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AMMVEPE

1968 - 2016

MEMORIAS DE LAS PONENCIAS


EN EL CURSO DE CARDIOLOGA
EN PERROS Y GATOS

MXICO, D. F., DICIEMBRE 8 Y 9 DE 2016


Asociacin Mexicana de Mdicos Veterinarios Especialistas en Pequeas Especies, S. C.
www.ammvepe.com.mx
PONENCIAS DEL CURSO
DE CARDIOLOGA EN PERROS Y GATOS


AMMVEPE

Diciembre 8 y 9 de 2016


MANAGEMENT OF CARDIAC ARRHYTHMIAS
John D. Bonagura DVM, MS, DACVIM

CARDIAC AUSCULTATION
John D. Bonagura DVM, MS, DACVIM

CONGENITAL HEART DISEASE
John D. Bonagura DVM, MS, DACVIM

PERICARDIAL DISEASES IN DOGS: DIAGNOSIS & MANAGEMENT
John D. Bonagura DVM, MS, DACVIM

RADIOGRAPHIC DIFFERENTIAL DIAGNOSIS OF CARDIOPULMONARY
DISORDERS
John D. Bonagura DVM, MS DACVIM


Asociacin Mexicana de Mdicos Veterinarios Especialistas en Pequeas Especies, S. C.
www.ammvepe.com.mx
MANAGEMENTOFCARDIACARRHYTHMIAS
REFERENCENOTES

JohnD.BonaguraDVM,DACVIM
VeterinaryClinicalSciences,OhioStateUniversity*

Heartrhythmdisturbances(arrhythmias,dysrhythmias)canbeclassifiedfollowingECGanalysisbased
on the heart rate (normal, bradyarrhythmia, tachyarrhythmia); anatomic origin of the rhythm disturbance
(sinoatrialnode,atrial,atrioventricularnodeorjunction,orventricle);andelectrophysiologicalmechanismif
evident(enhancedautomaticity,reentry,myocardialfibrillation).
Theunderlyingbasisforabnormalcardiacrhythmsincludeanumberofpossiblefactors.Evenwithout
overt cardiac disease, structural or physiologic abnormalities that alter normal cardiac cellular conduction
properties or excitability (automaticity) can predispose to arrhythmias. Such changes can occur during
cardiacremodelinginpatientswithheartdiseaseandfailure,orcanresultfromgeneticorenvironmental
factors.Myocytehypertrophy,abnormalionchannelstructureorfunction,tissueinflammationorfibrosis,
or other derangements may be involved. For example, in cardiomyopathy increasing heterogeneity of
repolarization and conduction velocity across the ventricular wall, from endocardium to epicardium,
increases the propensity for ventricular arrhythmia development. Yet even with such underlying
abnormalities, an arrhythmia may not occur unless provoked by some triggering event. For example, an
abruptchangeincardiaccyclelength(heartrate)oraprematurestimuluscantriggerasustainedarrhythmia
when the underlyingconditions are favorable. Additional modulating factors further influence whether an
arrhythmiaoccursorissustained.Thesefactorsmightincludechangesincardiacsympatheticorvagaltone,
circulatingcatecholamineconcentrations,electrolytedisturbances,andischemia.
The clinical association of most arrhythmias can be grouped into one of five general categories: 1)
Primary cardiac disease (structural or electrical diseases; often genetically predisposed); 2) Metabolic &
endocrinedisorders;3)Autonomicrelated;4)Drugs&toxins;and5)theUsualsuspects. Thelastgroup
referstoalargenumberofnoncardiacdisordersthatinducearrhythmiasbycausingischemiareperfusion,
releaseofcytokines,alteredautonomictraffic,orunknownmechanisms.Examplesincludegastricdilatation,
sepsis,anemia,andsplenicdiseaseindogs.Understandingthelikelyclinicalassociationofanarrhythmiacan
facilitatespecifictreatmentsandguidethedurationoftherapyandprognosis.
Clinical evaluation in most cases involves a complete physical examination including careful
cardiovascular (CV) evaluation, ECG, diagnostic imaging, and selected laboratory tests. When structural or
geneticallypredisposedcardiacdiseaseisthelikelycause,theworkupcanfocusonechocardiographyand
thoracic radiographs. If an acute insult or myocarditis is suspected, a cardiac troponin (cTnI) is
recommended, accepting that severe arrhythmias can lead to ischemia and secondary elevations in this
biomarker.Whenanoncardiacdisorderissuspectedorthereisnoclearevidenceofprimaryheartdisease,
theECG,CBC,routineserumchemistrieswithelectrolytes(especiallypotassiumandmagnesium),cTnI,and
atleastascreening2D Echoisadvised.Abdominal ultrasound oftenfocusedon thespleenisanother
usefultest.Insomelocationsandclinicalsettings,testsforinfectiousdiseaseagentsarealsoappropriate.
Nottobeoverlookedinthequestforanetiologyistheimportanceofcorrectlydiagnosingtheheart
rhythmdisturbance.Therearecertainlychallenges(asillustratedunderspecificrhythmdisturbances).ECG
recordings for rhythm analysis can be acquired from simple, singlelead recordings (typically lead II or a
thoracic lead from the ICU or a phone app), or multiplelead (6 or 9lead) recordings. Multiple lead
recordingscanberecordedsequentiallyorsimultaneously.Multipleleads,aswellasspecialleadssystems,
can be helpful when Pwaves are difficult to identify, as often occurs in cats or during narrowQRS
tachycardiasindogs.Sometimesjustmovingtheforelimbelectrodestothethorax(leftarmtoleftapexand
right arm to the craniodorsal right cardiac base and selecting lead I) and increasing the sensitivity of the
recordingto20mm/mVcanbehelpfulforidentifyingPwaves.

*ContributionsofDr.WendyA.Ware,DACVIM(Cardiology)tothisdocumentaregratefullyacknowledged
Specialized recordings using transesophageal or intracardiac electrode catheters also provide insight
regarding atrial activity, but these are rarely used. Ambulatory ECG recorders Holter monitors,18 event
monitors,1,9,10 and implantable loop recorders1114 all have their place in diagnosis, assessment and
managementofarrhythmiasandclinicalsignssuchasexertionalcollapseandsyncope.Someusesofthese
specializedrecordingdevicesarediscussedbelowunderspecificrhythmdisturbances.Forcertaincomplex
heart rhythm disturbances, multipolar intracardiac electrode catheters are needed for diagnosis; this
requiresacardiacelectrophysiologistandspecializedequipmentandtraining.Advancedanalysesincluding
signalaveragedECGandheartratevariability(HRV)areconsideredresearchtools.

NORMALELECTRICALACTIVITY
ThenormalcardiacrhythmbeginsintheSAnodeintherightatriumandthesubsequentdepolarization
proceeds from right to left and cranial to caudal generating positive Pwaves of <40 ms duration in most
dogs and cats in Leads I, II, and aVF. Assuming conduction across the AV node and HisPurkinje system is
normal,thePRintervalwillbe<130msfor(nongiant)caninebreedsand<100msformostcats.Thenormal
canineandtypicalfelineQRScomplexesarealsopositiveinleadsI,IIaVF,inthefrontalplaneandstrongly
positive in the lowerleft, precordial leads (V2V4). Ventricular depolarization is dominated and least
cancelledasitflowstowardstheleftapexindogs;accordingly,thelargest,positiveQRScomplexesinthe
limbleadsarefoundineitherleadII(60o)orleadaVF (90o)Thisfrontalaxisislessconsistentinnormalcats,
especiallythosewithsmallQRScomplexes.ThenormalQRScomplexisrelativelycompact(ornarrow)and
typically50msindogs(<60msingiantbreeds)and40msincats.TheSTsegmentusuallyfallswithin0.1
to.15mmfromthebaselineatstandardcalibration(withthebaselinereferencebeingthesegmentinfront
ofthePwave).However,ifthereisPRsegmentdepressionfromaprominentTa(atrialrepolarization)wave,
the reference baseline becomes the PR segment (from the end of Pwave to the onset of the QRS).
ProminentTawavesareoftenobservedindogswithatrialdilatation,duringsinustachycardia(whenthePR
abbreviates),andincompleteAVblock.15

APPROACHTOECGINTERPRETATION
A consistent approach to ECG interpretation is recommended. The recording/paper speed, lead(s)
used,calibration,aswellasthetracingquality(i.e.allcomplexeswithinthegrid,minimalartifact),should
firstbeidentified.Thentheheartrate(HR)andheartrhythmaredetermined.Ifmultiplefrontalplaneleads
are available, an estimate of mean electrical axis (MEA) can be obtained. Finally, individual waveform
durationandamplitude(inLeadII,byconvention)shouldbemeasured.
Because variation in HR is common, especially in dogs, estimating the average heart rate over
severalsecondsisusuallymoreaccurateandpracticalthancalculatinganinstantaneousheartrate.Simply
count the number of QRS complexes within a 3 or 6 second period andthen multiply by 20 or 10,
respectively.Iftheheartrhythmisregular,3000dividedbythenumberofsmallboxes(atpaperspeed50
mm/sec)betweentheonset(orRwavepeak)ofsuccessiveQRScomplexesequalstheapproximateheart
rate.
The heart rhythm is evaluated by scanning the ECG for patterns or irregularities and identifying
individualwaveforms.Commonrhythmabnormalitiesaredescribedbelow.Calipersareusefulforassessing
theregularityandinterrelationshipsofthewaveforms.Ectopiccomplexesaredescribedbytheirgeneralsite
oforigin(supraventricular[atrial,AVjunctional]orventricular)andtheirtiming(premature[earlierthanthe
next expected sinus impulse] or escape [late; after a longer pause]). The frequency and complexity of
ectopiccomplexesarealsoevaluated,e.g.whethertheyoccuroccasionallyorfrequently;assingles,pairs,
triplets,oratachycardia[paroxysmalorsustained];andwhethertheyappearuniform[monomorphic]orof
variableconfiguration[polymorphic,multiform].
TheabsenceofnormalPwavesmayindicateatrialfibrillation,sinusarrest,orfailureofintraatrial
conduction(atrialstandstillortheeffectsofhyperkalemia[silentatrium]).DisturbancesoftheAVnodaland
infranodal conduction system are common, and can cause various degrees of AV block, or just abnormal
intraventricular conduction (major bundle branch block or a nonspecific intraventricular conduction
disturbance). Marked bradycardia can occur from 3 and highgrade 2 AV block. Because AV nodal
conduction velocity normally is relatively slow, conditions that enhance vagal tone or otherwise further
reduce nodal conduction velocity tend to promote conduction failure. However, the AV block that occurs
when a supraventricular tachyarrhythmia such as atrial fibrillation or atrial tachycardia stimulates the AV
nodeataratefasterthanitcannormallyconductisconsideredphysiologic,notpathologic.
Keystodiagnosingacardiacarrhythmiaincludeananalysisofventricularandatrialrates,regularity
of the rhythm, patterns of arrhythmias, PQRS relationship, ECG waveform morphology, and conduction
intervals. The most important aspect of rhythm diagnosis involves identification of Pwaves and their
relationship to the QRS complexes. In terms of a methodological approach to rhythm diagnosis, it is
recommendedthatoneincludethe10stepsshowninTable1.Aftercompletingyouranalysis,interpret
theECGtracinginlightoftheclinical,imagingandlaboratoryfindings.

Table1.AnApproachtoECGRhythmAnalysis
1. Identifythepatient,lead(s),paperspeed,calibrationsignals,andartifacts
2. Decideiftheventricularrateisslow,normal,orfast(forthespecies;Table2)
3. Identifyiftherhythmisregular(RtoRintervalsevenlyspaced)orirregular
a. Ifirregular,searchforanyrecurringpatterns
4. IdentifyPwaves&QRSTcomplexesandtherelationshipbetweenthesewaveforms(PRandR
P)
a. Issinusrhythmpresent(withorwithoutotherabnormalities),oraretherenoconsistent
PQRSTrelationships?
b. AreallPwavesfollowedbyaQRSandallQRScomplexesprecededbyaPwave?
5. ScrutinizethemorphologyandconsistencyofthePwaves,QRScomplexes,andSTT
a. Ifpremature(early)complexesarepresent,dotheylookthesameassinusQRS
complexes,implyingatrialorjunctional(supraventricular)origin,oraretheywideandof
differentconfigurationthansinuscomplexes,implyingaventricularoriginor,possibly,
abnormal(aberrant)ventricularconductionofasupraventricularcomplex(e.g.bundle
branchblockpattern)?
b. AreprematureQRScomplexesprecededbyanabnormalPwave(suggestingatrial
origin)?
c. AretherebaselineundulationsinsteadofclearandconsistentPwaves,witharapid,
irregularQRSoccurrence(compatiblewithatrialfibrillation)?
d. Aretherelongpausesintheunderlyingrhythmbeforeanabnormalcomplexoccurs
(escapecomplexorrhythm)?
6. Considerconductionintervalsacrosstheatria(Pwaveduration),atrioventricularconduction
system(PRinterval),ventricles(QRSduration),andoverallrepolarizationtime(QTinterval,in
lightoftheheartrate)
a. IsanintermittentAVconductiondisturbancepresent?
b. IsconsistentrelationbetweenPwavesandQRScomplexestotallylacking,withaslow
andregularQRSoccurrence(implyingcompleteAVblockwithventricularescape
rhythm)?
7. Forsinusandsupraventricularcomplexes,estimatethemeanelectrical(frontal)axis(ifmultiple
limbleadsavailable;Figure1).
a. Notetheorientationofterminalelectricalactivityoftheventricle(last50%ofQRS)
8. EvaluatetheQRSmorphologyforpatternstypicalofintraventricularconductiondisturbances
includingbundlebranchandfascicularblocks
9. EvaluatethePwavesandQRScomplexesforpatternsconsistentwithcardiomegaly
10. AssesstheSTTforrepolarizationabnormalities;classifyasprimaryorsecondary(fromabnormal
QRScomplex)STTchanges

Table2.ECGReferenceRangesforDogsandCats
ECGVariable Dog Cat
60160beats/min,adults;upto
Heartrate 120240beats/min
220beats/mininyoungpuppies
Meanelectricalaxis(frontalplane) +40to+100degrees 0to+160degrees
Measurements(leadII)
0.04sec;to0.05secin
Pwaveduration(maximum) 0.0350.04sec
large/giantbreeds
Pwaveheight(maximum) 0.4mV 0.2mV
PRinterval 0.060.13sec 0.050.09sec
0.05sec(smallbreeds)to0.06
QRScomplexduration(maximum) 0.04sec
sec(largebreeds)
2.5mV(smallbreeds)to3mV 0.9mV,anylead;<1.2mVQRS
Rwaveheight(maximum)
(largebreeds)* totalexcursion,anylead
<0.2mVdepression;<0.15mV
STsegmentdeviation <0.1mVdeviation
elevation
usually<25%ofRwaveheight; maximum0.3mV;canbe
Twave canbepositive,negative,or positive(mostcommon),
biphasic negative,orbiphasic
0.120.18(range0.070.2)
QTintervalduration 0.150.25(to0.27)sec;varies
sec;varies
*
Maybegreaterinyoung,thin,deepchesteddogs
TablecompiledbyDrs.WendyAWareandJohnDBonagura.

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.

Supraventricular arrhythmias can be transient, recurrent, persistent, or permanent. In most cases,


recurrentorpermanentatrialarrhythmiasarecausedbystructuralheartdiseases27,75,7881,86,98100associated
with congenital, chronic valvular, myocardial, or pericardial disease. These arrhythmias are especially
frequent in the giant breeds and other dogs prone to dilated cardiomyopathy (DCM) such as the Irish
wolfhound,Newfoundlanddog,SaintBernard,GreatDaneandDobermanpinscher.Alargeatrialmass(size)
predisposestoatrialarrhythmiasin generalandto theperpetuationofatrialfibrillation(AF)in particular;
therefore,itislogicalthatthisrhythmismoreoftenobservedinlargerbreedsandwhenheartsareafflicted
bystructuraldiseaseandatrialdilatation.Atrialfibrillationisrelativelyuncommonincatsandmost(though
notall)also havesevere structuralheartdisease.101Somegiantbreedsdevelopchronicatrialarrhythmias
without overt structural disease (although this may eventually develop). Thus many dogs with socalled
loneAFarelikelytomanifestcardiomyopathyiffollowedoverasufficientlengthoftime.Transientatrial
arrhythmias often are observed in perioperative situations (often largebreed dogs), following opioid
administration, and with some gastrointestinal diseases (parasympathetic input shortens the atrial
refractory period, predisposing to AF). Other causes include intracardiac catheters, cardiac tumors
(especially right atrial hemangiosarcoma), and spontaneous and iatrogenic thyrotoxicosis.64,102 Many atrial
arrhythmias are shortlived and will revert to sinus rhythm; however, in other cases, the arrhythmia is
persistentorprogressiveandmightrequiredrugtherapyorDCcardioversion.
The ventricular response and regularity during an SVT is determined by the mechanism of the
arrhythmiaandAVconductionpattern:theventricularresponsecanbesloworfast;regularorirregular.In
highsympatheticstates,AVconductionofsupraventriculararrhythmiascanbeveryrapid,aswithAFinthe
setting of congestive heart failure (CHF). Organized, regular SVT associated with atrial tachycardia, atrial
flutterorreentrantSVTcaninduceventricularresponsesof300to400perminute!In2:1AVconductionof
atrialtachycardiaorflutter,theratemaysuddenlydoubleorhalfastheconductionratio(P:QRS)changes.
SubtleelectricalalternansisacommonfindingwithregularSVTsregardlessofmechanism,oftenappearing
attheonsetofanonsustainedarrhythmia.ThisfindingcanhelptoseparateapathologicSVTfromafast
sinus tachycardia (wherein alternans is uncommon). Supraventricular tachyarrhythmias also can be
conducted with bundle branch block, and the resultant QRS complexes can be confused with PVCs or
ventriculartachycardia(VT).
Therapy of supraventricular arrhythmias is often more challenging than for ventricular arrhythmias.
Premature atrial complexes are uncommonly treated other than to manage underlying heart disease. A
HolterECGcanbeusefulinassessingtheoverallseverityoftherhythmdisturbance.IfPACsarebothersome
(tothepatientordoctor)orassociatedwithparoxysmaltachycardias,abetablockersuchasatenololorthe
antiarrhythmicdrugsotalol(12mg/kgPOb.i.d.)canbeadministered.InthesettingofCHF,digoxin(starting
atapproximately0.005mg/kg,POb.i.d.)canbeconsidered.
Whenmanagingfocalatrialtachycardia,theclinicianshoulddecideifthearrhythmiaismorelikely
of recent onset or chronic in nature. Treatments that can suppress ectopic rhythms, including lidocaine
(effectiveonlyinacuteconditions),sotalol,amiodarone,andflecainide(orpropafenone)aremorelikelyto
besuccessfulinarrhythmiasofrecentonsetorinthesettingofanormalechocardiogram.Manyfocalatrial
tachycardias are relatively resistant to drug suppression and are bested treated with heart rate control.
DrugsthatblocktheAVnodediltiazem,betablockers,anddigoxinarethemainstays,asdiscussedbelow
forAF.Althoughratecontrolcanbeachievedinsomedogswithamiodarone,103thepotentialforadverse
effects outweigh the benefit. Thus if efforts to suppress an ectopic rhythm fails, or if the arrhythmia is
chronic,ventricularratecontrolisthemorelogicalgoal,especiallyinthesettingofstructuralheartdisease.
When atrial tachyarrhythmias are associated with CHF, digoxin is chosen first, but in all other cases,
diltiazemorabetablockeraloneorincombinationwillbemoreeffectiveforratecontrol,andsometimes
thesedrugswillconvertthearrhythmiabacktosinusrhythm.
Inthemanagementofatrialtachycardia,atrialflutterandatrialfibrillationtwogeneralapproachesare
taken: rhythm control with cardioversion and rate control with drugs. The issue of underlying structural
diseaseishighlyrelevantintermsofprognosisandtreatment.Despitereportsofsuccessfulcardioversionof
AFindogswithCHF,thegeneralexperienceisthatmostdogsrevertbacktoAFinarelativelyshorttime.
Accordingly, accepting some differences of opinion, it is difficult to justify the shortterm benefit of AV
synchronization with the risks and costs of the electrocardioversion procedure in a dog with CHF or
moderatetosevereatrialremodeling.Weneedmorecontrolled,prospectivestudiesofdogswithCHFwho
arecardiovertedandthenmaintainedwithdrugsthatpreventreversiontoAF.
Rhythmcontrolinatrialtachyarrhythmiasisappropriateforspecificcases.Intravenousdrugtherapyor
synchronizedDCcardioversionofatrialflutter/fibrillationisreasonableindogsifthearrhythmiaisknownto
havebegunduringaperioperativeperiodorisofrecentonset.Astructurallynormalheartshouldfirstbe
assured via echocardiography, and hypokalemia and hyperthyroidism should be excluded as predisposing
factors.WhentheonsetofAF(orflutter)iswitnessed,spontaneouscardioversioniscommonwithinafew
hours.Lidocaine(28mg/kgover10minutes)canbetried,especiallyifAFisvagallymediated,90andcarries
the potential for conversion with little downside on hemodynamics. Other options for intravenous
cardioversioninclude1)procainamide(2mg/kgIVover2minutes;upto20mg/kgcumulativedosage;with
QRS,QT,andBPmonitoring);2)IVamiodarone(useNexteroneonly!DonotusestandardIVamiodarone
withpreservatives;startNexteroneat23mg/kgIVinfusionover60to120minuteswithBPmonitoringand
continuetoacumulativedosageof5to6mg/kgiftolerated);3)ordiltiazem(startwith0.1mg/kgover5
minutes;repeatupto0.3to0.4mg/kgIVcumulativedosage;withBPmonitoring).Diltiazemisusedmainly
forventricularratecontrolwhentheheartrateisdangerouslyhigh(>250/minute)orBPislow;occasionally
diltiazemwillconvertAFtonormalsinusrhythm.Biphasic,DCcardioversionisveryeffectiveintreatinglone
AFofrecentonset.83,104,105Ifthecardioversionisplanned,oralamiodarone(loadingdoseof46mg/kgPO
b.i.d.) can be given for one week prior to conversion; alternatively intravenous Nexterone can be
administeredat46mg/kgIVover23hourspriortoelectrocardioversion.Eithergenericamiodarone(46
mg/kg PO once daily) or sotalol (1 to 2 mg/kg PO twice daily) is prescribed empirically after
electrocardioversion to maintain sinus rhythm. These drugs are usually continued for some months to
preventreversiontoatrialfibrillation;however,thebenefittoriskofsuchtherapyhasnotbeenestablished,
andamiodaronecarriestheriskofhepatotoxicityespeciallyaftermonthsoftherapy.
For chronic heart rate control of atrial tachyarrhythmias, the goal is blocking AV nodal conduction to
reducethetransmissionofatrialimpulses.Acombinedtreatmentwithdigoxinand diltiazem106 (abeta
blocker) is most often used in dogs with chronic AF associated with CHF. Rate control in cats is typically
attained with diltiazem, atenolol, or the combination. In the authors experience, optimal ventricular rate
controlindogsisachievedwithamodestdoseofdigoxin(startwith0.005mg/kgPOb.i.d.)andaimfora
troughbloodlevelof0.8to1.2ng/ml);moderatedosagesofdiltiazem(6to8mg/kg/day,POdividingthe
totaldosaget.i.d.orb.i.d.forstandardorlongactingpreparations,respectively);andlateraddinginalow
dose of carvedilol (starting at one 3.125 mg tablet twice daily for a largebreed dog). Higher dosages of
digoxinordiltiazemdefinitelyprovidebetterratecontrol,butattheexpenseofanorexiaorotheradverse
effects. The inclinic ECG heart rate overestimates the average home heart rate in dogs with AF.91 In the
authors experience, an inhospital ECG rate over 60 seconds of 120150/minute predicts good control;
optimally a Holter ECG should be recorded once the clinic ECG rate seems appropriate. It may take some
weekstoachieveoptimalratecontrol.
Genetically predisposed arrhythmias associated with abnormal electrical pathways (bypass tracts)9296
are observed in some breeds especially Labrador retrievers. These can predispose to very rapid SVT.
Reentrant SVTs employ circuits that develop at the micro (AV nodal/junctional) and macro (bypass tract)
levels.107Thebestcharacterizedonesindogsinvolveanelectricalcircuitconnectingtheatria,AVnode,and
an accessory AV pathway that bypasses (or longitudinally separates) the AV conduction system. The
tachycardiaisoften triggered byasuddenchangeinsinus cyclelength,by prematureatrialorventricular
complexes,orbyelectrophysiologicchangesintheelectricalpathwaysconstitutingthecircuit.Thispermits
currenttodescenddownonepathway(typicallyAVnode)andthetravelretrogradebacktotheatriaviathe
accessorypathway,creatingamacroreentryloop.InmostcasesthecircuitformsanorthodromicSVT:down
the AV node with an associated normal (narrow) QRS. Retrograde Pwaves may be identified in the ST
segment(anRP).Insome,butnotallcases,periodsofsinusrhythmareassociatedwithventricularpre
excitation,ahelpfulcluetothepresenceofanaccessorypathway.Preexcitationischaracterizedbyashort
PRintervalandearlyventricularactivation(thedeltawave)withnarrowtowideQRSandsecondaryTwave
changes. Delta waves can be discrete waves in dogs and cats96,108,109 or more typical of those observed in
humans (slurred upstroke of the Rwave, best seen in precordial leads). Management of reentrant SVT is
donewithdrugsinitially(diltiazemandprocainamidecanbetried),butreferraltoaspecialistforcatheter
ablationoftheaccessorypathisthebesttreatment.
Atrialstandstillisunrelatedtotheaforementionedatrialarrhythmias.Thetermindicatesthattheatrial
muscleisunexcitable,anditshouldnotbeconfusedwithsinusarrestinwhichatrialmuscleisresponsive,
but unstimulated. This condition is caused transiently by high serum potassium or persistently by atrial
musclediseaseorbysevereatrialdilation(incats).Inthesecases,noPwavesareevident(atrialstandstill)
or very tiny, nonconducted, or lowamplitude Pwaves are evident. With hyperkalemia the QRS complex
becomeswidenedandtheTwaveslargeandsometimestented(especiallyinVleads).Apitfallofdiagnosis
in cats, where heart rate may not decrease, is that hyperkalemia can be confused with ventricular
tachycardia.Persistentatrialstandstillcausedbyatrialmyocardialdiseaseandfibrosisismostcommonin
English Springer spaniels, but can also occur in larger retriever breeds and sporadically in others. On
echocardiographyoneorbothatriaaremarkedlydilatedandmostdogsalsodevelopCHF.Incatsapparent
atrial standstill can be observed with severe forms of cardiomyopathy and severe atrial dilatation. It is
sometimes, but not often, reversible. Treatment involves managing CHF medically and consideration of
endocardial ventricular pacemaker implantation, accepting the overall benefit varies widely with survival
timesrangingfrommonthstoyears.

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.

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CARDIAC AUSCULTATION
John D Bonagura DVM, MS, DACVIM (Cardiology, Internal Medicine)
Veterinary Clinical Sciences, Ohio State University College of Veterinary Medicine

CARDIAC AUSCULTATION INTRODUCTION


The stethoscope (and its clinical use) was first described by the French physician, Laennec
in 1816. He used a rolled tube of paper to transmit sounds from thorax to ear and subsequently
described the relationships between these sounds and underlying thoracic diseases in his
treatise De l'Auscultation Mediate. His observations, along with those of other clinical
investigators, continue to influence clinical decision-making. Auscultation of the heart and lungs
remains an important examination technique for the detection of thoracic disease. This
presentation reviews some of the key features of auscultation in dogs and cats, including
examination techniques and the interpretation of auscultatory findings relative to acquired and
congenital cardiac disorders.
The auscultatory exam is expedient and cost effective. When completed by an experienced
clinician, auscultation carries a high predictive value for identification of certain serious heart
diseases. Some diagnoses can be attained with high sensitivity and specificity through
auscultation. Two examples include the diagnosis of a patent ductus arteriosus (PDA) in a
puppy with a continuous murmur and the identification mitral regurgitation (MR) in the older dog
with a typical holosystolic, left apical murmur. Auscultation also carries high sensitivity, but lower
specificity, for the diagnosis of outflow tract obstructions, septal defects, and sustained or
recurrent cardiac arrhythmias. Often the results of auscultation, combined with the signalment,
clinical history, and findings on physical diagnosis point to a tentative cardiac or respiratory
diagnosis. This presumptive diagnosis is then confirmed, refined, or refuted through Doppler
echocardiography, radiography, or electrocardiography. It is emphasized that auscultation is less
sensitive for the recognition of patients with cardiomyopathies, pericardial diseases, pulmonary
hypertension, trivial valve lesions, or infrequent or sporadic arrhythmias. These are challenging
conditions to recognize or confirm without ancillary studies such as cardiac ultrasound or
ambulatory electrocardiography.
The essential abnormalities of cardiac auscultation include the following: abnormal heart
rate or irregular rhythm (arrhythmia); abnormal intensity of heart sounds (loud, soft, or variable);
extra sounds (gallops and clicks); split sounds; cardiac murmurs; and pericardial friction rubs.
Different classification systems for heart sounds and murmurs are designed to foster
communication among clinicians and carry clinical relevance. This subject is addressed below. A
respiratory examination is also performed using the stethoscope, and the breath sounds
detected should be classified and assessed as well (these are summarized at the end).

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.

TRANSIENT CARDIOVASCULAR SOUNDS


Transient sounds are vibrations of short duration because their genesis depends on abrupt
changes in pressure and blood flow. The transient sounds, as well as cardiac murmurs, are
timed relative to the first (S1) and second (S2) heart sounds. Following initial activation of the
ventricles and the rapid development of ventricular pressure, the first sound is heard indicating
the onset of systole for the clinician. At the end of ventricular ejection, the second sound is
generated, heralding the onset of diastole to the clinician. Any transient sounds detected during
systole or diastole are considered abnormal in small animals.
Both S1 and S2 are relatively high-frequency sounds. The first sound is associated with
vibrations of the cardiac structures and blood pool near the time of atrioventricular (AV) valve
closure, while the second sound is caused by vibrations occurring at the time of closure of the
aortic and pulmonic valves. The first sound is lower-pitched (duller), longer, and more obvious
over the left apex. The relatively sharper and shorter second sound is more prominent over the
aortic and pulmonic valve areas and in some normal dogs is closely split during inspiration.
These two transient sounds can become abnormal in certain conditions. Pericardial or pleural
effusions and myocardial failure (as with dilated cardiomyopathy) decrease the intensity of the
heart sounds. Conversely, both heart sounds tend to be relatively loud in healthy animals under
high sympathetic drive or those with thin body conformation.
Diastolic sounds or gallops are abnormal in dogs and in cats. These are audible
manifestations of filling sounds (that would be considered normal sounds in larger animal
species). Gallops are lower-frequency sounds and associated with vibrations surrounding either
sudden termination of early ventricular filling (S3) or atrial contraction and end-diastolic
ventricular filling (S4). These sounds indicate diastolic dysfunction when detected in dogs or
cats. A third sound is typical of a very diseased ventricle, reduced diastolic chamber compliance
with ventricular filling occurring under high venous pressures. Hence, a ventricular gallop is
sometimes considered a heart failure sound. An atrial gallop is typically associated with
impaired ventricular relaxation (as occurs with feline hypertrophic cardiomyopathy or
hypertensive heart disease) and probably stems from the brief, compensatory increase in atrial
pressure needed to fill the ventricle at end-diastole. This enhancement of end-diastolic filling
leads to an audible sound timed between the P-wave and QRS-complex of the ECG (it is called
S4 because it was the last sound discovered). If both filling sounds are present and the heart
rate is rapid, the gallops can be superimposed producing a summation gallop. In general, an
atrial gallop (S4) indicates less severe disease than an S3 gallop. Some otherwise healthy older
cats have this sound in the hospital when stressed; this is likely due to normal aging changes in
ventricular relaxation. However, in many cases, gallop sounds are the only auscultatory
abnormality of cardiomyopathy or hypertensive heart disease and these sounds will vary with
both heart rate and venous filling pressures. Thus in most cases a gallop sound prompts further
investigation with echocardiography.
Systolic clicks are extra systolic transient sounds. Mid-systolic clicks are common in dogs
with mitral or tricuspid valve disease and are probably indicative of prolapse from abnormal
chordae tendineae or valve redundancy. These high-pitched sounds can be fixed or labile within
the systolic period; single or multiple; louder of the left or right apex depending on the valve
source; and often come and go with changes in heart rate or ventricular volume. Isolated clicks
in a mature dog suggest early or mild degenerative disease. Systolic clicks become
superimposed with murmurs in dogs with advanced mitral regurgitation and can be difficult to
hear in that setting. Systolic clicks are also detected in some cats with hypertrophic
cardiomyopathy, but without a phonocardiograph recording, the distinction between an S4 and
early systolic click in a cat can be very challenging. These are also detected in some dogs and
cats with mitral valve dysplasia. Ejection clicks are infrequently detected in dogs affected by
valvular pulmonic stenosis or pulmonary hypertension; these tend to be loudest over the
pulmonic valve or pulmonary artery (left craniodorsal).
In many patients, the first recognition of a cardiac arrhythmia occurs during auscultation and
palpation of the femoral arterial pulse. Auscultatory findings in arrhythmias and conduction
disturbances include abnormal heart rate (bradycardia or tachycardia), irregular cadence to the
rhythm, variable intensity of the heart sounds, extra or absent heart sounds, or splitting of S1 or
S2. These findings indicate the need for an ECG. A cyclically irregular rhythm is very normal in
dogs and usually indicates (respiratory-related) sinus arrhythmia. In cats, sinus arrhythmia is
uncommon in hospital settings and represents another indication for an ECG. Many arrhythmias
lead to variable intensity of the first and second heart sounds caused by beat-to-beat variations
in ventricular preload. This affects the development of ventricular pressure and arterial pulse
pressure and therefore the loudness of the heart sounds and character of the following pulse. In
cases of premature ventricular activation, the ventricular pressure might be insufficient to open
the aortic valve and a single early sound along with a pulse deficit (S1 with a pulse) occurs. This
is often confused with an S3 gallop sound (the S1-S2prematureS1 is confused with an S1
S2S3). Most premature beats are followed by a pause. This is explained by penetration
(resetting) of the sinus node by the ectopic focus or to physiologic atrioventricular block of the
next sinus impulse by the premature ventricular activation. In cats, it may be more common to
recognize the post-extrasystolic pause rather than the actual premature heart sound. Pauses
also can be caused by sinus node disorders (sinus arrest) and by atrioventricular (AV) block.
A subtle sign of some arrhythmias is splitting of the heart sounds. This is usually due to
asynchronous ventricular activation as occurs with ventricular ectopia or bundle branch blocks
(splits are challenging to identify). Ventricular tachycardia for example, can lead to a series of
less distinct heart sounds when compared to those heard during normal sinus rhythm. Severe
pulmonary hypertension increases the intensity of S2 (by increasing the closing pressure on the
pulmonary root and eliminating physiologic splitting of the second sound). In advanced cases
audible splitting of the second sound can be detected should left and right ventricular ejection
times become widely disparate.
Although a cardiac murmur is often considered the hallmark auscultatory finding in heart
disease, as indicated above, some cardiovascular diseases might not be associated with this
finding. However, transient cardiac sounds can be abnormal in these patients and the clinician
should be vigilant for these abnormalities. Moreover, in the differential diagnosis for extra
sounds the clinician should consider true gallops (S3 and S4), clicks, widely split sounds, and
premature beats. An ECG can usually rule out an arrhythmia if the extra sounds are persistent.

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.

AUSCULTATION RESPIRATORY (BREATH) SOUNDS

Normal respiratory sounds include vesicular and bronchovesicular sounds, bronchial


breathing, and tracheal sounds (panting). Normal sounds can become accentuated or
decreased in diseases of the thorax or with left sided congestive heart failure (CHF). An
increase in bronchial sounds is often detected as a nonspecific finding of pulmonary disease
including pulmonary edema. Decreased sounds can indicate pleural fluid (ventral fluid line) or
air. Displaced sounds can occur with a mass lesion or diaphragmatic hernia. Normal sounds
and abnormal (adventitious) sounds might only become evident after enforcing deeper
breathing, which can be encouraged by closing the mouth and holding off one nostril or by
occluding both nostrils for a brief period to encourage deep breaths or sighs.

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.

Patent Ductus Arteriosus (PDA)

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.

Ventricular Septal Defect (VSD)

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.

Atrial Septal Defect (ASD)

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.

Pulmonic Stenosis (PS)

Overview PS is a congenital narrowing of the pulmonic valve, subpulmonic region, or


immediate supravalvular tissues. The components of valvular PS include valve thickening, fusion
along the valvular commissures, and varying degrees of hypoplasia of the valve. Subvalvular
obstruction can be fixed (fibrous) or related to dynamic obstruction due to muscular hypertrophy.
An unusual type of subvalvular PS is associated with a single origin of the coronary arteries (R2A);
this is most common in English bulldogs. The left coronary artery is located adjacent to a
subvalvular obstruction in this condition.
Pressure overload of the RV is created with increased systolic pressure needed to eject blood
across the stenotic valve. This pressure is generated by concentric hypertrophy of the ventricle.
High velocity ejection is needed to pump the RV stroke volume. This is associated with significant
post-stenotic turbulence in the great vessel. If there is a concurrent patent foramen ovale, ASD,
or VSD, right to left shunting can develop. Cardiac output is limited. Right-sided CHF can occur
from combinations of diastolic and systolic RV dysfunction, tricuspid regurgitation, and possibly
atrial fibrillation.
A genetic basis is responsible for most cases of canine PS, with higher prevalence in the
following breeds: terriers (multiple breeds), Beagle, Boykin spaniel, Boxer, Chihuahua, Cocker
spaniel, English bulldog, Mastiff, Samoyed, and schnauzers. PS is rare in cats. Most affected
dogs are asymptomatic, but tiring, exercise intolerance, and syncope can be observed in severe
cases. If CHF occurs, there will be abdominal distension from ascites.
Diagnosis The typical ejection murmur of PS is systolic and loudest over the pulmonary valve
and craniodorsal left base. The more severe the defect, the louder and later peaking the murmur.
An ejection sound can be detected in valvular PS. A loud holosystolic murmur on the right is
suggestive of tricuspid regurgitation from either right ventricular hypertrophy or concurrent
tricuspid valve malformation. Membranes should be pink unless there is a right-to-left shunt
across a PFO, ASD or VSD. A prominent jugular pulse can be identified. Right-sided CHF with
hepatomegaly and ascites will be found in a small percentage of cases. Rarely, pleural effusion
or chylothorax are identified in dogs with CHF.
The ECG, thoracic radiographs, and 2D echocardiogram will demonstrate RV enlargement and
often dilation of the right atrium. Imaging should reveal post-stenotic dilation of the pulmonary
artery in severe cases. The pulmonary circulation is normal to reduced. Doppler
echocardiography maps high-velocity, turbulent flow in the RV outflow tract and into the
pulmonary artery. Provided RV systolic function is normal (and the patient is not heavily sedated
or anesthetized), the peak velocity of ejection correlates with the severity of obstruction. Peak
velocities exceeding 5 m/s are considered severe (100 mm Hg peak pressure gradient), and carry
a guarded to poor prognosis. Velocities of <3.5 m/s indicate a relatively mild stenosis. Careful
examination of the atrial septum and ventricular septum with color Doppler is needed to exclude
a right to left shunt. A contrast echocardiogram is an efficient way to screen for a defect. Cardiac
catheterization is rarely needed to establish the diagnosis.
The differential diagnsosis includes other causes of CHD that create a systolic murmur or right
sided enlargement such as tetralogy of Fallot and ASD. Trivial PS may be difficult to distinguish
from a functional ejection murmur.
Therapy Mild PS (peak pressure gradients measured by Doppler studies of <50 mm Hg)
generally carries a good prognosis (survival of 8 years or more). Some dogs in the 50 to 100 mm
Hg range (moderate stenosis) do benefit from valvuloplasty in terms of exercise capacity, but
many of these dogs do well without intervention. Comparatively, severe disease (Doppler
echocardiographic gradient > 100 mmHg) increases the likelihood of sudden death or CHF.
Transcatheter balloon valvuloplasty is the treatment of choice for these dogs, especially when the
lesion is characterized by valvular thickening with commissural fusion. In experienced hands the
procedure mortality is <5% and the dilation results in a 50% or greater reduction of RV systolic
pressures. If the cases are chosen carefully, most treated dog will benefit. Therapy should not be
delayed as gradients and muscular hypertrophy can progress with time and growth. This
approach is generally unsafe in dogs with single origin of the coronary artery associated with
subvalvular stenosis. When PS is complicated by severe RV hypertrophy or subvalvular
fibromuscular obstruction, balloon valvuloplasty combined with propranolol or atenolol therapy (1
mg/kg PO, q12h). In some cases the dynamic muscular obstruction resolves over time; otherwise,
atenolol can be continued for life. Surgical techniques including patch grafting, pulmonary valve
repair or resection, or surgical dilation may help cases of severe (fibro-) muscular RV obstruction,
broad subvalvular fibrous ring, or when PS is complicated by marked pulmonary valvular
hypoplasia. Cutting balloons and catheter delivered stents have also been used in dogs with
subvalvular PS, but a limited annulus size usually limits this success. High pressure balloons can
sometimes be effective and are also useful for more typical valvular stenoses in some dogs. An
RV to pulmonary artery conduit can be placed surgically to bypass a hypoplastic valve or stenosis
due to an anomalous coronary artery, but surgical mortality is high. Instead we use a balloon
procedure but do not overize past the annulus. In cases that cannot be treated more definitively,
atenolol provides cardiac protection and is well tolerated. PS with patent foramen ovale, ASD, or
VSD can progress to right-to-left shunting with polycythemia, and is treated as described
previously.
In cases of mild stable PS, re-evaluation can not be necessary. The dog with moderate to
severe PS should have an annual examination and echocardiogram with Doppler study performed
by a cardiologist. This is especially true in large breed dogs where growth during the first year
may lead to a relative increase in severity of the obstruction. The pressure gradient, competency
of the tricuspid valve, and RV systolic and diastolic heart function should be followed.

Aortic Stenosis (AS)

Overview AS is typically related to developmental narrowing of the left ventricular outflow


tract. The most common location for obstruction is the subvalvular portion of the outflow tract
(subaortic stenosis or SAS), related to a fixed (fibrous) obstruction. The condition is common in
dogs and rare in cats. Valvular AS is observed in some dogs and is characterized by thick or
fused aortic valve leaflets, or by the presence of fused bicuspid leaflets. Dynamic obstruction of
the outflow tract also can occur due to malformation of the mitral valve allowing systolic anterior
motion of the mitral valve. This unusual form of SAS is labile and worsens with high sympathetic
tone (and benefits from beta-blockade). Additional features of AS include LV hypertrophy and
narrowing of the intramural coronary arteries, which reduces myocardial perfusion. Dogs with AS
are at a higher risk for infective endocarditis. The aorta is often abnormal with what has been
termed poststenotic dilation, but a primary aortopathy might also be pertinent to the further
development of this defect. For example, abnormal ventricular septal to aortic angles have been
identified in Boxers and in golden retrievers, even in very young dogs.
Pressure overload of the LV is created with increased systolic pressure needed to eject blood
across the stenotic zone. This pressure is generated by concentric hypertrophy of the LV. High
velocity ejection is needed to pump the LV stroke volume. This is associated with significant post-
stenotic turbulence in the great vessel. Coronary arterial insufficiency can lead to subendocardial
ischemia. This predisposes to exercise intolerance and cardiac rhythm disturbances. Cardiac
output is limited. Left-sided CHF can occur from combinations of diastolic and systolic LV
dysfunction, mitral regurgitation, and possibly atrial fibrillation. Syncope or sudden death can be
triggered by exertion. Ventricular arrhythmias or stimulation of ventricular mechanoreceptors
(cardiac baroreceptor reflex) can be responsible.
SAS is a genetic disorder in many canine breeds including the Golden retriever, Newfoundland,
Bull terrier, German shepherd, Boxer, English bulldog, among many. Most affected dogs are
asymptomatic, but tiring, exercise intolerance, and syncope can be observed in severe cases.
Should CHF develop, there will be tachypnea and other respiratory signs related mainly to
pulmonary edema.
Diagnosis The typical ejection murmur of AS is systolic and loudest over the aortic valve and
subaortic areas. In SAS, the more severe the defect, the louder and later peaking the murmur
and the more likely a prominent right-sided component will be evident (true valvular AS is often
loudest over the right dorsal base). A loud holosystolic murmur over the apex may be indicative
of concurrent mitral regurgitation. The femoral pulse is late-rising and weak in cases of moderate
to severe AS. Overt left-sided CHF will be found in a small percentage of cases.
The ECG, thoracic radiographs, and 2D echocardiogram will demonstrate LV enlargement and
less often dilation of the left atrium. Radiography shows a normal pulmonary circulation in most
cases. Imaging often reveals post-stenotic dilation of the ascending aorta (on the right of the
midline). The Echo finding of hyperechogenicity of the subendocardial myocardium and papillary
muscles indicates severe stenosis with ischemic fibrosis of muscle. The finding of left atrial dilation
is also a poor prognostic sign and stems from left ventricular failure; mitral valve disease; or an
(often overlooked) left-to-right shunt. Doppler echocardiography maps high-velocity, turbulent
flow in the LV outflow tract and into the ascending aorta. Generally the most accurate velocities
are obtained from a subcostal transducer position. Provided LV systolic function is normal (and
the patient is not heavily sedated or anesthetized), the peak velocity of ejection correlates with
the severity of obstruction. Peak velocities exceeding 4.5 to 5 m/s are considered severe (>80 to
100 mm Hg peak pressure gradient), and carry a guarded to poor prognosis. Cardiac
catheterization is rarely needed to establish the diagnosis.
The differential diagnosis includes other causes of CHD that create a systolic murmur or left-
sided enlargement, including VSD and mitral valve malformation. Pulmonic stenosis, atrial septal
defect, and functional murmurs are additional causes of left sided ejection murmurs. .
Therapy Transcatheter balloon dilation of the stenotic orifice has been performed and
successfully reduces LV pressure gradients by approximately 40 to 50%. However, this benefit
however becomes attenuated over time and the procedure has largely been abandoned, though
it can be a consideration for severe cases of SAS and is certainly beneficial in the patient with
valvular AS due to mobile, but fused valve leaflets. Recently clinicians have been using a
combination of a cutting balloon followed by a high-pressure balloon with the intent of scoring
the subvalvular lesion and then dilating it. It remains to be seen if this will be any more effective.
Open surgical resection of the stenotic lesion provides the best long term success in terms of
reduction of gradients, but it requires cardiopulmonary bypass, and long-term survival has been
disappointing. Beta-blockade with atenolol (1-2 mg/kg PO bid) seems to improve survival over
historical controls and a median survival of > 4 years has been observed in dogs from our hospital
with even severe SAS (gradients >120 mm Hg). Atenolol is recommended for all dogs with a peak
gradient >50 mm Hg. Beta-blockade is particularly helpful in the specific situation of dynamic SAS
caused by mitral valve malformation wherein beta-blockade can completely alleviate the
obstruction and allow regression of LV hypertrophy.
Unfortunately, severe SAS carries a discouraging prognosis owing to premature death. Sudden
arrhythmic cardiac death and progressive LV dysfunction with development of CHF are typical
outcomes. Mature dogs with mild SAS are more likely to live normal lives, though some still
experience sudden death. Dogs with even mild disease are at higher risk for development of
bacterial endocarditis. Therefore, prophylactic antibiotics should be administered during elective
surgical procedures or whenever wound contamination is an issue.
In cases of mild stable SAS, re-evaluation may not be necessary. The dog with moderate to
severe SAS should have an annual examination and echocardiogram with Doppler study
performed by a cardiologist. The pressure gradient, competency of the aortic and mitral valves,
and LV systolic and diastolic heart function should be followed. Giant breed dogs should be
evaluated just prior to full maturity, as the severity of the obstruction can increase dramatically
following rapid growth.

Atrioventricular Valvular Dysplasia

Overview Dysplasia or malformation of the mitral or tricuspid valves includes a number of


morphologic abnormalities of the atrioventricular valve apparatus including combinations of:
malformed papillary muscles; excessively short or long chordae tendineae; abnormal
development of the valve leaflets and cusps; and fusion along valve commissures. The functional
outcome of mitral or tricuspid dysplasia is either valvular regurgitation (most common) or valvular
stenosis with obstruction to ventricular filling. Both disorders can occur. Severity can range from
trivial to life-threatening. There can be concurrent defects such as atrial septal defect or patent
foramen ovale.
Dysplasia of the tricuspid valve is relatively common malformation of larger breeds of dogs
and especially of the Labrador retriever. In fullyformed tricuspid valve dysplasia the lesions are
dramatic. These can include: malformed and thickened leaflets; excessively long or short chordae
tendineae; either normal or ventral displacement (Ebsteins anomaly) of the annulus with leaflets
inserting beyond the normal apical offset; and prominent bridging between the medial and lateral
papillary muscles near the apex). In most cases the septal leaflet appears to be adhered to the
septum for a longer distance (failure to delaminate) and this is the cause of apical coaptation of
the valves. In severe cases massive RA dilation is expected along with significant RV eccentric
hypertrophy. Depending on the leaflet and chordal arrangements there may also be stenosis or
rarely atresia of the tricuspid valve. These lesions have also been observed in cats. In contrast,
mild tricuspid valve malformations are associated with subtler abnormalities in the valve
apparatus structure and motion and there is more controversy about these diagnoses because
some dysplastic valves might simply be variations on normal.
Both atrioventricular valvular regurgitation and valvular stenosis lead to atrial dilation on the
affected side and predispose to CHF and to atrial arrhythmias, including atrial fibrillation. If the
stenotic valve is competent, ventricular function is relatively normal. In cases of mitral stenosis,
reactive changes in the pulmonary vascular tree can lead to significant pulmonary hypertension
with right ventricular hypertrophy and limited exercise capacity; this is most common in cats. In
tricuspid stenosis (or severe regurgitation) there is a high potential for continued patency of the
foramen ovale. This can lead to right to left shunting, arterial hypoxemia, and create a form of
cyanotic heart disease.
Atrioventricular valve dysplasia is most likely a genetic disorder in a variety of breeds
particularly the Labrador retriever (tricuspid valve) and Bull terrier and Great Dane (mitral valve).
The precise mode of inheritance across various breeds has not been determined. Tricuspid
dysplasia in Labrador retrievers can be associated with anomalous conduction pathways
predisposing to reentrant supraventricular tachycardias. Clinical signs can be absent until the
onset of CHF or atrial fibrillation. Observant owners generally recognize some exercise
intolerance. In the case of trivial or mild malformation, the dog is normal. In the case of tricuspid
dysplasia with a patent foramen ovale, there can be tiring and obvious cyanosis.
Diagnosis The most common clinical sign is a systolic murmur of atrioventricular valvular
regurgitation over the affected valve area. Diastolic murmurs of atrioventricular valve stenosis are
usually very soft and easily missed. Membranes should be pink unless there is a right-to-left shunt.
Definitive diagnosis of mitral or tricuspid dysplasia requires careful 2D echo imaging of the
affected valve combined with Doppler studies that record transvalvular flow and identify valvular
regurgitation. There are characteristic Doppler flow patterns for valvular stenosis and
regurgitation, and severity of the disease can be gauged by an experienced examiner using
noninvasive ultrasound studies.
In mitral valve dysplasia signs are mainly left-sided, and with mitral regurgitation radiography,
ECG, and 2D echocardiography will demonstrate LV and left atrial dilatation. Marked left atrial
dilation is evident with mitral stenosis. Atrial fibrillation is common and can precipitate clinical
signs. CHF with Pulmonary edema is a common finding. In mitral stenosis there can be Doppler
echocardiographic evidence of pulmonary hypertension with secondary right ventricular
hypertrophy.
In tricuspid valve dysplasia with regurgitation, diagnostic examinations point to problems on the
right side of the heart including atrial and ventricular enlargement. Right-sided CHF with
hepatomegaly and ascites will be found in advanced cases. Atrial fibrillation is common. Rarely,
pleural effusion or chylothorax are identified in dogs with CHF due to tricuspid valve malformation.
A prominent jugular pulse can be identified. Notched or splintered R-waves can be observed in
dogs with tricuspid malformation. Re-entrant supraventricular tachycardias or ventricular pre-
excitation are occasionally observed on the ECG. Cyanosis, arterial hypoxemia, and polycythemia
are expected when severe tricuspid dysplasia is complicated by an atrial septal defect.
Dogs can survive for many years with atrioventricular valvular malformation, and therefore
acquired disorders such as valvular endocardiosis, dilated cardiomyopathy, and infective
endocarditis are considerations in the differential diagnosis of mitral dysplasia. Endocardiosis,
pulmonary hypertension, and right-sided cardiomyopathies can lead to tricuspid regurgitation and
must be distinguished from tricuspid dysplasia.In the setting of cyanotic heart disease, the
differential diagnosis is similar to that indicated above for tetralogy of Fallot. Atrioventricular
stenosis also can stem from an obstructive fibrous or fibromuscular ring situated above the mitral
or tricuspid valve (supravalvular mitral/tricuspid ring). Tricuspid stenosis can be confused with
(or occur along with) an obstructive partitioning of the right atrium termed cor triatriatum dexter.
In this malformation, the caudal right atrium is separated from the tricuspid orifice by a persistent
membrane with a small orifice. This situation obstructs caudal vena caval blood flow and leads to
hepatomegaly and ascites. A similar condition (though more rare) can occur in the left atrium (cor
triatriatum sinister), leading to pulmonary venous obstruction.
Therapy Balloon valvuloplasty has been performed with variable success in dogs with
tricuspid and mitral valvular or supravalvular stenosis. Surgical repair or annular support of
affected valves can be attempted. Replacement of dysplastic valves has been performed
successfully with cardiopulmonary by-pass. Most cases are treated medically when signs of CHF
or atrial fibrillation develop. Consideration should be given to ACE-inhibitor (enalapril) and to beta-
blocker therapy (carvedilol or metoprolol) for establishing cardioprotection in dogs with severe
mitral regurgitation and associated cardiomegaly. The benefit of such therapy in tricuspid
dysplasia is more uncertain.
Tricuspid malformation, associated with an ASD, can lead to right-to-left shunting; secondary
polycythemia should be managed (discussed above).
Mild mitral or tricuspid valvular dysplasia is often well-tolerated; however, severe lesions lead
to CHF and arrhythmias such as atrial fibrillation. Dogs with severe mitral disease usually develop
CHF in early to middle age, particularly when the valve is both stenotic and incompetent. Many
dogs with relatively severe tricuspid regurgitation survive for 7 or 8 years before CHF ensues.
It is more common for dogs with severe mitral valve dysplasia to develop left-sided CHF during
the first five years of life. Critical atrioventricular valvular stenosis is likely to cause signs within
the first one or two years of life. Asymptomatic dogs and cats with moderate to severe disease
should have a cardiology evaluation and echocardiogram yearly, or more often if warranted by
clinical findings.

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.

Congenital Heart Disease in Cats Data from Combined Studies

Ventricular septal defect (VSD) 80 18.4


Patent ductus arteriosus (PDA) 49 11.3
Tricuspid valve dysplasia (TVD) 47 10.8
Mitral valve dysplasia (MVD) 44 10.1
Atrioventricular septal defects (AVSD) 42 9.7
Aortic stenosis (AS) 31 7.1
Tetralogy of Fallot (ToF) 30 6.9
Atrial septal defect (ASD) 26 6.0
Persistent right aortic arch (PRAA) 23 5.3
Endocardial fibroelastosis (EFE) 21 4.8
Pulmonic stenosis (PS) 17 3.9
Other malformation 11 2.5
Double outlet right ventricle (DORV) 7 1.6
Cor triatriatum sinister 7 1.6

Total 435 100%


Pericardial Diseases in Dogs: Diagnosis & Management
John D Bonagura DVM, DACVIM (Cardiology, Internal Medicine)
Veterinary Clinical Sciences, Ohio State University

Congenital peritoneopericardial diaphragmatic hernia (PPDH) and acquired pericardial


effusions represent the most important disorders affecting the pericardium of dogs. Pericardial
effusion (PE) refers to the accumulation of an excessive volume or abnormal type of fluid within
the space bordered by the epicardium and parietal pericardium. Pericardial diseases impair
diastolic ventricular function. When the heart is compressed by a PE to the point that
intrapericardial pressures rise and cardiac filling is impaired, a state of cardiac tamponade is
present.
Important congenital forms of pericardial disease in dogs include congenital PPDH and the
rare cysts. Careful radiographic evaluation leads one to suspect the diagnosis. Findings include
altered radiographic density in the caudoventral portion of the pericardial space, often with cranial
displacement of the carina. A linear shadow ventral to the caudal vena cava represents the
persistent mesothelial remnant delineating the dorsal border of the communication.
Ultrasonography is diagnostic. The condition is treated surgically, but may be an incidental finding
in mature animals and not warrant intervention.

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

John D Bonagura DVM, MS, DACVIM (Cardiology, Internal Medicine)


Veterinary Clinical Sciences, The Ohio State University
Columbus, Ohio, USA

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

Initial Management: Dyspneic patients must be stabilized before radiography


Sedatives should be administered if restraint is difficult or the patient is distressed.
For cats: acepromazine (0.05 to 0.1 mg/kg) mixed with butorphanol (0.25 mg/kg) and
administered IM provides mild to moderate sedation. ACP should not be used in hypotensive
or hypothermic cats.
For dogs: one of the following protocols is usually effective: 1) butorphanol (0.25 to 0.5
mg/kg, IM); or 2) acepromazine (0.025 mg/kg) mixed with butorphanol 0.25 mg/kg IV or IM;
or 3) acepromazine (0.025 mg/kg) plus buprenorphine (0.0075 mg/kg), IV or IM.
Oxygen should be given by cage, tent, or mask (if tolerated). At a minimum, a fan should be
directed to the face to help relieve dyspnea and dissipate heat.
The clinical staff should be ready to perform tracheal intubation and positive pressure
ventilation should life-threatening dyspnea be evident and respiratory arrest imminent.
Obvious laryngeal or tracheal stridor may indicate airway obstruction that can be temporarily
managed by tracheal intubation.
Thoracocentesis should be performed if pleural effusion or pneumothorax is suspected.
For suspected pulmonary edema (when the patient cannot be examined by radiography)
administer parenteral furosemide (2 - 4 mg/kg IV or IM), oxygen, and nitroglycerine paste (
inch of 2% ointment for cats or small dogs; to 1-inch for large dogs).
For suspected feline asthma, use a pediatric spacer and a standard albuterol inhaler;
administer two puffs of albuterol into the spacer and allow the cat to breath through the
mask for 10 to 15 seconds. A positive response should provide a presumptive diagnosis of
reactive bronchospasm. If positive, administer short-acting glucocorticoids and oral airway
dilators (or continue using inhaled albuterol twice daily). Typical doses include:
dexamethasone Na phosphate - 0.5 to 1 mg/kg IV or IM; sustained release oral theophylline
25 mg/kg once daily; terbutaline sulfate (0.1 mg dose SQ or IV; or to of a 2.5 mg
terbutaline tablet PO 12h).
Page-1
Evaluation of Thoracic Radiographs Principles and Suggestions
Thoracic radiographs are essential in all cases of dyspnea or chronic cough. Good-quality
VD/DV and lateral films are needed to evaluate the trachea, bronchial tree, the lungs,
mediastinum, lymph nodes, and pleural space. A systematic approach should be taken as
suggested in Table 3. Interpret the radiographic findings in two ways: 1) Independently what
story can you make from the signalment and the radiographs? 2) Within the clinical context
how do the radiographic findings relate to known clinical problems & clinical examination
findings?
Cardiac Evaluation Assessment of the cardiac silhouette, great vessels, pulmonary
circulation, and veins is particularly important if heart failure, heartworm disease, or pulmonary
vascular disease is suspected. However, over-interpretation of cardiac size frequently misleads
the clinician to an erroneous diagnosis of heart failure, as with obese cats with intrapericardial
fat, toy breed dogs, and films exposed during expiration. A vertebral heart score may be
instructive when heart enlargement is in doubt (see Table). Cardiomegaly (left ventricular
dilation/hypertrophy) in cats is often manifested as elongation of the heart. A bulge in the 1 to 3
o'clock positions on the VD view is typical of left auricular dilation, and often suggests an
advanced form of feline cardiomyopathy. Apex shifting to the midline is also common in cats with
cardiomegaly. Cardiomegaly is also common with moderate to severe anemia, with
hyperthyroidism, with systemic hypertension, and with chronic respiratory disease. Pulmonary
edema in CHF is often more ventral than one might expect. Dilation of both lobar arteries and
veins is typical of left-sided CHF with pulmonary hypertension. The aorta is often dilated and
tortuous in older cats. Heartworm disease can lead to dilation of the lobar pulmonary arteries
(especially the right). Peracute heartworm death can cause a "white lung" with severe alveolar
infiltration.
Mediastinal Lesions Mediastinal widening is typical of fluid accumulation or mass lesions.
Pneumomediastinum suggests tracheal perforation (e.g. from trauma) or a lesion in the
esophagus. Lymphoma and thymoma are common mediastinal neoplasms in cats. It should
also be noted that benign mediastinal lesions can be encountered including mediastinal cysts in
young and older animals and mediastinal (thymic) hemorrhage in young dogs.
Pulmonary Densities If thoracic radiographs indicate abnormal thoracic densities,
characterize these as either increased or decreased thoracic density. If lung density is
decreased (air density) rule out an over-exposure problem, pneumothorax or
pneumomediastinum, or intrapulmonary gas trapping. The latter is typical of "asthma" in cats. If
lung density is increased, rule out expiratory film, (under-)exposure problem, motion, prominent
vessel margins, or true increase in fluid density within the thorax. If there is increased fluid
density, determine if it is within the pleural space, lung, or mediastinum.
If there are increased pulmonary densities, determine the distribution of densities (e.g.,
cranioventral, multifocal, right lobar, perihilar, accessory lobe [surrounds caudal vena cava], or
disseminated). Indicate the precise pattern of increased lung density (i.e., alveolar, interstitial
linear/unstructured or nodular, peribronchial, or mixed). Characteristic patterns may be
suggestive of specific diseases (for example, chronic bronchitis causes bronchial patterns;
atelectasis and pneumonia are common in the right middle lobe). Determine the presence or
absence of airway collapse or obstruction. Examine the thorax for mediastinal widening or
density changes. Inspect the film for hilar or mediastinal lymphadenopathy (typical of fungal
diseases, lymphoma, and pulmonary granulomatous diseases which are rare in cats). Mixed
pulmonary densities in multiple lobes are common with lungworms, atypical pneumonia,
disseminated neoplasia, fungal diseases, and Mycoplasma infection.
Pleural effusion typically obscures the borders of the heart and diaphragm (border effacement),
produces fissure lines, fills the costophrenic angles, and moves with gravity. Pleural effusion is
more obvious on the DV view, but the lungs will be better visualized in cases of pleural effusion
on the VD view. There are numerous causes of pleural effusion in cats (Table 2).

Additional Diagnostic Studies


Following physical diagnosis and radiography, a number of additional diagnostic studies can
be helpful in determining the underlying reason for respiratory signs.
Page-2
Routine laboratory tests are often obtained in animals with signs of thoracic disease (Table 1).
CBC abnormalities may be present to suggest infection, inflammation, or necrosis; however, the
neutrophil count can be very misleading and nearly normal in cases of significant pulmonary
infiltration. Eosinophilia, in the absence of intestinal or ectoparasitism, suggest the possibility of
heartworm disease, lungworms, allergic bronchitis, lymphoma, granulomatous disease, or
pulmonary infiltrates with eosinophils. Obtain a heartworm antigen test in areas where
heartworm is endemic (or an antibody/antigen test in cats, if indicated). Knowledge of the FeLV
and FIV status is always useful. Serologic testing for toxoplasmosis, systemic fungi, and feline
infectious peritonitis (FIP) is indicated in selected cases. If radiographs are compatible with
lungworm infection (e.g., paragonimiasis), use direct fecal studies including smears, routine
flotation, and sedimentation methods (Baermann) may be helpful in screening for lungworms.
Consider additional diagnostic tests (if indicated from the examination, prior test results, or lack
of response to prior treatment).

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.

Esophagoscopy is helpful in diagnosing esophageal-tracheal fistula or causes of aspiration


pneumonia.

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

Diseases of the Pleural Space


History and physical examination (observation, auscultation, percussion of the thorax)
Thoracic radiography (pre- and post-thoracocentesis)
Thoracocentesis with cytology of pleural effusate +/- culture and sensitivity of pleural effusate
Serological testing when appropriate (FIV, FIP)
Biochemical tests (e.g. serum/pleural effusion triglyceride concentration for chylothorax)
Ultrasound examination of pleural space, lungs, and mediastinum
CT or MRI of thorax
Lymphangiography

Diseases of the mediastinum


History and physical examination (observation, auscultation, percussion of the thorax)
Thoracic radiography
Ultrasound examination
CT or MRI of mediastinum
FNA of mediastinal masses
Esophageal contrast studies
Bronchoscopy

Page-5
Table 2. Differential Diagnosis of Pleural Effusion

Cardiac Causes Hemothorax


Congenital Heart Disease Bleeding Disorders, including
Valvular heart disease Rodenticide Toxicity
Pericardial Diseases Trauma
Canine Cardiomyopathy Neoplasia
(dilated in the dog)
Feline Cardiomyopathies (hypertrophic,
restrictive, dilated, right ventricular) Infectious Causes
Silent atrium Feline Infectious Peritonitis
Chronic bradycardia Pyothorax (Bacterial, Nocardia,
Chronic severe tachycardia Actinomycosis, Anaerobic Infections)
Advanced thyrotoxic Heart Disease Blastomycosis
Moderate To Severe Anemia Leading Penetrating trauma
To High Output Failure
Obstruction of Venous Return From The
Cranial Vena Cava Neoplastic Causes
Mediastinal Mass
Heart Based Tumors
Pulmonary Causes Primary Lung Tumors
Lung Lobe Torsion Disseminated Neoplasia
Pulmonary neoplasia
Pleuropneumonia (uncommon in cats) Other Causes
Atypical Pneumonia (Nocardiosis) Marked Hypoproteinemia
Pulmonary Thrombosis And Embolism Overinfusion of Fluids
Diaphragmatic Hernia
Thoracic Trauma
Chylous Effusion Central Venous Catheters
Idiopathic (Perforation or Thrombosis)
Obstructed or Traumatized Thoracic Thrombosis or Obstruction of The
Duct or cranial vena cava Cranial Vena Cava
Primary Lymphatic Disorder Abdominal Surgery
Congestive Heart Failure Pancreatitis
Pericardial Disease Idiopathic
Heart Base Tumor or Mass
Mediastinal Mass
Feline Heartworm Disease

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.

Examine the mediastinum


Identify widening cranially or caudally suggests mass lesions (ddx: thymus in young animal).
Identify mediastinal shifts that may suggest atelectesis.
Look for free air, especially in cases of pneumothorax.
Identify the trachea and follow its course to the carina. Recall breed variations (bulldogs
hypoplasia; basset hounds large)
Try to identify the main left and right bronchus; these bifurcate just cranial to the left atrium.
Identify any bronchial collapse or compression (as with enlarged left atrium or hilar
lymphadenopathy).
Identify tracheal deviation as might occur with cardiomegaly (dorsal deviation), persistent
right 4th aortic arch, mediastinal masses, or chemodectoma. Remember that tracheal
position depends greatly on head positioning and that in some breeds (bulldogs!) some
rightward deviation is normal on the VD projection.
Evaluate the tracheal lumen for narrowing, collapse, or abnormal densities (as with Oslerus
osleri nodules at the carina or the rare intraluminal neoplasm)
Examine the esophagus is it air-filled, dilated, or containing a foreign body or soft tissue
(as with gastroesophageal intussusception)
In cats especially remember to consider peritoneopericardial diaphragmatic hernia in the
differential diagnosis of cardiomegaly.

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.

Great Vessels and Pulmonary Vessels


Examine the great vessels. Inspect the aortic arch and descending aorta; examine the main
pulmonary artery and the lobar pulmonary artery branches. Identify any bulges or dilations
that might suggest congenital or acquired disease. Identify lobar vascular abnormalities.
Dilated aorta subaortic stenosis (ascending/arch), PDA (descending), generalized
dilation (hypertension), dilation/redundant (senile change in cats; idiopathic in dogs).
Dilated main PA pulmonic stenosis (post-stenotic dilation), left to right shunt (ASD,
VSD, PDA), or pulmonary hypertension (heartworm disease, idiopathic PH). Remember
that an oblique VD film will make the PA appear dilated.
Identify abnormal vascular patterns
Dilated pulmonary veins r/o left sided CHF; beware that superimposition of an artery
and vein can make the vessel appear large.
Dilated pulmonary arteries r/o pulmonary hypertension (heartworms,
thromboembolism)
Dilated arteries and veins r/o normal variation or magnification on the DV view (farther
from the cassette), high cardiac output (hyperthyroidism), left to right shunt, or
combination of left sided CHF + pulmonary hypertension.

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

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