cardaic arryhmia1

8/6/2019 cardaic arryhmia1

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Cardiac arrhythmiaCardiac arrhythmiaTherapeutic aspectTherapeutic aspect


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Learning ObjectivesLearning Objectives

know and understand the mechanismsknow and understand the mechanisms

underlying the generation of commonunderlying the generation of common

arrhythmiasarrhythmias

appreciate the concepts of the Vaughanappreciate the concepts of the Vaughan--Williams classificationWilliams classification

recognise and be able to discuss therecognise and be able to discuss the

mechanisms of action of key antiarrhythmicmechanisms of action of key antiarrhythmicdrugsdrugs


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IntroductionIntroduction

ArrhythmiaArrhythmia defined as abnormaldefined as abnormal

electrical activity in the heartelectrical activity in the heart

Can be categorized as too fastCan be categorized as too fast

(tachyarrhythmia) or too slow(tachyarrhythmia) or too slow

(bradyarrhythmia)(bradyarrhythmia)

Can also be divided by its originCan also be divided by its origin supraventricular or ventricularsupraventricular or ventricular


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ElectrophysiologyElectrophysiology -- resting potentialresting potential

A transmembrane electrical gradient (potential) isA transmembrane electrical gradient (potential) ismaintained, with the interior of the cell negative withmaintained, with the interior of the cell negative withrespect to outside the cellrespect to outside the cell

Caused by unequal distribution of ions inside vs. outsideCaused by unequal distribution of ions inside vs. outsidecellcell NaNa++ higher outside than inside cellhigher outside than inside cell

CaCa++ much higher much higher

KK++ higher inside cell than outsidehigher inside cell than outside

Maintenance by ion selective channels, active pumpsMaintenance by ion selective channels, active pumpsand exchangersand exchangers


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Cardiac Action PotentialCardiac Action Potential

Divided into five phases (0,1,2,3,4)Divided into five phases (0,1,2,3,4) Phase 4Phase 4 -- resting phase (resting membrane potential)resting phase (resting membrane potential)

Phase cardiac cells remain in until stimulatedPhase cardiac cells remain in until stimulated

Associated with diastole portion of heart cycleAssociated with diastole portion of heart cycle

Addition of current into cardiac muscle (stimulation)Addition of current into cardiac muscle (stimulation)causescauses Phase 0Phase 0 opening of fast Na channels and rapid depolarizationopening of fast Na channels and rapid depolarization

Drives NaDrives Na++ into cell (inward current), changing membrane potentialinto cell (inward current), changing membrane potential

Transient outward current due to movement of ClTransient outward current due to movement of Cl-- and Kand K++

Phase 1Phase 1 initial rapid repolarizationinitial rapid repolarization

Closure of the fast NaClosure of the fast Na++ channelschannels

Phase 0 and 1 together correspond to the R and S waves of thePhase 0 and 1 together correspond to the R and S waves of theECGECG


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Cardiac Na+ channelsCardiac Na+ channels


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Cardiac Action PotentialsCardiac Action Potentials


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Cardiac Action Potential (cont)Cardiac Action Potential (cont)

Phase 2Phase 2 -- plateau phaseplateau phase

sustained by the balance between the inward movement of Casustained by the balance between the inward movement of Ca++ andand

outward movement of Koutward movement of K ++

Has a long duration compared to other nerve and muscle tissueHas a long duration compared to other nerve and muscle tissue

Normally blocks any premature stimulator signals (other muscle tissueNormally blocks any premature stimulator signals (other muscle tissuecan accept additional stimulation and increase contractility in acan accept additional stimulation and increase contractility in asummation effect)summation effect)

Corresponds to ST segment of the ECG.Corresponds to ST segment of the ECG.

Phase 3Phase 3 repolarizationrepolarization

KK++ channels remain open,channels remain open, Allows KAllows K++ to build up outside the cell, causing the cell to repolarizeto build up outside the cell, causing the cell to repolarize

KK ++ channels finally close when membrane potential reaches certainchannels finally close when membrane potential reaches certainlevellevel

Corresponds to T wave on the ECGCorresponds to T wave on the ECG


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The Sodium ChannelThe Sodium Channel


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Refractory PeriodRefractory Period


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Mechanisms of ArrhythmiaMechanisms of Arrhythmia

Disturbances of impulse:Disturbances of impulse:

GenerationGeneration

Increased automaticityIncreased automaticity

Triggered impulse generationTriggered impulse generation

ConductionConduction

Simple conduction blockSimple conduction block

ReRe--entry (circus movement)entry (circus movement)

Combination of bothCombination of both


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Aim of Antiarrhythmic DrugAim of Antiarrhythmic Drug

TherapyTherapy Reduce abnormal pacemaker activityReduce abnormal pacemaker activity

modify cardiac conduction/refractoriness in remodify cardiac conduction/refractoriness in re--entrantentrantcircuitscircuits

Achieved by :Achieved by :

blockade of sodium channelsblockade of sodium channels

blockade of sympathetic nerve activityblockade of sympathetic nerve activity

prolongation of the effective refractory periodprolongation of the effective refractory period

blockade of calcium channelsblockade of calcium channels

NBNB Many antiarrhythmic drugs are not highly selective,Many antiarrhythmic drugs are not highly selective,@@ often block more than one channel typeoften block more than one channel type


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Antiarrhythmic drugsAntiarrhythmic drugs

Biggest problemBiggest problem antiarrhythmics canantiarrhythmics can

cause arrhythmia!cause arrhythmia!

Example: Treatment of a nonExample: Treatment of a non--life threateninglife threatening

tachycardia may cause fatal ventriculartachycardia may cause fatal ventricular

arrhythmiaarrhythmia

Must be vigilant in determining dosing, bloodMust be vigilant in determining dosing, bloodlevels, and in followlevels, and in follow--up when prescribingup when prescribing

antiarrhythmicsantiarrhythmics


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Vaughan Williams Classification:Vaughan Williams Classification:

ClassClass II Sodium Channel BlockersSodium Channel Blockers

Subdivided:Subdivided:

IAIA -- quinidine, disopyramidequinidine, disopyramide IBIB -- lignocainelignocaine

ICIC -- flecanideflecanide

All have similar effects on pacemaker cells:All have similar effects on pacemaker cells:

decrease slope of phase 4 (longer to reach threshold)decrease slope of phase 4 (longer to reach threshold)

increase threshold potentialincrease threshold potential

Difference occur wrt to effects on conductingDifference occur wrt to effects on conducting

cellscells


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Class IClass I

IA:IA: block phase 0,3; Slow conduction & prolong APD; someblock phase 0,3; Slow conduction & prolong APD; some

anticholinergic effectsanticholinergic effects

IB:IB: affinity for Na channel in depol tissue, little affinity in normalaffinity for Na channel in depol tissue, little affinity in normaltissue; shorten APDtissue; shorten APD

IC:IC: block phase 0 more that other agents; slow conduction; lessblock phase 0 more that other agents; slow conduction; less

effect on K than IAeffect on K than IA @@little effect on APD/QTlittle effect on APD/QT


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Classification of antiarrhythmicsClassification of antiarrhythmics(based on mechanisms of action)(based on mechanisms of action)

Class I AClass I A blockers of fast Nablockers of fast Na++ channelschannels

QuinidineQuinidine 11stst antiarrhythmic used, treat bothantiarrhythmic used, treat both

atrial and ventricular arrhythmias, increasesatrial and ventricular arrhythmias, increases

refractory periodrefractory period

ProcainamideProcainamide -- increases refractory periodincreases refractory period

but side effectsbut side effects

DisopyramideDisopyramide extended duration of action,extended duration of action,used only for treating ventricular arrthymiasused only for treating ventricular arrthymias


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Subclass IBSubclass IB

Weak Phase 0 depressionWeak Phase 0 depression

Shortened depolarizationShortened depolarization

Decreased action potential durationDecreased action potential duration

IncludesIncludes

LidocaneLidocane (also acts as local anesthetic)(also acts as local anesthetic) blocks Na+blocks Na+

channels mostly in ventricular cells, also good forchannels mostly in ventricular cells, also good for

digitalisdigitalis--associated arrhythmiasassociated arrhythmias

MexiletineMexiletine -- oral lidocaine derivative, similar activityoral lidocaine derivative, similar activity

PhenytoinPhenytoin anticonvulsant that also works asanticonvulsant that also works as

antiarrhythmic similar to lidocaneantiarrhythmic similar to lidocane


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Subclass ICSubclass IC Strong Phase 0 depressionStrong Phase 0 depression

No effect of depolarizationNo effect of depolarization

No effect on action potential durationNo effect on action potential duration

IncludesIncludes

FlecainideFlecainide (initially developed as a local anesthetic)(initially developed as a local anesthetic)

Slows conduction in all parts of heart,Slows conduction in all parts of heart,

Also inhibits abnormal automaticityAlso inhibits abnormal automaticity

PropafenonePropafenone

Also slows conductionAlso slows conduction

WeakWeak blockerblocker

Also some CaAlso some Ca2+2+ channel blockadechannel blockade


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Class IIClass II -- AtenololAtenolol

Inhibit symp. activation of cardiac automaticity & conductionInhibit symp. activation of cardiac automaticity & conduction

PPacemaker tissueacemaker tissue

HR (phase 4)HR (phase 4)

AV conduction velocityAV conduction velocity

AV refractorinessAV refractoriness

Little effect on ventricular conduction & repolarisation

Little effect on ventricular conduction & repolarisation


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Class IIIClass III

Block the delayed KBlock the delayed K++ currentcurrent

phase 3phase 3

prolong theprolong the APD (prolongsAPD (prolongs

QT) without affecting phaseQT) without affecting phase0 (cf amiodarone)0 (cf amiodarone)

DoesDoes NOTNOTaffect cardiacaffect cardiac

contractilitycontractility, ventricular, ventricular

conduction velocity orconduction velocity orincrease QRS intervalincrease QRS interval


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Class IIIClass III -- AmiodaroneAmiodarone

MechanismMechanism

BBlocks the delayed rectifier Klocks the delayed rectifier K++ current (Classcurrent (Class

III)III),, inward Nainward Na++ current (Class I)current (Class I), calcium current, calcium current

(class IV) and(class IV) and FF--adrenoceptors (class II)adrenoceptors (class II)

QT and QRS prolongation seen in the ECGQT and QRS prolongation seen in the ECG

Difficult to assign antiarrhythmic activity to aDifficult to assign antiarrhythmic activity to a

specific mechanismspecific mechanism SE: pulmonary fibrosis (5SE: pulmonary fibrosis (5--10% of patients &10% of patients &

is dose dependent)is dose dependent)


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Class IVClass IV -- Calcium ChannelCalcium Channel

BlockersBlockers -- VerapamilVerapamil Slow depolarisation in AV nodeSlow depolarisation in AV node

prolongsprolongs APDAPD

conduction velocityconduction velocity

Effects:Effects: decreased sinus ratedecreased sinus rate

slowed AV nodal conductionslowed AV nodal conduction

Decreases cardiac contractilityDecreases cardiac contractility


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AdenosineAdenosine Mechanism:Mechanism:

Activate PActivate P11--purinergicpurinergic

receptors to open a Greceptors to open a G--proteinprotein

coupled K channel causingcoupled K channel causing

hyperpolarisation & slowhyperpolarisation & slow

conductionconduction

inhibits cAMP dependentinhibits cAMP dependentCaCa2+2+ influx (suppresses Cainflux (suppresses Ca2+2+

dependent action potentials)dependent action potentials)

Effects:Effects:

slows AV nodal conductionslows AV nodal conduction

increases ERP of the AVincreases ERP of the AV

nodenode

Uses: supraventricularUses: supraventricular

tachycardiatachycardia


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MagnesiumMagnesium

Used in patients with:Used in patients with:

digitalis induced arrhythmiasdigitalis induced arrhythmias

ventricular tachycardiasventricular tachycardias Mechanism is unknownMechanism is unknown


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Atrial FibrillationAtrial Fibrillation

Afib results from random chaoticAfib results from random chaotic

depolarization of the atria leading todepolarization of the atria leading to

irregularly, irregular tachycardiairregularly, irregular tachycardia

Atrial rate usually 400Atrial rate usually 400--700 bpm700 bpm

but ventricular rate is limited by thebut ventricular rate is limited by the

refractory period at the AV noderefractory period at the AV node

so ventricular rate ranges from 140so ventricular rate ranges from 140--170170

bpmbpm


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Atrial FibrillationAtrial Fibrillation----ClassificationClassification

Paroxysmal afibParoxysmal afib Episodes that lasts less than 7 daysEpisodes that lasts less than 7 days

Terminate spontaneouslyTerminate spontaneously

Persistent afibPersistent afib Episodes lasting more than 7 daysEpisodes lasting more than 7 days

Require either pharmacologic or electrical intervention toRequire either pharmacologic or electrical intervention toterminateterminate

Permanent afibPermanent afib Continuous afib that has failed cardioversionContinuous afib that has failed cardioversion

Lone afibLone afib In individuals without structural or cardiac diseaseIn individuals without structural or cardiac disease

Low risk for thromboembolismLow risk for thromboembolism


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Atrial FibrillationAtrial Fibrillation--ClinicalClinical

featuresfeatures

Focus on hemodynamic stabilityFocus on hemodynamic stability

Duration and frequency of symptomsDuration and frequency of symptoms

Sx: palpitations, fatigue, poor exerciseSx: palpitations, fatigue, poor exercise

tolerance, syncope, dizzinesstolerance, syncope, dizziness

Risk factors:Risk factors:HTN, valvular heart diseaseHTN, valvular heart disease

CAD, DM, alcohol use, stimulant use,CAD, DM, alcohol use, stimulant use,

hyperthyroidismhyperthyroidism


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Atrial FibrillationAtrial Fibrillation --managementmanagement

New onset AFNew onset AF Rate control vs rhythm controlRate control vs rhythm control

Depends on duration of symptomsDepends on duration of symptoms

restoring and maintaining SR neitherrestoring and maintaining SR neither

improves survival rate nor reduces risk ofimproves survival rate nor reduces risk ofstrokestroke

Management of longManagement of long--standing afibstanding afib

Rate controlRate control

AnticoagulationAnticoagulation

AnticoagulationAnticoagulation


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Atrial Fibrillation managementAtrial Fibrillation management

Determined by hemodynamic stabilityDetermined by hemodynamic stability Unstable patients require immediateUnstable patients require immediate

cardioversioncardioversion Hypotension, decompensated CHF, ongoingHypotension, decompensated CHF, ongoing

ischemia/infarctionischemia/infarction

Stable patients require rate controlStable patients require rate control

with a target heart rate < 100 bpmwith a target heart rate < 100 bpm

Begin anticoagulation with eitherBegin anticoagulation with eitheraspirin or warfarinaspirin or warfarin


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Atrial Fibrillation managementAtrial Fibrillation management

New onset afibNew onset afib Symptoms < 48 hours: cardioversion (electrical orSymptoms < 48 hours: cardioversion (electrical or

pharmacologic) followed by anticoagulation for 4 wkspharmacologic) followed by anticoagulation for 4 wks

Stunning of atria and stasis can occur afterStunning of atria and stasis can occur aftercardioversion, and this can lead to thrombuscardioversion, and this can lead to thrombusformation even though patient is in NSRformation even though patient is in NSR

Symptoms > 48 hours:Symptoms > 48 hours: anticoagulation for 3 weeksanticoagulation for 3 weeks

prior to cardioversion OR heparinize, get TEE,prior to cardioversion OR heparinize, get TEE,

cardiovert if no thrombus detectedcardiovert if no thrombus detected

Anticoagulation for 4 wks afterward in both casesAnticoagulation for 4 wks afterward in both cases


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SVTSVT--treatmenttreatment

Carotid massage or adenosine commonlyCarotid massage or adenosine commonly

terminate the arrhythmia, esp, AVRT orterminate the arrhythmia, esp, AVRT or

AVNRTAVNRT

Can also use CCB or beta blockers toCan also use CCB or beta blockers to

terminate, if availableterminate, if available

Counsel to avoid triggers, caffeine, Etoh,Counsel to avoid triggers, caffeine, Etoh,

pseudoephedrine, stresspseudoephedrine, stress


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Treatment of VTTreatment of VT

1.1. Treat underlying diseaseTreat underlying disease

2.2. Cardioversion: Hemodynamic unstable VTCardioversion: Hemodynamic unstable VT(hypotension, shock, angina, CHF) or(hypotension, shock, angina, CHF) or

hemodynamic stable but drug was no effecthemodynamic stable but drug was no effect3.3. Pharmacological therapy:Pharmacological therapy: --blockers,blockers,

lignocain or amiodaronelignocain or amiodarone

4.4.RFCA, ICD or surgical therapyRFCA, ICD or surgical therapy

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cardaic arryhmia1