrial rate is 120 to 250 bpm. P-P intervals are equal

Conduction is commonly 1:1 (one P wave forevery QRS complex).

Conduction may be 2: 1 or greater especially inthe presence of digitalis toxicity.

(atrial tachycardia with AV block)


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ATRIAL TACHYCARDIA

PR interval is short when conduction through theAV node is 1: 1.

P wave morphology is often different from NSR

shape of the QRS is unchanged from NSR unlessconduction in the ventricles is disturbed.

Atrial tachycardia may occur in paroxysms;

when it terminates, there may be a long pausebefore NSR resumes.


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PAROXYSMAL SUPRAVENTRICULAR

TACHYCARDIA (PSVT)

DEFINITION

supraventricular impulses are conductedabnormally between atria and ventricles.

ventricles are depolarized 100 bpm.


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ETIOLOGY1. AV nodal reentry tachycardia (AVNRT)

Micro reentry circuit

A supraventricular impulse is conducted slowly

down one pathway in the AV node toward the

ventricles and is then conducted rapidly back

into the atria along a secondpathway within the

AV node.

The atria and ventricles are depolarized almost

simultaneously.

60-70% of PSVT


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ETIOLOGY2. Atrioventricular Reentrant Tachycardia

(AVRT) Uses a macro reentry circuit, such as bundle of

Kent, that bypasses the AV node to form anaccessory bridge from the atria to the ventricles

Most well known Wolff-Parkinson-White(WPW) syndrome

Manifest AP

Concealed AP

Less common form of PSVT

The atria and ventricles are depolarizedsequentially.

As with AVNRT, the cycle in AVRTperpetuates itself as the impulse repeatedlytravels the same route.


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ATRIAL FLUTTER

DEFINITION

a supraventricular dysrhythmia

characterized by the appearance of sawtooth-shaped flutter waves

rate between 250 and 350 bpm.

associated with a reentry mechanismwithin the atria esp around the pulmonaryveins


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CHARACTERISTICS1. P waves are absent.

2. flutter (F) waves represent abnormaldepolarization of the atria.

1. They assumed a saw tooth that is

2. most easily seen in leads II, III, and aVF, and V1.

3. The flutter waves appear contiguously with noisoelectric baseline visible.

Some flutter waves may be obscured by theQRS complex.

1. atrial rate (flutter rate) ranges btw 250 - 350 bpm(average is 300bpm).

2. The ventricular rate is usually slower than the

atrial rate


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CLINICAL TIP Flutter waves may be difficult to identify if 2:1 conduction Vent rate of 150 bpm

Vagal maneuvers like carotid sinus massage or drugs toincrease block at the AV node

slowing the ventricular resp enough to unmask hidden flutter waves.

Atril flutter must be differentiated from atrial tachycardiaby closely examine the P wave.

In atrial flutter, F waves is contiguous

In atrial tachycardia, ectopic P waves are separated by anisoelectric baseline.


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ATRIAL FIBRILLATION

DEFINITION

A supraventricular dysrhythmia

characterized bv multiple ectopic atrial foci,uncoordinated atrial contractions, and aclassically irregular ventricular rate.

May occur intermittently, (paroxysmal atrialfibrillation), but it frequently becomes achronic condition.


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CHARACTERISTICS

1. There are no P waves.2. fibrillatory (f) waves arise within the atria. small,

poorly defined, and distort the baseline, may be fine orcoarse in appearance.

3. R-R intervals are irregularbecause conduction throughthe AV node is highly variable.

4. QRS complexes are usually narrow unless conduction inthe ventricles is abnormal. As impulses are conductedirregularly through the AV node with some of these

impulses aberrantly conducted thru the ventricular5. Ashman's phenomenon (characterized by wide QRS

complexes that can easily be mistaken for (VPCs).


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JUNCTIONAL PREMATURE COMPLEXES

DEFINITION

a premature (ectopic) supraventricular

impulse that originates from the area

in and around the AV junction.

is also known as a premature

junctional complex (PJC).


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AV NODAL

EXTRASYSYTOLES

Conduction

1. Retrogadely to the

Atria and

2. Antegradely to theventricle

Antegrade conduction

To ventricle only

(retrograde conductionis blocked)


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CHARACTERISTICS R-R interval is irregular. The premature

complex disturbs the regularity of theunderlying rhythm.

A visible P wave may or may not be associatedwith a premature QRS complex

If the P wave is visible, commonly occurs eitherjust before or just after the QRS complex

usually inverted in II, III, aVF


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JUNCTIONAL PREMATURE

COMPLEXES

An inverted P wave implies that the ectopic impulsefrom the AV junction was conducted retrogradely(backward) into the atria.

If the P wave appears before the QRS complex, theatria were depolarized before the ventricles.

If the P wave occurs immediately after the QRScomplex, the atria were depolarized after theventricles.

If the P wave is buried in the QRS complex, it isassumed that the atria and ventricles weredepolarized simultaneously)


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JUNCTIONAL EXCAPE

RHYTHMDEFINITION

A passive escape rhythm that originates in

the AV junction and usually appearssecondary to depression of the higher sinus

pacemaker.


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CHARACTERISTICS1. The ventricular rate is between 40 and 60 bpm

2. The R-R interval is regular.

3. There is one P wave for every QRS complex (1: 1conduction). The P wave may appearbefore the QRSorafterthe QRS, or it may beburied within the QRS

complex.4. The P wave is usually inverted in the inferior leads (II,

III, aVF).

5. If the ectopic P wave precedes the QRS complex, theresultant PR interval is abnormally short-often less

than 0. 1 2 second.6. The QRS complex is narrow as long as intraventricular

conduction is undisturbed.


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ACCELERATED JUNCTIONAL

RHYTHM AND JUNCTIONAL

TACHYCARDIA

DEFINITION

Represent supraventricular dysrhythmias

arising from the AV junction at ratesexceeding the inherent junctional escape

rate of 40 to 60 bpm.


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CHARACTERISTICS

All the characteristics described for junctionalescape rhythm apply, except for ventricularrate.

In accelerated junctional rhythm theventricular rate is between 60 and 100 bpm.

Injunctional tachycardia the ventricular rate is

100 bpm or faster.


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Is there a normal looking QRS

complex ? If there is a abnormal looking QRS complex

considerVentricular arrhythmias.

If there is no QRS complexes at all,considerAsystole


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Ventricular Arrhythmias

VENTRICULAR PREMATURE BEAT (VPB)

VENTRICULAR ESCAPE COMPLEXES

VENTRICULAR TACHYCARDIA (VT)

TORSADE DE POINTES

ACCELERATED IDIOVENTRICULAR

RHYTHM

VENTRICULAR FIBRILLATION (VF)


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VENTRICULAR PREMATURE BEATS

early occurring widened QRS complexes

microreentry at the level of the Purkinje fiber

bizarre morphology QRS complex of a VPB is widened, bizarre, and often

notched, with a QRS duration >0.16 seconds

It may have a morphology which resembles a right or

left bundle branch block depending upon the location oforigin.


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Unifocal VPBs

all have a single morphology;

the interval between the VPB and the preceding sinus

beat is usually identical (fixed coupling cycle).

Multifocal VPBs

multiple different QRS morphologies

caused by various different reentrant circuits

varying coupling cycles between the sinus beat and theVPB.

In general there is no P wave identified before apremature QRS complex.


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A full compensatory pause usually follows theVPB;

interval between the QRS complexes before andafter the premature beat is 2X the interval btw twosuccessive sinus beats.

On occasion, the VPB may be interpolated,

ie, it occurs between two normal sinus QRScomplexes and does not alter the underlying sinusor ventricular rate.

Other findings on the ECG include markedrepolarization abnormalities, manifested as STsegment and T wave abnormalities.


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Ventricular bigeminy

ventricular premature beat follows each sinus

beat often becomes self perpetuating, asituation known as the rule of bigeminy. This

occurs because the long cycle length tends to

precipitate a VPB.


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Ventricular trigeminy

two sinus beats are followed by the ventricular

premature beat. Thus, every third beat is aventricular premature beat (show ECG 3).


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Ventricular couplets

two VPBs in a row (show ECG 4)

there is often a compensatory pause after the secondpremature beat

the two premature beats may have an identicalmorphology (unifocal couplet), or their morphologymay differ (multifocal couplet)

the RR interval between the two successive VPBs varies

widely.


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Interpolated VPBs

VPB may be interpolated between two successive sinusbeats without altering the underlying sinus RR interval(show ECG 5).


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VENTRICULAR ESCAPE


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VENTRICULAR ESCAPE

COMPLEXES OR RHYTHM when there is failure of the sinus and AV node togenerate an impulse

absence of P wave activity

associated with a widened QRS complex thatresembles a VPB and occurs after a pause ofvariable duration (but always greater than thenormal sinus RR interval)

persistence of this activity leads to multiplesuccessive ventricular complexes representing anescape ventricular rhythm with a rate that isslower than the normal sinus rhythm


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VENTRICULAR TACHYCARDIA

is defined as three or more successive ventricularcomplexes.

non sustained VT is a series of repetitive

ventricular beats which have a duration of lessthan 30 seconds; sustained VT lasts for more than30 seconds.

the rate of VT is generally greater than 100 beats

per minute, but may vary widely

the rhythm is usually regular, although there maybe slight irregularity of the RR intervals.


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features of ventricular tachycardia include:

abnormal morphology of the QRS complex, the QRS

axis is typically shifted (often to the left), the width of

the QRS complex is generally >0.16 sec.

positive or negative concordance of the QRS complex

across the precordial leads (eg, R waves or S waves

only)

a monophasic Rr' pattern in lead 1 (termed rabbit ears)with a taller left ear.

an indeterminate axis (between -90 and -180)


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Monomorphic VT

all QRS complexes of an episode are identical

often displays subtle changes of the QRScomplexes with regard to

morphology and

width


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Polymorphic VT

QRS complexes within each episode displaymarkedly different morphologies

the RR intervals may be grossly irregular(showECG 9).

The differences in QRS morphology result

from changes in the direction (vector) ofmyocardial activation due to markedheterogeneity of the electrophysiologiccharacteristics of the ventricular myocardium.


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Torsade de pointes

is an atypical, rapid, and bizarre form ofventricular tachycardia

it means "twisting of points" a name that refers to

the continuously changing axis of polymorphicQRS morphologies that are observed during eachepisode

the polymorphic VT is associated with a

congenital or acquired prolongation of the QTinterval, suggesting a prolonged refractory periodand repolarization time


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Torsade de pointes

there often is heterogeneity of repolarization

or dispersion of refractoriness.

Torsade is usually initiated by a long RRinterval (often a post VPB compensatory

pause) followed by a short RR cycle,

generally due to another VPB

ACCELERATEDIDIOVENTRICULAR RHYTHM


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IDIOVENTRICULAR RHYTHM

a repetitive ventricular rhythm occurring at a ratebetween 60 and 100 beats per minute

it may be the result of an accelerated ventricular

focus which generates an impulse faster than the

sinus node and therefore assumes control

if the idioventricular rhythm represents an escape

rhythm (generally the result of third degree AV

nodal block), the P waves are dissociated from the

QRS impulses and the atrial rate is faster than the

ventricular rate.


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VENTRICULAR FIBRILLATION complete absence of properly formed QRS complexes and

no obvious P waves

no uniform activation of the ventricular myocardium and

therefore no distinct ventricular complexes

coarse fibrillatory waves when the fibrillation is recent in

onset (eg, only a few minutes)

high amplitude oscillations occurring at rate greater than

320 beats per minute which manifest random changes in

morphology, width, and height, leading to the appearanceof a completely chaotic rhythm.

fibrillatory waves become fine when VF continues for a

longer time and may not be obvious; they may resemble

asystole in these cases.


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Class IA Quinidines, Procaninamide, Disopyramide

Class IB

Mexilitine, Lignocaine

Class IC Flecanide, Propafenone

Class II

Blocker

Class III

Sotalol, amiodarone

Class IV

Diltiazam, Verapamil

Anti Arrhythmic


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Heart Block

SA Block AV Block

First degree

Second degree

Third degree

Bundle Branch Block

LBBB

RBBB

Fascicular Block

Anterior

Posterior


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Atrioventricular block

FIRST DEGREE ATRIOVENTRICULARBLOCK

SECOND DEGREEATRIOVENTRICULAR BLOCK

Mobitz type I (Wenckebach)

Mobitz type II

THIRD DEGREE ATRIOVENTRICULARBLOCK

FIRST DEGREE


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FIRST DEGREE

ATRIOVENTRICULAR BLOCK defined as a prolonged PR interval(>0.20

seconds)

most often occurs when there is a prolongation or

delay in impulse conduction through the AV node

(show ECG 1).

The PR interval generally varies with the heart

rate; in the presence of sinus bradycardia (usually the result

of enhanced vagal tone), the PR interval lengthens.

the PR interval becomes shorter during sinus

tachycardia.


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SECOND DEGREE


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SECOND DEGREE

ATRIOVENTRICULAR BLOCK Mobitz type I (Wenckebach) or Mobitz type II.

Mobitz type I

Wenckebach second degree AV block

result of an intermittent block of the impulse within the

AV node, with subsequent failure to conduct an atrialimpulse from the atria to the ventricles.

SECOND DEGREE


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SECOND DEGREE

ATRIOVENTRICULAR BLOCK The ECG correlates of these electrical eventsinclude the following (show ECG 2):

There is a progressive lengthening of the PR interval

unti l a normally occurr ing P wave is not followed by

a QRS complexbecause of failure of the node to

conduct the impulse to the ventricle.

The completely blocked P wave is on time; the

surrounding RR interval is prolonged. The impulse that arrives at the node following the

completely blocked beat is conducted normally again

because the node has had time to become totally

repolarized.


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SECOND DEGREE


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SECOND DEGREE

ATRIOVENTRICULAR BLOCK Mobitz type IIusually indicative of underlying structural

disease involving the AV node that is

characterized by episodic and unpredictablefailure of the node to conduct the impulse fromthe atria to the ventricles.

The block occurs below the AV node in some

cases, within the bundle of His, or within bothbundle branches.

SECOND DEGREE


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SECOND DEGREE

ATRIOVENTRICULAR BLOCKIn contrast to Mobitz type I, there is no changein the PR intervalprior to or after the non-conducted P wave (show ECG 3).

There may be more than one successive non-conducted P wave, resulting in several P wavesin a row without QRS complexes.

An escape ventricular focus may generate a

QRS complex in some cases after a variableduration


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THIRD DEGREE


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THIRD DEGREE

ATRIOVENTRICULAR BLOCK occurs when there is complete failure of the AVnode to conduct any impulses from the atria to theventricles.

Causes: intrinsic AV nodal disease.

Drugs that depress and block nodal conduction such asdigoxin, beta blockers, or calcium channel blockers

Enhanced vagal tone, such as that occurring duringsleep

Infrequently it is congenital.

result of infranodal block occurring within the bundleof His or in both bundle

THIRD DEGREE


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THIRD DEGREE

ATRIOVENTRICULAR BLOCK The P waves are completely dissociatedfrom the QRS complexes on the ECG (showECG 4).

Thus, the PR intervals are irregularlyvariable.

The atrial and ventricular rates are both

stable; the former is faster than the latter.


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ECG l i


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ECG analysis

Rate

Rhythm

AxisInterval & Morphology

P, PR, QRS duration & Amplitude, Q, ST, T, QT,

Ischaemia, infarction

ECG l i


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ECG analysis

Three simple questions:

(1) Is there a normal looking QRS complex ?

(2) Is there a P wave ?(3) What is the relationship between the P

wave and QRS complexes ?

I th P ?


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Is there a P wave ?

If the QRS complexes are normal proceed

to examine P wave

If P wave is normal, consider sinus rhythmand its variants

If P wave is absent or abnormal, consider

supraventricular tachycardia.


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P l l El t i l A ti it


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Pulseless Electrical Activity

Electrical Mechanical Dissociation

Any rhythm or electrical activity that fails

to generate a palpable pulse The one major action is to search for

reversible cause while non-specific

interventions is administered


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D fib ill ti


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Defibrillation

Therapeutic use of electric current delivered

in large amounts over very brief periods of

time The defibrillation shock temporarily

STUNS an irregularly beating heart and

thus allows normal electrical activity to

occur (more coordinated contractile activity

to resume)

R ti l f l d fib ill ti


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Rationale for early defibrillation

The most frequent initial rhythm in suddencardiac arrest is VF

The only effective treatment for VF iselectrical defibrillation

The probability of successful defibrillationdiminishes rapidly over time

VF tends to convert to asystole within a fewminutes


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Cardio ersion


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Cardioversion

Cardioversion is the delivery of energy

that is synchronized to the QRS

complex, while defibrillation isnonsynchronized delivery of energy, ie,

the shock is delivered randomly during

the cardiac cycle.

Cardioversion


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Cardioversion

terminates arrhythmia by the delivery of asynchronized shock that depolarizes thetissue involved in a reentrant circuit and make

the tissue refractory (the circuit is no longerable to propagate or sustain reentry).

terminates those arrhythmias resulting from asingle reentrant circuit (as atrial flutter,

atrioventricular nodal reentrant tachycardia,atrioventricular reentrant tachycardia ormonomorphic ventricular tachycardia.)

FACTORS AFFECTING

DEFIBRILLATION AND


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DEFIBRILLATION AND

CARDIOVERSION SUCCESSElectrodes The placement of defibrillation electrodes on

the thorax, while determining the

transthoracic current pathway for externaldefibrillation, may have only a minimal effecton the myocardial distribution of the 4 to 5percent of energy that actually reaches the

heart There are two conventional positions:

Anterolateral orientation

Anteroposterior orientation

Several studies have suggested that less


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Several studies have suggested that lessenergy is required and the success rate is

higher with the anteroposterior electrodeposition in patients cardioverted for atrialfibrillation

In some patients one, but not the other position,

may be effective; thus, it has been suggestedthat if initial shocks are unsuccessful interminating the arrhythmia, the electrodesshould be relocated and cardioversion repeated

FACTORS AFFECTING

DEFIBRILLATION AND


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DEFIBRILLATION AND

CARDIOVERSION SUCCESS Electrode pad size is an importantdeterminant of transthoracic current flowduring external countershock

A larger pad or paddle surface is associatedwith a decrease in resistance and increase incurrent

However, there appears to be an optimal

electrode size (approximately 12.8 cm); anincrease in electrode area beyond this sizecauses a decline in current density

Transthoracic impedance


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During transthoracic defibrillation, a

considerably larger current must be

delivered to the thorax to compensate

for transthoracic impedance.

Impedance results in the dissipation of

energy due to shunting to the lungs, the

thoracic cage, and other elements of the

chest.



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Transthoracic impedance is determined bymultiple factors including: Energy level

Electrode size

Electrode-to-skin interface

Interelectrode distance

Electrode pressure

Phase of ventilation

Thoracic impedance

Myocardial tissue and blood conductive properties



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To reduce impedance, the operator should

always apply electrode gel or specifically

made paste/ gelled pad

Asystole


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Asystole

No evidence to support the use of

defibrillation in asystole

Empiric shocks of asystole can inhibit therecovery of natural pacemakers in the heart

and completely eliminate any chance of

recovery

Ventricular Asystole


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(Cardiac Standstill)

Total absence of ventricular electricalactivity and subsequently no ventricularcontraction.

May occur as primary event or follow VF orpulseless electrical activity

Can occur also in patients with compete

heart block without escape pacemaker Must always differentiate it from fine VF

(different management)

What is the relationship between the

P d QRS l ?


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P wave and QRS complexes ?

In the normal ECG every QRS complexes is

preceded by a P wave

The interval between P and QRS is less than0.21 second

Consider heart block when the above

relationship is disturbed.

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ACLS Arrhythmias & Defibrillation