Vol. 22, No.
1 January 2000 V
CE Refereed Peer Review
FOCAL POINT
★ Arrhythmias are common in
the perianesthetic period and
should be recognized, thus
the electrocardiograph is an
important monitoring device
that should be used in all
anesthetized patients.
KEY FACTS
■ Preanesthetic and induction
agents can alter autonomic
balance, which can result in
a variety of arrhythmias that
may or may not be clinically
significant.
■ Bradyarrhythmias and heart
blocks may often result
from opioid and tranquilizer
administration but may not be
clinically significant if cardiac
output is not adversely affected.
■ Anticholinergics may produce
such arrhythmias as complex
second-degree atrioventricular
block and extrasystoles.
■ Ventricular premature complexes
can have a variety of noncardiac
causes and often do not require
specific antiarrhythmic drug
administration but may require
changes in anesthetic
management to prevent serious
consequences.
Perianesthetic
Arrhythmias
Mississippi State University University of Georgia
Lynne I. Kushner, DVM Clay A. Calvert, DVM
ABSTRACT: The patients discussed in this article were presented to the Veterinary Teaching
Hospital at Mississippi State University for a variety of surgical or medical procedures requir-
ing anesthesia. The electrocardiograms of all patients were monitored during induction and
maintenance of anesthesia. A variety of arrhythmias were recorded, including heart blocks, ex-
trasystoles, escape complexes, and accelerated junctional or ventricular rhythms. Noncardiac
causes were implicated in all cases. Some arrhythmias may produce hemodynamic instability,
whereas others may not. Although specific antiarrhythmic agents were not required, alteration
in anesthetic management was necessary in these patients to resolve the arrhythmia and avert
serious consequences.
T
he incidence of cardiac arrhythmias in the perioperative period in human
patients ranges from 18% to 70%.1,2 Incidence varies with degree of
monitoring, type of anesthetic, presence or absence of preexisting disease,
and ventilatory status. Although specific statistics are unknown, cardiac arrhyth-
mias are also common in anesthetized veterinary patients.3,4
Causes of arrhythmia during anesthesia and surgery include altered physio-
logic states, autonomic imbalance, and adverse effects of drugs and drug interac-
tions.2,3 In humans, arrhythmias may be more common when heart disease is
present2; in our opinion, most arrhythmias in veterinary patients have a noncar-
diac cause. Although most arrhythmias are often benign (i.e., causing no physio-
logic or circulatory impairment), some may result in significant cardiovascular
impairment if unrecognized or potentiated by anesthetic agents.
The following electrocardiogramsa (ECGs) and case descriptions are of pa-
tients presented to the Veterinary Medical Teaching Hospital at Mississippi State
University. All patients were either normal and healthy or had only mild sys-
temic disease and were presented for routine medical or surgical procedures.
None of the patients had documented cardiac disease. This article describes
some common arrhythmias, speculates on their causes, and discusses their rele-
vance and possible treatment.
CASE 1
A 5-year-old Boston terrier required anesthesia for dental cleaning and tooth
extraction. The dog was premedicated with acepromazine (0.05 mg/kg intra-
muscularly [IM]), oxymorphone (0.05 mg/kg IM), and glycopyrrolate (0.01
mg/kg IM) 40 minutes before the preinduction ECG was recorded (Figure 1).
aAllECGs were recorded in lead II at a paper speed of 25 mm/second; they were not stan-
dardized for sensitivity.
Small Animal/Exotics
Figure 1—Second-degree atrioventricular (AV) block. The atrial and ventricular rates block.5
are 100 and 60 beats/min, respectively. The P-R interval preceding the nonconduct-
ed P wave (0.14 seconds) is slightly longer than the first P-R interval (0.12 seconds) of the atria, sinus arrest/block often
of the pair. This describes a Mobitz type 1 (Wenckebach phenomenon) second-de- occurs with sinus arrhythmia caused
gree AV block.5
Second-degree atrioventricular (AV) block is charac-
terized by an interruption of AV conduction that re-
sults in one or more P waves that are not followed by a
QRS-T complex.5 When found in normal dogs, it is
most often associated with sinus arrhythmia and other
5
causes of increased vagal tone. Brachycephalic breeds
as well as young or athletic dogs may have hyperactive
vagal reflexes.6,7 Response to anticholinergic drug ad-
ministration would verify a vagal cause and an anti-
cholinergic drug is indicated if bradycardia adversely
affects cardiac output. Although an ECG was not re-
corded before premedication in this patient, ausculta-
tion did not indicate preexisting bradyarrhythmia.
Many drugs, including α2 agonists (e.g., xylazine8)
9 10
and opioids (e.g., oxymorphone, butorphanol ), pro-
duce bradyarrhythmias as a result of increased vagal
outflow. Acepromazine may either increase or not have
a significant effect on heart rate (HR) but may produce
profound bradycardia in susceptible dogs by increasing
11
central cholinergic outflow. Acepromazine’s role in
potentiating vagal activity in brachycephalic breeds has
been reviewed.12,13
Oxymorphone was the most likely cause of the ar-
rhythmia in this patient, with acepromazine being a
potentiating factor. Glycopyrrolate was apparently inef-
fective in producing vagal blockade. Although anti-
cholinergic administration would increase HR and re-
store rhythm, the dog was hemodynamically stable and
induction with thiopental proceeded with no complica-
tions. The HR remained around 80 beats/min with no
further evidence of heart block.
CASE 2
Anesthesia and surgery were planned for a healthy, 7-
year-old dachshund. The patient was premedicated
with butorphanol (0.3 mg/kg IM) and midazolam (0.2
mg/kg IM), and a preinduction ECG was recorded
(Figure 2A). Because of the low HR, atropine (0.02
mg/kg) was administered intravenously (IV).
In sinus block, the sinoatrial (SA) node discharges
SECOND-DEGREE ATRIOVENTRICULAR BLOCK ■ OXYMORPHONE ■ SINUS BLOCK
Compendium January 2000
but does not depolarize the atria; si-
nus arrest occurs because no sinus im-
pulse is formed.5 Electrocardiographi-
cally, sinus block and sinus arrest are
difficult to differentiate; however, a
pause that encompasses exact multi-
ples of R-R intervals suggests sinus
In addition to pathologic conditions
by increased vagal tone.5 The brady-
cardia (Figure 2A) may be attributed
to butorphanol, an opioid with mixed agonist–antago-
nist activity. Butorphanol produces bradycardia similar
to that caused by oxymorphone in acepromazine-sedat-
ed dogs.9 Midazolam, a water-soluble benzodiazepine
with twice the potency of diazepam,14 was added in this
case to improve the sedative effects of butorphanol. An
escape complex occurs when lower pacemakers dis-
charge to rescue the heart.
Atropine, a competitive muscarinic-receptor antago-
nist, is used to correct vagally mediated bradycardia.
However, atropine often produces initial slowing of HR,
with or without AV block, especially at low dosages15;
the causative mechanism initially proposed was central
stimulatory effects on vagal centers.15,16 Recent evidence,
however, suggests a peripheral mechanism involving
augmentation of acetylcholine release by high-affinity
presynaptic muscarinic receptors, followed by blockade
of low-affinity postsynaptic muscarinic-receptor sub-
types, which results in parasympatholytic effects.17 In
addition, current hypotheses include a difference in sen-
sitivity or distribution of muscarinic receptors at the SA
and AV nodes, which may account for the differential
response in SA and AV nodal activity.16,17
A recent study demonstrated this biphasic response
in HR after IM and IV administration of atropine.17
This effect was also demonstrated in this case. After
several minutes, the HR and rhythm improved and in-
duction proceeded without complication or further
heart block.
CASE 3
A healthy, 1.5-year-old Labrador retriever was anes-
thetized for surgical correction of osteochondritis desic-
cans. After moderate sedation with acepromazine (0.05
mg/kg IM) and oxymorphone (0.05 mg/kg IM), anes-
thesia was induced with thiopental (12 mg/kg IV admin-
istered to effect) and maintained with halothane and
oxygen. Approximately 3 to 5 minutes after inhalation
anesthesia began, an arrhythmia was noted (Figure 3).
Ventricular premature complexes (VPCs) arise from
Compendium January 2000 Small Animal/Exotics

Figure 2A

Figure 2B
Figure 2—(A) Marked sinus arrhythmia with a ventricular rate of 60 to 80 beats/min. Sinus block/arrest results in long pauses
equal to or greater than two R-R intervals. An escape complex, probably either atrioventricular (AV) nodal or high septal in ori-
gin, interrupts the block. The P wave can be seen after the QRS complex (arrow). (B) An advanced second-degree AV block oc-
curs. More than one consecutive P wave is not conducted. The atrial rate is 130 beats/min, and the ventricular rate is 60
beats/min. Escape beats, which may be AV nodal or high ventricular in origin, occur independent of the rhythm of sinoatrial
node depolarization. P waves occur before, within, and after the QRS of the escape complexes.

ectopic foci in the ventricles and result in bizarre, wid-
ened QRS complexes that are not associated with P waves.5
Classification of the severity of VPCs is based on (1)
the number of single VPCs per minute; (2) whether
they are multiform or uniform in appearance; (3) if
they occur early on the preceding T wave (i.e., R-on-T
phenomenon); or (4) if they occur in pairs, runs, or
paroxysms.5 If VPCs occur frequently enough to pro-
duce circulatory impairment, treatment should be insti-
tuted.
In addition to cardiac disease, VPCs can have numer-
ous noncardiac causes, including electrolyte and acid–
base imbalance, autonomic imbalance, hypoxia, and
hypercapnia.5 Circulating catecholamines can increase
because of stress, pain, and excitement and exert their
potential arrhythmogenic effects by binding to α- and
β-adrenergic receptors within the myocardium.18 The
myocardial sensitization to epinephrine by anesthetic
agents has recently been reviewed.19 The arrhythmo-
genicity of a drug can be measured by determining its
effect on the arrhythmogenic dose of epinephrine
(ADE). One study determined the receptor mechanism
that mediates epinephrine-induced arrhythmias during
halothane administration; the ADE was increased the
greatest after α1 blockade, suggesting that mediation of
sensitization by halothane is predominantly an α1 re-
ceptor–effector mechanism.18 Anesthetic agents that have
lowered the ADE include thiobarbiturates, 20,21 pro-
pofol,22 and halothane.23 Xylazine and ketamine may or
may not enhance arrhythmogenicity.24–27
Thiopental or halothane administration, hypoxia,
and hypercapnia are potential precipitating causes in
this healthy dog. It is well established that thiopental
potentiates halothane-epinephrine–induced arrhyth-
mias.20,21 In addition, the duration of this potentiation
can exceed 4 hours, well beyond thiopental’s clinical ef-
fects.20,21 This arrhythmia was noticed soon after halo-
thane was administered, but anesthetic concentrations
of halothane were not measured. Myocardial epi-
nephrine sensitization may occur with halothane con-
centrations as low as 0.1%.28
Because oxygen–hemoglobin saturation and partial
pressure of arterial carbon dioxide concentrations were
not measured, it cannot be stated with certainty wheth-
er hypoxia and/or hypercapnia played a role in the
genesis of this arrhythmia. The dog was immediately
ventilated with several breaths to ensure adequate oxy-
genation and ventilation, but normal rhythm was not
restored and ventricular ectopic beats continued with
similar frequency. Because the dog’s mucous membrane
color, capillary refill time, pulse quality, and depth of
anesthesia were assessed as adequate, surgery proceeded
with vigilant monitoring. Halothane was replaced with
isoflurane with little response in the frequency of the

VENTRICULAR PREMATURE COMPLEXES ■ ARRHYTHMOGENIC DOSE OF EPINEPHRINE ■ HALOTHANE

Small Animal/Exotics Compendium January 2000

Figure 3—Heart rate is 160 beats/min with ventricular premature complexes (arrows). These complexes are not followed by a
pause and are called interpolated; they do not disrupt the ventricular rhythm.

Figure 4—Ventricular trigeminy (two sinus beats followed by ventricular premature complexes [arrows] in a repetitive pattern).
The ventricular rate is 140 beats/min. The arrhythmia persisted for approximately 10 minutes.

arrhythmia. Although indirect blood pressure remained
satisfactory, lidocaine (2 mg/kg IV) was eventually ad-
ministered and was successful in restoring normal sinus
rhythm.
CASE 4
A healthy, 3-year-old, 32-kg rottweiler was presented
for ovariohysterectomy. Because of a history of potential
aggression, heavy sedation was accomplished with xy-
lazine (0.3 mg/kg IM), butorphanol (0.2 mg/kg IM),
and glycopyrrolate (0.015 mg/kg IM). An IV catheter
was placed with little physical restraint. A preinduction
ECG (not depicted) revealed sinus rhythm with an HR
of 140 beats/min. Induction with thiopental was about to
begin when an arrhythmia suddenly emerged (Figure 4).
In bigeminal or trigeminal rhythms, the interval be-
tween the sinus and ectopic beat is constant (fixed cou-
pling). This indicates that the sinus beat controls the
discharge of the ectopic focus by a reentry mechanism in
the myocardium.29
Noncardiac causes were considered in this normal,
healthy dog. Drugs administered to this dog that could
be implicated in the genesis of ventricular extrasystoles
include glycopyrrolate and xylazine. Dogs receiving gly-
copyrrolate, xylazine, and butorphanol exhibited de-
creases in cardiac index with ST segment depression,
pulsus alternans, and occasional VPCs.30
Xylazine either decreased 8,24 or did not alter the
ADE25 in anesthetized dogs, but differences in method-
ologies and end points may have accounted for dis-
agreement in the results. Dexmedetomidine, a highly
selective α2 agonist, inhibited the arrhythmogenic effect
of epinephrine in halothane-anesthetized dogs.31 Bilat-
eral vagotomy abolished this antiarrhythmogenic effect,
suggesting protection from parasympathetic tone.32
Parasympatholytics may induce autonomic imbal-
ance, resulting in extrasystoles. Atropine administration
in dogs resulted in a higher frequency of ectopic
rhythm disturbances than in control dogs that did not
receive atropine.15 However, in a recent study, choliner-
gic blockade increased the threshold to epinephrine-in-
duced arrhythmias in halothane- and isoflurane-anes-
thetized dogs.33
In this case, induction was delayed while the ECG,
which improved over several minutes, was observed.
Because the dog’s mucous membrane color, capillary re-
fill time, and pulses were good, induction was still
planned but thiopental was no longer considered be-
cause of its potential arrhythmogenicity. Diazepam
(0.3 mg/kg IV) followed by ketamine (2 mg/kg IV)
was administered, and intubation was easily accom-
plished. Normal sinus rhythm remained, and no fur-
ther arrhythmia was observed.
CASE 5
A 13-year-old cocker spaniel required anesthesia for
mammary tumor removal. A preoperative radiographic
evaluation for possible metastasis revealed no signifi-
cant abnormalities of the lung fields or cardiac silhou-
ette. The dog was premedicated with oxymorphone
(0.05 mg/kg IM), midazolam (0.2 mg/kg IM), and gly-
copyrrolate (0.015 mg/kg IM). Normal sinus rhythm
was noted immediately before induction with thiopen-
tal (10 mg/kg IV to effect). During endotracheal intu-

VENTRICULAR TRIGEMINY ■ XYLAZINE ■ PARASYMPATHOLYTICS

Compendium January 2000 Small Animal/Exotics

Figure 5A

Figure 5B

Figure 5C
Figure 5—(A) Ventricular premature complexes (VPCs; arrows) occur regularly following three sinus complexes. The ventricular
heart rate (HR) is 170 beats/min. (B) There are supraventricular complexes of either atrial or atrioventricular nodal origin (small
arrows) occurring in a bigeminal pattern; T waves preceding each supraventricular beat appear deeper, suggesting an additive neg-
ative P-wave effect. VPCs are also present (large arrows). (C) Immediately after intubation, the HR is 100 beats/min with no pre-
mature complexes.

bation, an arrhythmia was noted and recorded (Figures
5A and 5B). Immediately after intubation, normal si-
nus rhythm was restored (Figure 5C).
Supraventricular premature complexes originate in
atrial or AV nodal tissue.5 The P waves, if visible, should
differ slightly from the sinus P waves and can occur be-
fore, during, or after the QRS complex. The QRS com-
plex should usually have a similar conformation to that
associated with sinus beats. When AV nodal premature
beats are indistinguishable from those of atrial origin,
supraventricular is the appropriate terminology. Atrial
premature complexes are often associated with heart dis-
ease, although they can occur in normal dogs.5 In one
experimental study, atrial arrhythmias preceded ventric-
ular arrhythmias during epinephrine-induced sensitiza-
tion with halothane and isoflurane.21
The fact that the arrhythmia resolved immediately
after intubation argues strongly for laryngeal stimula-
tion as the precipitating cause. Stimulation of the lar-
ynx by laryngoscopy and intubation can cause tachy-
cardia, hypertension, and cardiac arrhythmias by an
absolute or relative increase in sympathetic tone. How-
ever, parasympathetic stimulation is also possible.1,4 Ec-
topic complexes resolved after the HR decreased (180
to 100 beats/min), which supports a mechanism of au-
tonomic imbalance from increased sympathetic stimu-
lation.
Hypoxia and hypercapnia can induce cardiac ar-
rhythmia indirectly by release of catecholamines or di-
rectly by depression of cardiac cells and stimulation of
the vasomotor centers of the brain.4 However, manual
ventilation was not required to restore the rhythm in
this case. If intubation had not been initially successful,
ceasing attempts at intubation would have been advis-
able. Delivery of oxygen via a face mask using high
oxygen flow rates before further attempts at intubation
may help avoid a more serious arrhythmia and its con-
sequences. After intubation, no further arrhythmia was
observed and surgery and recovery were uneventful.
CASE 6
A 10-month-old cat was administered tiletamine–zo-

SUPRAVENTRICULAR PREMATURE COMPLEXES ■ ATRIAL ARRHYTHMIAS ■ LARYNGEAL STIMULATION

Small Animal/Exotics Compendium January 2000

reflex or jaw tone, and the va-

porizer was turned off tem-
porarily. Because there was
no patent airway, the cat was
immediately intubated. Sinus
rhythm was restored with the
administration of one or two
Figure 6—The ventricular rate is 170 beats/min. In addition to sinus complexes, there are mul-
breaths. Surgery and recovery
tiform ventricular complexes with both right (1) and left (2) bundle branch block patterns.
Fusion beats (F) resemble both forms of ventricular premature complexes.
proceeded uneventfully.
Although the cat was nei-
ther apneic nor cyanotic, res-
lazepam (4 mg/kg IM), intubated, and maintained with piration was assumed to be inadequate because the ar-
halothane for ovariohysterectomy. Approximately 30 rhythmia disappeared immediately after intubation. If an
minutes later, during surgery, abnormal complexes were ECG had not been eventually monitored, change in
noted on the ECG (Figure 6). management may have been unlikely. Rapidly occurring
Fusion beats are the result of simultaneous activation multiform VPCs may lead to ventricular tachycardia and
of the ventricle by impulses from the SA node and ven- fibrillation.5 This case demonstrates the importance of
29
tricular ectopic foci. The QRS is intermediate in form adequate oxygenation, supportive care, and monitoring.
between the sinus and ectopic QRS. Ventricular ectopic
beats were not noted until the viscera was manipulated. CASE 8
Catecholamine release from painful stimuli, especially A 10-year-old Labrador retriever with upper airway
in the presence of halothane, can result in ventricular stridor was to be anesthetized for possible laryngoplasty.
arrhythmias.4,34 Palpebral reflex and jaw tone suggested After premedication with butorphanol and diazepam,
a light plane of anesthesia. Attempts were made to in- the ECG was monitored in preparation for induction.
crease the anesthetic plane by increasing ventilation and An irregular rhythm with abnormal complexes was
vaporizer concentration. Because isoflurane was readily recorded (Figure 8). The surgeon’s concern that heart
available, halothane was discontinued. The rhythm was disease was present prompted cancellation of surgery
quickly restored with no further abnormalities. Discon- until cardiac evaluation was completed.
tinuation of halothane may not have been necessary— Right bundle branch block (RBBB) is a delay or in-
increasing halothane concentration has been shown to terruption of conduction through the right bundle
result in resolution of ventricular arrhythmias.34 branch. Normally, the right ventricle is activated by an
Tiletamine–zolazepam is an unlikely factor in the gen- impulse that passes from the bundle of His to the right
esis of this arrhythmia. It did not affect ADE in cats bundle branch. With RBBB, the right ventricle is acti-
anesthetized with halothane.35 vated by an impulse that passes from the left bundle
branches to the right side of the septum below the
CASE 7 block, with delay causing the QRS to be wide and
A 1-year-old domestic shorthair cat was given tile- bizarre.36 In this case, P-P intervals become progressive-
tamine–zolazepam (4 mg/kg ly shorter and P-R intervals
IM) for castration and ony- remain the same. The AV
chectomy. Because the anes- impulse enters the conduct-
thetic depth was judged to ing system before the right
be inadequate, halothane was bundle branch has a chance
administered by face mask. to repolarize, thereby pro-
During surgery, an abnormal ducing aberrant conduction.
rhythm was noted on the ul- This pattern persisted through-
trasonic Doppler flow detec- out the ECG.
tor, which was recording pulse Figure 7—In a repetitive pattern, triplets of multiform ven- Criteria of complete RBBB
rhythm at the metatarsal ar- tricular premature complexes (large arrows) can be seen fol- includes a QRS complex
tery. An ECG was recorded lowing two possible sinus complexes. However, the second longer than 0.08 seconds; a
(Figure 7). “sinus beat” (small arrow) may be an atrial premature com- right axis deviation; and
Vital signs and anesthetic plex because, compared with the previous sinus beat, the P deep S waves in leads I, II,
depth were quickly evaluat- wave is smaller and there is no S wave on the subsequent III, and aVF. RBBB can be
QRS complex.
ed. There was no palpebral associated with heart disease

FUSION BEATS ■ CATECHOLAMINE RELEASE ■ OXYGENATION

Small Animal/Exotics Compendium January 2000

ing an AV junctional or ventricular focus to

Figure 8—Intermittent right bundle branch block (RBBB). QRS duration is
0.12 seconds with deep S waves (arrows). This is an example of phasic aber- healthy cat during inhalation anesthesia.
rant conduction taking the usual form of rate-dependent RBBB. The R-R in-
tervals preceding the RBBB become progressively shorter until RBBB occurs. discharge by direct and indirect effects on
A marked sinus (vagal) arrhythmia is also evident. The ventricular rate is 80 to SA node automaticity.40 In addition, isoflu-
100 beats/min.
but also can occur in normal, healthy dogs or as an in-
cidental finding in dogs with noncardiac diseases.36
RBBB alone does not require treatment, produces no
hemodynamic problems, and should not present a con-
cern for anesthesia. It is important not to confuse
RBBB with VPCs; the former can be distinguished by
preceding consistent P-R intervals.
An echocardiogram demonstrated normal cardiac di-
mensions and function. Anesthesia and surgery pro-
ceeded without complication.
CASE 9
A 6-year-old cat was diagnosed with leukocytopenia
of undetermined cause. An echocardiogram revealed no
significant findings. Months later, the cat was presented
for an ovariohysterectomy and follow-up bone-marrow
biopsy. There were no significant findings on physical or
hematologic examination. Ketamine (5 mg/kg), butor-
phanol (0.2 mg/kg), and midazolam (0.1 mg/kg ) were
administered IM and produced adequate sedation. A
preinduction ECG was not recorded. Thiopental was
administered IV to effect for intubation, and anesthesia
was maintained with isoflurane. An ECG was recorded
during surgical preparation (Figure 9A).
A pararrhythmia is an abnormal rhythm in which
two pacemakers discharge independently of each other,
and each can activate the ventricle at different times.38
AV dissociation is one example in which the dominant
pacemaker (AV junction or ventricle) controls ventricu-
lar activation and another pacemaker (SA node or atri-
al) controls the atria. Incomplete AV dissociation oc-
curs if an impulse from the SA node conducts to the
ventricle, producing a ventricular capture beat. This oc-
curs after every second or third QRS complex (Figure
9A). AV dissociation is a sign of a primary disturbance
and is not an ECG rhythm diagnosis. This disturbance
can result from depressed SA node automaticity allow-
take over, increased AV junctional or ven-
tricular automaticity, disturbed AV conduc-
tion, or a combination of mechanisms.37
Decreased SA node automaticity and an ac-
celerated ventricular rhythm may be the
mechanisms involved in this case. Although
AV dissociation may be associated with
heart disease, it has been reported in a
39
Isoflurane slows the rate of SA pacemaker
rane at increased concentrations lengthens
AV nodal conduction time. The depressant
effects of anesthetics on AV nodal conduc-
tion with depression of sinus nodal automaticity could
favor an occurrence of AV dissociation.40
AV dissociation resulting from accelerated junc-
tional rhythms can be caused by sympathetic stimula-
tion of AV nodal pacemaker cells or parasympathetic
overriding of the sympathetic nervous system as a re-
sult of autonomic imbalance. These arrhythmias have
been successfully treated with propranolol41 and at-
ropine.42 Atropine was administered in the cat in this
case because of the low HR and marginally low sys-
tolic pressures. Although atropine increased HR to
only 100 beats/min, sinus rhythm was restored (Fig-
ure 9C).
CASE 10
A 6-year-old Brittany spaniel was admitted for surgery
1 day after being hit by a car. The dog, which had an
open fracture of the radius and ulna, was bright and alert.
Radiographs of the thorax revealed mild changes consis-
tent with heartworm disease; there were no significant
findings on abdominal films. Minimal laboratory data,
consisting of packed cell volume, total protein, blood urea
nitrogen, and glucose estimation, were within reference
ranges.43
The following day, surgery was scheduled for internal
fixation of the radius and ulna. The dog was premedi-
cated with acepromazine (0.05 mg/kg IM) and oxy-
morphone (0.05 mg/kg IM). A preinduction ECG was
normal (not depicted). Anesthesia was induced with
thiopental and maintained with isoflurane. Forty-five
minutes after surgery began, bradycardia with first- and
second-degree AV block (not depicted) was noted. HR
and indirect blood pressure began to drop quickly over
10 minutes. P waves were no longer recognized (Figure
10A). Atropine (0.02 mg/kg IV) was administered,
producing electrocardiographic changes (Figure 10B).
Blood was collected for electrolyte, chemistry, pH, and

RIGHT BUNDLE BRANCH BLOCK ■ ATRIOVENTRICULAR DISSOCIATION ■ ISOFLURANE

Compendium January 2000 Small Animal/Exotics

blood gas determinations.

Chemistry results that were
not within reference ranges43
included potassium (9.89
mEq/L), blood urea nitro-
gen (90 mg/dL), creatinine
(3.9 mg/dL), and albumin
(1.4 g/dL). Blood gas re- Figure 9A
sults using lingual venous
blood were also out of ref-
erence range43 and indicat-
ed a respiratory and meta-
bolic acidosis (pH, 7.14;
partial pressure of carbon
dioxide, 66 mm Hg; par-
tial pressure of oxygen, 450 Figure 9B
mm Hg; bicarbonate, 23
mEq/L; base deficit, 8.3
mEq/L).
Regular insulin (20 units)
and 5% dextrose were add-
ed to normal saline and ad-
ministered at a rate of 20
ml/kg IV. Sodium bicar-
bonate (0.5 mEq/L IV) was
administered slowly. Twen- Figure 9C
ty minutes after the treat- Figure 9—(A) The ventricular rate is 100 beats/min. The dominant rhythm occurs regularly at
ment, P waves were notice- 80 beats/min, with abnormal QRS morphology suggesting a ventricular origin. P waves (arrows),
able and a normal ECG was although not clearly visible, may be present and are dissociated from the dominant rhythm. Oth-
restored 30 minutes there- er leads might better delineate their presence. A P wave is also barely visible (arrow) in the T
after (not depicted). waves preceding the capture beats (C). Capture beats are sinus impulses that occasionally capture
Loss of P-wave morphol- the ventricles, making this a type of incomplete atrioventricular dissociation.37 (B) After atropine
ogy with spiked T waves is (0.02 mg/kg IV) is administered, P waves are more clearly evident—demonstrating their occur-
highly suggestive of hyper- rence before, within, and after the QRS. The ventricular rate is 80 beats/min, and another cap-
ture beat can be seen after the fourth complex. (C) After atropine is readministered, the ventricu-
kalemia. 44,45 The resting lar rate increases to only 100 beats/min but sinus rhythm is restored.
membrane potential (RMP)
of cardiac muscle depends
on a normal ratio of extracellular:intracellular potassium that the SA node continues to discharge and impulses are
concentration.44 During hyperkalemia, the RMP is raised transmitted to the AV node, and thereby to the ventri-
(becomes less negative). Fewer sodium channels are open, cles, by specialized internodal conducting pathways. The
and thus depolarization to threshold potential (TP) is re- atria are not activated, and thus no P wave is recorded.45
duced. The action potential duration is shortened, and This is termed sinoventricular conduction.
the rate of repolarization increases. The earliest manifes- Insulin administration with glucose will result in
tations of hyperkalemia on the ECG are peaked, narrow- movement of potassium into the cells. Sodium bicar-
based T waves. The RMP decreases with further increas- bonate also induces an intracellular potassium shift.
es in potassium concentration, which in turn slows Calcium can be administered in severe cases to restore a
intraventricular conduction and increases the duration of normal gradient of RMP to TP and to increase myocar-
the QRS complex. Automaticity, conductivity, contrac- dial conduction and contractility.46
45
tility, and excitability are decreased. The fracture in this patient was quickly repaired. A
Various cardiac cells have a differential sensitivity to ruptured bladder was suspected and confirmed by ultra-
rising extracellular potassium. Purkinje fibers and my- sound. Potassium enters the abdominal cavity from a rup-
ocardial cells are the most sensitive, atrial cells more so tured bladder and is reabsorbed, causing serum potassium
than ventricular.44,45 Experimental studies have shown to increase. A celiotomy was performed, and approxi-

HYPERKALEMIA ■ RESTING MEMBRANE POTENTIAL ■ THRESHOLD POTENTIAL

Small Animal/Exotics Compendium January 2000

mately 1 L of fluid was suc-

tioned from the abdomen. A
3-cm rent was observed in the
bladder and repaired. Serum
potassium was 6.1 mmol/L at
the completion of surgery, and
recovery occurred with support-
ive care without further com- Figure 10A
plications.
A ruptured bladder was not
expected either at the time of
admission or on the day of
surgery because of the dog’s
bright attitude and lack of ra-
diographic and clinical signs.
More complete hematologic
and biochemical evaluation
may have induced suspicion
of a ruptured bladder. The Figure 10B
relatively high fluid rate of 10 Figure 10—(A) The ventricular rate of 50 to 60 beats/min with absence of P waves suggests ei-
ml/kg/hour during anesthesia ther sinoventricular conduction or a junctional rhythm. The QRS morphology is abnormal,
most likely produced rapid which could be the result of aberrant conduction from increased serum potassium. T waves
urine production and bladder are more than half the size of the R wave. (B) Because of the sudden development of brady-
distention to maintain paten- cardia, atropine is administered, after which the complexes are more aberrant, particularly at
cy of the tear in the bladder. the faster rates (i.e., S waves are deeper and wider [arrows] ); this may be caused by rate-de-
pendent aberrant conduction in addition to that caused by the increased serum potassium.
Atropine was administered for
the sudden bradycardia but
produced a more aberrant cardiac rhythm. and dogs. JAVMA 185(6):643–646, 1984.
5. Tilley LP: Analysis of common canine cardiac arrhythmias,
SUMMARY in Tilley LP (ed): Essentials of Canine and Feline Electrocar-
It is hoped that these cases demonstrate the impor- diography Interpretation and Treatment. Philadelphia, Lea &
Febiger, 1992, pp 127–207.
tance of ECG monitoring in anesthetized patients. Al- 6. Bolton GR: Bradycardia, in Kirk RW (ed): Current Veteri-
though it is not a substitute for simple clinical assess- nary Therapy VII. Small Animal Practice. Philadelphia, WB
ments of pulse quality, mucous membrane color, and Saunders Co, 1980, pp 376–380.
respiration, ECG monitoring provides important infor- 7. Branch CE, Robertson BT, Williams JC: Frequency of sec-
ond-degree atrioventricular heart block in dogs. JAVMA 36:
mation not available by any other means. Most of the 925–929, 1975.
arrhythmias described in this article did not require spe- 8. Muir WW, Werner LL, Hamlin RJ: Effects of xylazine and
cific treatment, but some required alteration in manage- acetylpromazine upon induced ventricular fibrillation in
ment that may have prevented serious consequences. dogs anesthetized with thiamylal and halothane. Am J Vet
Res 36(9):1299–1303, 1975.
9. Cornick JL, Hartsfield SM: Cardiopulmonary and behav-
ACKNOWLEDGMENT ioral effects of combinations of acepromazine/butorphanol
The authors thank Mr. Tom Thompson for his pho- and acepromazine/oxymorphone in dogs. JAVMA 200(12):
tographic assistance. 1952–1956, 1992.
10. Trim CM: Cardiopulmonary effects of butorphanol tartrate
in dogs. Am J Vet Res 44(2):329–331, 1983.
REFERENCES 11. Muir WW: Anesthetics and techniques, in Slatter D (ed):
1. Katz RL, Bigger JT: Cardiac arrhythmias during anesthesia
Textbook of Small Animal Surgery. Philadelphia, WB Saun-
and operation. Anesthesiology 23(2):193–213, 1970.
2. Atlee JL: Perioperative cardiac dysrhythmias: Diagnosis and ders Co, 1993, pp 2245–2250.
management. Anesthesiology 86(6):1397–1424, 1997. 12. Brock N: Acepromazine revisited. Can Vet J 35:458–459,
3. Cohen RB, Tilley LP: Cardiac arrhythmias in the anes- 1994.
thetized patient. Vet Clin North Am Small Anim Pract 9(1): 13. Dodman NH, Court MH: Questions about ECG interpre-
155–162, 1979. tations. JAVMA 197(2):169–170, 1990.
4. Hubbell JAE, Muir WW, Bednarski RM, Bednarski LS: 14. Reves JG, Fragen RJ, Vinik RH, Greenblatt DJ: Midazolam:
Change of inhalation anesthetic agents for management of Pharmacology and uses. Anesthesiology 62(3):310–324, 1985.
ventricular premature depolarizations in anesthetized cats 15. Muir WW: Effects of atropine on cardiac rate and rhythm in

SINOVENTRICULAR CONDUCTION ■ RUPTURED BLADDER

Compendium January 2000
dogs. JAVMA 172(1):917–921, 1978.
16. Kantelip JP, Alatienne M, Gueorguiev G, Duchene-Marul-
laz P: Chronotropic and dromotropic effects of atropine and
hyoscine methobromide in unanesthetized dogs. Br J
Anaesth 57:214–219, 1985.
17. Rishniw M, Tobias AH, Slinker BK: Characterization of
chronotropic and dysrhythmogenic effects of atropine in
dogs with bradycardia. Am J Vet Res 57(3):337–341, 1996.
18. Maze M, Smith CM: Identification of receptor mechanism
mediating epinephrine-induced arrhythmias during halo-
thane anesthesia in the dog. Anesthesiology 59(4):322–326,
1983.
19. Lemke KA, Tranquilli WJ: Anesthetics, arrhythmias, and
myocardial sensitization to epinephrine. JAVMA 205(12):
1679–1684, 1994.
20. Bednarski RM, Majors LJ, Atlee JL: Epinephrine-induced
ventricular arrhythmias in dogs anesthetized with halothane:
Potentiation by thiamylal and thiopental. Am J Vet Res
46(9):1829–1832, 1985.
21. Atlee JL, Malkinson CE: Potentiation by thiopental of
halothane-epinephrine-induced arrhythmias in dogs. Anes-
thesiology 57(4):285–288, 1982.
22. Kamibayashi T, Hayashi Y, Sumikawa K, et al: Enhance-
ment by propofol of epinephrine-induced arrhythmia in
dogs. Anesthesiology 75(6):1035–1040, 1991.
23. Zink J, Sasyniuk BI, Dresel PE: Halothane-epinephrine-in-
duced cardiac arrhythmias and the role of heart rate. Anes-
thesiology 43(5):548–555, 1975.
24. Tranquilli WJ, Thurmon JC, Benson GJ: Alterations in
epinephrine-induced arrhythmogenesis after xylazine and
subsequent yohimbine administration in isoflurane-anes-
thetized dogs. Am J Vet Res 49(7):1072–1074, 1988.
25. Lemke KA, Tranquilli WJ, Thurmon JC, et al: Alterations
in the arrhythmogenic dose of epinephrine after xylazine or
medetomidine administration in isoflurane-anesthetized
dogs. Am J Vet Res 54(12):2139–2144, 1993.
26. Bednarski RM, Sams RA, Majors LJ, Ashcraft S: Reduction
of the ventricular arrhythmogenic dose of epinephrine by
ketamine administration in halothane-anesthetized cats. Am
J Vet Res 49(3):350–354, 1988.
27. Bednarski RM, Majors LJ: Ketamine and the arrhythmo-
genic dose of epinephrine in cats anesthetized with halo-
thane and isoflurane. Am J Vet Res 47(10):2122–2126, 1986.
28. Hayashi Y, Sumikawa K, Yamatodani A, et al: Myocardial
epinephrine sensitization with subanesthetic concentrations
of halothane in dogs. Anesthesiology 74(1):134–137, 1991.
29. Goldman MJ: The ventricular arrhythmias, in Goldman MJ
(ed): Principles of Clinical Electrocardiology. Los Altos, CA,
Lang Medical Publications, 1986, pp 260–277.
30. Jacobson JD, McGrath CJ, Ko JCH, Smith EP: Cardiore-
spiratory effects of glycopyrrolate-butorphanol-xylazine com-
bination with and without nasal administration of oxygen in
dogs. Am J Vet Res 55(6):835–841, 1994.
31. Hayashi Y, Sumikawa K, Maze M, et al: Dexmedetomidine
prevents epinephrine-induced arrhythmias through stimula-
tion of central α2 adrenoceptors in halothane-anesthetized
dogs. Anesthesiology 75(1):113–117, 1991.
32. Kamibayashi T, Hayashi Y, Sumikawa K, et al: A role of va-
gus nerve in antiarrhythmic effects of doxazosin and
dexmedetomidine on halothane-epinephrine arrhythmias.
Anesthesiology 77(3A):A642, 1992.
33. Lemke KA, Tranquilli WJ, Thurmon JC, et al: Influence of
cholinergic blockade on the development of epinephrine-in-
Small Animal/Exotics
duced ventricular arrhythmias in halothane and isoflurane
anesthetized dogs. Vet Surg 23:61–66, 1994.
34. Muir WW, Hubbell JAE, Flaherty S: Increasing halothane
concentration abolishes anesthesia-associated arrhythmias in
cats and dogs. JAVMA 192(12):1730–1736, 1988.
35. Bednarski RM, Muir WW: Ventricular arrhythmogenic
dose of epinephrine in dogs and cats anesthetized with tile-
tamine/zolazepam and halothane. Am J Vet Res 51(9):1468–
1470, 1990.
36. Tilley LP: Analysis of P-QRS-T deflections, in Tilley LP
(ed): Essentials of Canine and Feline Electrocardiography Inter-
pretation and Treatment. Philadelphia, Lea & Febiger, 1992,
pp 59–123.
37. Tilley LP: Interpretation of complex arrhythmias, in Tilley
LP (ed): Essentials of Canine and Feline Electrocardiography
Interpretation and Treatment. Philidelphia, Lea & Febiger,
1992, pp 385–416.
38. Goldman MJ: The pararrhythmias, in Goldman MJ (ed):
Principles of Clinical Electrocardiology. Los Altos, CA, Lang
Medical Publications, 1986, pp 271–281.
39. Gaynor JS, Mason DE: ECG of the month. JAVMA 199
(11):1574–1575, 1991.
40. Atlee JL, Brownlee SW, Burstrom RE: Conscious-state com-
parisons of the effects of inhalation anesthetics on specialized
atrioventricular conduction times in dogs. Anesthesiology
64(6):703–710, 1986.
41. Breslow MJ, Evers AS, Lebowitz P: Successful treatment of
accelerated junctional rhythm with propranolol: Possible
role of sympathetic stimulation in the genesis of this rhythm
disturbance. Anesthesiology 62(2):180–182, 1985.
42. de Leon-Casasola OA, Lema MJ: Atrioventricular dissocia-
tion resulting from combined thoracic epidural and general
anesthesia. Acta Anaesthesiol Scand 36:165–169, 1992.
43. DiBartola SP, Autran de Morais HS: Appendix, in DiBarto-
la SP (ed): Fluid Therapy in Small Animal Practice. Philadel-
phia, WB Saunders Co, 1992, pp 599–688.
44. Rardon DP, Fisch C: Electrolytes and the heart, in Hurst JW,
Schlant RC, Rackley CE, et al (eds): The Heart Arteries and
Veins. New York, McGraw-Hill Inc, 1990, pp 1557– 1570.
45. Goldman MJ: Miscellaneous abnormal electrocardiographic
patterns, in Goldman MJ (ed): Principles of Clinical Electro-
cardiology. Los Altos, CA, Lang Medical Publications, 1986,
pp 297–322.
46. Senior DF: Fluid therapy, electrolytes and acid base control,
in Ettinger SJ (ed): Textbook of Veterinary Internal Medicine.
Philadelphia, WB Saunders Co, 1989, pp 429–449.
About the Authors
At the time this article was submitted for publication, Dr.
Kushner was affiliated with the Animal Health Center,
Mississippi State University, Mississippi State, Mississip-
pi. Dr. Kushner is currently affiliated with the Veterinary
Hospital of the University of Pennsylvania, Philadelphia,
Pennsylvania; she is a Diplomate of the American Col-
lege of Veterinary Anesthesiologists. Dr. Calvert is affiliat-
ed with the Department of Small Animal Medicine, Col-
lege of Veterinary Medicine, University of Georgia, Athens,
Georgia; he is a Diplomate of the American College of
Veterinary Internal Medicine.