Beruflich Dokumente
Kultur Dokumente
1968 - 2016
Meanelectricalaxis
TheMEAdescribestheaveragedirectionoftheventriculardepolarizationprocessinthefrontalplane.It
represents the summation of the instantaneous depolarization boundaries during ventricular activation
(QRS complex). Estimation of the MEA helps the clinician identify major intraventricular conduction
disturbancesorwithlesssensitivityventricularenlargementpatternsthatshifttheaveragedirectionof
ventricularactivation.SincetheMEAisdeterminedinthefrontalplane,onlythesixfrontalleadsareused
(notchestorbaseapexleads).Byconvention,theleadsreferencepositionsaredefinedbydegrees(from0
to180)aroundacircle(seefigurebelow).Thepositivepole(electrode)ofmostleadsliesonthepositive
side of the circle; however, it is important to note that the positive pole of leads aVR and aVL lie on the
negativesideofthecircle.TheMEAcanbeestimatedbyeitherofthefollowingmethods:
Find the lead (I, II, III, aVR, aVL, or aVF) with the largest R wave (or more precisely, the greatest net
positive QRS area)). The location of the positive electrode of this lead along the frontal axis is the
approximateMEA.
Findthelead(I,II,III,aVR,aVL,oraVF)withthemostisoelectricQRS(positiveandnegativedeflections
areaboutequal).Thenidentifytheleadperpendiculartothisleadonthehexaxialleaddiagram.Ifthe
QRSinthisperpendicularleadismostlypositive,theMEAistowardthepositivepoleofthislead.Ifthe
QRS in the perpendicular lead is mostly negative, the MEA is oriented toward the negative pole. If all
leads appear isoelectric, the frontal axis is indeterminate. Normal MEA ranges for dogs and cats
generallyorienttowardsleadsIIandaVF.
ECGcomplexmeasurement
Abnormalcomplexmeasurementsmayindicatespecificchamberenlargementorhypertrophy,aswell
as conduction or repolarization abnormality. Waveform amplitudes are recorded in millivolts (mV) and
durationsinseconds.Onlyonethicknessoftheinscribedpenlineshouldbeincludedforeachmeasurement.
Atatracespeedof25mm/sec,eachsmall(1mm)boxontheECGgridis0.04secondsindurationfromleft
to right. At a paper speed of 50 mm/sec, each small box equals 0.02seconds. At standard calibration, a
deflectionupordownof10smallboxes(1cm)equals1mV.
COMMONECGARTIFACTS
Artifacts complicate ECG interpretation and can mimic arrhythmias. Common ECG artifacts include
intermittent shivering or muscle tremor artefact, purring in cats, respiratory motion or limb movement
artifacts, and 60Hz electrical interference. ECG artifacts are sometimes confused with arrhythmias, but
artifacts do not disturb the underlying cardiac rhythm. In contrast, ectopic complexes often disrupt the
underlying rhythm and are followed by a T wave. Identifying whether the ECG deflection in question
changes the underlying rhythm and also is followed by a T wave usually allows differentiation between
intermittent artifacts and arrhythmias. Evaluating more than one simultaneouslyrecorded lead is also
helpful.
HEMODYNAMICCONSEQUENCESOFARRHYTHMIAS
The hemodynamic effects of an arrhythmia depend on a number of factors. These include whether
underlyingdiseaseispresentandtheeffectitmighthaveoncardiacfunction,theventricularactivationrate,
the duration of the arrhythmia, the temporal relation between atrial and ventricular activation, the
sequenceorcoordinationofventricularactivation,drugtherapy,andtheanimalsactivitylevel.Arrhythmias
that compromise cardiac output and coronary perfusion promote hypotension, myocardial ischemia,
impaired pump function, and, sometimes, sudden death. These arrhythmias tend to be either very rapid
(e.g.sustainedventricularorsupraventriculartachycardias)orveryslow(e.g.advancedAVblockwithaslow
orunstableventricularescaperhythm).
Rapidtachycardiaspromotemyocardialischemiabecausetheyreducecoronaryperfusionpressureand
shorten diastole (when most coronary blood flow occurs). Rapid ventricular tachycardia can quickly
degenerateintofibrillation.Supraventriculartachycardiacouldpromotesecondaryventriculararrhythmias
related to poor myocardial perfusion, ischemia, and increased sympathetic stimulation. Persistent
tachycardiaofeithersupraventricularorventricularorigin(e.g.ventricularratesof180200beats/minute)
willcausemyocardialfailurewithinafewweeks.Theresultingcardiacenlargement,functionalchanges,and
neurohormonal activation that occur mimic spontaneous cardiomyopathy. This tachycardiainduced
cardiomyopathyisreversibleifheartrateiscontrolledwithinafewweeksofonset.
AF and atrial standstill cause loss of effective atrial contraction (the atrial kick). This can negatively
affectventricularfilling(preload).Atslowerheartrates,therelativeimportanceofatrialcontractiontototal
ventricularfillingissmall,soanynegativeeffectoncardiacoutputislikelytobeclinicallyinconsequentialat
rest. However, as heart rate increases, the importance of atrial contraction increases; the atrial kick can
contributeupto30%oftotalventricularenddiastolicvolumeathighheartrates.Duringexerciseorwith
heartfailure,thelossofatrialcontractioncanhaveapronouncednegativeeffectoncardiacoutput.
Cardiac output also can be impaired by loss of AV synchronization, as well as by ventricular
dyssynchrony. AV synchrony is lost when the atria and ventricles beat at different rates, as occurs with
various premature beats and abnormal tachycardias, during 3rd degree AV block (with ventricular escape
rhythm), and also with accelerated ventricularorigin rhythms, including an artificially paced ventricular
rhythm. Ventricular dyssynchrony involves delayed or uncoordinated activation and contraction of one
ventricle compared to the other, or septum compared to free wall. Ventricular tachyarrhythmias typically
causesomedegreeofventriculardyssynchrony,whichcanexacerbatethearrhythmiasnegativeimpacton
cardiac output at any given HR. Major bundle branch blocks also cause dyssynchronous ventricular
contraction that could reduce cardiac output depending on HR and myocardial function. Especially in
animals with underlying myocardial disease, ventricular dyssynchrony can contribute to deteriorating
cardiacfunction,evenwithoutovertintraventricularconductiondelayorventriculartachyarrhythmias.
ARRHYTHMIAS:WHENTOTREAT?
The arrhythmias ofgreatest concern are those that cause hemodynamic compromise such as
hypotension during anesthesia or clinical signs like syncope. Some arrhythmias associated with breed
relateddilatedcardiomyopathyareknowntobeassociatedwithsuddendeath;thisisanissueinDoberman
pinschers. Conversely, especially in asymptomatic animals with a structurallynormal heart, the risk of an
arrhythmia might be very low. Such arrhythmias can include isolated premature beats, accelerated
idioventricularrhythm,briefepisodesofparoxysmaltachycardia,andintermittentlowgradeAVblock.The
question of whether to use antiarrhythmic drug therapy for arrhythmias that cause no clinical signs is
controversialandinfluencedbyindividualcircumstances.Nevertheless,inallcasesasearchforunderlying
abnormalitiespotentiallyassociatedwiththearrhythmia,aswellasmonitoringofthepatientsrhythmand
clinicalstatusarewarranted.
Arrhythmiascausingacuteclinicalsignsshouldbetreated,asshouldpersistenttachycardias,because
of their negative longterm effect on myocardial function. Successful therapy often means reduction in
frequencyorrepetitiverateofectopicbeatstorestorenormalhemodynamicstatusandeliminateclinical
signs.Someantiarrhythmictherapiesarethoughttoreducetheriskforsuddendeath;however,thereisno
clinicaltrialevidencethatreductionofarrhythmiafrequencywilltranslatetoimprovedsurvivalorreduction
in the risk for sudden cardiac death. Besides their expense, antiarrhythmic drugs have multiple adverse
effectsthatcanincludeprovokingnewarrhythmias(proarrhythmia).
Exercise restriction and stress avoidance are important to reduce sympathetic nervous activation
(which can exacerbate arrhythmias) and as well as cardiac workload. Treatment for concurrent cardiac or
extracardiac disease is the best management for some arrhythmias. For example, in the setting of
congestive heart failure (CHF) isolated arrhythmias are usually ignored and the heart failure managed
medically.
NORMALANDABNORMALCARDIACRHYTHMS
The predominant rhythm in most healthy dogs evaluated by ambulatory monitoring1,2,5,1619 is sinus
arrhythmia with a daily average heart rate of about 70 to 85/minute, seemingly varying with breed.
Wandering atrial pacemaker is commonly observed in dogs and transient second degree AV block is
sometimespresent;thesearemanifestationsofvagotoniaindogs.Forcatsthedailyaverageheartrateis
typically 150 to 170 per minute on 24h Holter recordings with significant variation in average heartrate
among cats.6,8,20,21Althoughsinusarrhythmiais uncommonin hospitalizedcats,thosemonitoredat home
oftenexhibitperiodsofthisrhythm.
The number of ventricular and atrial ectopic complexes considered normal is a source of some
controversy in both dogs and in cats. Multiple studies show very small numbers in most healthy dogs
typically <10 PACs and <10 PVCs in 24h in healthy subjects but again, there is individual variation. The
assessment of normal with respect to ectopy is complicated by the frequent occurrence of escape
complexes during sleep and our inability to compare Holter data to a true gold standard of (genetic)
normalcy.Echocardiographyistypicallyusedbutisaninferiormethodfordecidingiftheheartiselectrically
or genetically normal. This issue becomes especially obvious in canine breeds prone to heart rhythm
disturbances associated with cardiomyopathies (including Doberman pinschers 3,22,23, Boxers,24,25 English
bulldogs,26Irishwolfhounds,27,28andgreatDanes29).Asimilarconcernarisesincatsowingtothehighdegree
ofocculthypertrophiccardiomyopathy(HCM)inthisspecies.30
SinusRhythms
Thenormalsinusnodecandischargeregularly(normalsinusrhythm),andirregularlyduetoautonomic
influence (sinus arrhythmia). Sinoatrial discharge rate also can be slower or faster than normal for the
species(sinusbradycardiaandsinustachycardia,respectively).Eachoftheserhythmsischaracterizedbya
normalPwaveprecedingtheQRScomplex.Undersomeconditionssinusbradycardiaandsinustachycardia
are physiological, as with sleep or exercise; however, these rhythms can also arise from number of
influencesandmedicaldisordersasindicatedbelow.Sinoatrial exitblock,sinusarrest,and sinusnodere
entry are considered abnormal rhythms involving the sinus node (see Table 3). Physiologic sinus rhythms
duringroutineclinical(hospital)examinationsincludenormal(regular)sinusrhythmandsinusarrhythmiain
dogs. Sinus arrhythmia does occur in unstressed cats but is uncommon in the clinic due to sympathetic
dominanceinthatsetting.
It also should be noted that sinus node activity usually persists in the presence of functional or
anatomical impairment of atrioventricular (AV) conduction. This is a useful diagnostic feature especially
when atrial activity is driven by the sinus node during periods of AV block, nodal (junctional) rhythm,
ventricular tachycardia (VT) or ventricular pacing. These rhythms often lead to socalled AV dissociation,
which is simply a description of two independent pacemaker foci one driving the atria and one
depolarizingtheventricles.AVdissociationitisnotarhythmdiagnosispersebutaconsequenceofanother
rhythm disturbance. Although retrograde atrial activation can occur during AV dissociation,31 leading to
capture(depolarizationorsuppression)oftheSAnode,thisisrelativelyuncommonindogsandcats.
Intheclinicalsettingnormalsinusrhythmindogsoccursatrelativelyhigherratesofapproximately60
to180perminutewhenrecordedbyECGandwiththedoginlateralrecumbency.Theheartrateforcatsin
normalsinusrhythmisusually160to240perminute,again,withtherecordingdoneinlateralrecumbency
(andundoubtedlyinducingstress).Sinusarrhythmiaindogsischaracterizedbysimilarratesbutwithcyclic
variationintheatrialrateandoftenawanderingatrialpacemaker(withPwavesbecomingtallerduringthe
shortercyclesintheleftcaudalleads).Althoughmostsinusarrhythmiastendtodevelopatrelativelyslow
heartratesindogs,concurrentsympatheticandparasympatheticsurgescanoccurresultinginarelatively
fast, but irregular rhythm. Most sinus arrhythmias in dogs are ventilation related, with heart rate
acceleratingthroughinspiration;however,thisrelationshipisnotalwaysobvious,especiallyinpantingdogs
orwhentheoverallsinusrateisrelativelyhigh.Inthesecases,otherfactors,suchasbaroreceptorreflexes,
might also be operational. Dogs with respiratory disease often show pronounced sinus arrhythmia with a
wandering pacemaker. The short cycles in these cases can resemble premature atrial complexes (PACs)
althoughtheearlierPwavesarerarelysummatedonthepriorTwaveduringsinusarrhythmia(incontrast
toPACs).Asageneralrule,vagallyinducedarrhythmiasshouldabateorbecomemoreregularwithexercise
orothercausesofsympathetictone.
FailureofsinusnodedischargeleadstoatransientabsenceofPwavesandtherhythmiscalledsinus
arrestwhentheensuingpauseexceedsattwonormalPPintervals.Briefpausesaresometimesreferredto
as sinus pause and this might represent a variant of sinus arrhythmia, sinoatrial block, or sinus arrest. In
cases of recurrent sinus arrest the heart will usually be rescued by pacemaker cells located in the atrial
tissues,AVjunction,orHisPurkinjesystem.Thesesubsidiarypacemakerscaninitiateescapecomplexesor
an escape rhythm. Chronic, progressive, sinus node dysfunction is especially prevalent in miniature
schnauzers, West Highland white terriers, and Cocker spaniels, but also observed in other breeds. With
sufficientescapeactivitymostdogsareasymptomatic,butfailureofsubsidiarypacemakersasignofmore
diffuseconductionsystemdiseasecanresultincollapseorsyncopecreatingthesicksinussyndrome.3240
Additionally some dogs with sinus node disease experience atrial or other types of paroxysmal
supraventriculartachycardiasthatcanoverdrivethesinusnodeandpromoteperiodsofsinusarrest.Thisis
the socalled bradycardiatachycardia syndrome of sick sinus syndrome. Most of these cases are easily
diagnosedfromastandard2to5minuteECG,especiallyincasesofsymptomaticsinusnodedysfunction.
Sinus arrest is often confused (and might overlap with) the vagallymediated sinus bradycardia and
arrest associated with an exaggerated baroreceptor reflex. This reflexmediated (vasovagal,
neurocardiogenic)syncopegenerallystemsfromacombinationofvagallyinducedcardiacdepressionand
thesimultaneouswithdrawalofsympatheticstimulationtobloodvessels.Classically,weaknessorcollapseis
induced by sudden sympathetic stimulation of the heart associated with a stressor. This reflex involves
activationofcardiacmechanoreceptors(Cfibers)leadingto(inappropriate)activationofthebaroreceptor
reflex.Thereflexismostoftenprecededbyaperiodofsinustachycardiafollowedquicklybysuddensinus
node slowing, transient AV block, sinus arrest, and junctional or ventricular escape activity. These can be
readilyobservedonaneventmonitor.Inhumans,vasodepressoreffects(vasodilation)canpersistevenafter
recoveryoftheheartrate;thus,thediagnosiscanbeelusivewithoutanexcellenthistoryandeventmonitor
recording.(Frequently,recordingstakenjustafterthefaintingarenormal).Althoughthisconditionisbarely
mentionedinveterinaryliterature,itislikelythediagnosisinmanycasesofsocalledsicksinussyndrome
whensinusarrestisrecordedduringexercise/excitementinducedsyncope.
Table3.SinusRhythms
Rhythm Comments
Normalsinusrhythm PtoPintervalsvaryby<10%;normalHRforspecies
CyclicspeedingandslowingatnormaltoslowHRforspecies.Often
Sinusarrhythmia synchronizedtoventilation.Wanderingatrialpacemakercommonly
observed.
Sinusbradycardia Slowsinusrhythm;regularorirregular.
FastsinusrhythmwithsubtlevariationinPtoP(RR)intervals;vagal
maneuversmighttransientlyalterthecyclelength.
Sinustachycardia
Fastsinustachycardia,over~240to250/min,canresultinTwave/Pwave
fusion,confusingtherhythmdiagnosis.
Longpausesduringsinusarrhythmia;canbenormal(vagal)orearlysignof
Sinuspause
sinusnodedysfunction.
Termedsicksinussyndrome(SSS)whenassociatedwithclinicalsignsand
nottriggeredonlybyexcitement.SignsinSSSusuallydependonalackof
Sinusarrest
escapeactivity.Sinusarrestcanalsooccurwithinappropriateactivationofa
baroreceptorreflex(reflexmediatedsyncope).
Rareindogsandonlytenableasadiagnosiswhentheinteratrial(Pwave)
intervalboundingalongpauseisexactlytwicetothreetimesthenormal
PPinterval.Nearlyimpossibletodiagnoseinthesettingofsinusarrhythmia.
Sinoatrialblock
AnothervariantisSAWenckebachperiodicity;thisisconsideredwhentheP
Pintervalprogressivelydecreasesfollowedbyarelativelylongpause(this
mightbeanormal,vagallyinducedrhythm).
Difficulttodiagnosiswithcertainty;thecoupledPwavesshouldbenearly
identical.Canbeconfusedwithsinusarrhythmiaoccurringinpaired
Sinusnodereentry complexesfollowedbyapause.Alsocanbeconfusedwithatrialbigeminy
(sinuscomplexfollowedbyanectopicatrialcomplex)iftheectopyoriginates
nearthecristaterminalis(i.e.,closetotheSAnode).
In considering the differential diagnosis of sinus rhythm disturbances, it is emphasized that most are
causedbyeitherexaggeratedvagalorsympathetictone.Forexample,anathleticdogislikelytohaveavery
low resting heart rate, often falling into the 40s or lower, a physiologic sinus bradycardia. Patients with
elevated CSF pressure can develop sinus bradycardia through activation of the baroreceptor reflex
(Cushingsreflex)andsecondaryincreasesinvagaltone.Paradoxically,manycausesofshockincatsare
associated with sinus bradycardia. Conversely, predictable causes of reflex sinus tachycardia include pain,
anxiety,hypotension,andheartfailure.Additionally,drugssuchasanesthetics,digoxin,dexmedetomidine,
phenylephrine, theophylline, and catecholamines (acting directly or via autonomic effects); plant, animal,
prescription and illicit drug toxicities body temperature; and endocrine status (especially thyroid and
adrenal) can positively or negatively modify sinus node discharge rate. Thus the management of sinus
rhythmdisturbancesisfocusedinitiallyonidentifyingandtreatinganyunderlyingconditions.
In most situations sinus tachycardia means activation of the sympathetic nervous system. A rapid
volume or colloid infusion will slow the heart rate in many cases of reflex sinus tachycardia due to
hypovolemiaoranothercauseofreducedventricularpreload.Thisisoftenafirsttreatmentincriticalcare
andperioperativesettings(forpatientsnotincongestiveheartfailureorCHF).Pain controlorrelieffrom
anxiety often reduces a physiological sinus tachycardia, and successful therapy of heart failure usually
reducessinusnoderateaswell.Occasionally,inappropriatesinustachycardiaistreatedwithabetablocker
such as esmolol (IV) or atenolol (PO). This is especially relevant when the sinus rate persistently exceeds
~240/minuteindogsor~280/minuteincatsandnodefinableetiologyhasbeenfound.Althoughatenolol
therapycanbeadministeredtobluntthesinustachycardiaofcatswiththyrotoxicosis,inmostcatstheheart
rateslowswithmethimazoletherapy.Drugtherapyofsinustachycardiamightalsobeappropriatewhena
sympathomimetic toxin (e.g. Bakers chocolate) has been ingested and the heart rate does not slow with
volumeinfusionandsedation.
Sinus bradycardia can be treated and sometimes prevented in the hospital with atropine or
glycopyrrolate.Catswithcardiogenicshockrarelyrespondtoatropineandarebesttreatedwithaninotropic
drugwithsympathomimeticproperties(forexample,dobutamineat2.5to5mcg/kg/minforinitialtherapy).
Withincreasedcardiacoutputandpassivewarmingtheheartratewillincreaseincatsthatsurviveandoften
Pwaveswillbecomemoreobvious.Shorttermmanagementofsinusbradycardiathatisrefractorytodrugs
can involve temporary pacing by transvenous, transesophageal, or transcutaneous methods4149 provided
thesedationoranesthesianeededtomaketheseprocedurestolerableandhumaneisgiven.
The best longterm therapy for sick sinus syndrome (SSS) is permanent transvenous pacing. In
bradycardiatachycardiasyndrome,antiarrhythmicdrugsthateithersuppressatrialectopyorblocktheAV
node can also be given once pacing has commenced (see next section on atrial arrhythmias). Pacemaker
programming is critical for optimal system performance (e.g. VVIR or rateresponsive demand mode) 5056
andlongtermoutcomesaregenerallyverygoodwithsinglechamberatrialorventricularpacing(thelatter
islesscomplicated).Althoughoftenprescribed(andanecdotallyappeartoreducelethargyandweaknessin
somedogswithearlystageSSS),anticholinergicdrugssuchashyoscyamine(Levsin)orsympathomimetic
drugssuchasterbutalineandtheophyllinelongactingarerarelyeffectiveinpreventingrecurrentboutsof
sinoatrial syncope. These drugs generally are only used if pacing cannot be performed for some reason.
Importantly,pacemakertherapyshouldntbedelayedfordrugtrialsunlessthediagnosisisuncertainorthe
symptomsinfrequent.
Optimal treatment for sinus node depression related to documented reflexmediated syncope is
unknown. For those with predominately cardiodepressor activity (sinus slowing/AV block) cardiac pacing
with hysteresis might help; however, if there is a prominent vasodilator component, pacing could be
insufficient to prevent collapse or syncope. This has not been studied in veterinary medicine. In these
patientstreatmentisdirectedinitiallytocontrollingcircumstancesthatprecipitatesyncopeandmanaging
any identified comorbidity (such as heart failure, pulmonary hypertension or respiratory disease). Beta
blockadegiventopreventtheinitialcardiactriggeringofthereflexhasbeendisappointing,oftenmakes
thingsworse.Medicaltherapywithhyoscyamine,theophyllinelongacting,orterbutalinecanbetriedas24
weektrials.
SupraventricularArrhythmias
Atrial and other supraventricular rhythm disturbances are among the most common and difficult to
treat of all ECG diagnoses These supraventricular arrhythmias include the following: premature atrial
complexes(PACsorAPCs),focalandreentrantatrialtachycardias,11,5759atrialflutter,57,6068atrialfibrillation
(AF),28,6991 reentrant supraventricular tachycardia (SVT) using an accessory bypass tract,9296 nodal
(junctional)rhythms,31andatrialstandstill(Table4).Theauthorshaveexcludedsinusrhythmdisturbances
inthisclassificationalthoughothersincludesinustachycardiaasaformofSVT.
Conceptually it is helpful to consider the most common atrial arrhythmias as interrelated. These
include recurrent PACs, focal and microreentrant atrial tachycardias,97 atrial flutter,63,65 and AF. Some
patients exhibit all of these rhythm disturbances at one point or another. The diagnosis of PACs and
nonsustained(paroxysmal)atrialtachycardiaisrelativelystraightforward(seeTable4),butthedifferences
betweensustainedatrialtachycardiaandatrialfluttercanbesubtle;withoutelectrophysiologicalstudies,is
sometimesdifficult totell onefromtheotherandwedonotyet havefirmcriteriaforthesediagnosesin
small animals. In general, atrial flutter is observed in dogs with dilated right atrial chambers and is
characterized by sawtoothed flutter waves in the baseline and the lack of an isoelectric shelf. Atrial
tachycardias in dogs often fit the human criteria for focal atrial tachycardia and many exhibit positive P
waves in the caudal limb leads creating some diagnostic confusion with sinus tachycardia. Furthermore,
largeTawavesinatrialtachycardiacanmimicflutterwaves.Theatrialrateinatrialtachycardiaisoftenin
the250to300perminuterange(orfaster)andphysiologicalAVblockiscommon.97Withatrialflutterthe
atrialrateisusuallyinthe260360/minuterangebutthemacroreentryloopintherightatriumcanresultin
slowerorfastercyclelengths.63Therecognitionofatrialtachycardiaorfluttercanbechallengingifthereisa
regularconductionsequence,especiallywith1:1atrioventricularconduction,asectopicPwavesorFwaves
areburiedintheQRScomplexesorSTT.Incasesofregular,narrowQRStachycardia,theECGdifferential
diagnosisisusuallyoneoffourSVTs:(1)sinustachycardia(typically<300/min);2)focalatrialtachycardia;3)
atrial flutter; or 4) AV nodaldependent, orthodromic reentrant SVT using an accessory pathway or
longitudinal dissociation of the AV node. Blocking the AV node is especially helpful in confirming the
diagnosis and can be attempted with a vagal maneuver, diltiazem, or esmolol (see below).
Table4.Atrial&SupraventricularRhythms
Rhythm Comments
Mustdistinguishfromsinusarrhythmia
Prematureatrialcomplexes PrematurePoftenburiedinthepriorSTT
Atrialechoes(retrogradeactivity) AlongerPRintervaliscommonwithPACs
Retrograde(negative)Pwaveswithatrialechoes
Atrialtachycardia Canresemblesinustachycardia
Focalmostcommonindogs Typicallyrelatedtoatrialdilatation
Regularconductionsequencescanleadtodifficultiesin
Atrialflutter diagnosis;blockingtheAVnode(vagalmaneuverordiltiazem)
usuallyrevealsflutterwaves
Irregularventricularresponseisexpectedexceptincasesof
Atrialfibrillation
concurrentAVconductiondisease
Presenceofventricularpreexcitationduringsinusrhythmisa
Orthodromicsupraventricular
tipoff(WPW);however,electrophysiologicstudymightbe
tachycardia(accessorypathway)
neededfordiagnosis.RetrogradePwavesinSTsegment.
Nodal(junctional)rhythms EscaperhythmsaresecondarytosinusnodedysfunctionorAV
Junctionalescapes block
Junctional(nodal)tachycardia Nodaltachycardiasrareexceptwithdigitalistoxicity
MostcommonabsenceofPwaves,increasedamplitudeT
Atrialstandstill
waves(positiveORnegative)&wideningofQRScomplex.
Transient(hyperkalemia)
Cats:oftenmisdiagnosedasventriculartachycardia.
Persistent
Sinewaveswithbradycardia=nearterminalrhythm.
VentricularArrhythmias
Arrhythmiasarisingintheventricleparallelthoseoftheatriaintermsofnomenclature.Bothtypesof
arrhythmias can be hemodynamically destabilizing, but there are important differences: 1) the AV node
need not be activated to generate a QRS complex so that heartrate control is generally not an effective
strategy; and 2) there is greater potential for sudden death if the rhythm degenerates to ventricular
fibrillationorasystole.Unfortunatelyitisdifficulttopredictwhichpatientswilldiesuddenlyorwillbenefit
fromtherapy.
In terms of etiology, the aforementioned categories listed in the Introduction and the various
etiologies mentioned under atrial arrhythmias also apply to ventricular ectopy. Some breeds especially
boxers or English bulldogs (with arrhythmogenic right ventricular cardiomyopathy = ARVC), and many
Doberman pinschers with occult DCM are prone to ventricular ectopy as part of a genetic/breed
predisposition.AnotherexampleisDuchennecardiomyopathyingoldenretrievers.110Thesearrhythmiascan
develop within or before the development of overt ventricular dysfunction. Other breeds develop
ventricularectopyasacomponentof dilated cardiomyopathy. Someofthesedogshave relatively normal
echocardiogramsatthetimeoffirstrecognitionofthearrhythmiaandexhibitclinicalfindingsofDCMonly
further down the road. There are sporadic cases of myocarditis seen in dogs (postviral(?); septicemia;
Chagas myocarditis), and cats have a wellrecognized endomyocarditis that is difficult to diagnosis
antemortem.Nodoubttherealsoaremanyundiscovered,geneticallyprogrammedchannelopathiesindogs
that can serve as a substrate for ventricular ectopy but are as yet unrecognized. One wellcharacterized
example of genetic electrical disease is the inherited ventricular ectopy seen in certain lines of German
shepherds.111 When ventricular ectopic complexes are recognized in a canine breed that is atypical for a
geneticcardiomyopathy,ordiagnosedinadogwithnoothersignsofheartdisease,theclinicianalsomust
considerahostofpotentialnoncardiaccauses,includinghypokalemia,autonomicimbalance,112myocardial
ischemia,coronarythrombosis,andotherusualsuspectssuchassplenicmasses,anemia,infections,and
drugs.Veterinarianshavelearnedtoexpectsomeconditions,suchasgastricdilatationvolvulus,toinduce
ventriculararrhythmias.
AclassificationofventricularrhythmsislistedinTable5.Idioventricularrhythmsarisefromnormally
present pacemakers in the HisPurkinje system. When activated, these escape complexes are rescue
mechanisms for sinus node arrest or AV block and should not be suppressed. The typical idioventricular
(escape)rhythminthedogdischargesat20to40/minute;however,inthecattheescaperateismuchfaster
(typically110to120/minute)andoftenapproaching130/minuteincatswithchroniccompleteAVblock.113
The socalled accelerated idioventricular rhythm (AIVR) is thought to indicate normal pacemaker cells
hastenedbysomeinjurythathasalteredtransmembranepotentialsorpacemakercurrents.Inthisregard,
sympathetic activity and enhanced calcium transits are relevant factors. These are quite common in dogs
following various ischemiareperfusion injuries or after general anesthesia. These rhythms are faster than
escape rhythms and tend to initiate in late diastole, warmup for a few beats, then manifest at normal
heartrates(typically60to180perminute).TheslowVTsoftencompetingwiththesinusrhythmsuchthat
fusion complexes (from combined ectopic and sinus impulses) are common in AIVR. In general these
rhythmsarewelltoleratedandleftuntreated,infavorofaddressinganyunderlyingmedicalissues.
Table5.VentricularRhythms
Rhythm Comments
Ventricularescapes Secondarytosinusbradycardia,sinusarrest,orAVblock;
Ventricularescaperhythm idioventricularrhythmcanalsobeaterminalrhythmfrom
(idioventricularrhythm) downwarddisplacementofthepacemaker.
TimingofPVCsshouldconsiderRonTandlatediastolicPVCs
(distinguishfromescapecomplexes)
Prematureventricularcomplexes
Distributionalpatternsincludehaphazard,bigeminy,trigeminy(two
(PVCs,VPCs)
variants),couplets,triplets
Morphologyincludesuniform(unifocal)&multiform
Variouscategorizationsbasedonrateandmorphology
Ventriculartachycardia(VT) AcceleratedIdioventricularrhythmsgenerallybenign
VTmonomorphic,bidirectional,polymorphic,torsade
Ventricularflutter Signwavelike;cannotdistinguishRfromTwave
Noconsistentlyformedwaveforms;coarseorfineVF
Ventricularfibrillation
FineVFcanbeconfusedwithasystole
Absentrhythm
Asystole(ventricularstandstill)
CanoccurinDCMorinchroniccongestiveheartfailure
In contrast to idioventricular rhythms, premature ventricular complexes (PVCs, VPCs) and most
ventricular tachycardias (VTs) arise early in the cardiac cycle (i.e. compared to the dominant RR cycle);
these ectopic complexes can be uniform or multiform in morphology. (Note: a fusion complex between a
PVCandasinusimpulsealsocancreateintermediateQRSformsandshouldnotbeviewedasamultiform
complex). In Holter ECG systems, 3 (or more often 4) linked PVCs constitute a run of VT. Ventricular
tachycardias can be slow or fast; paroxysmal or sustained; monomorphic or polymorphic; or rapidly
varyinginorientation(torsadedepointes).Theventriclesalsocanflutter(creatingsinewaves),orfibrillate
(disorganizedandlethalactivation).InverysickanimalsorinthosewithCHF,deathcanoccurfromasystole,
whichisessentiallyventricularstandstill.
The ECG diagnosis of PVCs or of VT is generally straightforward, although it can be confused by
supraventricular tachycardias conducted with aberrancy (bundle branch block) or by hyperkalemia. A full
workup includes drug and medical history, consideration of clinical signs (weakness, collapse or syncope),
Echofindings,laboratorytests(CBC,chemistries,cardiactroponinI),andoftenabdominalultrasound.These
areobtainedtodeterminethemostlikelycauseandoverallclinicalsignificanceofthearrhythmia.AHolter
ECGcancontributetoassessingtheseverityandcomplexityofthePVCs,aswellasprovideabaselineand
objective measure of response to therapy. Although some cardiologists always perform a baseline Holter
before starting antiarrhythmic therapy, in dogs with syncope or dangerousmorphology rhythms, there is
someriskofdelayingtherapy(andasinglesuddendeathduringthatshorttherapydelaycanbeenoughto
modifyonesviewaboutalwayshavingabaseline!).Asdiscussedearlier,theabsolutenumberofnormal
PVCs per day is controversial, and related in part to classification of some late ventricular ectopic
complexes(abnormalvs.escapes).BasedonsomeHolterECGstudies,>10/dayincatsand>50to100/dayin
dogswouldbeconsideredabnormal114(butthesearearbitrarynumbersandmanycardiologistsuselower
limits). Spontaneous daily variation24,115 is common (up to ~85%); this should be taken into account when
assessingtherapyaswell.Anabsolutenumberofcomplexesper24hisnotveryimportantwhenthetotal
countislow.Recallthereare1440minutesperdaysoatotalof1000PVCs,whileclearlyabnormal,isstill
<1/minute on average. More critical to consider are: the impact of the underlying cause, the rate and
complexityofthearrhythmia(modifiedLowncriteria),andthepresenceofclinicalsigns.
Theassessmentandtherapyofventriculararrhythmiasisbothcontroversialandconfusing.Thepatient
history (collapse or syncope), signalment, and underlying cause should factor into the assessment. For
example, most cats with chronic ventricular ectopy have structural heart disease (cardiomyopathy) or at
least an elevated serum troponin suggestive of active myocardial injury, infarction, or myocarditis. A
DobermanpinscherwithPVCsonaroutineECGislikelytoprogresstowardsovertdilatedcardiomyopathy.
WhenanECGdemonstratesevenafewPVCsinadogofthisbreedthathascollapsedorfainted,theriskof
sudden cardiac death is also very high, although that might not be the case for a boxer dog. Thus clinical
signsmightpromptantiarrhythmictherapyinaDobermanpinscher,recognizingthereisnoprooftreatment
willprolonglife.Conversely,manyasymptomaticboxershavePVCsforyearswithoutattendantsignsand
arebestassessedbyhistoryandambulatory(Holter)ECGmonitoringbeforeinitiatinganytreatment.When
VTorPVCsoccurafteranacutenoncardiacdisorder,suchasgastricdilationortrauma,shorttermtherapy
mightormightnotbeneeded.Incontrast,thesyncopalboxerorgiantbreeddogwithwellcharacterizedVT
willlikelyreceivelifelongtreatment.Whenventricularectopyisidentifiedinthesettingofheartfailureitis
worthhavingareasoneddiscussionwiththeclients.Manyclientsoptfornoantiarrhythmictherapyevenin
dogswithrunsofVT.Thisisnotunreasonableconsideringthelackofefficacydata,thepotentialfordrug
sideeffectsandnegativeinotropy,andthesimplefactthatmanypetownerswouldpreferasuddendeath
tomakingadecisionforeuthanasia.Forthesereasons,indogswithCHF,theauthorsoftenignorePVCs
andshortrunsofVT,especiallyiftheserunsarenotinducingclinicalsigns.
Managementofventricularectopicrhythmsinvolvesdeterminingthemostlikelycause,advancingan
educated guess about the clinical significance of the rhythm disturbance (often after a Holter ECG),
consideringtheneedfortherapy,andpossiblychoosingoneormoredrugs.Allantiarrhythmicdrugscarry
the potential for adverseeffects and worsening of the arrhythmia (proarrhythmia). For acute hospital
managementindogs2%lidocaineremainsthedrugofchoice(2mg/kgIVbolusover2minutes;repeatedup
to 8 mg/kg over 10 minutes stop if vomiting or tremors). Lidocaine can also be used at the 12 mg/kg
dosage in cats with slow administration to prevent seizures or asystole. Second line drugs include IV
procainamide (2 mg/kg IV over 2 minutes; up to 20 mg/kg cumulative dosage in dogs; up to 10 mg/kg
cumulativedosageincats;withQRS,QT,andBPmonitoring);esmolol(loadingdoseof50to100mcg/kg
over5minutes;thereafter25to50mcg/kg/minute,IV;catswithoutCHFcantolerateloadingdosagesatthe
higher range), magnesium salts, and preservativefree amiodarone (Nexterone; see dosage under atrial
arrhythmias)asbackuptreatments.Premixed(preservativefree)Nexteroneisanexcellentantiarrhythmic
drugfordogsinhospitalsettings,andthedrugisunderused;inourhospitalitisoftenchoseniflidocaine
fails.ElectrocardioversionofVTalsocanbeeffective116butrequiresgeneralanesthesia.Forchronichome
therapy of PVCs and VT, sotalol (12 mg/kg PO b.i.d.) is generally the best tolerated (beware: negative
inotropic effects in CHF), but it is not always as effective as mexiletine (48 mg/kg PO t.i.d.) plus sotalol,
mexiletine plus atenolol (0.5 to 1 mg/kg PO bid), or oral amiodarone (46 mg/kg PO b.i.d. for one or two
weeks; then 46 mg/kg PO once daily). Amiodarone deserves respect, especially in terms impairing liver
function.Flecainide(1to2mg/kgPOb.i.d.)isapotentiallyusefuldrugbutexperienceindogsislowandthe
drugcanleadtoproarrhythmiainhumans(andpossiblydogs),especiallyinsettingsofafailingheart.We
avoidthedruginthesettingofCHForimpairedLVfunction.Theadditionofafishoilsupplementtothe
treatmentplanresultedinastatisticallysignificantreductioninthefrequencyofPVCsinBoxerdogs117and
isareasonableaddin.
ConductionDisturbances
In addition to sick sinus syndrome, persistent atrial standstill, and ventricular preexcitation (each
discussedabove),conductiondisturbancesincludetheAVblocks;bundlebranchblocks,andintraventricular
conductiondisturbances.TheAVblocksareclassifiedasfirst,second(MobitzIorWenckebachtype,Mobitz
IIA and IIB), and complete (thirddegree block). The finding of second degree block with a concurrent
intraventricular conduction disturbance (Type IIB) indicates a high risk for advancement to complete AV
block. Treatment of symptomatic AV blocks generally involves referral for permanent pacing and in the
authors opinion this should be done transvenously in most canine cases. Single or dual chamber pacing
systems can be used,45,52,53,117130 depending on a variety of patient, technical, and experience factors.
Permanent epicardial pacing has some indications, but these are best discussed with a cardiologist
experienced in pacing. Longterm prognosis depends mainly on etiology of the bradyarrhythmia (with the
best prognosis for SSS and AV block without other structural diseases and the worst for persistent atrial
standstill).
Persistent bundle branch block or phasic aberrant ventricular conduction (generally heart rate/cycle
length dependent) can be encountered in structurally normal hearts or in those with diseases of the
conductionsystem. Theseconduction disordersdo notrequire therapybut caninformfurther diagnostics
andwhenpresentduringasupraventriculartachycardiacanbereadilyconfusedwithVT.
Table6.SomeStrategiesforRefractoryVentricularTachycardia
ReevaluatetheECGcouldtherhythmhavebeenincorrectlydiagnosedinitially?Forexample,SVT
with aberrancy (intraventricular conduction disturbance) can mimic ventricular tachycardia. In
thesecases,IVdiltiazemisusuallymoreeffectivethanlidocaine.
Assess serum K+ (and Mg++) concentration. Hypokalemia reduces the efficacy of class I
antiarrhythmicdrugsandcanpredisposetoarrhythmiadevelopment.
o ForserumK+concentration<3mEq/L,KClcanbeinfusedat0.5mEq/kg/hr.
o ForserumK+between3and3.5mEq/L,KClcanbeinfusedat0.25mEq/kg/hr.
o AserumK+concentrationinthehighnormalrangeisthegoal.
o If the serum Mg++ concentration is <1.0 mg/dl, MgSO4 or MgCl2, diluted in D5W, can be
administeredat0.75to1.0mEq/kg/daybyCRI.
Trysotalol(PO),oramiodarone(IVorPOloading),orabetablockerinconjunctionwithaclassI
drug(e.g.,propranolol,esmololoratenololwithlidocaine,procainamideorquinidine)oraclassIa
drugwithaIbdrug(e.g.,procainamidewithlidocaineormexiletine).
Consider that the antiarrhythmic drug might be exacerbating the rhythm disturbance
(proarrhythmiaeffect).
o Polymorphic ventricular tachycardia (or torsade de pointes) has been associated with
quinidine,procainamide,andotherdrugtoxicities.
MgSO4 may be effective in animals with ventricular tachyarrhythmias associated with digoxin
toxicityorwithsuspectedtorsadedepointes.
o Administer MgSO4 as a slow IV bolus of 25 to 40 mg/kg, diluted in 5% dextrose in water
(D5W),&followedbyaninfusionofthesamedoseover12to24hours
o MgSO4contains8.13mEqmagnesiumpergram,soasimilarmagnesiumdoseisprovided
bycalculating0.15to0.3mEq/kg.
If the animal is tolerating the arrhythmia well, continue supportive care, correct other
abnormalitiesaspossible,andcontinuecardiovascularmonitoringaloneorwiththemosteffective
antiarrhythmicdrug.
ConsiderDCcardioversion,ifavailable.
ANTIARRHYTHMICDRUGS(thissectioniscourtesyofDr.WendyAWare)
Antiarrhythmic drugs can serve to slow a tachycardias rate, terminate a reentrant arrhythmia, or
preventabnormalimpulseformationorconduction. These effectscanoccur through modulationoftissue
electrophysiologicpropertiesand/orautonomicnervoussystemeffects.
ClassIAntiarrhythmicDrugs
TheseagentsblockmembraneNa+ channelsanddepressaction potentialupstroke (phase 0). This
slows conduction velocity and can interrupt reentrant rhythms. Their membranestabilizing effects also
includedecreasingexcitabilityandautomaticity.Theyaresubclassifiedaccordingtootherelectrophysiologic
characteristics. Class Ia agents moderately slow conduction, increase action potential duration, and can
prolong QRS complex and QT interval durations. Class Ib agents cause little change in conductivity; QRS
complexandQTintervaldurationsremainunchanged.ClassIcdrugsmarkedlyslowconduction,generally
withoutchangeinactionpotentialduration.
The electrophysiologic effects of class I drugs are extremely dependent on extracellular K+
concentration; hypokalemia may render these drugs ineffective, whereas hyperkalemia intensifies their
depressant effects on cardiac membranes. All these agents are contraindicated in animals with complete
heartblockandshouldbeusedonlycautiouslyinanimalswithsinusbradycardia,SSS,and1or2AVblock.
Lidocaine (Class Ib) has little effect on sinus rate, AV conduction rate, and refractoriness at standard
doses.ItsuppressesautomaticityinnormalPurkinjefibersanddiseasedmyocardium,slowsconduction,and
reducesthedispersionofrefractoriness.Itseffectsaregreaterondiseasedandhypoxiccardiaccellsandat
faster stimulation rates. While lidocaine often is effective against VT, it usually is ineffective against
supraventriculararrhythmias.HoweveritmayinduceconversionofSVTandrecentonset,vagallymediated
AF, in some dogs90. Lidocaine produces little or no depression of contractility when given slowly IV at
therapeuticdoses.Toxicconcentrationscancausehypotension.ThetoxiceffectsusuallyrelatetotheCNS,
includingagitation,disorientation,mentaldepression,ataxia,muscletwitches,nystagmus,andgeneralized
seizures(whichmayrequirediazepam[0.250.5mg/kgIV]orashortactingbarbiturate).Nauseacanalso
occur.
Procainamide(ClassIa)prolongstheeffectiverefractoryperiodandslowsconductionintheaccessory
pathwayofdogswithorthodromicAVreciprocatingtachycardia.Procainamidehasbothdirectandindirect
(vagolytic) effects. It is indicated for ventricular (and sometimes supraventricular) tachyarrhythmias, but
generally is less effective than quinidine for atrial tachyarrhythmias. Procainamide should be used only
cautiouslyinhypotensiveanimals.RapidIVinjectionofprocainamidecanproducehypotensionandcardiac
depression, although to a much lesser degree than quinidine; IM administration does not cause marked
hemodynamiceffects.ProcainamideCRIisusefulforarrhythmiasresponsivetoanIVbolus.Toxiceffectscan
includeGIupset,QRSorQTprolongation,AVblock,andproarrhythmia.
Quinidine(ClassIa)isnotoftenusednow,butmaybehelpfulforventricularandsomesupraventricular
tachyarrhythmiasifotherstrategiesarenotavailableoreffective.Quinidinemustbegivenwithcautionto
animals with heart failure or abnormal serum K+ concentration. Quinidine depresses automaticity and
conductionvelocityandprolongseffectiverefractoryperiod.Correspondingdosedependent ECG changes
(e.g. prolonged PR, QRS, and QT intervals) result from direct electrophysiologic and vagolytic effects;
however,atlowdosesthedrugsvagolyticeffectscanoffsetitsdirecteffectsandincreasethesinusrateor
the ventricular response rate to AF. Because of its propensity to cause vasodilation (via alphareceptor
blockade),cardiacdepressionandhypotension,quinidineisnotusedIVindogsandcats.Quinidinetoxicity
extendsfromthedrugselectrophysiologicandhemodynamiceffects.ProlongationofECGintervalsoccurs
in a doserelated manner. Marked QT prolongation, right bundle branch block, or QRS widening >25% of
pretreatmentvaluesuggesttoxicity.AVconductionblockandandventriculartachyarrhythmiascanresult.
Marked QT prolongation implies increased temporal dispersion of myocardial refractoriness, which
predisposestoTdPandVF.OtheradverseeffectsincludeGIsigns.
Mexiletine (Class Ib) is similar to lidocaine in its electrophysiologic, hemodynamic, toxic, and
antiarrhythmic properties. It is used for ventricular tachyarrhythmias in dogs. It can reduce arrhythmias
associatedwithrepolarizationabnormalities,bydecreasinglateNa+influxduringrepolarizationandthereby
decreasingEADs.ThecombinationofabetablockerorclassIIIagentwithmexiletinemaybemoreeffective
and cause fewer adverse effects than mexiletine alone. When used together, mexiletine counteracts the
action potential prolongation caused by sotalol. Sotalol, administered with mexiletine, appears to mildly
increase mexiletine plasma concentration. Adverse effects of mexiletine can include vomiting, anorexia,
tremor, ataxia, disorientation, sinus bradycardia, and thrombocytopenia; administration with food can
reduceGIsideeffects.
Class Ic agents slow cardiac conduction velocity markedly but have minimal effect on sinus rate or
refractoriness. However, high doses depress automaticity in the sinus node and specialized conducting
tissues. Proarrhythmia is a serious potential adverse effect of the class Ic agents. Flecainide prolongs the
sinuscyclelengthandAVnodalconductiontimeandrefractoriness.Flecainidehasablockingeffectonthe
delayedrectifierpotassiumcurrent(IK)similartoclassIIIagents,butthisrepolarizationprolongingeffectis
mitgatedbyitsNa+channelblockingeffect,solittlechangeinactionpotentialdurationoccurs.However,at
high plasma concentrations flecainide can prolong QT interval. Adverse effects can include GI signs,
hypotension, bradycardia, AV blocks, and sudden death. Propafenone increases AV nodal functional
refractory period, slows intraatrial conduction, and reduces ventricular excitability and triggered activity.
Propafenone also has weak beta and calcium channel blocking activity, and a vagolytic effect. It may be
effective for both atrial (including incessant atrial tachycardia) and ventricular tachyarrhythmias.
Propafenone can cause GI side effects, proarrhythmia, and increase concurrent digoxin serum
concentration.
ClassIIAntiarrhythmicDrugs
Betablockersactbyinhibitingcatecholamineeffects.ThesedrugsslowHR,reducemyocardialoxygen
demand,andincreaseAVconductiontimeandrefractoriness. Theyareunlikelytoaffectrepolarization.The
antiarrhythmic effect of betablockers relates to beta1receptor blockade rather than direct
electrophysiologiceffects.Mostoftenusedarethebeta1selectiveagentsatenolol,metoprolol,andesmolol.
Thenonselectivedrugpropranololalsoiscommonlyused.Becauseofpossiblebetareceptorupregulation
during longterm betablockade, abrupt discontinuation of therapy could result in serious cardiac
arrhythmias;gradualdosagereductionpriortodiscontinuationisrecommended.Betablockersaregenerally
contraindicatedwithsinusbradycardia,SSS,highgradeAVblock,orsevereCHF.Nonselectivebetablockers
may increase peripheral vascular resistance, because of unopposed alpha effects, and promote
bronchoconstriction by beta2 antagonism. Lipophilic betablockers, such as propranolol, can cause
depressedattitudeanddisorientation.Otheradverseeffectsofbetablockerscanincludelethargy,fatigue,
anorexia, vomiting, diarrhea, hypotension, onset or recurrence of CHF, sinus bradycardia, and AV block.
Betablockers also can mask early signs of acute hypoglycemia in diabetics (e.g. tachycardia and blood
pressurechanges),andreduceinsulinreleaseinresponsetohyperglycemia.
ClassIIIAntiarrhythmicDrugs
These agents prolong action potential duration and effective refractory period without decreasing
conductionvelocity.TheyactmainlybyinhibitingtherepolarizingpotassiumchannelIK(delayedrectifier).
The effects of some drugs in this class (e.g. amiodarone) are greater at higher HRs (usedependence),
although others exhibit reverse usedependence (e.g. sotalol). They are useful for refractory ventricular
arrhythmias,especiallythosecausedbyreentry. Thesedrugscanhaveantifibrillatoryeffectsonatrialand
ventricular tissues. Currently available agents share some characteristics of other antiarrhythmic drug
classesinadditiontotheirclassIIIeffects.
Sotalol HCl is a nonselective betablocker with class III effects at higher doses. It has been effective
againstventriculartachyarrhythmiasinmanydogsandsomecats.ItmaybemoreeffectiveinpreventingAF
than terminating it because its refractory period prolongation is more pronounced at slower heart rates
(reverse usedependence). However, its betablocking effect helps control ventricular rate in animals with
AF.Sotalolhasalsobeenusedincatswithsevereventriculartachyarrhythmias. Sotalol(disomer)prolongs
therefractory period by selectively blocking the rapidcomponent (IKr) of the delayed rectifier current
responsible forrepolarization. Sotalol can increase triggered activity (early afterdepolarizations) and can
cause TdP at high doses, or with hypokalemia at slow heart rates. Coadministration with mexiletine may
reducesotalolsproarrhythmicpotential.However,sotalolwasshowntoinduceventriculartachycardiain
young German Shepherd Dogs affected with inherited ventricular tachyarrhythmias131, and should be
avoidedasasoleagentintheseanimals.SotalolalsoisnotadvisedforBoxerswithbradycardiaassociated
syncope. Adverse effects of sotalol can include reduced myocardial contractility, hypotension, depression,
nausea,vomiting,diarrhea,andbradycardia.Thereareafewanecdotalreportsofaggressionthatresolved
aftersotalolwasdiscontinued.
Amiodarone is a unique Class III agent. While it prolongs the action potentialduration and effective
refractory period in both atrial and ventricular tissues, it also sharesproperties with all three other
antiarrhythmicdrugclasses.AmiodaroneisaniodinatedbenzofurancompoundthathaseffectsonNa+,K+,
andCa++channels,andhasnoncompetitivealpha1andbetablockingproperties. Itsbetablockingandclass
Iblike effects occur soon after administration, but maximal class III effects, with prolongation of action
potential and QTinterval durations, and reduced Purkinje fiber automaticity, are achieved after weeks of
administration. In contrast to other class III drugs which tend to induce early afterdepolarizations (EADs),
amiodarone can abolish EADs. Its Ca++ channelblocking effects may contribute to the reduced triggered
activity.Amiodaronesprolongationofactionpotentialdurationismoreuniformacrossventriculartissues
thanthatofotheragents,andtheoccurrenceofTdPassociatedwithamiodaroneislow.Amiodaronehas
beeneffectiveinconvertingAFtosinusrhythminsomedogs103.Amiodaronehasadelayedonsetofaction
and prolonged time to steady state (>10 weeks). Slow intravenous bolus administration may suppress
ventricular arrhythmias in dogs. However, use of the standard (older) IV formulation often precipitates
hypotension and anaphylactoid reactions, related to solvents (polysorbate 80 and benzyl alcohol) used to
keep the drug in solution. Acute hypersensitivity reaction therapy includes stopping IV amiodarone, and
using diphenhydramine (e.g. 1 mg/kg IV), a corticosteroid (e.g. prednisolone 12 mg/kg IV), IV fluids and
other supportive care as needed. Although antihistamine pretreatment, conservative dosing, and slow
injection over 1020 minutes have been helpful in some cases, use of standard amiodarone IV is not
currentlyrecommended.Aneweramiodaroneformulation(Nexterone)withoutpolysorbate80andbenzyl
alcoholisavailableandshouldbesafer,butisquiteexpensive.Manypotentialsideeffectsoccurwithlong
term amiodarone use, including depressed appetite, GI upset, pneumonitis leading to pulmonary fibrosis,
hepatopathy, thyroid dysfunction, positive Coombs test, thrombocytopenia, and neutropenia. Some of
these resolve with drug discontinuation or dosage reduction. Hepatotoxicity appears common and
somewhat dose related in Dobermans. Other adverse effects noted with longterm use in people include
corneal microdeposits, photosensitivity, bluish skin discoloration, and peripheral neuropathy; however,
amiodaronemayhavealesserproarrhythmiceffectthanotheragentsandreducetheriskofsuddendeath.
Amiodarone can increase serum concentrations of digoxin, diltiazem, and, possibly, procainamide and
quinidine.
Ibutilide fumarate is used for converting recent onset AF in people, but there is little veterinary
experiencewithit;ibutilideconvertedonly~50%ofacutelyinducedAFinadogstudy.Indogstudies,SA
and AV nodal suppression, increased atrial and ventricular refractoriness, QT duration prolongation,
increasedrepolarization dispersion,andinduction ofEADswereshown. Experimentally, doseseffectivein
terminatingAFalsoincreasedmyocardialrefractorinessandQTdurations.IbutilidehascausedTdPindogs
withexperimentalAVblockandcardiomyopathy. Dofetilideisanotherdrugthatselectivelyblockstherapid
componentoftherepolarizingK+current.ItalsohasbeenusedinpeopletoconvertAFandmaintainsinus
rhythm.However,itsefficacymaydependonthedurationandunderlyingmechanismofAF,anditmaybe
more effective in preventing rather than terminating AF. Dofetilide also tends to induce EADs and TdP,
especiallywithcardiacremodelingandincreasedrepolarizationvariability.Experimentallyitappearstohave
greatereffecttoprolongQTintervalindogs.
ClassIVAntiarrhythmicDrugs
This diverse group of drugs reduces cellular Ca++ influx by blocking transmembrane Ltype Ca++
channels.Diltiazemandverapamil(nondihydropyridines)haveantiarrhythmiceffects,especiallyontissues
dependentontheslowinwardCa++current,particularlythesinusandAVnodes.Theyslowthesinusrate,
increaseAVnodalrefractoryperiod,andcaninterruptsomearrhythmiascausedbyabnormalautomaticity,
triggered mechanisms, and reentry. These agents are most effective against supraventricular
tachyarrhythmias, although they might suppress ventricular arrhythmias dependent on abnormal Ca++
fluxes. Verapamil should not be used in animals with heart failure, and is rarely used clinically in other
animals. Sideeffects of these agents can include reduced contractility, vasodilation, hypotension,
depression, anorexia, lethargy, bradycardia, and AV block. They are usually not prescribed with a beta
blocker,butifso,onlywithcaution.Adverseeffectsofdiltiazemareuncommonattherapeuticdoses,but
anorexia, nausea, bradycardia, and, rarely, other GI, cardiac, or neurologic effects may occur. Cats
sporadically develop liver enzyme elevation with anorexia. Anecdotally, some cats become aggressive or
showotherpersonalitychangewhentreatedwithdiltiazem.
ClassVAntiarrhythmicDrugs
`ThedesignationofClassVissometimesusedtogroupantiarrhythmicdrugsthatworkbymechanismsother
thatdescribedintheoriginalfourclasses.Digoxin,althoughprimarilyconsideredapositiveinotropicdrug,is
useful for slowing the ventricular response rate in AF. Digoxin also may suppress some supraventricular
premature depolarizations. These effects are mediated by an increase in parasympathetic tone, which
mainlyaffectstheSAandAVnodesandatrialtissue,anddirecteffectswhichprolongAVnodalconduction
and refractory period. Anticholinergic agents, such as atropine sulfate and glycopyrrolate, increase sinus
rateandAVconductionwhenexcessivevagaltoneispresent.Bradyarrhythmiasresponsivetoparenteral
atropine or glycopyrrolate sometimes also respond to oral anticholinergic agents (such as propantheline
bromideorhyoscyaminesulfate).
AtropineResponseTest:thisisusedtodeterminethedegreeofvagalinfluenceonsinusandAVnodal
function.ResponsetoatropinechallengeismostconsistentwithIVadministrationof0.04mg/kg.AnECGis
recordedwithin510minutesafteratropineinjection.IftheHRhasnotincreasedbyatleast150%,theECG
isrepeated15(to20)minutesaftertheatropineinjection;sometimes,aninitialvagomimeticeffectonthe
AV node lasts longer than 5 minutes. The normal sinus node response is a rate increase to 150160
beats/minute(or>135beats/minute).Apositiveresponsemaynotpredictresponsetooralanticholinergic
therapy.
Sympathomimeticdrugssuchasterbutalinesulfate,abeta2receptoragonist,andthemethylxanthine
bronchodilators aminophylline and theophylline can increase HR in some animals with bradyarrhythmias
whenusedathigherdoses.
Ivabradineisaselectiveinhibitorofthesocalled funny current (If),whichis mainlyresponsiblefor
(initial)slowdiastolicdepolarizationofsinusnodecells.Byreducingthisrateofdiastolicdepolarization,the
drugdecreasesheartrate;slowerheartratesreducemyocardialoxygenrequirementandimprovecoronary
perfusion. Ivabradines reduction in the sinus rate is dosedependent. The drug does not appear to
significantly affect conductivity, repolarization, or refractoriness of the AV node, atrial or ventricular
myocardium,orHisPurkinjesystem.IthasrecentlybecomeavailableintheUS,butisquiteexpensive;there
islittleclinicalveterinaryexperiencewiththisagent.
VagalManeuver
A vagal maneuver is usually tried initially for rapid supraventricular tachycardias (e.g. during
preparationsforIVcatheterplacement).Itisperformedbymassagingthecarotidsinusregion(withgentle
continuouspressureoverthecarotidsinuses,justcaudodorsaltothelarynx),orbyapplyingfirm(butgentle)
bilateral ocular pressure, over closed eyelids, for 1520 seconds; (ocular pressure technique is
contraindicatedinanimalswitheyedisease).Althoughavagalmaneuveroftenisineffectiveatfirst,itmay
beeffectivewhenrepeatedafterantiarrhythmicdrugadministrationiftherhythmdisturbancepersists.An
IV drug that increases vagal or decreases sympathetic tone can potentiate the vagal maneuver in cases
whereitwasinitiallyunsuccessful.
Increasing vagal tone should temporarily slow the rate of sinus tachycardia and allow normal P
wavestobeseen,althoughsomeatrialtachycardiasalsoslow.ReentranttachycardiasinvolvingtheAVnode
aresometimesabruptlyterminatedbyavagalmaneuver,asanincreaseinAVrefractorinessblocksfurther
conductionaroundthereentrycircuit.ThevagalmaneuvermaytransientlysloworintermittentlyblockAV
conductiontoexposeabnormalatrialPwavesfromanautomaticectopicatrialfocus.
Table7.CommonDosagesofAntiarrhythmicDrugs
Drug Dosage
ClassI
Lidocaine Dog:initialbolusesof2mg/kgslowlyIV(over2minutes),upto8mg/kg(over
10min;stopifvomitingortremors);orrapidIVinfusionat0.8mg/kg/minute;
ifeffective,then2580g/kg/minuteCRI;canalsobeusedintratracheallyfor
CPR.
Cat:initialbolusof0.250.5(or1.0)mg/kgslowlyIV;canrepeatbolusesof
0.150.25mg/kg,uptototalof4mg/kg;ifeffective,1040g/kg/minuteCRI
Mexiletine Dog:46(8)mg/kgPOq8h
Cat:*
Procainamide Dog:2mg/kgIVover2minutes;repeatifnecessary,uptocumulativedoseof
20mg/kg;1050g/kg/minuteCRI;620(upto30)mg/kgIMq46h
Cat:1.02.0mg/kgIVover2minutes,repeatifnecessary,uptocumulative
doseof10mg/kg;1020g/kg/minuteCRI;7.520mg/kgIMq(6)8h
Quinidine Dog:620mg/kgIMq6h(loadingdose,1420mg/kg);616mg/kgPOq6h;
sustainedactionpreparations,820mg/kgPOq8h
Cat:616mg/kgIMorPOq8h
Flecainide Dog:12(upto5?)mg/kgPOq12h(notadvisedifCHForimpairedLVfunction
present)
Cat:*
Propafenone Dog:24(upto6)mg/kgPOq8h(startlow)
Cat:*
ClassII
Atenolol Dog:0.21.0mg/kgPOq12(24)h;startlow
Cat:?sameor6.25(12.5)mg/catPOq12(24)h
Carvedilol Dog:0.10.5mg/kgPOq12h(upto1.0mg/kgifnormalLVfunction;startlow)
Cat:same?
Esmolol Dog:0.10.5mg/kgIVover1minute(loadingdose),followedbyinfusionof
0.0250.2mg/kg/minute
Cat:same
Metoprolol Dog:initialdose,0.10.2mg/kgPOq24(12)h,upto1mg/kgq8(12)h;start
low
Cat:2upto15mg/catPOq8(12)hr;startlow
Propranolol Dog:0.02mg/kginitialbolusslowlyIV(uptomaximumof0.1mg/kg);initial
POdose,0.10.2mg/kgPOq8h,upto1mg/kgq8h
Cat:SameIVinstructions;2.5upto10mg/catPOq812h
ClassIII
Amiodarone Dog:6(upto10)mg/kgPOq12hfor7(to14)days(loading),then46mg/kg
POq24h;ForIVadministrationuseNexterone(notstandardamiodaronesee
text):23mg/kgslowIVinfusionover12hoursandmonitorBP;(cancontinue
tocumulativedoseof5to6mg/kg,iftolerated).
Cat:*
Sotalol Dog:12.5(5?)mg/kgPOq12h
Cat:1020mg/catPOq12h(or24mg/kgPOq12h)
ClassIV
Diltiazem Dog:AcuteIVforrapidratecontrolofAF:0.050.15mg/kgIVover23
minutes,canrepeatifneeded.AcuteIVforSVT:0.1(0.2)mg/kgover(3)5
minutesIV,canrepeattocumulativeIVdoseof0.30.4(0.7)mg/kg;monitor
BP.CRI:0.020.08mg/kg/min.Oralloadingdose:0.5mg/kgPOfollowedby
0.25mg/kgPOq1htoatotalof1.5(2.0)mg/kgorconversion.Oral
maintenance:(standardformulation)initial0.51mg/kg(upto23mg/kg)PO
q8h.Extendedrelease(diltiazemER):1.54(upto6)mg/kgPOq12h
Cat:Same?;oralmaintenance:1.52.5mg/kg(or7.510mg/cat)POq8h;
Extendedrelease(diltiazemER),30mg/cat/day(onehalfofa60mginternal
tabletwithinthe240mgcapsule),canincreaseto60mg/dayinsomecatsif
necessary
Verapamil Dog:initialdose,0.020.05mg/kgslowlyIV,canrepeatq5minuptoatotalof
(note:diltiazemis 0.15(0.2)mg/kg;0.52mg/kgPOq8h(diltiazempreferred)
preferred) Cat:initialdose,0.025mg/kgslowlyIV,canrepeatevery5minutesuptoa
totalof0.15(0.2)mg/kg;0.51mg/kgPOq8h
Anticholinergic
Atropine Dog:0.020.04mg/kgIV,IM,SC;0.04mg/kgPOq68h
Cat:same
Glycopyrrolate Dog:0.0050.01mg/kgIVorIM;0.010.02mg/kgSC
Cat:same
Hyoscyamine Dog:0.0030.006mg/kgPOq8h
Cat:*
Propantheline Dog:0.250.5mg/kg,or3.737.5mg/dog,POq812h
Cat:*
Sympathomimetic
Dobutamine Dog:2.5to5mcg/kg/min,initial(upto20mcg/kg/min)CRI
Cat:2.5to5mcg/kg/minCRI,startlow
Isoproterenol Dog:0.040.08g/kg/minuteCRI
Cat:same
Theophylline(ext. Dog:10mg/kgPOq12h
release) Cat:1015mg/kgq24h
Terbutaline Dog:0.14mg/kg,or2.55mg/dog,POq812h
Cat:0.10.2mg/kg,or0.6251.25mg/cat,POq12h
OtherAgents
Digoxin Dog:Maintenancedosefordogs<22kg,0.0050.008mg/kgPOq12h;dogs
>22kg,0.0030.005mg/kg(or0.22mg/m2)POq12h.
Cat:0.007mg/kg(or1/4of0.125mgtab)POq48h.
TablecompiledbyDrs.WendyAWare(IowaStateUniv)andJohnBonagura(OhioStateUniversity)
*=effectivedosagenotknown;BP=bloodpressure;CHF=congestiveheartfailure;CRI=constantrate
infusion;CPR=cardiopulmonaryresuscitation;LV=leftventricular.
REFERENCES
1. Goodwin JK. Holter monitoring and cardiac event recording. Vet Clin North Am Small Anim Pract.
1998;28(6):13911407,viii.
2. Miller RH, Lehmkuhl LB, Bonagura JD, Beall MJ. Retrospective analysis of the clinical utility of
ambulatory electrocardiographic (Holter) recordings in syncopal dogs: 44 cases (19911995). J Vet
InternMed.1999;13(2):111122.
3. Calvert CA, Jacobs GJ, Smith DD, Rathbun SL, Pickus CW. Association between results of ambulatory
electrocardiography and development of cardiomyopathy during longterm followup of Doberman
pinschers.JAmVetMedAssoc.2000;216(1):3439.
4. CalvertCA,WallM.ResultsofambulatoryelectrocardiographyinovertlyhealthyDobermanPinschers
with equivocal echocardiographic evidence of dilated cardiomyopathy. J Am Vet Med Assoc.
2001;219(6):782784.
5. Petrie JP. Practical application of holter monitoring in dogs and cats. Clin Tech Small Anim Pract.
2005;20(3):173181.
6. HanasS,TidholmA,EgenvallA,HolstBS.TwentyfourhourHoltermonitoringofunsedatedhealthycats
inthehomeenvironment.JVetCardiol.2009;11(1):1722.
7. Wess G, Schulze A, Geraghty N, Hartmann K. Ability of a 5minute electrocardiography (ECG) for
predicting arrhythmias in Doberman Pinschers with cardiomyopathy in comparison with a 24hour
ambulatoryECG.JVetInternMed.2010;24(2):367371.
8. Ware WA. Twentyfourhour ambulatory electrocardiography in normal cats. J Vet Intern Med.
1999;13(3):175180.
9. Eastwood JM, Elwood CM. Assessment of an ECG event recorder in healthy dogs in a hospital
environment.JSmallAnimPract.2003;44(4):161168.
10. BrightJM,CaliJV.Clinicalusefulnessofcardiaceventrecordingindogsandcatsexaminedbecauseof
syncope, episodic collapse, or intermittent weakness: 60 cases (19971999). J Am Vet Med Assoc.
2000;216(7):11101114.
11. FerasinL.RecurrentsyncopeassociatedwithparoxysmalsupraventriculartachycardiainaDevonRex
catdiagnosedbyimplantablelooprecorder.JFelineMedSurg.2009;11(2):149152.
12. James R, Summerfield N, Loureiro J, Swift S, DukesMcEwan J. Implantable loop recorders: a viable
diagnostictoolinveterinarymedicine.JSmallAnimPract.2008;49(11):564570.
13. MacKie BA, Stepien RL, Kellihan HB. Retrospective analysis of an implantable loop recorder for
evaluation of syncope, collapse, or intermittent weakness in 23 dogs (20042008). J Vet Cardiol.
2010;12(1):2533.
14. SantilliRA,FerasinL,VogheraSG,PeregoM.Evaluationofthediagnosticvalueofanimplantableloop
recorderindogswithunexplainedsyncope.JAmVetMedAssoc.2010;236(1):7882.
15. Perego M, Skert S, Santilli RA. Analysis of the atrial repolarization wave in dogs with thirddegree
atrioventricularblock.AmJVetRes.2014;75(1):5458.
16. Rasmussen CE, Falk T, Domanjko Petric A, Schaldemose M, Zois NE, Moesgaard SG, et al. Holter
monitoring of small breed dogs with advanced myxomatous mitral valve disease with and without a
historyofsyncope.JVetInternMed.2014;28(2):363370.
17. MotskulaPF,LinneyC,PalermoV,ConnollyDJ,FrenchA,DukesMcEwanJ,etal.Prognosticvalueof24
hourambulatoryECG(Holter)monitoringinBoxerdogs.JVetInternMed.2013;27(4):904912.
18. Rasmussen CE, Vesterholm S, Ludvigsen TP, Haggstrom J, Pedersen HD, Moesgaard SG, et al. Holter
monitoring in clinically healthy Cavalier King Charles Spaniels, Wirehaired Dachshunds, and Cairn
Terriers.JVetInternMed.2011;25(3):460468.
19. CrosaraS,BorgarelliM,PeregoM,HaggstromJ,LaRosaG,TarducciA,etal.Holtermonitoringin36
dogswithmyxomatousmitralvalvedisease.AustVetJ.2010;88(10):386392.
20. Jackson BL, Lehmkuhl LB, Adin DB. Heart rate and arrhythmia frequency of normal cats compared to
catswithasymptomatichypertrophiccardiomyopathy.JVetCardiol.2014;16(4):215225.
21. Abbott JA. Heart rate and heart rate variability of healthy cats in home and hospital environments. J
FelineMedSurg.2005;7(3):195202.
22. Calvert CA, Jacobs G, Pickus CW, Smith DD. Results of ambulatory electrocardiography in overtly
healthy Doberman Pinschers with echocardiographic abnormalities. J Am Vet Med Assoc.
2000;217(9):13281332.
23. Calvert CA, Hall G, Jacobs G, Pickus C. Clinical and pathologic findings in Doberman pinschers with
occultcardiomyopathythatdiedsuddenlyordevelopedcongestiveheartfailure:54cases(19841991).
JAmVetMedAssoc.1997;210(4):505511.
24. SpierAW,MeursKM.Evaluationofspontaneousvariabilityinthefrequencyofventriculararrhythmias
in Boxers with arrhythmogenic right ventricular cardiomyopathy. J Am Vet Med Assoc.
2004;224(4):538541.
25. MeursKM,SpierAW,MillerMW,LehmkuhlL,TowbinJA.Familialventriculararrhythmiasinboxers.J
VetInternMed.1999;13(5):437439.
26. Santilli RA, Bontempi LV, Perego M, Fornai L, Basso C. Outflow tract segmental arrhythmogenic right
ventricularcardiomyopathyinanEnglishBulldog.JVetCardiol.2009;11(1):4751.
27. Brownlie SE, Cobb MA. Observations on the development of congestive heart failure in Irish
wolfhoundswithdilatedcardiomyopathy.JSmallAnimPract.1999;40(8):371377.
28. Brownlie SE. An electrocardiographic survey of cardiac rhythm in Irish wolfhounds. Vet Rec.
1991;129(21):470471.
29. MartinMW,StaffordJohnsonMJ,StrehlauG,KingJN.Caninedilatedcardiomyopathy:aretrospective
studyofprognosticfindingsin367clinicalcases.JSmallAnimPract.2010;51(8):428436.
30. CoteE,JaegerR.Ventriculartachyarrhythmiasin106cats:associatedstructuralcardiacdisorders.JVet
InternMed.2008;22(6):14441446.
31. PeregoM,RameraL,SantilliRA.IsorhythmicatrioventriculardissociationinLabradorRetrievers.JVet
InternMed.2012;26(2):320325.
32. HamlinRL,SmetzerDL,BreznockEM.SinoatrialsyncopeinMiniatureSchnauzers.JAmVetMedAssoc.
1972;161(9):10221028.
33. FoxPR.ECGofthemonth:sinoatrialblock.JAmVetMedAssoc.1980;176(10Pt1):978979.
34. MillerMS,TilleyLP.ECGofthemonth.Sicksinussyndrome.JAmVetMedAssoc.1984;184(4):423425.
35. Bonagura JD, DiBartola SP. ECG of the month. Sick sinus syndrome. J Am Vet Med Assoc.
1983;183(4):420421.
36. MonevaJordan A, Corcoran BM, French A, DukesMcEwan J, Martin MW, Luis Fuentes V, et al. Sick
sinussyndromeinnineWestHighlandwhiteterriers.VetRec.2001;148(5):142147.
37. KavanaghK.Sicksinussyndromeinabullterrier.CanVetJ.2002;43(1):4648.
38. SaundersAB.ECGofthemonth.Sicksinussyndrome.JAmVetMedAssoc.2005;227(1):5152.
39. Gladuli A, Moise NS, Hemsley SA, Otani NF. Poincare plots and tachograms reveal beat patterning in
sick sinus syndrome with supraventricular tachycardia and varying AV nodal block. J Vet Cardiol.
2011;13(1):6370.
40. EstradaAH,PariautR,HemsleyS,GatsonBH,MoiseNS.Atrialbasedpacingforsinusnodedysfunction
indogs:initialresults.JVetInternMed.2012;26(3):558564.
41. Sanders RA, Chapel EH. Effect of pulse width on transesophageal atrial pacing in dogs. Vet Anaesth
Analg.2015.
42. GreenHW,3rd,SandersRA,RamosVaraJ,HoganDF,BatraAS.Safetyoftransesophagealpacingfor24
hoursinacaninemodel.PacingClinElectrophysiol.2009;32(7):888893.
43. Chapel EH, Sanders RA. Efficacy of two commercially available cardiac pacing catheters for
transesophagealatrialpacingindogs.JVetCardiol.2012;14(3):409414.
44. SchmidtM,EstradaA,VangilderJ,MaisenbacherH,ProsekR.Safetyandfeasibilityoftransesophageal
pacinginadog.JAmAnimHospAssoc.2008;44(1):1924.
45. CoteE,LasteNJ.Transvenouscardiacpacing.ClinTechSmallAnimPract.2000;15(3):165176.
46. Sanders RA, GreenHW,3rd,HoganDF,Sederquist K. Useoftransesophagealatrialpacingtoprovide
temporary chronotropic support in a dog undergoing permanent pacemaker implantation. J Vet
Cardiol.2011;13(3):227230.
47. DeFrancesco TC, Hansen BD, Atkins CE, Sidley JA, Keene BW. Noninvasive transthoracic temporary
cardiacpacingindogs.JVetInternMed.2003;17(5):663667.
48. SandersRA,GreenHW,3rd,HoganDF,TrafneyD,BatraAS.Efficacyoftransesophagealandtransgastric
cardiacpacinginthedog.JVetCardiol.2010;12(1):4952.
49. Noomanova N, Perego M, Perini A, Santilli RA. Use of transcutaneous external pacing during
transvenouspacemakerimplantationindogs.VetRec.2010;167(7):241244.
50. Visser LC, Keene BW, Mathews KG, Browne WJ, Chanoit G. Outcomes and complications associated
withepicardialpacemakersin28dogsand5cats.VetSurg.2013;42(5):544550.
51. WardJL,DeFrancescoTC,TouSP,AtkinsCE,GriffithEH,KeeneBW.Complicationratesassociatedwith
transvenouspacemakerimplantationindogswithhighgradeatrioventricularblockperformedduring
versusafternormalbusinesshours.JVetInternMed.2015;29(1):157163.
52. JohnsonMS,MartinMW,HenleyW.Resultsofpacemakerimplantationin104dogs.JSmallAnimPract.
2007;48(1):411.
53. SissonD,ThomasWP,WoodfieldJ,PionPD,LuethyM,DeLellisLA.Permanenttransvenouspacemaker
implantationinfortydogs.JVetInternMed.1991;5(6):322331.
54. Thomason JD, Fallaw TL, Calvert CA. ECG of the month. Pacemaker implantation for sick sinus
syndrome.JAmVetMedAssoc.2008;233(9):14061408.
55. BurrageH.Sicksinussyndromeinadog:treatmentwithdualchamberedpacemakerimplantation.Can
VetJ.2012;53(5):565568.
56. Wess G, Thomas WP, Berger DM, Kittleson MD. Applications, complications, and outcomes of
transvenouspacemakerimplantationin105dogs(19972002).JVetInternMed.2006;20(4):877884.
57. de Madron E, Kadish A, Spear JF, Knight DH. Incessant atrial tachycardias in a dog with tricuspid
dysplasia.Clinicalmanagementandelectrophysiology.JVetInternMed.1987;1(4):163169.
58. WillisR,WottonPR,LittleCJ.TachyarrhythmiainaStBernarddog.JVetCardiol.1999;1(2):2731.
59. Harmon MW, Fine DM. ECG of the month. Atrial tachycardia. J Am Vet Med Assoc. 2012;240(6):668
670.
60. RiepeRD,GompfRE.ECGofthemonth.JAmVetMedAssoc.1993;202(3):374376.
61. Cunningham SM, Rush JE. ECG of the month. Atrial flutter. J Am Vet Med Assoc. 2005;226(12):1986
1988.
62. TyszkoC,BrightJM,SwistSL. Recurrentsupraventriculararrhythmiasinadogwithatrial myocarditis
andgastritis.JSmallAnimPract.2007;48(6):335338.
63. Santilli RA, Perego M, Perini A, Carli A, Moretti P, Spadacini G. Radiofrequency catheter ablation of
cavotricuspidisthmusastreatmentofatrialflutterintwodogs.JVetCardiol.2010;12(1):5966.
64. FineDM,TobiasAH,BonaguraJD.Cardiovascularmanifestationsofiatrogenichyperthyroidismintwo
dogs.JVetCardiol.2010;12(2):141146.
65. Santilli RA, RameraL,PeregoM,MorettiP,SpadaciniG. Radiofrequency catheterablationofatypical
atrialflutterindogs.JVetCardiol.2014;16(1):917.
66. MachenMC,EstradaAH,ProsekR.ECGoftheMonth.Atrioventricularblockandatrialflutter.JAmVet
MedAssoc.2008;233(11):16941696.
67. ArmentanoRA,SchmidtMK,MaisenbacherHW.ECGoftheMonth.Atrialflutter.JAmVetMedAssoc.
2010;236(1):5153.
68. Nakamura RK, Russell NJ. ECG of the month. Atrial flutter in dog. J Am Vet Med Assoc.
2013;242(12):16501652.
69. Buchanan JW. Spontaneous arrhythmias and conduction disturbances in domestic animals. Ann N Y
AcadSci.1965;127(1):224238.
70. Martin RH, Lim ST, Van Citters RL. Atrial fibrillation in the intact unanesthetized dog: hemodynamic
effectsduringrest,exercise,andbetaadrenergicblockade.JClinInvest.1967;46(2):205216.
71. EttingerS.Conversionofspontaneousatrialfibrillationindogs,usingdirectcurrentsynchronizedshock.
JAmVetMedAssoc.1968;152(1):4146.
72. BohnFK,PattersonDF,PyleRL.Atrialfibrillationindogs.BrVetJ.1971;127(10):485496.
73. BoltonGR,EttingerS.Paroxysmalatrialfibrillationinthedog.JAmVetMedAssoc.1971;158(1):6476.
74. Hilwig RW. Hemodynamic relationships in dogs with sinus arrhythmia and atrial fibrillation. Am J Vet
Res.1972;33(3):475483.
75. TilleyLP,LiuSK.Cardiomyopathyinthedog.RecentAdvStudCardiacStructMetab.1975;10:641653.
76. ZenobleRD,HillBL.Hypothermiaandassociatedcardiacarrhythmiasintwodogs.JAmVetMedAssoc.
1979;175(8):840842.
77. MuirWW,BonaguraJD.Treatmentofcardiacarrhythmiasindogswithgastricdistentionvolvulus.JAm
VetMedAssoc.1984;184(11):13661371.
78. TidholmA,JonssonL.Aretrospectivestudyofcaninedilatedcardiomyopathy(189cases).JAmAnim
HospAssoc.1997;33(6):544550.
79. VollmarAC.TheprevalenceofcardiomyopathyintheIrishwolfhound:aclinicalstudyof500dogs.JAm
AnimHospAssoc.2000;36(2):125132.
80. Meurs KM, Miller MW, Wright NA. Clinical features of dilated cardiomyopathy in Great Danes and
resultsofapedigreeanalysis:17cases(19902000).JAmVetMedAssoc.2001;218(5):729732.
81. MoralesM,YnarajaE,MontoyaJA.DilatedcardiomyopathyinPresacanariodogs:ECGfindings.JVet
MedAPhysiolPatholClinMed.2001;48(10):577580.
82. TakemuraN,NakagawaK,HiroseH.Loneatrialfibrillationinadog.JVetMedSci.2002;64(11):1057
1059.
83. Gelzer AR, Kraus MS. Management of atrial fibrillation. Vet Clin North Am Small Anim Pract.
2004;34(5):11271144,vi.
84. Menaut P, Belanger MC, Beauchamp G, Ponzio NM, Moise NS. Atrial fibrillation in dogs with and
without structural or functional cardiac disease: A retrospective study of 109 cases. J Vet Cardiol.
2005;7(2):7583.
85. MoiseNS,PariautR,GelzerAR,KrausMS,JungSW.Cardioversionwithlidocaineofvagallyassociated
atrialfibrillationintwodogs.JVetCardiol.2005;7(2):143148.
86. BorgarelliM,SantilliRA,ChiavegatoD,D'AgnoloG,ZanattaR,MannelliA,etal.Prognosticindicators
fordogswithdilatedcardiomyopathy.JVetInternMed.2006;20(1):104110.
87. Oyama MA, Prosek R. Acute conversion of atrial fibrillation in two dogs by intravenous amiodarone
administration.JVetInternMed.2006;20(5):12241227.
88. RiesenSC,LombardCW.ECGoftheMonth.Atrialfibrillationsecondarytohypoadrenocorticism.JAm
VetMedAssoc.2006;229(12):18901892.
89. Bright JM, zumBrunnen J. Chronicity of atrial fibrillation affects duration of sinus rhythm after
transthoracic cardioversion of dogs with naturally occurring atrial fibrillation. J Vet Intern Med.
2008;22(1):114119.
90. Pariaut R, Moise NS, Koetje BD, Flanders JA, Hemsley SA, Farver TB, et al. Lidocaine converts acute
vagally associated atrial fibrillation to sinus rhythm in German Shepherd dogs with inherited
arrhythmias.JVetInternMed.2008;22(6):12741282.
91. GelzerAR,KrausMS,RishniwM.Evaluationofinhospitalelectrocardiographyversus24hourHolterfor
ratecontrolindogswithatrialfibrillation.JSmallAnimPract.2015;56(7):456462.
92. SantilliRA,CritelliM,BaronToaldoM.ECGoftheMonth.Accessoryatrioventricularpathwaymediated
tachycardia.JAmVetMedAssoc.2010;237(10):11421144.
93. SantilliRA,DianaA,BaronToaldoM.Orthodromicatrioventricularreciprocatingtachycardiaconducted
withintraventricularconductiondisturbancemimickingventriculartachycardiainanEnglishBulldog.J
VetCardiol.2012;14(2):363370.
94. SantilliRA,SantosLF,PeregoM.Permanentjunctionalreciprocatingtachycardiainadog.JVetCardiol.
2013;15(3):225230.
95. AtkinsCE,KanterR,WrightK,SabaZ,BatyC,SwansonC,etal.Orthodromicreciprocatingtachycardia
and heart failure in a dog with a concealed posteroseptal accessory pathway. J Vet Intern Med.
1995;9(1):4349.
96. WrightKN,AtkinsCE,KanterR.Supraventriculartachycardiainfouryoungdogs.JAmVetMedAssoc.
1996;208(1):7580.
97. Santilli RA, Perego M, Perini A, Moretti P, Spadacini G. Electrophysiologic characteristics and
topographicdistributionoffocalatrialtachycardiasindogs.JVetInternMed.2010;24(3):539545.
98. BonaguraJD,WareWA.Atrialfibrillationinthedog:clinicalfindingsin81cases.JAmAnimHospAssoc.
1986;22:110120.
99. TidholmA,JonssonL.DilatedcardiomyopathyintheNewfoundland:astudyof37cases(19831994).J
AmAnimHospAssoc.1996;32(6):465470.
100. BorgarelliM,ZiniE,D'AgnoloG,TarducciA,SantilliRA,ChiavegatoD,etal.Comparisonofprimary
mitralvalvediseaseinGermanShepherddogsandinsmallbreeds.JVetCardiol.2004;6(2):2734.
101. Cote E, Harpster NK, Laste NJ, MacDonald KA, Kittleson MD, Bond BR, et al. Atrial fibrillation in
cats:50cases(19792002).JAmVetMedAssoc.2004;225(2):256260.
102. Peterson ME, Keene B, Ferguson DC, Pipers FS. Electrocardiographic findings in 45 cats with
hyperthyroidism.JAmVetMedAssoc.1982;180(8):934937.
103. Saunders AB, Miller MW, Gordon SG, Van De Wiele CM. Oral amiodarone therapy in dogs with
atrialfibrillation.JVetInternMed.2006;20(4):921926.
104. Bright JM, Martin JM, Mama K. A retrospective evaluation of transthoracic biphasic electrical
cardioversionforatrialfibrillationindogs.JVetCardiol.2005;7(2):8596.
105. Estrada AH, Pariaut R, Moise NS. Avoiding medical error during electrical cardioversion of atrial
fibrillation:preventionofunsynchronizedshockdelivery.JVetCardiol.2009;11(2):137139.
106. Gelzer AR, Kraus MS, Rishniw M, Moise NS, Pariaut R, Jesty SA, et al. Combination therapy with
digoxinanddiltiazemcontrolsventricularrateinchronicatrialfibrillationindogsbetterthandigoxinor
diltiazem monotherapy: a randomized crossover study in 18 dogs. J Vet Intern Med. 2009;23(3):499
508.
107. SantilliRA,SpadaciniG,MorettiP,PeregoM,PeriniA,CrosaraS,etal.Anatomicdistributionand
electrophysiologic properties of accessory atrioventricular pathways in dogs. J Am Vet Med Assoc.
2007;231(3):393398.
108. Hill BL, Tilley LP. Ventricular preexcitation in seven dogs and nine cats. J Am Vet Med Assoc.
1985;187(10):10261031.
109. Rishniw M. ECG of the month. Ventricular preexcitation in a cat. J Am Vet Med Assoc.
2000;216(5):667668.
110. ValentineBA,WinandNJ,PradhanD,MoiseNS,deLahuntaA,KornegayJN,etal.CanineXlinked
musculardystrophyasananimalmodelofDuchennemusculardystrophy:areview.AmJMedGenet.
1992;42(3):352356.
111. Moise NS, MeyersWallen V, Flahive WJ, Valentine BA, Scarlett JM, Brown CA, et al. Inherited
ventriculararrhythmiasandsuddendeathinGermanshepherddogs.JAmCollCardiol.1994;24(1):233
243.
112. MoiseNS.Fromcelltocageside:autonomicinfluencesoncardiacrhythmsinthedog.JSmallAnim
Pract.1998;39(10):460468.
113. Kellum HB, Stepien RL. Thirddegree atrioventricular block in 21 cats (19972004). J Vet Intern
Med.2006;20(1):97103.
114. Stern JA, Meurs KM, Spier AW, Koplitz SL, Baumwart RD. Ambulatory electrocardiographic
evaluationofclinicallynormaladultBoxers.JAmVetMedAssoc.2010;236(4):430433.
115. MeursKM,SpierAW,WrightNA,HamlinRL.Useofambulatoryelectrocardiographyfordetection
ofventricularprematurecomplexesinhealthydogs.JAmVetMedAssoc.2001;218(8):12911292.
116. Prosek R. Electrical cardioversion of sustained ventricular tachycardia in three Boxers. J Am Vet
MedAssoc.2010;236(5):554557.
117. Bonagura JD, Helphrey ML, Muir WW. Complications associated with permanent pacemaker
implantationinthedog.JAmVetMedAssoc.1983;182(2):149155.
118. FoxPR,MatthiesenDT,PurseD,BrownNO.Ventralabdominal,transdiaphragmaticapproachfor
implantationofcardiacpacemakersinthedog.JAmVetMedAssoc.1986;189(10):13031308.
119. Flanders JA, Moise NS, Gelzer AR, Waskiewicz JC, MacGregor JM. Introduction of an endocardial
pacingleadthroughthecostocervicalveininsixdogs.JAmVetMedAssoc.1999;215(1):4648,34.
120. OyamaMA,SissonDD,LehmkuhlLB.Practicesandoutcomeofartificialcardiacpacingin154dogs.
JVetInternMed.2001;15(3):229239.
121. van Loon G, Fonteyne W, Rottiers H, Tavernier R, Jordaens L, D'Hont L, et al. Dualchamber
pacemakerimplantationviathecephalicveininhealthyequids.JVetInternMed.2001;15(6):564571.
122. Bulmer BJ, Oyama MA, Lamont LA, Sisson DD. Implantation of a singlelead atrioventricular
synchronous(VDD)pacemakerinadogwithnaturallyoccurring3rddegreeatrioventricularblock.JVet
InternMed.2002;16(2):197200.
123. BuchananJW.Firstpacemakerinadog:ahistoricalnote.JVetInternMed.2003;17(5):713714.
124. PetrieJP.Permanenttransvenouscardiacpacing.ClinTechSmallAnimPract.2005;20(3):164172.
125. Bulmer BJ, Sisson DD, Oyama MA, Solter PF, Grimm KA, Lamont L. Physiologic VDD versus
nonphysiologic VVI pacing in canine 3rddegree atrioventricular block. J Vet Intern Med.
2006;20(2):257271.
126. CunninghamSM,RushJE.Transvenouspacemakerplacementinadogwithatrioventricularblock
andpersistentleftcranialvenacava.JVetCardiol.2007;9(2):129134.
127. Estrada AH, Maisenbacher HW, 3rd, Prosek R, Schold J, Powell M, VanGilder JM. Evaluation of
pacingsiteindogswithnaturallyoccurringcompleteheartblock.JVetCardiol.2009;11(2):7988.
128. Hildebrandt N, Stertmann WA, Wehner M, Schneider I, Neu H, Schneider M. Dual chamber
pacemakerimplantationindogswithatrioventricularblock.JVetInternMed.2009;23(1):3138.
129. Maisenbacher HW, Estrada AH, Prosek R, Shih AC, Vangilder JM. Evaluation of the effects of
transvenouspacingsiteonleftventricularfunctionandsynchronyinhealthyanesthetizeddogs.AmJ
VetRes.2009;70(4):455463.
130. LichtenbergerJ,Scollan KF,BulmerBJ,SissonDD.LongtermoutcomeofphysiologicVDDpacing
versus nonphysiologic VVI pacing in dogs with highgrade atrioventricular block. J Vet Cardiol.
2015;17(1):4253.
131 MerotJ,ProbstV,DebailleulM,etal.Electropharmacologicalcharacterizationofcardiacrepolarization
in German shepherd dogs with an inherited syndrome of sudden death: abnormal response to
potassiumchannelblockers.JAmCollCardiol2000;36:939947.
CARDIAC AUSCULTATION
John D Bonagura DVM, MS, DACVIM (Cardiology, Internal Medicine)
Veterinary Clinical Sciences, Ohio State University College of Veterinary Medicine
METHODS
Heart sounds are generally too low in frequency or amplitude to be detected by the human
ear. Accordingly, careful auscultation is necessary to identify the limited vibrations that fall within
our audible frequency-amplitude spectrum. This requires a stethoscope to transfer (not amplify)
the sounds from the patient to the examiner.
The choice of a stethoscope is one of personal preference, and there is no best model for
everyone. Some reasonable stethoscope choices advocated by the author are included in this
section. The traditional stethoscope design has a diaphragm and shallow bell (selected by
twisting the chest piece head). Many of these instruments permit an exchange to a different-
sized (pediatric) diaphragm or (deep) bell (Tycos Harvey Elite; MDF Procardial C3). Newer
stethoscope models carry one or two tunable diaphragms. A single tunable diaphragm is found
on some instruments (3M Littman Master Classic II and Master Cardiology models); this chest
piece is acoustically superior in many ways. However, it is designed for adults and is somewhat
large for cats and smaller dogs so the examiner must learn to place it carefully. Another popular
stethoscope (3M Littman Cardiology III) uses both adult and pediatric sized tunable
diaphragms in a single rotating head. For clinicians preferring a light pediatric stethoscope with
a small footprint there are very good and economical models available (e.g. 3M Littman Classic
II Pediatric Stethoscope; MDF Pediatric Stainless Steel Dual Head Stethoscope). These
pediatric scopes are especially good for small dogs, cats, ferrets, and birds. While amplified
stethoscopes generally are not recommended because of the potential for artifacts and
distortion, they can be useful for those hard of hearing or for recording documenting sounds (3M
Littman Electronic 3000 series). Ultimately, the most important part of the stethoscope are the
bits between the earpieces! A practiced and knowledgeable examiner will succeed with any
number of stethoscope models.
Stethoscope designs have improved the acoustics of the instrument, but it must be used
properly to obtain optimal clinical results. Of importance are acquiring an instrument of
acceptable quality and tube length (typically 22 to 28 inches; longer tubes are not better);
directing the binaurals rostrally (towards the nose) and aligning these to the ear canals by gently
adjusting the headset; inserting comfortable earpieces snugly to obtain an airtight seal; and
applying the chest pieces with proper technique. The stethoscope chest pieces include two
general types: traditional and tunable. A traditional flat diaphragm is applied gently but firmly to
the chest to accentuate higher frequency sounds such as normal heart and breath sounds. This
chest piece is used for 90% of the examination. The traditional shallow or deep bell chest pieces
are applied lightly to achieve an airtight seal and enhance auscultation of lower pitched sounds.
Examples of the latter include the third and fourth heart sounds and some diastolic murmurs.
Combination chest pieces (tunable diaphragms) change their frequency response with varying
pressure such that flattening the chest piece accentuates higher-pitched sounds (like a typical
diaphragm) while gentle pressure brings out the lower pitched sounds like a traditional bell.
There are also intermediate levels of pressure that can optimize certain sounds and murmurs;
however, careful attention must be directed to subtle pressure changes to optimize the chest
piece functionality.
The conditions for auscultation exert a substantial influence on the results of the
examination. The room must be quiet, the patient gently restrained by an assistant, and the
examiner relaxed. It is preferable for the dog to stand in order to locate the valve areas
accurately. A cat can be gently restrained with one hand under the caudal abdomen; this
encourages the cat to rest on the forelimbs. The patient must be calm and ventilation and
purring controlled if possible. Ventilation (especially panting) that is synchronous to the heart
rhythm can mimic cardiac murmurs. Gently holding the mouth closed, whistling, or briefly
obstructing the nares are effective maneuvers for reducing ventilation artifacts in dogs. Showing
a cat water dripping in a sink, holding the cat, or gently pressing the larynx might reduce the
degree of purring. Sound artifacts can be misinterpreted as abnormal heart or lung sounds.
These include ventilation and panting (mimics murmurs); twitching (sounds like an extra heart
sounds or premature beats); and friction from rubbing the chest piece across hair (sounds like
pulmonary crackles or rales). Excessive pressure on the chest can distort the thorax of small
animals and create abnormal flow patterns and murmurs.
The clinical examination method involves integration of auscultation with palpation of the
precordium and examination of the pulses. Auscultation is preceded by palpation of the arterial
pulse to estimate heart rate, regularly, and pulse strength and character. Ideally, the jugular
venous pulse should also be inspected, but practically this is rarely done in healthy patients
because of the need to clip neck hair. The thoracic wall over the heart (precordium) is palpated
on both sides in order to assess the apical beats. The prominent left apical impulse occurs
coincident with opening of the semilunar valves (a systolic thrust). The impact is normally
strongest at the left fifth intercostal space near the costochondral junction. A weaker impulse is
normally palpable on the right hemithorax at approximately the right third to fourth ICS.
Dilatation of the left ventricle displaces the apex beat caudoventrally. Hypertrophy of the left or
the right ventricle can produce an impulse more prominent than normal; this is termed a
precordial heave. Interpretation of these changes requires considerable experience and
practice. Of great value is the identification of a precordial vibration or thrill. A precordial thrill is
the palpable manifestation of a loud murmur and it typically indicates the point of maximal
murmur intensity, a descriptor that informs the differential diagnosis.
The entire precordium is examined, with particular attention directed to the cardiac valve
areas and the first and second heart sounds, which indicate the onset of systole and diastole,
respectively. While the exact anatomic location of the valve areas depends on the species,
breed, chest conformation, and size of the heart, a common relative location can be identified.
From caudal to cranial are the mitraltricuspidpulmonicaortic with the tricuspid valve on the
right side and other valves areas on the left. The author approaches the patient from the caudal
perspective, allowing the stethoscope to follow the natural curve of the arm; if one can learn to
be ambidextrous in holding the chest piece, the examination can be very efficient. A useful
approach in dogs begins with palpation of the left apical impulse where mitral sounds radiate
well and the lower-pitched, first heart sound is best heard. The mitral listening area is there and
immediately dorsal to the apex. Other valve areas are found from this point. The aortic valve
area is located one or two intercostal spaces craniodorsal to the mitral area, and the sharper,
higher-pitched second heart sound is usually loudest at that location. Once the aortic second
sound is identified, the stethoscope can be moved one interspace cranial and slightly ventral
(over the pulmonary valve area). The tricuspid valve area is over the right hemithorax, cranial to
the mitral area, and covers a relatively wide area. The pulmonary artery extends dorsally from
the pulmonic valve. The left ventricular outflow tract (LVOT) is located near the center of the
heart and aortic sounds and aortic ejection murmurs usually radiate to each hemithorax,
although these are usually loudest over the aortic area and craniodorsal to the valve.
Cardiac apex and cardiac base are commonly used expressions to designate the region
ventral (ventricles) and dorsal to the atrioventricular groove but are not specific for any cardiac
valve. Mitral and tricuspid valve sounds and murmurs generally project ventrally to the apical
regions. Ventricular septal defects are also louder ventrally (along the sternal edges) in most
patients. In contrast, murmurs originating at the semilunar valves or the great arteries are
detected best over the base, generally over the left, craniodorsal cardiac base. Murmurs that
originate in the subvalvular regions of the outflow tracts are often heard both ventrally and
craniodorsally. For example, it is common for a loud murmur of subvalvular aortic stenosis
(SAS) in dogs to radiate to be well detected at aortic valve area, the mitral valve area, and in the
ascending aorta on both left and right sides of the chest.
Valve areas in cats are less distinct and the edges of the chest piece usually cover multiple
valves. Consequently, most clinicians do not identify specific feline valve areas but instead use
descriptors such as apical, caudal, cranial, and sternal. In many cats, the apical impulse is
located close to the midline and most auscultation is conducted along the left and the right
sternal borders. The first sound is loudest along the left apical (caudal) sternal border. The
normal second sound is louder over the left cranial sternal border. A typical murmur of mitral
regurgitation is loudest over the caudal left sternal border (apex) whereas typical ejection and
functional murmurs are loudest along the left or right cranial sternal borders. However, these are
generalizations and distinguishing the source and cause of feline heart murmurs is quite
challenging.
CARDIAC MURMURS
Cardiac murmurs are prolonged audible vibrations. Although murmurs are a hallmark of
many cardiac diseases, very often murmurs are innocent or functional (i.e., the heart is
structurally normal). Murmurs are associated with high velocity blood flow (typically >1.6 m/sec)
and vibrations that develop about disturbed or turbulent flow; these generate changes in the
flow stream capable of generating audible sound waves. Turbulence and wake fluctuations are
more common when flow velocity increases, viscosity of the blood decreases, or when flow
moves through a larger blood vessel.
Clinically the causes of cardiac murmurs relate to a number of common conditions.
Adrenergic stimulation, secondary to anxiety, fear, exercise, fever, drugs, or hyperthyroidism, is
a common denominator underlying many functional heart murmurs. Both sympathomimetic
activation (by increasing contractility) and peripheral vasodilation (by reducing afterload) can
increase ventricular systolic function. This can lead to higher ejection velocity into the great
vessels, dynamic obstruction in either ventricle and foster high-velocity or turbulent blood flow.
Anemia decreases viscosity of blood and like hyperthyroidism is associated with increased
sympathetic activity and peripheral vasodilation. Increased ventricular stroke volume can cause
mild-to-moderate increases in ejection velocities and result in an ejection murmur in the
absence of any valvular obstruction. Examples include bradycardias (pronounced sinus
arrhythmia, AV block, and athletic heart) and atrial septal defect. Structural heart lesions offer
pathways for blood to flow from high to low-pressure zones; this pathophysiology represents the
most common explanation for pathologic (organic) murmurs. Examples include flow across a
restrictive ventricular septal defect (VSD), a stenotic valve, an incompetent valve, or through an
aortic to pulmonary shunt (as with PDA). A common reason for heart murmurs in cats are the
primary or secondary cardiomyopathies; murmurs stem from either secondary mitral
regurgitation or dynamic ventricular obstruction. Another common cause of murmurs in older
cats is aortic dilatation (aortoannular ectasia) with discrete upper septal thickening (in the
subaortic ventricular septum).
Cardiac murmurs should be described based on timing and shape, intensity (loudness),
and point of maximal intensity (PMI). Additional qualifiers include the murmur radiation, pitch
and quality. The general timing of the murmur is designated as systolic, diastolic, continuous, or
to-and-fro (systolic diastolic with a pause a S2). The adjectives proto, meso, and tele are
sometimes used to indicate early, middle, and late. Within this timing are descriptions qualifying
the onset/end and relative loudness of the murmur as characterized by a phonocardiographic
recording. This creates an impression of the murmurs shape. For example, ejection murmurs
cannot begin until after S1 and must end by S2 and peak in early to mid-systole unless caused
by a severe obstruction to flow. The shape of ejection murmurs is crescendo-decrescendo
(diamond-shaped). In contrast, loud holosystolic murmurs of mitral regurgitation (MR) and
tricuspid regurgitation (TR) usually obliterate the first and second sounds and are plateau-
shaped. The intensity or loudness of the murmur is arbitrarily graded on a 1-6 scale; we use the
following convention in our practice:
Grade 1 Very soft, localized murmur detected only in a quiet room after intense listening.
Grade 2 Soft murmur, heard immediately but relatively localized to a single area.
Grade 3 Moderate intensity murmur that is evident at more than one location.
Grade 4 Moderate intensity to loud murmur that radiates well but without a consistent
precordial thrill
Grade 5 Loud, widely radiating heart murmur with a precordial thrill.
Grade 6 Loud murmur with a precordial thrill, audible with stethoscope off the thorax
The point of maximal intensity is communicated by indicating the location, valve area, or
intercostal space where the murmur is loudest. A murmur usually projects from the PMI in the
direction of abnormal blood flow. Murmurs can also radiate through solid structures to the chest
wall, as often occurs with MR radiating to the left apex. The radiation of a loud cardiac murmur
can be extensive and can off some clues about the genesis of the murmur. However, very loud
murmurs tend to radiate widely and can sometimes be confusing. Pitch and quality pertain to
the frequency and subjective assessment of the murmur by the examiner. Murmurs consisting of
one fundamental frequency with overtones are described as musical, whereas murmurs of
mixed frequencies are typically noted to be harsh. Most murmurs are of mixed frequency.
Functional Murmurs are those unassociated with obvious cardiac pathology. These murmurs
arise from physiologic changes (see above) or undefined causes (so-called innocent murmurs).
In small animals, nearly all functional murmurs are systolic and the murmur is typically ejection
in shape, meaning it begins after S1 and ends prior to S2. The PMI of the functional ejection
murmur is at or adjacent to the aortic or the pulmonary valve and the murmur radiates
craniodorsally into the aorta or pulmonary artery. In general, functional murmurs are soft, grade
1-2/6, and relatively brief with both heart sounds evident. In puppies, most innocent murmurs
become softer during the vaccination sequence and eventually disappear (at about 4 months of
age). A classical innocent murmur has a humming or musical character likely related to a
vibrating intracardiac structure. Functional ejection murmurs in larger canine breeds can persist
throughout life. In many of these dogs, the murmur is protomesosystolic, grade 2 to 3/6 in
intensity, and transiently accentuates following exercise to a grade 3 to 4/6 intensity. These
ejection murmurs are evident without any accompanying structural lesions on 2D
echocardiography. In fact echocardiographic correlates to a functional murmur are inconsistent
with the most frequent being mildly increased aortic ejection velocity on spectral Doppler
imaging (1.7 to 2.4 m/s). It is nearly impossible to distinguish functional ejection murmurs from
those due to trivial LVOT stenosis based on velocity alone. Some breeds, such as boxers and
bull terriers, have a relatively narrow aorta, and ejection murmurs in some of these dogs could
represent the effect of ventricular-annular disproportion as opposed to true subvalvular aortic
stenosis (SAS). This issue is controversial and largely unresolved. It should be noted, however,
that in breeds rarely affected by SAS (such as greyhounds), functional ejection murmurs are
also associated with mildly elevated aortic ejection velocities. Systolic murmurs over the cranial
sternal borders are common in cats without echocardiographic evidence of significant heart
disease. Many of these murmurs arise from flow across the LVOT (often in to a dilated aorta).
Others are caused by dynamic intra-ventricular obstruction (see next section).
Dynamic mid-ventricular and outflow tract obstructions are another potential cause of
systolic murmurs in dogs and cats. The classic auscultatory feature is a mid-to-late systolic
murmur associated with emptying of ventricular blood and physical contract between cardiac
walls, papillary muscle, or mitral valve elements. The Doppler signal is dagger-shaped, typical of
obstruction that begins dynamically, as ejection progresses and ventricular volume decreases.
The heart can be structurally normal or hypertrophied in these cases. Mid-ventricular obstruction
of the left ventricle (LV) is often from dehydration or concentric hypertrophy of the chamber.
When the murmur arises in the right ventricle (RV), the obstruction is often between the free-
wall and the supraventricular crest and is often explained by high sympathetic tone, ventricular
septal thickening, or right ventricular hypertrophy. Dynamic RV obstruction is especially common
in stressed and dehydrated cats.
Whether these murmurs should be considered functional or a consequence of pathology
depends largely on the findings on 2D echocardiography. Some cats with hypertrophic
cardiomyopathy (HCM) have prominent mid-ventricular obstruction. The finding is also common
in cats with hypertrophy thickening from systemic hypertension and hyperthyroidism. Mid-
ventricular obstruction differs from dynamic LVOT obstruction caused by systolic anterior motion
of the mitral valve associated with HCM in cats and mitral valve malformations in cats and dogs.
In that situation, elements of the anterior (septal) mitral leaflet are pulled towards the ventricular
septum creating both dynamic obstruction and an eccentric jet of MR.
Aortic Stenosis Obstruction in the LVOT is most often causes by subvalvular aortic stenosis
(SAS) in dogs and by HCM in cats. The lesions of SAS include a congenital, subvalvular, fibrous
obstruction below the aortic valve that can be discrete or envelop the outflow tract to the base of
the aortic valve proper. Other causes of LVOT obstruction are valvular aortic stenosis (AS),
mitral valve malformations, and chronic infective endocarditis of the aortic valve. Depending on
the lesion, aortic regurgitation (AR) will occur to varying degrees. In most cases, AR is a
Doppler diagnosis and the regurgitation is silent to auscultation.
The murmur of (S)AS is systolic, flow dependent, and crescendo-decrescendo in
configuration. As with most ejection murmurs, the murmur intensifies following exercise,
inotropic stimulation, a ventricular premature beat, a long pause in sinus arrhythmia, or with
increases in venous return and stroke volume. The typical PMI of SAS is over the left thorax at
the aortic/subaortic region with strong radiation of the murmur apically towards the mitral area
and craniodorsally into the ascending aorta. The murmur tends to project into the carotids and
even radiate to the skull. The murmur of SAS can be loudest over the right dorsal cardiac base
owing to radiation into a dilated ascending aorta. In pure valvular or rare supravalvular AS, the
murmur can be loudest on either side of the thorax. With moderate to severe (S)AS the murmur
peaks later in systole sounding more holosystolic than ejection in configuration; at the same
time the arterial pulses are hypokinetic and late-rising. If a diastolic murmur of aortic
regurgitation develops with (S)AS, both a systolic and a decrescendo diastolic murmur are
evident. This leads to the to-and-fro murmur of AS/AR and to bounding arterial pulses.
Pulmonic Valve Stenosis (PS) is a congenital malformation of the pulmonary valve
characterized by varying degrees of valve thickening, leaflet fusion and tethering, and
hypoplasia of the annulus or along the base of the valve. It is most common in dogs and
relatively rare in cats (and more likely to be infundibular in this species). The resultant murmur is
systolic, crescendodecrescendo, and loudest over the pulmonary valve (at the left second to
third ICS) with strong radiation dorsally into the post-stenotic dilatation of the main pulmonary.
Thus, the murmur tends to be heard very well over the left, cranial to dorsal cardiac base and is
sometimes confused with a PDA for this reason. An early systolic ejection click might be
detected with careful auscultation (from a fused but mobile valve). A concurrent murmur of
tricuspid regurgitation (TR) is often heard over the tricuspid valve area caused by secondary
right ventricular enlargement or tricuspid dysplasia. Pulmonary regurgitation is invariably
present on Doppler studies but rarely audible. However, following successful balloon catheter
valvuloplasty, there is often moderate to severe pulmonary insufficiency creating an early to mid-
diastolic decrescendo murmur of pulmonary regurgitation. Rarely severe pulmonary
regurgitation is present with native valvular dysplasia and the associated to-and-fro murmur of
PS/PR is easily confused with a PDA. Congenital PS is often associated with a prominent
jugular pulse (giant A-wave). In contrast to dogs with SAS, the arterial pulses should be normal
in character unless there is heart failure.
Mitral Regurgitation is one of the most common and important flow disturbances responsible
for a pathologic systolic heart murmur. MR develops secondary to malfunction of any portion of
the mitral apparatus. Causes include congenital mitral dysplasia, myxomatous degeneration of
the valve (endocardiosis) in the dog, infective endocarditis, redundancy or rupture of a chordae
tendineae (in the dog), and causes of left ventricular dilatation or hypertrophy, such as
cardiomyopathy, hyperthyroidism, systemic hypertension, and PDA. This murmur is loudest over
the mitral valve area or the palpable left apex where it is projects well (or near the left sternal
edge in cats). MR murmurs radiate both dorsally and to the right (usually one grade softer on
the right hemithorax). The MR murmur can be decrescendo in peracute leakage (from
equilibration of LV-LA pressures) or in mild cases (as the regurgitant orifice closes in late
systole). The murmur is soft in hypotensive patients; alternatively, systemic hypertension can
amplify the intensity. The musical systolic whoop is a striking frequency phenomenon in some
dogs. Progressive increase in the intensity of the first heart sound is a unique feature of MR in
dogs with valvular endocardiosis and probably indicates cardiac dilatation with maintenance of
left ventricular systolic function. Additionally, the intensity of the MR murmur usually increases
with the degree of valvular incompetency (assuming normal ABP) in dogs with myxomatous
disease. The intensity of a MR murmur in other causes of MR is not as reliably correlated to the
severity. Cats with hypertrophic cardiomyopathy often have a labile murmur of MR related to
dynamic left ventricular outflow tract obstruction and systolic anterior motion of the mitral valve.
Tricuspid regurgitation is another common cardiac murmur and in many ways is similar to
mitral regurgitation. Causes include valve malformation, degenerative valve disease
(endocardiosis), right ventricular enlargement (from pulmonic valve stenosis, right sided
cardiomyopathy, chronic bradycardia, or pulmonary hypertension), dirofilariasis, transvenous
pacing leads, and (very rarely) tricuspid endocarditis. The PMI of this murmur is the tricuspid
valve area on the right, and dorsal radiation is typical. In young puppies with TV dysplasia (e.g.,
Labrador retrievers), the murmur can be very soft and readily missed. It can be difficult to
distinguish TR from the radiating murmur of MR. The following support concurrent TR in the this
setting: a prominent jugular pulse, right precordial thrill, different frequency murmur than that
heard at the left side, louder right than left-sided murmur, or right-sided CHF. The murmur of TR
is often very loud in the setting of pulmonary hypertension. Eccentric jets of TR from
degenerative TV prolapse can also lead to very prominent murmurs of TR along with a right
sided thrill.
Ventricular Septal Defect is the most common congenital heart malformation of cats, and also
occurs with some frequency in dogs. A large nonrestrictive VSD (i.e., no substantial pressure
difference between the ventricles) is also part of the tetralogy of Fallot. When the defect
communicates the left ventricular outlet with the perimembranous ventricular septum, the
murmur is loudest just below the tricuspid valve, along the right sternal border. When the defect
is subarterial, communicating the subaortic septum with the subpulmonary septum, the murmur
may is most prominent over the craniodorsal left cardiac base (similar to PS). If the aortic valve
has prolapsed into the ventricular septal defect, there may be a diastolic murmur of aortic
regurgitation as well.
Aortic Regurgitation is the most important diastolic cardiac murmur. Causes include infective
endocarditis, congenital aortic valve disease, prolapse of an aortic valve cusp into a subaortic
ventricular septal defect, and aortic root dilatation in aged cats. This murmur is a long, diastolic,
decrescendo murmur heard best over the aortic valve at the left hemithorax. The murmur is also
well heard at the right cardiac base.
Diastolic murmurs are otherwise rare in dogs and cats. Differential diagnosis includes the
soft, low-pitched rumble of congenital mitral or tricuspid stenosis but these are very rare
conditions. There is often concurrent atrioventricular valvular regurgitation, which may lead to a
systolic murmur.
Patent Ductus Arteriosus is the most important cause of a continuous murmur and is
described as distant and machinery (like a machine shop) in quality. The murmur must be
carefully located dorsally on the cranial left base, over the main pulmonary artery (which is the
sink for the shunt). Although it is continuous, the murmur does vary and loudness peaks around
the time of S2. Often there is concurrent mitral regurgitation (due to left ventricular dilatation)
which can be responsible for a systolic murmur over the left apex. The stethoscope should be
inched up and back from the left apex to the PMI of the continuous murmur at the left base. In
terms of differential diagnosis, continuous murmurs (bruits) can be detected over congenital or
acquired arteriovenous fistulas, including those associated with thyroid carcinomas or limb
injuries. Within the thorax, coronary artery to pulmonary artery fistulas and systemic arterial to
pulmonary artery vascular malformations can result in a continuous cardiac murmur. Rare cases
of reversed PDA usually have no murmur or a soft ejection murmur with a tympanic and
sometimes split second heart sound.
Abnormal upper airway sounds include: 1) tracheal snaps (tracheal collapse); 2) stertor
(inspiratory snoring) typical of pharyngeal or nasopharyngeal diseases, and 3) stridor, an
inspiratory wheeze loudest over the larynx. Stridor or altered inspiratory pitch is typical of upper
airway obstruction. Low-pitched inspiratory noise can also indicate upper airway obstruction.
While upper airway obstruction is classically inspiratory, fixed obstructions can lead to airway
noise during both phases of ventilation.
Abnormal lower airway (adventitious) sounds include rhonchi, wheezes, and crackles. A
sonorous rhonchus is an inspiratory or expiratory noise (r/o transmission of upper respiratory
stertor) which suggests the presence of fluid or exudate in larger airways, as with bronchitis or
pneumonia. Wheezes (sibilant rhonchi) are high-pitched expiratory sounds typical of bronchial
narrowing. The usual associations are bronchial disease (bronchitis, asthma) or attenuation of a
main bronchus caused by left atrial dilation, hilar lymphadenopathy, primary bronchial collapse,
or a pulmonary mass lesion. Crackles (rales) are discontinuous sounds similar to radio static
or the sound of Velcro pulled apart. These sounds are caused by the explosive opening of
collapsed small airways. Though there is a tendency to relate these to fluid in the lungs, there
is not a consistent correlation as crackles might be detected with pulmonary edema,
pneumonia, bronchitis, or pulmonary fibrosis. The loudest crackles are typically detected in
primary lung diseases. Subtle crackles are evident only after a deep breath.
References
1. Detweiler DK, Patterson DF. A phonograph record of heart sounds and murmurs of the dog. Ann N Y
Acad Sci. 1965;127(1):322-40
2. Vrs K, Nolte I, Hungerbhler S, et al.: Sound recording and digital phonocardiography of cardiac
murmurs in dogs by using a sensor-based electronic stethoscope. Acta Vet Hung. 2011; 59(1):23-35.
3. Wagner T, Fuentes VL, Payne JR, McDermott N, Brodbelt D. Comparison of auscultatory and
echocardiographic findings in healthy adult cats. J Vet Cardiol. 2010; 12(3):171-82.
4. Little CJ, Ferasin L, Ferasin H, Holmes MA. Purring in cats during auscultation: how common is it, and
can we stop it? J Small Anim Pract. 2014;55(1):33-8. 5. Blass KA, Schober KE, Bonagura JD, Scansen
BA, et al.: Clinical evaluation of the 3M Littmann Electronic Stethoscope Model 3200 in 150 cats. J Feline
Med Surg. 2013 Oct;15(10):893-900. 6. anagement of incidentally detected heart murmurs in dogs and
cats.
Ct E, Edwards NJ, Ettinger SJ, et al.: Working Group of the American College of Veterinary Internal
Medicine Specialty of Cardiology on Incidentally Detected Heart Murmurs. J Am Vet Med Assoc. 2015
May 15;246(10):1076-88.
CONGENITAL HEART DISEASE
John D. Bonagura, DVM, MS, DACVIM (Cardiology, Internal Medicine)
Veterinary Clinical Sciences, The Ohio State University
Principles
Cardiac malformations are developmental lesions of the heart or great vessels present at birth.
CHD can be caused by genetic, environmental, chromosomal, infective, toxicologic, or nutritional
factors or develop from teratogenic effects of drugs. Most defects are considered genetic in origin,
but the precise mode of inheritance often is unknown. There are numerous examples of breed-
related predispositions to specific cardiac malformations (see Tables at the end of these reference
notes). Penetrance of a lesion can be incomplete, making clinical recognition difficult or
impossible.
The pathophysiology of CHD can be classified arbitrarily as: left-to-right shunts, right-to-left
shunts, outflow tract stenosis, atrioventricular valve malformations, and complex malformations.
Left-to-right shunts, outflow tract stenosis, and valvular malformations are likely to cause
congestive heart failure (CHF), arrhythmias, syncope, or sudden cardiac death. Right-to-left
shunts and complex malformations create hypoxemia and secondary polycythemia with clinical
complications related to tissue hypoxia and blood hyperviscosity. A number of uncommon
complications also can develop, including hypertrophic osteopathy.
The first step in the management of congenital heart disease involves recognition of a
congenital malformation of the heart. This must be done by the family veterinarian, so emphasis
here is placed on honing auscultation skills, distinguishing functional murmurs from those caused
by CHD, and developing a general understanding of the cardiac malformations affecting dogs and
cats. Unless the family veterinarian identifies and refers the patient (or accurately diagnoses the
situation in the practice), appropriate management can never be accomplished. Since thoracic
surgery and cardiac catheterization/intervention are not part of routine veterinary practice, most
patients are referred to a cardiology specialist for management.
The actual therapy of heart malformation can involve surgical, catheter-based, or medical
treatments. Some disorders are relatively mild and require no treatment, but many are severe and
life-shortening. Prior to any therapy, a definitive diagnosis must be established. This requires a
complete echocardiographic study with Doppler and an advanced knowledge of the different
variations of heart and vascular malformations. Many cases of CHD are complicated by multiple
issues that must be considered before an accurate diagnosis, prognosis, and therapy plan and
be advanced. Heart surgery is difficult as it may require cardiopulmonary bypass (making
treatment impractical in many cases, even in referral situations). Thus, definitive surgical repair
of CHD is rarely accomplished except for extracadiac procedures like closure of patent ductus
arteriosus (PDA) or reduction of a congenital peritoneopericdardial diaphragmatic hernia.
Similary, catheter-based interventions need sufficient equipment for quality angiography and
intervention. Catheter-based treatments for PDA or pulmonary stensois (PS) can end badly if the
operating clinician is inexperienced. Thus it is strongly recommended that surgical or
interventional management of cardiac defects be undertaken only by those with appropriate
training.
Symptomatic medical therapy also can be needed for complications of CHD, namely control of
CHF, cardiac arrhythmias, PH, or secondary polycythemia. Such treatment can be directed by
the general practitioner provided the disorder is well characterized and the complications and
management issues understood.
Congestive heart failure is a consequence of progressive volume or pressure overload of the
affected ventricle. With time, diastolic and systolic ventricular function decline and cardiac output
becomes limited. This situation is worsened by development of mitral or tricuspid valvular
regurgitation or atrial fibrillation. The end-result is development of left- or right-sided CHF. Initial
management of left sided CHF involves treatment with furosemide (2-4 mg/kg IV, IM, or SQ),
oxygen, and possibly 2% nitroglycerine ointment. Sedation with butorphanol (0.1 to 0.25 mg/kg
IM or SQ) can be added if necessary. Pimobendan (0.25 to 0.3 mg/kg PO q12h) is often included
in therapy of CHF due to CHD. If this approach fails to control the CHF, and the cause is a left to
right shunt, sodium nitroprusside (0.5 to 2.5 micrograms/kg/min infusion) can be used to reduce
the arterial blood pressure and magnitude of shunting. Alternatively, hydralazine (0.5 to 2 mg/kg
PO q12h) or enalapril (0.25 to 0.5 mg/kg PO q12h) or other angiotensin converting-enzyme (ACE)
inhibitor can be initiated to reduce afterload and reduce left-to-right shunting. Care must be taken
to maintain systolic blood pressure in the 80 to 120 mm Hg range, particularly in cases of aortic
stenosis where hypotension can reduce coronary perfusion.
Chronic medical therapy of CHF includes furosemide, an ACE-inhibitor, spironolactone, and
pimobendan (see elsewhere in this Program).. The use of beta-blockers in treatment of dogs with
CHF due to CHD is unresolved, and care must be used to avoid bradycardia, especially in dogs
with fixed obstructions such as SAS and PS, as cardiac output in these conditions is relatively
heart rate dependent. For dogs already taking beta-blockers as cardioprotection, once CHF
develops, the beta blocker should be continued, the dosage reduced if needed to obtain a target
examination heart rate in the 100 to 140/minute range. In some cases, medical therapy for CHF
can be discontinued if definitive repair of the defect can be successfully performed. This is
particularly true in young animals with PDA.
Controlling arrhythmias in the setting of severe CHD can help to maintain a compensated state
and can prevent sudden death. Atrial fibrillation is particularly destabilizing to dogs with CHD and
established heart failure. Heart rate control can be achieved with digoxin, diltiazem, and a beta-
blocker. Electrical cardioversion is another option to restore sinus rhythm, unless atrial
enlargement is severe, in which case it is not likely to yield long-term success. Re-entrant SVT
due to an accessory pathway can be encountered and radiofrequency catheter ablation of the
anomalous pathway can eliminate the arrhythmia substrate. In the interim, diltiazem (to block the
AV node) and flecainide or another antiarrhythmic drug given to block the accessory pathway.
Ventricular arrhythmias are often recognized in canine SAS and PS. Holter ECG monitoring can
be indicated to screen for rhythm disturbances, especially in dogs with exertional symptoms.
Chronic therapy of important ventricular tachycardia can include sotalol, mexiletine plus a beta
blocker (including sotalol), amiodarone, or procainamide.
Management of pulmonary hypertension due to high pulmonary vascular resistance is difficult
as the anatomic vascular changes responsible often are irreversible. The evaluation of PH usually
requires referral to a specialist experienced in CHD. PH usually develops rapidly in dogs with
large left-to-right shunts (prior to six months of age). In cats development is more gradual, and if
caught in time, can be arrested by closure of the defect or management of a stenotic mitral valve.
When a reactive component of vasoconstriction is identified, drugs that reduce pulmonary
vascular resistance such as sildenafil at initial doses of 1 to 2 mg/kg q12h PO can be beneficial.
Currently this therapy is very expensive. Arterial blood pressure must be monitored as reduced
systemic resistance will lead to greater right-to-left shunting. Controlled exercise is important to
prevent exertional collapse or dyspnea. This can be difficult to achieve in puppies or kittens.
Management of polycythemia can be required. This condition is usually a consequence of
complex malformations (double outlet right ventricle; tricuspid or pulmonary atresia) or of right-to-
left shunting across a PDA or septal defect related to an obstructive lesion of the right heart (PS,
double-chambered right ventricle, tricuspid stenosis) or pulmonary hypertension. Balloon
valvuloplasty or surgery can decrease right-sided pressures and reduce shunting in the case of
an anatomic obstruction; drugs can be tried to reduce pulmonary vascular resistance (see above).
Care must be exercised in the setting of a large VSD as florid left-to-right shunting can develop if
RV pressures approach normal. Phlebotomy can be required in patients with right-to-left shunting
and secondary polycythemia. While a PCV of 62 to 65% often is well tolerated, values exceeding
68 to 70% are likely to cause exercise difficulties or predispose to thrombotic stroke or sudden
death. Periodic phlebotomy with replacement by IV or subcutaneous crystalloid fluid. When the
need for phlebotomy becomes too frequent, bone marrow suppression can be attempted using
hydroxyurea (10 to 20 mg/kg PO daily). Treatment can not work, and anorexia, GI disturbances,
and skin rash can limit tolerability of the drug. A CBC and platelet count should be performed
regularly.
Overview PDA is a persistent patency of the fetal ductus arteriosus. The ductus connects the
descending aorta and the main or adjacent left pulmonary artery. This defect is reported to be
present in approximately 2.5 of 1000 live canine births. Left to right shunting leads to pulmonary
overcirculation, volume overload of the left heart, and progressive LV dysfunction. Left sided CHF
can develop. Cardiomyopathy of chronic volume overload and atrial fibrillation are common in
larger breeds with untreated PDA. In a small percent of cases, reversed shunting is caused by
pulmonary vascular injury (Eisenmengers physiology). Most puppies are apparently
asymptomatic. Once tachypnea and exercise intolerance develop, left-sided CHF is likely.
Exertional rear limb weakness is typical of reversed PDA.
PDA is a genetic disorder in many breeds, including: Bichon frise, Chihuahua, Cocker spaniel,
Collie, English Springer spaniel, German shepherd, Irish and Gordon setters, Poodles, Maltese,
Kerry blue terrier, Keeshond, Labrador retriever, Newfoundland, Pomeranian, Shetland
sheepdog, and Yorkshire terrier. The precise mode of inheritance is undetermined, likely related
to multiple or modifying genes. Females are predisposed, but both sexes are affected. PDA is
rare in cats.
Diagnosis The most striking diagnostic finding during physical examination is a continuous
cardiac murmur loudest over the left craniodorsal cardiac base. The diastolic component of the
murmur is less prominent or absent in very young puppies, in cats, or in cases of progressive
pulmonary hypertension. Arterial pulses are typically hyperkinetic as the arterial pulse pressure
is wide. This is explained by the large LV stroke volume and low diastoic pressure associated with
pressure run off across the ductus. The LV can be palpably enlarged with caudoventral apical
displacement. Pelvic limb weakness that improves with rest, differential cyanosis, loss of the
continuous murmur, and a loud second heart sound are typical of reversed PDA. Radiographs
and 2D echocardiography demonstrate dilation of the left atrium, LV, ascending aorta, descending
aorta (ductus bump), and main pulmonary artery. Radiographs identify pulmonary
overcirculation in left to right shunting PDA. Doppler studies reveal continuous blood flow in the
main pulmonary artery. Mitral regurgitation and pulmonic insufficiency are commonly found due
to chamber dilatation. Echocardiography can document reduced LV systolic function. The typical
ECG findings are enlargement of the LV and possibly the left atrium. In reversed PDA, the
diagnostic studies demonstrate mainly right heart enlargement, dilation of the main pulmonary
artery, and reduced pulmonary blood flow. Contrast echocardiography following cephalic vein
injection will demonstrate contrast in the descending aorta.
The differential diagnoses includes aortopulmonary window, a congenital connection between
the ascending aorta and pulmonary artery; ventricular septal defect with aortic regurgitation; and
aortic stenosis/regurgitation. Multiple bronchial artery to pulmonary fistulas can create a PDA like
situation in terms of lung circulation and left-sided volume overload; however, a continuous
murmur may not be evident mandating, angiography for diagnosis. The signs of reversed PDA
can mimic those of neuromuscular diseases, particularly myasthenia gravis.
Therapy Closure or occlusion is strongly recommended in left-to-right shunting defects as the
one-year mortality for untreated dogs probably exceeds 60%. In the reversed (right-to-left)
shunting PDA, closure of the defect is contraindicated. Thoracotomy and surgical ligation of the
ductus is a very successful with a perioperative mortality that should be <5% at experienced
surgical centers, and is <2% in the best hands. Closure generally results in complete resolution
of signs. A post-operative murmur of mitral regurgitation is common due to LV stretch, but is
generally gone by the time of suture removal. Less-invasive transcatheter techniques for closure
of PDA have gained significant popularity and have superseded surgery at many hospitals. As
with surgery, success is highest in the hands of experienced operators. Embolization coils
(Gianturco) are best suited for small diameter defects with a gradually tapering diameter; the
various Amplatzer occluding devices has been modified for both small and larger diameter (>5
mm) defects. The current Amplatz Canine Ductal Occluder is highly effective and only limited by
the size of the patient in terms of vascular access (more challenging in dogs <3 kg). When CHF
complicates PDA, medical management is needed (discussed previously). Reversed PDA has a
poor prognosis though with vigilant therapy some patients live beyond 5 years of age, affected
mainly by rear limb weakness during exercise. Management of pulmonary hypertension and
polycythemia were discussed previously.
Early therapeutic intervention can slow or eliminate irreversible myocardial damage and prevent
heart failure. For example, after successful closure of a PDA, most dogs will live a normal life
without need for cardiac follow-up. The prognosis following isolated closure of a PDA is excellent.
A normal life-span can be anticipated, and most cases do not require any cardiac follow-up.
Exceptions to this rule include dogs with marked LV systolic dysfunction (by Echo), dogs with
prior CHF, or dogs with atrial fibrillation. Such patients should be referred to a cardiologist for
evaluation. Follow reversed PDA dogs by monitoring clinical signs and the PCV.
Overview A VSD is a communication between the left and right ventricles. Unless there is a
reason for elevated right ventricular pressure, shunting proceeds from LV to RV. The location of
a VSD determines the classification of the defect. This is generally defined by 2D
echocardiographic and color coded Doppler studies studies as paramembranous
(perimembranous), inlet, muscular (trabecular), or subarterial (subpulmonic, supracristal, doubly-
committed). Large defects are sometimes associated with malalignment of the aorta. These
lesions are likely to cause aortic root prolapse and permit aortic valvular regurgitation. A large
VSD also forms one component of the tetralogy of Fallot. VSD shows a genetic predisposition in
some breeds, including English bulldogs and Springer spaniels.
The shunting physiology of VSD is similar that of PDA, representing a left to right shunt with
pulmonary overcirculation and volume overload of the left atrium and LV. Large septal defects
usually progress to left-sided CHF. This is particularly true when there is complicating aortic
regurgitation. The degree of RV overload depends on the size of the defect, the presence of RV
outflow tract obstruction, the location of the defect, and pulmonary vascular resistance.
Concurrent PS, a double-chambered RV (a midventricular fibromuscular obstruction), or
development of Eisenmengers physiology can lead to reversed shunting. Most dogs and cats are
asymptomatic. Occasional cases show signs of CHF or pulmonary hypertension. Cyanosis
indicates a complicated VSD.
Experimentally, VSD in various species can be associated with a number of drugs, infections,
or environmental factors. Most cases of uncomplicated VSD in dogs are well tolerated so long as
the defect is restrictive. Defects <50% of the aortic root area are restrictive in nature. Very large
defects are likely to cause CHF and death at approximately one to two months of age as
pulmonary vascular resistance drops; puppies and kittens are uncommonly presented to
veterinarians at this age.
Diagnosis A systolic murmur, generally loudest over the cranial right sternal edge, is typical
of the membranous VSD. However, if the defect is located elsewhere in the septum, or if fibrous
tissue proliferation partially occludes the defect, the jet of flow can be diverted resulting in a
systolic murmur that is apical or loudest over the left sternal edge. In the setting of concurrent
aortic regurgitation, a diastolic murmur may be audible, and this usually indicates a clinically-
relevant complication that will shorten lifespan. Results of radiography are quite variable, but
overcirculation of the lungs is common. Various combinations of left and right heart enlargement
are typical. The main pulmonary artery can be dilated from increased flow or PH. The ECG can
be normal, LV enlargement or wide or splintered Q-wave in leads I, II, and aVF may be observed.
Echocardiography is diagnostic with 2D imaging and Doppler studies delineating the location,
direction and velocity of shunting. Restrictive defects are characterized by high velocity (>4 m/s)
shunting, indicating maintenance of left-to-right ventricular pressure gradient. It is important to
scrutinize the right ventricle for obstructive lesions and the LV outflow tract for aortic root for
malalignment or aortic regurgitation.
The differential diagnosis includes other causes of systolic murmurs, particularly tricuspid valve
dysplasia, aortic stenosis and some cases of double-chambered right ventricle. Mitral
regurgitation can create a similar murmur in terms of timing. Subpulmonic defects create left
basilar murmurs that can be confused with pulmonic or aortic stenosis.
Therapy Most dogs and cats with an isolated, uncomplicated VSD (without severe aortic
regurgitation or other lesions) that survive to 4 months of age will not require any treatment.
Surgical closure of septal defects is the definitive treatment but requires cardiopulmonary by-pass
and open heart surgery. While this has been successfully performed in dogs and cats, it is not a
common practice in veterinary medicine. Palliative pulmonary arterial banding is available to
create a supravalvular PS and reduce the magnitude of left-to-right shunting. This procedure is
recommended only for those animals with rapidly progressive cardiomegaly and with overt or
impending CHF. Simple cardiomegaly is not an indication for banding. A cardiologist should be
consulted. Transcatheter and perventricular occlusion devices (hybrid surgery) can be applied
to dogs.
If CHF does develop, medical management is indicated (discussed previously). Right to left
shunting can develop in dogs or cats with VSD due to PH, valvular or subvalvular PS, or
progressive, midventricular fibromuscular obstruction (so called double-chambered RV). Exercise
intolerance and polycythemia can develop. Treatment is as described above for polycythemia.
A small, restrictive VSD carries an excellent prognosis for longevity. CHF associated with VSD
is actually uncommon in most small animals with VSD as they are naturally-selected and rarely
require intervention. CHF should be anticipated in the dog with a VSD and aortic root prolapse
and audible aortic regurgitation. In these cases, CHF can develop in middle-age from LV volume
overload. The author empirically treats these patients with ACE-inhibitors. CHF also develops in
some cats with VSD, especially when the defect is non-restrictive. Not infrequently a VSD will be
observed to close from fibrous tissue proliferation or adherence of the septal leaflet of the tricuspid
valve. This can lead to a septal aneurysm but without significant shunting. These lesions are
essentially closed.
Overview An ASD is a communication between the left and right atria. Unless there is a
reason for elevated right ventricular pressure, shunting generally proceeds from left to right. The
location of an ASD determines the classification of the defect. These are generally defined by
detailed 2D echocardiographic and color Doppler studies as a secundum, primum, or sinus
venosus defect. A defect in the ventrally-located atrioventricular septum, or of the embryonic
endocardial cushions, can lead to a complicated situation of a primum (ventral) ASD, inlet septal
VSD, and malformation of the septal leaflets of the atrioventricular valves with atrioventricular
valvular regurgitation. This latter situation is terms (a complete) atrioventricular septal defect. A
patent foramen ovale is created when the two atrial septal membranes (I and II) are either pulled
or pushed apart. Patency can be maintained by either severe left atrial stretch or from a higher
than normal right atrial pressures that push the membranes apart. The latter is caused by some
other form of right-sided disease. ASD is sometimes recognized in dogs with advanced mitral
regurgition and probably represents an atrial tear in the thin-walled fossa ovalis.
The pathophysiology of ASD is that of a left to right shunt with volume overload of the right
atrium and right ventricle. There is also pulmonary overcirculation, but the left atrium typically
decompresses to the right atrium and can be normal in size (except with an endocardial cushion
defect). A large ASD can cause right-sided CHF or lead to pulmonary vascular injury with
pulmonary hypertension. An endocardial cushion defect can cause left-sided or biventricular CHF.
Right to left shunting can occur across an ASD (or PFO) in the setting of PH, or from obstructive
lesions on the right side of the heart. Severe tricuspid regurgitation also can cause cyanosis by
raising right atrial pressure.
ASD is genetic predisposed in some breeds and family lines (e.g., standard poodles in North
America). Most dogs and cats with an isolated ASD appear asymptomatic. There are no specific
signs of an ASD. The pressure difference across an ASD is relatively small; therefore, the defect
does not cause a murmur aside from that of increased flow across the pulmonary valve (relative
PS). Classically the second heart sound will be split, owing to a longer duration of right ventricular
ejection. Occasional cases show signs of CHF or of pulmonary hypertension. Cyanosis indicates
a complicated ASD.
Diagnosis The identification of a systolic murmur creates suspicion for CHD. Careful
auscultation should reveal a splitting of the second heart sound owing to delayed pulmonary valve
relative to aortic valve closure. Radiography of a secundum ASD demonstrates right heart
enlargement, dilation of the pulmonary artery, and overcirculation of the lungs. Left atrial size is
variable. With a complete endocardial cushion defect (atrioventricular septal defect), significant
mitral or AV valve regurgitation can occur. This can lead to left atrial enlargement and eventually
signs of left-sided or biventricular CHF. The ECG generally shows RV and usually right atrial
enlargement with right axis deviation. A left cranial frontal axis is more typical of a primum ASD
or an endocardial cushion defect. Echocardiography is diagnostic with 2D imaging demonstrating
the septal defect and Doppler studies delineating the direction of shunting, which is often bi-
directional. It is important to scrutinize the right ventricle for obstructive lesions and the
atrioventricular valves for malformation and valvular regurgitation. Differential diagnosis includes
other causes of systolic murmurs in young dogs including functional murmur, valvular pulmonic
stenosis, and aortic stenosis. Anomalous pulmonary venous drainage can create a similar
physiology but appears rare in animals. This lesion can be associated with a sinus venosus type
ASD.
Therapy There is little experience in the management of ASD in dogs and cats as this defect
is relatively uncommon. In the case of patent foramen ovale, treatment of the related lesion can
cause the defect to functionally close. Transcatheter atrial septal occlusion devices have been
developed for closure of septal defects in children and have been applied to dogs. Open-heart
surgery has been used for successful closure of ASDs, but is not readily available. If CHF does
develop, medical management is indicated (discussed previously). Right to left shunting ASD will
likely create exercise intolerance and polycythemia. Treatment is as described above for
polycythemia. A yearly cardiologist examination with an echocardiogram is recommended for
most dogs and cats with an ASD. Late-onset pulmonary vascular disease with PH can occur.
Tetralogy of Fallot
Overview The tetralogy of Fallot is defined by the following anatomical defects: pulmonic
stenosis (PS), large (unrestrictive) VSD, dextropositioned aorta, and right ventricular hypertrophy.
This condition represents one of the most common causes of cyanotic CHD. The presence of PS
increases RV systolic pressure and allows shunting of blood from right to left. Depending on the
severity of RV outflow obstruction and the systemic vascular resistance, blood will shunt from
right to left, left to right, or (most commonly) in a bi-directional manner. Right to left shunting leads
to hypoxemia, cyanosis, and secondary polycythemia. There is a genetic basis for tetralogy of
Fallot in some breeds including the English bulldog and Keeshond. The history can include
exercise intolerance, syncope, or tachypnea. When the PS is not severe, the condition can be
well tolerated and shunting is predominately left to right (pink tetralogy).
Diagnosis A systolic murmur of PS is typically detected over the left base. Cyanosis is typical,
especially after exercise. Pulse oximetry can identify clinically significant desaturation (<90%).
Blood gas analysis reveals hypoxemia, often with pO2 < 65 mm Hg. Right ventricular hypertrophy
is evident by ECG and imaging studies. Radiographs demonstrate right ventricular rounding, a
small and straight left heart border on the VD projection, and pulmonary under-circulation. The
ascending aorta can be widened ventrally on the lateral projection (over-riding aorta). 2D
echocardiography is diagnostic and demonstrates the four components of the malformation.
Doppler studies show low velocity (bidirectional) shunting across the VSD over the cardiac cycle,
while high velocity flow of PS (typically 4 to 5 m/s) is evident across the proximal pulmonary artery.
The PCV may indicate polycythemia; pulse oximetry can show desaturation of hemoglobin.
Cardiac catheterization is rarely needed to establish the diagnosis.
The differential diagnosis for the various signs of tetralogy includes tricuspid atresia, pulmonary
atresia (pseudotruncus arteriosus), and PS with a VSD or an ASD (or patent foramen ovale).
Complex malformations such as double outlet RV can lead to cyanotic heart disease.
Therapy Animals with a sedentary lifestyle will often tolerate this disease well, especially if
the PS is not too severe. Some will live for 5 or more years. Exercise creates vasodilation in
skeletal muscle and increases tissue oxygen demands; accordingly, most affected animals have
signs of tachypnea and exercise intolerance with exertion. Sudden death is common consequent
to progressive hypoxemia, polycythemia and cardiac arrhythmias. Drugs that cause systemic
vasodilation should be avoided in these patients as right-to-left shunting can be exacerbated.
Beta-blockage with the nonspecific beta-blocker propranolol (starting at 0.25 mg/kg PO q8h and
up-titrating over 4 weeks to 1 mg/kg PO q8h) can be beneficial by reducing exercise-induced RV
hyper-contractility, an event that can add a dynamic component to RV outflow obstruction. The
beta2 blocking effect should theoretically benefit by preventing some exercise induced peripheral
vasodilation. Definitive surgical treatment for tetralogy of Fallot includes closure of the VSD and
removal or bypass of the stenosis under cardiopulmonary by-pass. Palliative surgery involves
creation of an extra-cardiac shunt between the systemic and pulmonary circulations (e.g., Blalock-
Tausig shunt). Such shunts increase pulmonary flow, improve arterial saturation, and can produce
significant clinical improvement. The major limitation is the extent to which these shunts will
remain patent. Aspirin or another drug that inhibits platelet activation (such as clopidogrel) is
indicated. Balloon valvuloplasty of a stenotic pulmonary valve can reduce RV pressures, but
complete resolution of the PS will generally allow for marked left to right shunting. Polycythemia
should be managed as described previously.
Follow-up evaluation should emphasize clinical signs, PCV, and arterial oxygen saturation.
Yearly reevaluation is indicated. If a palliative shunt has been created, Doppler evaluation of shunt
patency should be undertaken.
Reference
1. Oyama MA, Sisson DD, Thomas WP, Bonagura JD: Congenital heart disease. In: Ettinger SJ,
Feldman EC (eds): Textbook of Veterinary Internal Medicine, 6th ed. St Louis: Elsevier
Saunders, 2005; and 2009.
Some Canine Breed Predilections to Congenital Heart Disease
Basset Hound PS
Beagle PS
Bichon Fris PDA
Boxer SAS, PS, ASD
Boykin Spaniel PS
Bull Terrier MVD, AS
Chihuahua PDA, PS
Chow Chow PS, CTD
Cocker Spaniel PDA, PS
Collie PDA
Doberman Pinscher ASD
English Bulldog PS, VSD, ToF
English Springer
PDA, VSD
Spaniel
German Shepherd
SAS, PDA, TVD, MVD
Dog
German Shorthaired
SAS
Pointer
Golden Retriever SAS, TVD, MVD
Great Dane TVD, MVD, SAS
Keeshond ToF, PDA
Labrador Retriever TVD, PDA, PS
Maltese PDA
Mastiff PS, MVD
Newfoundland SAS, MVD, PS
Pomeranian PDA
Poodle PDA
Rottweiler SAS
Samoyed PS, SAS, ASD
Schnauzer PS
Shetland Sheepdog PDA
Terrier breeds PS
Weimaraner TVD, PPDH
Welsh Corgi PDA
West Highland White
PS, VSD
Terrier
Yorkshire Terrier PDA
AS, Aortic stenosis; ASD, atrial septal defect; CTD, cor triatriatum dexter; MVD, mitral
valve dysplasia; PDA, patent ductus arteriosus; PPDH, peritoneopericardial
diaphragmatic hernia; PS, pulmonic stenosis; SAS, subaortic stenosis; ToF, tetralogy of
Fallot; TVD, tricuspid valve dysplasia; VSD, ventricular septal defect.
Congenital Heart Disease in Dogs Data from Combined Studies
Numbe Percentag
Defect r e
Patent ductus arteriosus (PDA) 1207 25.7
Subaortic stenosis (SAS) 1102 23.5
Pulmonic valve stenosis (PS) 1039 22.1
Ventricular septal defect (VSD) 413 8.8
Tricuspid valve dysplasia (TVD) 216 4.6
Mitral valve dysplasia (MVD) 204 4.3
Other defects 160 3.4
Persistent right aortic arch or other vascular ring anomaly
(PRAA) 155 3.3
Tetralogy of Fallot (ToF) 110 2.3
Atrial septal defect (ASD) 89 1.9
Total 4694 100
Reprinted from Scansen BA, Cober RE, Bonagura JD. Congenital heart disease. In: Bonagura
JD, Twedt DC, editors. Kirk's Current Veterinary Therapy XV (15th ed). St. Louis,
Elsevier/Saunders; 2014. p. 756-761.
Etiology
Acquired pericardial effusions are common in dogs. The pericardial fluid is typically classified
using clinicopathologic methods. Causes of transudates include right-sided CHF, PPDH, cysts,
and hypoalbuminemia. Exudates are caused by pericarditis, including that associated with
perforating foreign bodies. Sterile (inflammatory) pericarditis can complicate recurrent, idiopathic
intrapericardial hemorrhage. Hemorrhagic pericardial effusions are the most common fluid type
collected from dogs. In patients <6 years, idiopathic pericardial hemorrhage predominates. In
older dogs, hemangiosarcoma of the right atrium, aortic body tumor (chemodectoma), ectopic
thyroid carcinoma, and pericardial mesothelioma are major causes. The latter is a difficult and
sometimes controversial histopathological diagnosis. Metastatic pericardial neoplasia is
recognized at necropsy but is an uncommon antemortem diagnosis. Uncommon causes of
pericardial hemorrhage include left atrial tearing from mitral regurgitation; blunt trauma;
coagulopathy, and complicated thoracocentesis. Chyle is a very rare fluid type.
Pathophysiology
Pericardial effusion leads to clinical signs by compressing the heart. Cardiac tamponade refers
to "the decompensated phase of cardiac compression resulting from an unchecked rise in the
intrapericardial fluid pressure." The normally negative intra-pericardial pressure becomes positive
relative to atmosphere and pressures rise quickly once elastic limits of the pericardium are
reached. Tamponade can develop quickly with sudden hemorrhage into the space, as with a
bleeding tumor. In chronic cases, larger volumes can be accommodated before intrapericardial
pressures rise. The pathophysiology can be summarized as: Increased (positive) intrapericardial
pressure diastolic collapse of the thinner-walled right atrium and ventricle along with
compression of the proximal vena cava reduced right ventricular filling decreased preload
decreased stroke volume and cardiac output and arterial hypotension if compensatory
mechanisms (heightened sympathetic activity, vasoconstriction, and renal retention of sodium and
water) are insufficient.
Clinical signs
The clinical consequences of tamponade are straightforward. Syncope, collapse or even
sudden death can occur if hypotension is acute and severe. Given sufficient time, compensatory
measures are activated to maintain arterial blood pressure (BP). Congestive heart failure, with a
predominately right-sided component is the most common consequence of chronic cardiac
tamponade. Dogs become exercise intolerant, develop abdominal distension, lose muscle mass,
and might become tachypneic if pleural effusion supervenes.
Breed predispositions to specific neoplasm types are relevant in the differential diagnosis, as
with golden retrievers (idiopathic hemorrhage, hemangiosarcoma), St. Bernard dogs (idiopathic
hemorrhage) and brachycephalic breeds (chemodectoma). Fever or thoracic pain could indicate
inflammatory pericarditis; occasionally other signs of systemic disease such splenomegaly might
be noted. Overt right-sided CHF is characterized by elevated jugular venous pressure, muffled
(distant) heart sounds, ascites, and possibly signs of pleural effusion. If superficial venous
distension is missed, a diagnosis of liver disease or abdominal neoplasia might be erroneously
entertained. Arterial hypotension or pulsus paradoxicus, a marked inspiratory fall in BP is often
detected; this is caused by respiratory variation in ventricular filling that becomes exaggerated
within an encased heart. Pulsus paradoxicus is identified using a Doppler flow detector or by
careful palpation/observation. Breath sounds are muffled with tachypnea or respiratory distress if
there is moderate to large pleural effusion.
Electrocardiogram (EKG)
The EKG can be normal, but any of the following might be observed: decreased amplitude
QRS complexes; electrical alternans with large effusates and swinging of the heart; ST-segment
elevation from epicardial injury (indicating pericarditis); sinus tachycardia; vagal reflexes that
induce sinus arrhythmia or sinus bradycardia; or heart rhythm disturbances. The latter include
atrial and ventricular premature complexes secondary to epicarditis, invasive cardiac neoplasia,
ischemia from tamponade, concurrent heart disease, or splenic disease.
Diagnostic Imaging
As the cardiac silhouette enlarges, thoracic radiographs will be suggestive of the diagnosis but
have relatively low sensitivity and specificity. The size increases and cardiac borders lose their
angles and waists, eventually becoming globular in shape. The cardiac outline might be especially
sharp, presumably from diminished motion of the distracted pericardium. The left atrial border
on the lateral view may become rounded. This and the common finding of diminished pulmonary
vascularity help to distinguish cardiac tamponade from cardiomegaly due to cardiomyopathy or
chronic valvular disease. If CHF has developed, there may be increased pulmonary interstitial
densities, distension of the caudal vena cava, hepatomegaly, or pleural effusion. Heart base
tumors can deviate the trachea. Metallic densities (such as a shotgun pellet) should be taken as
risk factors for pericarditis. Fluoroscopy reveals reduced cardiac motion.
Echocardiography is a highly sensitive test for detecting pericardial effusion and most cardiac
mass lesions. Abnormal fluid accumulation is evident as a sonolucent (generally black) space
between the epicardium and pericardium, extending from apex to base. A mixed echogenic fluid
suggests cellular exudate or recent hemorrhage. The effusion can be loculated (localized) in
inflammatory diseases or following a surgical pericardial window. A tumor of the right atrium or
along the right atrioventricular groove is suggestive of hemangiosarcoma. A heart base mass
around the aorta is typical of chemodectoma or ectopic thyroid carcinoma. Thickened pericardium
with tumors on the parietal surface may suggest mesothelioma, but these are difficult to discern.
False positives for mass lesions can stem from clot formation and the fat pad normally present
between the pulmonary artery and aorta. Pleural effusions, ascites, dilated caudal vena cava, and
distended hepatic veins also may be observed. Diastolic collapse of the right atrium or right
ventricular wall is supportive of increased intrapericardial pressure and corresponds to effusion
with tamponade. Inversion of the atrial wall and protracted collapse of the ventricular wall are
more specific signs. However, both false positives (from massive pleural effusions) and false
2
negatives (from concurrent elevated CVP expanding the cardiac chambers) do occur. The
distinction between idiopathic hemorrhagic pericardial effusion and bleeding from a tumor is
crucial in terms of prognosis and might require a high-resolution, technically-proficient,
echocardiogram recorded from each side of the thorax using multiple views. In some cases,
exploratory surgery or advanced imaging (CT, MRI) will be needed to exclude a mass lesion.
Clinical Laboratory
Serum biochemistries usually reflect the heart failure; cardiac troponins can increase from
myocardial ischemia. The CBC may suggest inflammation, hemorrhage, or hemangiosarcoma
(nucleated RBCs). Pleural and peritoneal effusions are obstructive (transudate, modified
transudate). Pericardial effusions are typically hemorrhagic; reactive mesothelial cells are
common (but not diagnostic of mesothelioma). Most heart base tumors exfoliate poorly so
cytological diagnosis in unreliable. Flow cytometry has been positive in some cases. Cultures are
usually negative.
Pericardiocentesis
Needle or catheter drainage of the pericardial space is the initial treatment for cardiac
tamponade. Intrapericardial pressures fall rapidly with removal of ~1/2 of the volume. The steps
can be summarized as follows and are demonstrated in the lecture.
Prepare patient:
o Left-lateral recumbency (spine elevated)
o IV catheter
o BP cuff
o ECG electrodes
o Sedation (butorphanol 0.1 to 0.2 mg/kg).
o Identify puncture site over right thorax
o Clip/prepare target area
o Infiltrate ~3 ml of 2% lidocaine, skin to pleura
Glove and prepare catheter (14 to 20 gauge Angiocath) with extra side holes
Perform centesis
o Insert catheter in a controlled motion into the pericardial space
o Once fluid exits freely, advance catheter over needle
o Connect tubing & aspirate
o Collect clot and EDTA tubes
o Monitor for extrasystoles & hypotension
o Recheck ultrasound
Follow-up Care
Other medical therapies are rarely administered. Judicious doses of furosemide (post-
pericardiocentesis) will hasten mobilization of ascites. Chemotherapy is recommended for optimal
palliation of hemangiosarcoma. Treatments involving corticosteroids or colchicine require study.
Surgical procedures
A number of different procedures can be performed in carefully selected cases. Right
auriculectomy is performed rarely for isolated hemangiosarcoma. Major thoracic surgery with
subtotal pericardiectomy is indicated for recurrent idiopathic pericardial hemorrhage and for
infective pericarditis (to prevent constrictive pericarditis). Less-invasive procedures (via balloon
pericardiotomy, thoracoscopy, or mini-thoracotomy) involve creation of windows for palliation of
heart base masses along with visualization and pericardial biopsy in older dogs with recurrent
effusions. These have also been used for recurrent idiopathic hemorrhage but substantial long-
3
term follow up on these cases is still needed to gauge the risk of constriction.
References:
Atencia S1, Doyle RS, Whitley NT. Thoracoscopic pericardial window formanagement of pericardial effusion in 15
dogs. J Small Anim Pract. 2013 54(11):564-9
Case JB, Maxwell M, Aman A, Monnet EL. Outcome evaluation of a thoracoscopic pericardial window procedure or
subtotal pericardectomy via thoracotomy for the treatment of pericardial effusion in dogs. J Am Vet Med Assoc. 2013
Feb 15;242(4):493-8
Ct E1, Schwarz LA, Sithole F. Thoracic radiographic findings for dogs with cardiac tamponade attributable to
pericardial effusion. J Am Vet Med Assoc. 2013 Jul 15;243(2):232-5..
Nelson OL, Ware WW: Pericardial Effusion, in Bonagura JD and Twedt DC (eds): Current Veterinary Therapy XV, St.
Louis, Elsevier/Saunders, 2014.
MacDonald KA, Cagney O, Magne ML. Echocardiographic and Clinicopathologic Characterization of Pericardial
Effusion in Dogs: 107 cases (1985-2006). J Am Vet Med Assoc. 2009; 15;235(12):1456-61.
Stafford Johnson M, Martin M, Binns S, Day MJ. A retrospective study of clinical findings, treatment and outcome in
143 dogs with pericardial effusion. J Small Anim Pract. 2004; 45(11):546-52.
4
RADIOGRAPHIC DIFFERENTIAL DIAGNOSIS
OF CARDIOPULMONARY DISORDERS
The clinical signs of cardiac and respiratory diseases are similar and the clinician must be
adept at distinguishing heart from respiratory diseases. Knowledge of common (and less
common) diagnoses, skill in orchestrating a logical workup, and ability to interpret thoracic
radiographs are keys to success.
Most bronchopulmonary disorders, as well as problems within the mediastinum and pleural
space, are identified because of the initial signs of cough, tachypnea, or respiratory distress
(dyspnea). The clinician must have an appreciation of the numerous causes of these clinical
signs and the resources to evaluate these problems. The clinical work-up is summarized in
Table 1. In addition to the history and physical examination, radiographic examination of the
thorax is critical, and the clinician must learn to identify common patterns of thoracic disease.
The causes of acute and chronic respiratory disease can be classified simply, as follows:
Mechanical or obstructive lesions causing major-airway obstruction or compression
Cardiac diseases
Pulmonary vascular diseases
Bronchial diseases including bronchitis and asthma
Infectious and noninfectious pulmonary parenchymal diseases -
including edema, hemorrhage, and pneumonia
Tumors and mass lesions of the bronchopulmonary tree
Mediastinal diseases
Pleural space disorders (causing respiratory distress) see Table 2
Alternative imaging can be quite helpful in some cases. Fluoroscopy is useful for identifying
dynamic collapse of the larger airways (trachea and main bronchi). Ultrasonography of the
thorax is indicated in cases of suspected heart disease, pericardial effusion, heart base or
mediastinal mass, diaphragmatic hernia, consolidated lung, or large pleural effusion. Pleural
effusion - in the absence of enlarged jugular veins, cardiomegaly, or distended hepatic veins -
usually indicates a noncardiac condition.
Computerized tomography (CT) can be very helpful in assessing the lung for
metastasis, pulmonary infiltrates, bronchial lesions, and pulmonary vascular lesions that
cannot be seen radiographically. The method is also helpful for identifying mediastinal
masses or hilar lymphadenopathy. This examination is made less useful when there is pleural
effusion or pulmonary atelectasis. Some studies (with fast imagers) can be done with sedation.
The electrocardiogram (ECG) and echocardiogram are appropriate for assessing patients with
suspected heart failure or pericardial disease.
Endoscopy provides for direct visualization of the upper airways, trachea, and proximal bronchi
and is indicted when intraluminal masses, foreign body, or other causes of unexplained airway
obstruction or inflammation is suspected. Endoscopes must be appropriate size for cats and
small dogs, and often these are unavailable. Following initial visual inspection, airway culture is
performed, generally with a guarded culture swab designed for endoscopes or airway cultures.
This is followed by a detailed examination of the trachea and bronchial tree followed by
bronchial washing, brush cytology, mucosal biopsy, or bronchoalveolar lavage.
Airway cytology is a helpful examination in many noncardiac thoracic diseases. If clinical signs
and prior laboratory test results inadequately explain cough or dyspnea, or the reason for
increased pulmonary density, the clinician should obtain a lower airway tissue sample for culture
and cytology or cytology of pleural fluid should that be present. The method of choice for
obtaining airway samples depends on experience, availability of equipment, and the nature of
pulmonary infiltration. Endotracheal washes and brush cytology are should be evaluated by a
clinical pathologist for predominant cell type, presence or absence of microorganisms, and other
cytologic features which can contribute to the diagnosis. A bronchoalveolar lavage is treated in a
similar qualitative manner, but it is also important to request a quantitative cell count. The wash
sample is divided for culture, requesting aerobic culture and sensitivity, +/- anaerobic culture,
and special culture media for Mycoplasma (especially in cats). In general, any upper airway
inflammation (e.g. mucous from bronchitis) will contaminate lower airway samples of a BAL, and
this should be appreciated when interpreting a BAL.
A modified approach for obtaining respiratory cytology in cats and very small dogs is to first
Page-3
intubate with a sterile tube (2.3 to 3 Fr), place the patient in right or left lateral recumbency,
hyperoxygenate, give two puffs of albuterol from an inhaler, then remove the adaptor from the
tube and obtain a culture through the endotracheal tube using a guarded brush). Next, use a 3-
way stopcock as an adaptor in the end of the inflated endotracheal tube to obtain a
tracheobronchial wash. Sterile saline (5-6 cc) is quickly flushed into the side port, and then
aspirated back preferably with suction and a mucous trap. The cat is turned to the other side,
the wash procedure is repeated, and the fluid samples pooled. If a second stopcock is attached
to the first one, the cat can be ventilated with oxygen between the two washes. This approach
seems to represent a hybrid of a tracheal wash and a BAL, but clearly samples the most distal
airways.
Fine needle lung aspirate (FNA) is another alternative for assessment of the dyspneic or
coughing patient with multifocal, diffuse, or lobar infiltrates. This method, like the BAL, may be
especially helpful if the cat is not coughing and producing bronchial exudate or if pulmonary
infiltrate is limited to the interstitial space. Pneumothorax is a common complication.
Inspection of the thorax and biopsy of the lung or pleura by thoracotomy or thoracoscopy is
sometimes the only method for attaining a diagnosis in disseminated pulmonary disease (e.g.,
neoplasia, granulomatous disease). Thoracoscopy is particularly useful in experienced hands
and avoids the morbidity of traditional thoracotomy (which is also problematic in terms of
approach and degree of invasiveness needed for suitable exploration). Lung biopsy is especially
helpful in diseases characterized by marked interstitial infiltration or disorders unexplained by
prior, less-invasive tests. When a singular localized lung lesion is evident from radiographs, and
either a foreign body or tumor is suspected, consider surgical removal and biopsy of the
affected lobe. Optimally, exploratory procedures for solitary lung masses should be preceded by
detailed noninvasive imaging, including CT of the chest.
Notes:
Page-4
Table 1. Diagnosis of Respiratory Disease
Bronchopulmonary Diseases
History and physical examination (observation, auscultation, percussion of the thorax)
Thoracic radiography
Complete blood count
Heartworm tests (ELISA antigen tests, HW antibody test for cats)
Fecal examinations (flotation and Baermann sedimentation to detect lung parasites)
Serologic testing when appropriate (e.g., immunodiffusion or urinary antigen tests for systemic
mycoses, IgM ELISA for Toxoplasmosis, etc.)
Arterial blood gas | Pulse oximetry
Culture of tracheobronchial secretions (transtracheal, endotracheal using a guarded swab, or
aspiration through sterile tubing placed down a sterilized endoscope port)
Endotracheal aspiration cytology
Bronchoscopy (visual examination and cytology)
Bronchial brushing
Bronchial aspiration cytology
Bronchoalveolar lavage with a wedged bronchoscope
Ultrasound examination of the heart and mediastinum or of consolidated lung tissue
Fine needle aspiration (FNA) of the lung or mass lesion
Lung biopsy
Pulmonary function testing
Page-5
Table 2. Differential Diagnosis of Pleural Effusion
Page-6
Table 3. Thoracic Radiography:
Some Guidelines for Evaluation of Thoracic Radiographs
Initial Steps
Identify the films, case number and date
If analog films, place the films on the view box correctly (if digital, insure proper labels):
Cranial is oriented to your left side on the lateral X-ray film; the patients right side is oriented
to your left side on the VD or the DV view
Remember there is substantial variation among species and breeds.
For example, cats have more horizontally oriented hearts on the lateral view and the
heart takes up less space in the thorax.
Deep-chested dogs, such as the Doberman pinscher, have a more upright-oriented
cardiac axis.
There are also differences between left and right lateral projections and VD and DV films.
This is useful to remember when evaluating serial studies.
Start with a system.try P-E-P
Positioning is the patient straight (sternum on spine on the VD/DV; not excessively
rotated on the lateral). Is the beam properly centered over the thorax?
Exposure is the exposure sufficient to allow you to follow vascular structures and does
the technique penetrate (but still allow you to see) the ribs? Remember: underexposure
makes the lung parenchyma appear too dense; overexposure burns out subtle
pulmonary densities.
Phase of Ventilation were the films exposed during inspiration? Expiratory films cause
the pulmonary parenchyma to appear more dense leading one to over-diagnose
interstititial patterns. Furthermore, the heart may appear more enlarged if the thorax is
not sufficiently expanded.
Examine the extrathoracic structures and bones for disease, organomegaly, rib destruction,
and other lesions. Remember that dyspnea or vigorous coughing can lead to rib fractures or
movement of the stomach into the esophagus (hiatal hernia or G-E intussusception) . Do not
mistake calcification of the costochondral junction for disease. Pectus excavatum may be
identified in cats and dogs and will often lead to a mediastinal shift on the VD/DV
projections.
Page-7
Identify Cardiomegaly
Obtain an overall opinion of cardiac size on both views. Enlarged or not? If so, is the
cardiomegaly mild, moderate or severe? Measure the Vertebral Heart Score if you are
uncertain about the presence of cardiomegaly. A VHS that exceeds 8.0 in a cat is
suspicious for cardiomegaly (average value is 7.5 vertebral bodies). A VHS that exceeds
10.5 to 11 in a dog is likely to indicate cardiomegaly; even more useful are serial evaluations
in a dog. There are some breed variations in VHS nicely summarized on Dr. Jim
Buchanans web site, see: http://www.vin.com/library/general/JB111VHS.htm
Measure the apical-basilar length from the ventral border of right bronchus at level of
circular carina to the apex of the heart. This is the major axis measurement.
Then draw a line perpendicular to your first measurement, extending from the cranial to
caudal heart border. This is the minor cardiac axis. Select the greatest length but do not
extend the measurement into the caudal vena cava or left atrium.
Identify the 4th thoracic vertebral body inspect the dorsal spinous processes (the fourth
TV is the 4th one with a tall dorsal spinous process; you can also count the ribs as they
insert on the spine)
Measure the VHS from the cranial edge of T4 caudally.
Count the number of vertebral bodies encompassed in the major + minor axis lengths.
Extrapolate to the nearest decimal point.
Cardiac elongation on the lateral or DV views is typically due to LV enlargement.
Widening: Either RV or LV enlargement can cause cardiac widening.
Note if there are any distinctive bulges or rounded borders that suggest specific chamber
enlargements?
Be familiar with the location of the cardiac chambers around the perimeter of the heart.
One species difference: on the VD/DV view the 1-3 oclock border in cats is usually the left
auricle; in dogs 1-2 oclock is the main PA and 2-3 oclock represents the left auricle.
Key to the diagnosis of left sided CHF is assessment of the left atrium. Estimate left atrial
enlargement as mild, moderate or severe. Mild is a slight separation of the bronchi or
prominence of the LA. Moderate is prominence with moderate separation or a distinct
auricular bulge and/or squaring of the caudal atrial border. Severe is caudal bulging of the
left atrium on the lateral view and prominent rounding on the VD projection. The left auricle
in cats is often quite prominent on the VD view, but on the lateral the left atrium is more
difficult to assess.
Page-8
Pleural Space
Inspect the pleural surface for mass lesions, especially if there is rib destruction.
Evaluate the thorax for pleural effusion, a sign of right sided, left sided, or biventricular CHF
(as well as many noncardiac conditions). Remember that the DV will show the effusion more
readily but also obscure the lung to a greater degree.
Diagnostic criteria for pleural effusion include: increased fluid density, blunting of
costophrenic angles, identification of two or more fissure lines, border effacement
(silhouetting or obscuring) of the diaphragm or cardiac borders, and widening of the
mediastinal recesses. A horizontal beam may be helpful in selected cases.
Dont be confused by ventral subcutaneous fat on the lateral view verify the diagnosis on
the VD view (fissure lines, blunted angles)
Rounding of the lung borders suggests chronicity of the effusion of inflammatory response
(as with chylothorax in cats).
Pneumothorax often occurs from trauma (including iatrogenic barotraumas from ventilation),
needle puncture during diagnostic procedures, consequent to pneumomediastinum, and
following rupture of lung cysts or bullae.
Pulmonary Parenchyma
Identify abnormal pulmonary densities. If increased, note the distribution. Classify when
possible as:
Interstitial nodular or linear (obscures blood vessels). Linear interstitial density is over-
interpreted. If you can see vessel walls clearly, the lung is probably normal.
Alveolar generally a very dense infiltrate that will silhouette or efface part of the heart or
diaphragm. Air bronchograms are classic findings.
Bronchial The bronchial walls are evident from thickening or infiltration.
Note: Pulmonary edema can cause a mixed pulmonary pattern including interstitial fluid
accumulation around blood vessels and airways and later progressing to an alveolar
infiltrate classically bilateral (may be slightly worse on right), caudal, and perihilar.
Notes:
Page-9
Asociacin Mexicana de Mdicos Veterinarios Especialistas en Pequeas Especies, S. C.
www.ammvepe.com.mx