Non cardaic surgery preoperative cardiac evaluation aha esc guideline 2015
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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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Classification of antiarrhythmicsClassification of antiarrhythmics(based on mechanisms of action)(based on mechanisms of action)
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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Classification of antiarrhythmicsClassification of antiarrhythmics(based on mechanisms of action)(based on mechanisms of action)
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