Management of perioperative arrhythmias - medIND

15 Pages·2007·6.84 MB·English

IndianJournalofAnaesthesia2007;51(4):310-323 Indian Journal of Anaesthesia, August 2007
Management of Perioperative Arrhythmias
N. Dua1, V.P. Kumra2
Key words Perioperative, Arrhythmias
Definition Pathogenesis
Arrhythmia is defined as “Abnormality of cardiac 1. Injuryordamage(pathology) tothecardiaccon-
rate,rhythmorconductionwhichcanbeeitherlethal(sud- ductionsystems.
den cardiac death), or symptomatic (syncope, near syn-
2. Re-entry: Reentry is a mechanism that may pre-
cope,dizziness,orpalpitations)orasymptomatic”.Imme-
cipitateawidevarietyofsupraventricularandven-
diatediagnosisandinterventionwithappropriatetherapy
triculararrhythmias.
often will prevent degeneration of an arrhythmia into a
3. Automaticity:Abnormaldepolarizationofatrialor
life-threateningevent.
ventricularmusclecellduringtheperiodsofaction
Cardiac arrhythmias are the most frequent
potentialcanleadtoarrhythmias.
perioperativecardiovascularabnormalitiesinpatientsun-
dergoing both cardiac and non-cardiac surgery.The oc- 4. Mutations in ion channels: Since these channels
currenceofarrhythmiashavebeenreportedin70.2%of aremainlyresponsiblefordepolarization,mutation
patientssubjectedtogeneralanaesthesiaforvarioussur- canleadtoarrhythmias.
gicalprocedures.1,2Theincidenceofarrhythmiasvaries 5. Ectopic foci/ irritable foci
frompatientsundergoingcardiacornon-cardiacsurgery
The mechanismof arrthythmogenesis has been il-
aswellasonmonitoringmodality.Theincidencehasbeen
lustrated6inFig.1
reportedtovaryfrom16.3to61.7%withintermittentECG
monitoring3and89%withcontinuousholtermonitoring4
inpatientsundergoingnon-cardiacsurgery,whilepatients
undergoing cardiac surgery are more prone to develop
arrhythmiawithreportedincidenceofmorethan90%.5
Regardlessoftheterminology(arrhythmiaordys-
rhythmia),cardiacrhythmdisturbancerepresentsoneof
themostmisunderstood,frustratingandpotentiallydev-
astating problems faced by the general or cardiac
anaesthesiologist.Thefirstbasicprincipleofanti-arrhyth-
mictherapyistoidentifyandcorrectpossibleprecipitat-
ing factors related to the administration of anaesthesia.
Arrhythmias in the presence of cardiovascular disease
aremoredangerousandattimesmaybelifethreatening
unlikethoseoccurringinhealthypatientswhichareusu-
ally of little clinical consequence. Pacemakers and im-
plantablecardioverter-defibrillators(ICD)arebeingused
inthetreatmentoftachyarrhythmiasandbradyarrhythmias
nowadays very frequently. The basic understanding of
theirperioperativefunctionandmanagementneedstobe
highlighted.Thistextwillprovideasimplerwaytodiag-
noseandmanagearrhythmiasintheperioperativeperiod. Fig 1. Mechanism of arrthythmogenesis
1.M.D.,Consultant,2.M.D.,D.A.,D.Ac.,M.Ac.F.I.,EmeritusConsultant,DepartmentofAnaesthesiology,Pain&PerioperativeMedicine,
SirGangaRamHospital,SirGangaRamHospitalMarg,NewDelhi-110060,INDIA. Correspondenceto:NareshDua,Departmentof
Anaesthesiology,PainandPerioperativeMedicine,SirGangaRamHospital,SirGangaRamHospitalMarg,NewDelhi-110060,INDIA.
Email:[email protected]
310
N. Dua et al. Perioperative arrhythmias
a) Increasedautomaticityduetoreducedthresholdpo- b. Central nervous system disease - Patients with in-
tentialor anincreasedslope ofphase 4depolariza- tracranial disease especially sub-arachnoid
tion haemorrhagemayshowECGabnormalitiessuchas
changes in QT intervals, development of Q waves,
b) Triggeredactivitydueto‘after’depolarizationsreach-
ST-segment changes, and occurrences of U waves.
ingthresholdpotential
c. Oldage-Postoperativeatrialfibrillation(AF)isafre-
c) Mechanismofcircusmovementorreentry.Inpanel
quentcomplicationintheelderlypatients3undergoing
(1)theimpulsepassesdownbothlimbsofthepoten-
thoracicsurgery.Agingcausesdegenerativechangein
tial tachycardia circuit. In panel (2) the impulse is
blockedinthepathwaybutproceedsslowlydown atrial anatomy and is also accompanied by relative
the pathwayandreturnsalongthepathway. In changesinatrialpathology.Theinjurytosympathovagal
fibersofcardiacplexusduringsurgeryandpreexisting
panel (3) the impulse travels so slowlyalongthe 
atrialelectricalchangesinthesepatientspredisposethem
pathwaythatwhenitreturnsalongthepathwayto
topostoperativeatrialfibrillation
itsstartingpointitisabletotravelagaindownthe 
pathway,producingacircusmovementtachycardia.
2.Anaesthesiarelatedfactors
Factors and causes- There are several contribut-
a. Tracheal intubation – It is one of the most com-
ingfactors.Thecausesmainlyresponsibleforarrhythmias
monestcausesofarrhythmiasduringinductionaswell
arelistedinTable1.
asduringtheperioperativeperiod,mostoftenasso-
Table 1. Contributing factors and causes ciatedwithhaemodynamicdisturbances.
b. General anaesthetics – The drugs used for induc-
Hypovolemia  Cardiacischaemia
tion,maintenanceaswellasforreversalofgeneral
Hypoxia  Lightplaneofanaesthesia/pain
anaesthesia are not primarily arrhythmogenic, but
Hypo/Hyperkalemia  Toxins/Drugs arrhythmias can be produced in the presence of a
Hypomagnesaemia/  Tamponade,Cardiac variety of triggering agents and clinical situations
Hypocalcaemia  Tensionpneumothorax generatinghigh catecholaminessuch aslight plane
Hypoglycemia  Thrombosis (Coronary or pul- of anaesthesia with hypertension and tachycardia,
Hypothermia monary) hypoxaemia,hypercarbia,exogenousepinephrineand
Acidosis aminophylline. Halothane or enflurane produces
 Trauma
Mechanical arrhythmias,probablybyareentrantmechanism.3
 Surgicalcause(Tractiontointes-
Irritation(e.g.centralvenous tine,oculocardiacreflex,neuro- c. Local anaesthesia – Regional anaesthesia (epidu-
lines,pulmonaryart.catheter, surgicalcauses,cardiaccompres- ralanaesthesia)followedbycentralneuraxialblock-
siononbeatingheartbypasssur-
chesttube) ade may be associated with pharmacological sym-
geryetc.)
pathectomyleadingtoparasympatheticnervoussys-
Thesefactorscangrosslybedividedintofollowing tempredominancecausingbradyarrhythmias.Itmay
categories: bemildtoverysevereinnature.7
1. Patient related factors d. Electrolyteimbalanceandabnormalarterialblood
gases –Abnormalbloodgasessuchashypercarbia,
2. Anaesthesia related factors
hypoxaemia or electrolyte imbalance produce
3. Surgeryrelated factors
arrhythmiaseitherbyproducingreentrantmechanism
orbyalteringphasedepolarizationofconductingfi-
1.Patientrelatedfactors
bers.Hypokalemiaorhyperkalemiamayalsoleadto
a. Preexisting cardiac disease - The patients with
arrhythmias.
knowncardiacdisease(e.g.myocardialischaemia-
e. Central venous cannulation – Stimulation of carotid
MI)havemuchhigherincidenceofarrhythmiasdur-
sinusreflexesmayoccurduetopressurefromfingers
inganaesthesiathanpatientswithoutknowncardiac
duringjugularveincannulationasexcessinsertionof
disease1.The arrhythmias are more fatal in patients
thecentralvenouscatheterintotherightatriumduring
withassociatedcardiacpathology.
centralvenouscannulationmayalsoleadtoarrhythmias.7
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Indian Journal of Anaesthesia, August 2007
3. Surgeryrelatedfactors raisedintracranialpressure
a. Cardiac surgery – A spectrum of cardiac 5. Chronicdegenerativechangesuchasfibrosisofthe
arrhythmias can be observed during the immediate atriumandsinusnode
period following the release of aortic cross clamp
Treatment:
whenmyocardiumisrecoveringfromtheischaemic
Asymptomaticbradycardiausuallydoesnotrequire
insult and regainingnormal sinus rhythm. Surgical
treatment.Symptomaticbradyarrhythmiasshouldbedi-
manipulation such as retraction of the heart during
agnosedandimmediatetherapyshouldfollow.Inpatients
operationonbeatingheart,venouscannulationortak-
who manifest haemodynamic compromise such as hy-
ing sutures over the atrium can also precipitate
potension,atropineisthefirstlineoftreatment.Itcanbe
arrhythmias.
used in the dose of 0.5 to 1.0 mg (IV bolus), repeated
b. Non-cardiacsurgery–Vagalstimulationduetotrac-
every3to5minutes,ifrequired(maximumdose=0.04
tionontheperitoneumordirectpressureontheva-
mg.kg-1). However, it should be used cautiously in pa-
gusnerveduringcarotidarterysurgerymayproduce
tients with CAD, since excessive increase in heart rate
bradycardiaoratrioventricular(AV)blocks,oreven
mayworsenischaemiabecauseofincreasedmyocardial
asystole. Dental surgery causes profound stimula-
oxygenconsumptionorreduceddiastolicfillingtime.If
tion of both sympathetic and parasympathetic ner-
bradycardiastillpersistsdespitetreatment,isoprenaline
vousstimuli.
canbeadministeredasanIVbolusof5to10gfollowed
Arrhythmiasarebroadlyclassifiedas by an infusion of 2 to 10g.min-1. Other alternative is
dopamineinfusion5to20g.min-1.
Table 2 : Classification of arrhythmias
Whiletreatingsinusbradycardia,variouscausesor
1. Bradyarrhythmia 2. Tachyarrhythmia factors contributing should be searched and treatment
i.SinusBradycardia i.NarrowQRS ii.WideQRS started.Bereadyforpercutaneousandtransvenouspac-
complex (SVT) complex
ii. Various forms of tachycardias (QRS tachycardias (QRS > ing.8(FlowChart1)
heart block
<0.12 second) 0.12 second) Expertcardiologistopinionmustbesoughtforfur-
a. First degree
a. Sinus tachycardia ther management.
b.Seconddegree a. Ventricular prema-
b. Atrial premature
c. complete beat turebeat(VPB)/Ven- ii. Various forms of heart block: Heart blocks
tricular extrasystole
(AVHB)arebroadlyclassifiedintothreecategories
c.Atrial tachycardia
b. Ventricular tachy-
a) Firstdegreeheartblock
d.Atrial flutter cardia (VT)
e.Atrial fibrillation c. Ventilation fibrilla- b) Seconddegreeheartblock
tion c) Completeheartblock
d.Torsadesdepointes Anatomicalorfunctionalabnormalitiesunderlieatrio-
1.Bradyarrhythmia ventricularheartblock(AVHB).Thesemaybetransient
orpermanent.TransientAVHBcanbeproducedbyacute
i. Sinus bradycardia – bradycardia is generally de-
MI and general anaesthetics such as enflurane or hal-
finedasaheartrateoflessthan60beatsperminute.
othane in patients using calcium channel blocker drug
Inpatientsonchronicbeta-blockertherapysuchas
(CCB) or amiodarone. Permanent AVHB, on the other
thosesufferingfromcoronaryarterydisease(CAD),
handisusuallyidiopathic,othercausesincludeCADand
itisdefinedasaheartrateoflessthan50beats/min.
Lev’sorLenegredisease,wherefibrosisoftheconduct-
Causes ingsystemoccurs.
Thecausesofsinusbradycardiaareasfollows: a) Firstdegreeheartblock:Thisissimpleprolonga-
tionofthePRintervaltomorethan0.22sec.Every
1. Drugeffects: blockers,digitalisandotheranti-ar-
atrialdepolarizationisfollowedbyconductiontothe
rhythmicdrugs
ventriclebutwithdelay.Thetreatmentisusuallynot
2. Acutemyocardialischaemia
necessaryhowever,thepatientsshouldbecarefully
3. Hypothermia
observedforprogressiontoahigherdegreeofblock,
4. Underlyinghypothyroidism,cholestaticjaundiceor thatrequiresprompttreatment.(Fig.2)9
312
FlowChart1
ae)noSsegno)rerm:seceMIoednoAnPtVodnhwboidbisatltv.etozyegcTpTrskehecyeoeoprnfeedhAaIeuVrcaBeHtrlBetsole,ecbvtckheltoe(rrWciarceklae:filonsaprcTmcrkohtisegivbrsoaeaoftsiccssoiehcvnc’ueasornppsnddrhwoeodlhnoteheno--nm--gTtiwlatIhtthsereaenahauhnmmtecasegnaitrourptPttiaetrnaoRhoihybleanralepaolM.tnloiyfnPrcTrricooytPRnoognhkepgnRoip.briritsevtanoinrIiisctefatatnnsszlecieetctbssercohtmviauTercereoladavfillynosPdlseekasopreaaRdewapleefrnrrty.uriitltethiIeny(nhhnIeFrnteedotaatxe“iBiiunbhrgcllMcvtdl.leiaoeaa4onaobutc)pecb‘lsi9lnk,Ptouokieicbtpcbn’:nzwurdaskeTntefesToaPdlqhdboivwouyrceectpewePacthreunieeavwvvftIsaeIeesavie”piiseivnollldsynetns.npamt.thrcoti(aoroFeeciuTlilcpuncmccrgyourelho.oaolmtmea3hannrglt)eoretdmprrenrnucalo9escogeoeftsenennttiieat-..rs,ve
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Indian Journal of Anaesthesia, August 2007
Note Note
Progressive lengthening of PR interval  Regular P waves (normal atrial depolarization)
One non-conducted P wave  P wave rate 145/min
Next conducted beat has a shorter PR interval than the preceding  QRS complexes highly abnormal because of abnormal conduction
through ventricular muscle
Fig 3. Second degree heart block (Wenckebach type)
 QRS (ventricular escape) rate 15/min
 No relationship between P waves and QRS complexes
Fig 6. Complete heart block
 Broad complex: This occurs because of disease in
the Purkinje system. The escape pacemaker arises
fromthe distal Purkinje network or the ventricular
myocardium. The resulting rhythm is slow (15-40
Note
b.p.m)andrelativelyinsignificantorunharmful.In
 PR interval of the conducted beats is constant
theelderly,itisusuallycausedbydegenerativefibro-
 One P wave is not followed by a QRS complex and here second
sisandcalcificationofthedistalconductionsystem
degree block is occurring
(Lenegre’s disease) or the more proximal conduc-
Fig 4. Second degree heart block (Mobitz type 2)
tion system(Lev’s disease).It mayoccur after clo-
eitherbroad(>0.15)ornarrow(<0.15)QRScom- sure of ventricular septal defect (VSD) and some-
9
plexes.(Fig.5&6) timesfollowingaorticvalvereplacement(AVR).In
younger patients, broad complexAVblock may be
causedbyperioperativemyocardialischaemia.
Management:Treatmentisnotrequiredinnarrow
complex3°blockexceptforeradicationoftoxiccauses.
Occasionally, permanent pacingis advocated for symp-
tomatic,isolatedAVblock.Whileinbroadcomplex,pac-
ingisindicatedtomaintainthenormalhaemodynamics.
Note
2.Tachyarrhythmia
 P wave rate 90/min
 QRS complex rate 36/min Thetachycardiacanbeclassifiedbasedontheap-
 No relationship between P waves and QRS complex pearance of the QRS complex as tachycardia, narrow
 Abnormally-shaped QRScomplexes becauseof abnormal spread of complex supraventricular tachycardia (SVT), and wide
depolarization from a ventricular focus
complex tachycardia. Most wide complex (broad com-
Fig 5. Third degree block plex)tachycardiasareventricularinorigin.Symptomatic
tachy-arrhythmias should be monitored and immediate
 Narrow complex: This is due to disease in theAV therapy should be done.8 (Flow Chart 2)
node or the proximal bundle of His. The escape
Tachyarrhythmiasareclassifiedintwocategoriesdepend-
rhythmoccurswithanadequaterate(50-60b.p.m.) ingupontheQRScomplexes.
and is relativelyreliable.It occurs because of infe-
i. Narrow QRS complex (QRS<0.12): In these
riorwallMIandtoxicconcentrationofdrugssuchas
type of arrhythmias the QRS complex is less than 0.12
digitalis,verapamilorblockersinperioperativepe-
sec.
riod.
314
N. Dua et al. Perioperative arrhythmias
Flow Chart 2
FlowChart3
diltiazem - blockers
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Indian Journal of Anaesthesia, August 2007
N. Dua et al. Perioperative arrhythmias
a. Sinus tachycardia: it is defined as an increase
inthesinusrateofmorethan100beats/minute.Prolonged
tachycardiaforlongdurationcaninduceischaemiaincoro-
naryarterydiseasedpatients.
Causes: It includes
Note
 Anaemiabecauseofbloodloss
 Afterone sinus beat the SAnodefails todepolarize.Aftera delay,
 Pain an abnormal P wave is seen because excitation of the atrium has
begunsomewhereawayfromtheSAnode.TheabnormalPwaveis
 Inadequate anaesthesia followed bya normal QRS complex, because excitation has spread
normallydown the His bundle. The remaining beats showa return
 Hypovolaemia to sinus arrhythmia.
 Fever Fig 7. Arial premature beat
 Hypercarbia
 Thyrotoxicosis/thyroidcrisis
 Cardiacfailurewithcompensatorysinustachy-
cardia
 Catecholamines excess Note :
Treatment: Before instituting pharmacological
 Afterthreesinusbeats, atrialtachycardia developsat a rateof150/
treatmentforsinustachycardia,precipitatingfactorsmust min. P waves can be seen superimposed on the T waves of the
precedingbeats.TheQRScomplexeshavethesameasthoseofthe
be identified and corrected. Drug therapy is especially
sinusbeats.
required in patients with ischaemic heart disease who
Fig 8. Atrial tachycardia
developSTsegmentchangestopreventfurthermyocar-
dialischaemia.Tachyarrhythmiashouldbemanagedac- fasterusuallylessthan130beats/min,itistermedasaccel-
cordingtoFlowChart2.Beta-blockerssuchasesmolol eratedAVjunctionalrhythm.Thosearrhythmiascanlead
ispreferreddrugformanagingit.Ithashalf-lifeof10min tofallinbloodpressureupto15%inpatientswithoutcar-
withbolusdoseof500mcg.kg-1over1min,followedby diacdiseaseandupto30%indiseasedheart.11 Usuallyno
aninfusionof50-300mcg.kg-1.min-1.Ifcontinuoususeis treatmentisrequired;carotidsinusmassageandverapamil
required,itmaybereplacedbylongerlastingcardiose- areoftenhelpfulinsymptomaticpatients.Intravenousad-
lectivedrugssuchasmetoprololinthedoseof5to10mg enosinein6to12mgdosesisanotheralternative.Treat-
givenslowlyintravenously(IV)at5minintervaltoatotal mentwithclassIa,IcorIIIdrugsisusuallysuccessfule.g.
doseof15mg.10Anotherdrugcanbeusedispropranolol disopyramide2mg.kg-1over10min.(Fig.8)9
0.1 mg.kg-1.
d.Atrialflutter
b.Atrialprematurebeat:Itrepresents10%ofall
Thisisarhythmdisturbancethatisusuallyassociated
intraoperative arrhythmias. On the ECG they appear as
withorganicischaemicheartdisease.Theatrialratevaries
early and abnormal ‘P’ waves and are usually but not
between280and350min-1butisusuallyaround300min-1.
always,followedbynormalQRScomplexes.Thedura-
tionofQRSwaveisnormalbutwideQRSwavemaybe Mostofteneverysecondflutterbeatconductsgivinga
present due to aberrant ventricular conduction, which ventricularrateof150min-1.Occasionallyeverybeatcon-
mimicsprematureventricularbeat.Treatmentisnotnor- ducts,producingaheartrateof300min-1.Moreoften,espe-
mallyrequiredunlesstheectopicbeatsprovokemoresig- ciallywhenpatientsarereceivingtreatment,AVconduction
nificantarrhythmias,whereblockademaybeeffective. blockreducestheheartratetoapproximately75min-1.
(Fig.7)9
ECG:TheECGshowsregularsawtooth-likeatrial
c.Atrialtachycardia:Thesearrhythmiasarefound flutterwavesbetweenQRSTcomplexes.Iftheyarenot
in 6% of patients undergoingnon cardiac surgery.2 It is clearlyvisible,AVconductionmaybetransientlyimpaired
nonparoxysmal, narrow QRS rhythm with retrograde or bycarotidsinusmassageorbytheadministrationofAV
nonapparentPwavesandaratelessthan70beats/min.if nodalblockingdrugssuchasverapamil.(Fig.9)9
316
N. Dua et al. Perioperative arrhythmias
naryembolisation.Successfulcardioversionisrelatively
rareinchronicAF.Thecontrolofventricularrateisthe
preferredapproachinthesecases.Themostusefuldrug
forthispurposeisdigoxin.ThepatientswithchronicAF
undergoing noncardiac surgery should be evaluated for
Note
 P waves can be seen at a rate of 300 min-1, giving a saw-toothed thepresenceofatrialclotbyechocardiogrampriortosur-
appearance. There are four P waves per QRS complex, and ven- gery.Inthepresenceofatrialclot,controlofventricular
tricular activation is perfectly regular at 75min-1. response rate with appropriate medication is instituted
Fig 9. Atrial flutter
duringperioperativeperiod,ifnecessary.
Treatment: Treatment of an acute paroxysm is
ii. Wide QRS complex (QRS>0.12): In these
electricalcardioversion.Prophylaxisisachievedwithclass
types of arrhythmias the QRS complex is usually more
Ia,Icor IIIdrugsindiseased heartpatients.
than 0.12 sec.
e.Atrialfibrillation(AF)
Itaccountsformorethan90%ofsupraventricularta-
chycardia(SVT)intheperioperativesetting.Itiscausedby
araisedatrialpressure,increasedatrialmusclemass,atrial
fibrosisorinflammationandinfiltrationoftheatrium.Rheu-
maticdiseaseisoftenassociatedwithcardiaccausessuch
Note
asmitralvalvedisease,myocarditisandcoronaryarterydis-
 No Pwaves – irregular baseline
ease.Systemicdiseasesincludehyperthyroidism,pulmonary
 Irregular QRS complexes
embolismandelectrolyteimbalance.Whencausedbyrheu-
 Normally shaped QRS complexes
maticmitralstenosis,theonsetofatrialfibrillationresultsin
 InleadV wavescanbeseenwithsomeresemblancetothoseseenin
considerableworseningofcardiacfailure. 1
atrial flutter this is common in atrial fibrillation
Clinicallythepatienthasaveryirregularpulse,as Fig 10. Atrial fibrillation
opposed to a basicallyregular pulse with an occasional
a.Ventricularprematurebeat(VPB)/Ventricular
irregularity(extrasystoles)orrecurringirregularpattems.
extrasystole
TheECGshowsfineoscillationsofthebaseline(socalled
fibrillation) and no clear P waves. The QRS rhythm is VPB results from ectopic foci arising from below
usually 160-180min-1 but it slows with treatment. ECG AVnode and give rise to wide (>0.12 sec) bizarre QRS
changesaremoreindicativeinleadII(Fig.10) 9.AFmay complex. They account for 15% of the observed
be acute or recent onset (<48 hrs) and chronic. In the arrhythmias,morecommoninanaesthetizedpatientswith
recentonsetAF,initialtreatmentisdirectedtowardsthe pre existing cardiac disease. New onset of VPB, may
controlofventricularresponseratewithagentsthatslow occur in the presence of coronary artery insufficiency,
AVnodeconduction.Theprecipitatingorprovokingagents myocardialinfarction,digitalistoxicitywithhypokalemia
should be removed or treated first. Intravenous beta- and hypoxaemia.On the ECG,the premature beathas a
blockersorcalciumchannelblockersproducerapidcon- broad(>0.125)andbizarreQRScomplexbecauseitarises
trol of rate, regardless of the level of sympathetic tone. froman abnormal (ectopic) site in the ventricular myo-
Howeverbeta-blockersarepreferredovercalciumchan- cardium.Followingtheprematurebeatthereisusuallya
nel blocker (CCB) during intraoperative period due to completecompensatorypausebecausethetimingofsinus
shorter duration of action and lesser negative inotropic rhythmisnotinducedbytheprematurebeat.(Fig.11&12)9
effects.10,12Inhaemodynamically-compromisedpatients,
Treatment: Underlyingabnormalitiesinthesepa-
DC cardioversion is the most effective method of con-
tients should be corrected immediately. No treatment is
vertingAFtosinusrhythm.ChronicAFisoftenfoundin
generallyrequiredforisolatedVPBinasymptomaticand
patientswithrheumaticheartdiseaseundergoingcardiac
healthy patients. However VPBwhich are multiple (>5
surgery and may have atrial thrombi, therefore, any at-
beats/min),multifocal,orbigemminaloroccurnearthe
tempttorestoresinusrhythmbyDCcardioversionmay
vulnerableperiodoftheprecedingventricularrepolariza-
beassociatedwith increasedriskofsystemic orpulmo-
317
Indian Journal of Anaesthesia, August 2007
blood pressure are very depressed, emergency DC-
cardioversionmustbeconsidered.Ontheotherhand,if
thebloodpressureandcardiacoutputarewellmaintained,
intravenoustherapywithclassIdrugsisusuallyadvised.
First-linedrugtreatmentconsistsoflidocaine(50-100mg
i.v. over 5 min) followed by a lidocaine infusion (2-4
mg.min-1 i.v.). DC-cardioversion may be necessary if
medical therapy is unsuccessful. The administration of
multipleantiarrhythmicdrugsshouldbeavoided.
Patientswithrecurrentepisodesorunresponsiveto
lidocaine,mayrequiretherapywithprocainamide(10-15
Note mg.kg-1 loading dose followed by an infusion of 2 to 6
 The upper trace shows five sinus beats, then an early beat with a mg.min-1)orbretylium(5to10mg.min-1over2to5min
wide QRS complex and an abnormal T wave: this is a ventricular
theninfusionof1-2mg.min-1)oramiodaroneinthedose
extrasystole. In the lower trace, the ventricular extrasystole occur
(arrows) at the peak of the T waves of the preceding sinus beats: of150mgIVover10minutesfollowedbyaninfusionof
this is the ‘R on T’ phenomenon. 1 mg.min-1 for 6 hours and 0.5 mg.min-1 thereafter. IV
Fig 11. Ventricular extrasystole amiodaronehasbeenshowntobeaseffectiveasbretylium
with added advantage of less hypotension as compared
toIVbretylium.(Fig.13)9
Note
 Three sinus beats are followed by a ventricular extrasystole. No P
wave is seen afterthis beat, but the next P wave arrives on time.
Fig 12. Ventricular extrasystole
Note
tion(thesocalledRonTphenomenon),associatedwith  After two sinus beats, the rate increases to 150/min. The QRS
complexes become broad, and theTwavesare difficult to identify.
haemodynamic disturbance or convert to worse
The final beat shows a return to sinus rhythm.
arrhythmiasrequireprompttreatment.Lidocainewithan
Fig 13. Ventricular tachycardia
initialbolusdoseof1.5mg.kg-1followedbyinfusionof1
C.Ventricularfibrillation(VF)
to4mg.min-1canbegiven.OtherdrugsfromclassI,IIor
IIIare used to treat these types of arrhythmias. Itisveryrapidandirregularventricularactivationwith
nomechanicaleffect.Itisusuallyintiatedfromanischaemic
b.Ventriculartachycardia
myocardium or an aberrant foci (especially in acute
This is defined as three or more ventricular beats perioperativemyocardialinfarction),ventriculartachycar-
occurringatarateof120bpmormore.Itmaybepoten- diaortorsadesdepointes.OnECG, thereareno defined
tiallylifethreatening.Examinationrevealspulserateof QRScomplexes,showsshapelessrapidoscillationsandon
pulseoximetry,thereisacutefallinSpO becauseoflow
120-220bpm.Usuallythereareclinicalsignsofatrioven-
2
ornocardiacoutput.Causesincludemyocardialischaemia,
triculardissociationi.e.intermittentcannon'a'wavesand
hypoxaemia,electrolyteimbalanceanddrugeffects.
variableintensityofthefirstheartsound.TheECGshows
a rapid ventricular rhythm with broad (often 0.14s or Treatment:Cardiopulmonaryresuscitationmustbe
more), abnormal QRS complexes. Dissociated P waves performedasrapidlyaspossible.Asynchronousexternal
defibrillationshouldbeperformedusing200-360J.Apre-
activitymaybeseen andhave nofixed relationto wide
cordialthumpisoccasionallyeffectiveinterminatingVF,
QRScomplex.
butshouldbeattemptedonlyifadefibrillatorisnotavail-
Treatment may be urgent depending on the
ableimmediately.Intravenousbretyium5-10mg.kg-1over
haemodynamic situation. If the cardiac output and the
5mincanbeusefulonsomeoccasion.Supportingphar-
318
N. Dua et al. Perioperative arrhythmias
macological therapysuch as lidocaine, amiodarone and positive electrode on the cardiac chamber being paced.
procainamideareusedonlytopreventrecurrenceofVF. Thecombinationofwiresallowsatrial,ventricular,oratrial
ventricularsequentialpacingwhenusedincombination
d.Torsadesdepointes
withadualoutput(atrialandventricular)sequentialex-
Thesearrhythmiasareusuallyshortindurationand
ternal pacemaker. 13
spontaneouslyreverttosinusrhythm.Occasionallyitcan
change to VF. On ECG, it is characterized by rapid, ir- Prophylactic transvenous pacing is recommended
regularsharpcomplexesthatcontinuouslychangefrom inpatientswhoareconsideredathighriskfordeveloping
anuprighttoaninvertedposition.Betweenspellsofta- haemodynamicallysignificantbradycardiaduetoAVheart
chycardia the ECG shows a prolonged QT interval; the
blockorsinusnodedysfunction.Whereas,directcardiac
correctedQTisequalto orgreaterthan0.44s.
pacingmethodsarepreferredforthepatientshavingcar-
Treatment: diacsurgery,especiallyinthepostbypassperiod.Inthese
Thearrhythmiaistreatedasfollows patients, current output of the pacemaker is slowly in-
creaseduntildesiredcardiacchambercontractioniscap-
1. Anyelectrolytedisturbanceiscorrected.
tured(usually5-10milliamperes),thencurrentoutputis
2. Causative drug and precipitating factors should be
furtherincreasedby5moremilliamperestoassurecon-
stoppedandremoved.
tinuedcapture.Whenatrialventricularsequentialpacing
3. IntravenousisoprenalinemaybeeffectivewhenQT
isrequired,theoptimalPRintervalwillneedtobedeter-
prolongationisacquired.
mined.Itisgenerally150msecbutcanvarybetween120
4. BlockadeisadvisediftheQTprologationiscon-
to200msecsoastooptimizeventricularfillingandcar-
genital.
diacoutput.Ifextensiveelectrocauteryisbeinguseddur-
Collapserhythm- ThereisnoECGrhythminthe
ingtheoperation,pacemakermayhavetobeputonasyn-
case of cardiac arrest or asystole. Immediate manage-
chronousmodetopreventinhibitionofthepacemakerby
mentshouldbedoneaccordingtoFlowChart3.
electrocauteryradiofrequencycurrent.(Fig.14) 9
Pacemaker
New or worse cardiac arrhythmias in the
perioperativeperiodareusuallytemporaryoccurrences,
oftenduetotheresultoftransientphysiologicorpharma-
cologicimbalance.Antiarrhythmicdrugshavethepoten-
Note
tialtofurtheraggravatethisimbalance.Therefore,early
 OccasionalPwavesarevisible,but arenot relatedtotheQRScom-
useoftemporarypacemakerduringperioperativeperiod
plexes.TheQRScomplexesarepreceded byabriefspike,represent-
is preferred nowadays. More than 90% of pacemakers ingthepacemakerstimulus.TheQRScomplexesarebroad.Because
pacemakersstimulatetherightventricleandcause‘ventricular’beats.
are inserted for the treatment of bradyarrhythmias oc-
Fig 14. Pacemaker
curring either after tachycardia (bradytachy syndrome)
Anaestheticconsiderations
orAVconductiondisordersorbythemselves(sicksinus
All patients undergoing anaesthesia and surgery
syndrome).
should have ECG monitoring. Lead II and V are supe-
5
Temporarypacemakermaybeinvasive(epicardial riorforarrhythmiadetectionanddiagnosisbeforetheap-
and endocardial) or non-invasive (transcutaneous and pearanceofphysicalsignse.g.changesinBP,heartrate
transesophageal).Thepacingmayalsobeunipolarorbi- or heart sounds. After establishing from ECG that ar-
polar. Unipolar pacing describes the placement of the rhythmiaispresent,itiscrucialtoevaluatepatient’sre-
sponse to altered rhythm in rate and type of treatment
negative(stimulation)electrodeintheatriumorventricle
required.Correctionofcontributingcauseandfinalline
andthepositive(ground)electrodedistantfromtheheart.
oftreatmentfollowsthereafter.Routinemeasuresforall
Bipolar pacingdescribes placementof thenegative and
intraoperativearrhythmiasareasfollows(Table3&4)
319