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Israel Journal of Veterinary Medicine  Vol. 70 (3)  September 2015 Oron, L. 58
Transient Atrioventricular Block Associated with Acute Pancreatitis
in a Japanese Chin Dog
Oron, L., Ohad, D., Kelmer, E., Dahan, Y. and Bruchim, Y.
Veterinary Teaching Hospital, Koret School of Veterinary Medicine, Robert H. Smith Faculty of Agriculture, Food and
Environment, Te Hebrew University of Jerusalem, P.O. Box 12, Rehovot, 76100, Israel.
*
Corresponding Author: Dr. Liron Oron, DVM, Small Animal Emergency and Critical Care, School of Veterinary Medicine, Te Hebrew University of
Jerusalem, P.O. Box 12, Rehovot 76100, Israel. Tel: 972-3-9688588, Fax: 972-3-9604079. Email: dr.liron.oron@gmail.com
ABSTRACT
Electrocardiographic changes (ECG) are a common complication of acute pancreatitis (AP), although their
etiology and pathogenesis remain unclear. Commonly reported electrocardiographic changes in human
beings with AP include non-specifc changes of the ventricular repolarisation process, and various kinds of
conduction and/or rhythm anomalies. Te association between AP and ECG abnormalities has not been
investigated in the veterinary literature. We report a case of a previously healthy Japanese Chin dog with
acute pancreatitis demonstrating severe bradycardia, ST-segment depression, atrial standstill, 2
nd
and then 3
rd
degree atrioventricular block, all of which were resolved once the pancreatitis ameliorated. We conclude that
due to the transient nature of such ECG fndings in patients with AP, as long as haemodynamics remain or
can be maintained stable, decisions regarding permanent pacemaker therapy or euthanasia should be made
with caution.
Keywords: Atrial standstill; Atrioventricular block; Bradycardia; Canine; ECG; Pancreatitis.
INTRODUCTION
Acute pancreatitis (AP) is an acute infammatory process of
the pancreas associated with local and systemic manifesta-
tions (1). Te clinical course of pancreatitis varies between
patients from mild clinical signs such as vomiting and
abdominal discomfort to severe fulminating sequels such
as systemic infammatory response syndrome (SIRS) and
multiple organ dysfunction syndrome (MODS) (1, 2).
Systemic complications of AP include acute kidney injury
(AKI), coagulopathy, acute respiratory distress syndrome and
cardiac arrhythmia (1).
Tachyarrhythmia (such as supraventricular premature
complexes, atrial futter or atrial fbrillation) bradyarrhythmia,
and bundle branch block, have all been associated with AP
in human beings (2). Although veterinary textbooks mention
arrhythmia as a potential sequel of pancreatitis (1), to the
best of the authors’ knowledge the veterinary literature lacks
clinical case reports that describe this phenomenon.
Te present report describes the clinical course of a 7 year
old intact female Japanese Chin dog with AP, complicated
by AKI and multiple electrocardiographic (ECG) changes,
including bradyarrhythmia, ST-segment depression, atrial
standstill, and atrio-ventricular (AV) block, all of which
resolved once pancreatitis ameliorated.
CASE SUMMARY
A 7 year old intact female Japanese Chin dog was referred
to a Koret School of Veterinary Medicine university teach-
ing hospital emergency department with chief complaints
of vomiting, anorexia, weakness and depression of 3 days
duration. Te dog was treated by the referring veterinarian
Case Reports
Israel Journal of Veterinary Medicine  Vol. 70 (3)  September 2015 59 Atrioventricular block and Acute Pancreatitis
with intravenous (IV) fuids and broad-spectrum antibiotics,
with no signifcant improvement over the following two days.
Physical examination at presentation revealed hypother-
mia with a rectal temperature of 36.4°C, a normal respiratory
rate of 20 breaths/minute, normal mucous membrane color
with a prompt capillary refll time, and a normal heart rate
(HR) of 100 beats/minute) (BPM) with an auscultated ar-
rhythmia. Te dog was in good body condition (BCS=4 / 9,
body weight = 5.2 kg), estimated to be 6% dehydrated, not
ambulatory and depressed. Pain and discomfort were noted
upon cranial abdominal palpation.
A complete blood count (CBC) showed mild leukocytosis
(22.0 x 10
3
/µL, Reference interval (RI): 8.0-17.0), with a
mild mature neutrophilia (19.0 x 10
3
/µL, RI: 3.6-13.1)
and hemoconcentration (Hematocrit 60.8%, RI: 37.0-55.0;
RBC 9.4 x 10
6
/µL, RI: 5.0-8.1). No toxic changes of the
neutrophils were noted on a direct blood smear microscopic
examination.
A complete serum biochemical panel taken by the refer-
ring veterinarian a day before admission revealed elevations
in albumin and total protein (4.7 g/dl, RI: 2.3-4.5, and 8.5
g/dl, RI: 4.9-7.2, respectively), elevated alanine transaminase
(ALT, 124 U/L, RI: 6-70), aspartate transaminase (AST, 65
U/L, RI: 10-43), creatinine (2.3 mg/dl, RI: 0.5-1.5) and urea
(201.7 mg/dL, RI 10-60). Electrolyte abnormalities included
hypocalcemia (7.9 mg/dL, RI: 9.1-11.7), hyperkalemia (6.6
mmol/L, RI: 3.5-5.4) and hyperphosphatemia (10.6 mg/
dL, RI: 2.3-6.4). Sodium and chloride levels were normal
(149 mmol/L, RI: 139-150 and 102 mmol/L, RI: 97-120,
respectively). Sodium to potassium (Na : K) ratio was low
at 22.
On presentation, creatinine was further elevated at 2.5
mg/dl and the hyperkalemia began to resolve with a potas-
sium of 5.5 mmol/L. Sodium and chloride concentrations
decreased (133 and 96 mmol/L, respectively). Urinalysis
showed isosthenuria with hyaline and granular casts, indicat-
ing renal tubular damage, attributed to AKI. Based on the
low Na:K ratio an ACTH stimulation test was performed
to rule out hypoadrenocorticisim (Base cortisol - 11.6 µg/
dL, RR:1.3-7.2).
Abdominal ultrasound revealed a corrugated and thick-
ened duodenal wall and a hypo-echoic pancreas, both of
which were strongly suggestive of AP. No chronic structural
changes were demonstrated in the kidneys and there was no
evidence of free abdominal fuid. Te ultrasonographic fnd-
ings, combined with the clinical history, physical examination
and blood work abnormalities, were indicative of primary AP,
with AKI suspected to be a secondary complication.
Te dog was treated with an IV bolus of 20 ml/kg
Lactate Ringers Solution (LRS) (Teva Medical, Ashdod,
Israel), followed by 5ml/kg/hr, metoclopramide (Pramin,
Rafa laboratories, Jerusalem, Israel, 1mg/kg/day, for 4 days),
an H2 blocker (Famotidine, West-Ward, United states, New
Jersey, 1 mg/kg, IV, q24h), ampicillin (Penibrin, Sandoz,
Pyrmont, Australia, 20mg/kg, IV, q12h) and buprenorphine
(Siegfried, Switzerland) 0.01 mg/kg, IV, q6h). Due to its low
body temperature the patient was warmed with a blower.
Vital signs, semi-quantitative urine output, body weight,
indirect blood pressure and ECG were all monitored.
Eight hours after admission, breathing rate increased
to 60 breath/minute along with a decreased HR of 35-40
BPM. A Lead-II ECG rhythm strip performed over 120
consecutive seconds in right lateral recumbency at 25 mm/s
and 10mm/mV, with no fltering (Nihon Kohden, Cardiofax
GEMECG-9029K, Japan), revealed a slow, irregular rhythm
lacking P waves, with ST-segment depression (0.3 millivolts)
as well as T-wave inversion (discordant to the dominant
R-wave of the QRS complex) (Figure 1). Tese fndings were
compatible with atrial standstill along with a junctional es-
cape rhythm. However, as many of the pauses were recorded
Figure 1: An ECG rhythm strip (Lead II, 25 mm/sec, 10 mm/mV.) of
a 7-year-old female Japanese Chin dog presented for AP, recorded on
day 1. Note the irregular heart rhythm with a heart rate of 72 BPM,
the absence of P waves, an ST-segment depression (0.3 millivolts)
(black arrows), and T-waves (arrowheads) of two separate amplitudes
(labeled A and B).
Case Reports
Israel Journal of Veterinary Medicine  Vol. 70 (3)  September 2015 Oron, L. 60
to be as long as an exact multiplication (x2) of the R-to-R
interval, a sino-atrial block could not be ruled out.
Furosemide (Fusid, Alfasan, Woerden, Te Netherlands, 2
mg/kg, IV, once) was empirically administrated to relieve pul-
monary edema, suspected based on the documented tachy-
pnea, and oxygen was administered via a mask. Immediately
following atropine sulphate administration (Atropine, Teva
pharmaceuticals, Israel, Petach Tikva, 0.02 mg/kg, IV, once)
a repeated ECG rhythm strip showed occasional re-initiation
of P waves followed by QRS complexes with a persistent PR
interval. However, the only occassional repetitive PR-interval
may have been incidental and these complexes were noncon-
secutive and were therefore not necessarily consistent with
capture beats. Also, in this strip, some of the T waves were
deeper than others in peak amplitude, potentially suggestive
of more than a single escape focus (Figure 2).
Over the next day the dog improved clinically, vomiting
ceased and body temperature and breathing rate normalized.
Repeat creatinine, potassium, sodium and ionic calcium all
measured within normal RI’s. Electrocardiography, how-
ever, demonstrated the same pattern of bradycardia and ST-
segment depression with occasional non-conducted P waves.
In this strip (Figure 3), couplets with a fxed coupling interval
appeared with the second complex demonstrating a deeper
T-wave peak, similarly suggestive of two separate foci. Within
each pair, the second complex appeared to be an “echo beat”
compatible with re-entry as the underlying electrophysiological
mechanism (3). Tree of these couplets involved a constant
PR interval, which may attest to a fusion process, where two
separate depolarization fronts propagated simultaneously from
two (a ventricular and a sino-atrial) foci, and collided to gener-
ate a “merged” QRS complex morphology (Figure 3).
At this point treatment with atropine (0.02mg/kg IV
q6h) was restarted. On the next day (day 3), the dog had re-
gained its appetite. It was still bradycardic at 30 BPM, and a
3
rd
degree atrioventricular block with ventricular escape beats
of the deeper T-wave amplitude were recorded (Figure 4).
On day 4, HR was 33 BPM. Electrocardiography revealed
a low grade, 2
nd
degree, Mobitz Type II, atrioventricular block
(Figure 5) with ventricular escape beats of the deeper-T wave
morphology. To increase the sympathetic tone, beta adren-
ergic agonists, terbutaline (Terbutaline sulphate, Vitamed,
Binyamina, Israel, 0.2 mg/kg, PO, q8hr), and isoproterenol
(Isoprenalina cloridato, Monico spa, Italy, Venezia, 0.4 mg in
250 mL d5W, SIV), and theophylline, a phosphodiesterase
inhibitor (Teotrim, Trima, Kibbutz Maabarot, Israel, 6
mg/kg, PO, q12h) were added to the treatment regimen.
Twelve hours later the dog had a grand mal seizure which
was controlled by an IV bolus of diazepam (Assival, Teva
pharmaceuticals, Petach Tikva, Israel, 2.5 mg, IV). Treatment
Figure 2: An ECG rhythm strip (Lead II, 25 mm/sec, 10 mm/mV.)
of a 7-year-old female Japanese Chin dog presented for AP, recorded
on day 1, following intravenous administration of atropine (0.02 mg/
kg). Note the occasional re-initiation of P waves followed by QRS
complexes with only occassional repeated PR interval (black arrows)
and deepening of some of the T waves (arrowheads), compatible with
the morphology labeled B in Figure 1 (see text for details).
Figure 3: An ECG rhythm strip (Lead II, 25 mm/sec, 10 mm/mV.) of a
7-year-old female Japanese Chin dog presented for AP, recorded on day
2. Note the initiations of couplets with a fxed coupling interval (three of
which are underlined by horizontal brackets). Te second complex in each
such couple demonstrates a relatively deeper T-wave peak, compatible
with the morphology labeled B in Figure 1 (see text for details).
Case Reports
Israel Journal of Veterinary Medicine  Vol. 70 (3)  September 2015 61 Atrioventricular block and Acute Pancreatitis
with isoproterenol and theophylline was discontinued and
the dog was discharged with only oral terbutaline for 3 more
days.
Upon follow-up examination on day 7, the owner re-
ported that the dog has made a complete recovery. Pulse
rate had increased to 80 BPM and an ECG rhythm strip
revealed normal sinus arrhythmia, with a single non-con-
ducted P-wave and no ST-segment depression (Figure 6).
Unfortunately, repeated ultrasound or blood-work was not al-
lowed. A repeated ECG a month later was similarly normal.
DISCUSSION
Pancreatitis is an infammation of the pancreas which is
commonly associated with severe systemic complications
(1). Te exact prevalence in dogs is unknown but the condi-
tion is considered relatively common (1). Although several
etiologies have been suggested, including dietary changes,
a fat-rich diet, obesity, use of drugs such as potassium bro-
mide, L-asparginase, tetracycline and azathioprine, surgical
manipulation, or blunt abdominal trauma and shock, in most
cases the etiology remains unknown (1, 4).
Acute pancreatitis develops as a result of premature acti-
vation of zymogens, which leads to auto-digestion, resulting
in stimulation of an infammatory reaction. Most dogs with
AP present with weakness, vomiting, depression, abdominal
pain and diarrhea (5). Systemic manifestation such as shock,
dehydration, jaundice, respiratory distress, bleeding disorders
and cardiac arrhythmia are also seen in the more severe cases
(1).
Diagnosis of AP in dogs is challenging due to a low
sensitivity and specifcity of the available diagnostic tests (1,
Figure 4: An ECG rhythm strip (Lead II, 25 mm/sec, 10 mm/
mV.) of a 7-year-old female Japanese Chin dog presented for AP,
recorded on day 3, following intravenous atropine (0.02 mg/kg)
administration. Note the isolated, generally evenly-spaced P-waves
(often superimposed on the descending limb, peak, or ofset of the
T-wave) with no constant PR-interval, consistent with a 3
rd
degree
atrioventricular block with escape beats (arrowheads).
Figure 5: An ECG rhythm strip (Lead II, 25 mm/sec, 10 mm/mV.)
of a 7-year-old female Japanese Chin dog presented for AP, recorded
on day 4. Sinus beats are presented with ventricular escape beats of the
deeper-T wave type (arrowheads) following longer pauses, compatible
with the diagnosis of a 2
nd
degree, Mobitz Type II, atrioventricular
block (see text for details).
Figure 6: An ECG rhythm strip (Lead II, 25 mm/sec, 10 mm/mV.) of
a 7-year-old female Japanese Chin dog presented for AP, recorded on
day 7. Normal sinus arrhythmia is present, (including transient, second
degree atrio-ventricular block, recorded following the third complex)
with a normal heart rate, and normal amplitudes and intervals (see
text for details).
Case Reports
Israel Journal of Veterinary Medicine  Vol. 70 (3)  September 2015 Oron, L. 62
6). Terefore, signalment, clinical signs, blood work, as well
as imaging diagnostics should all be taken into account (6).
Te gold standard is considered histopathology. However,
acquiring a pancreatic biopsy requires an invasive procedure.
In addition determining the clinical signifcance of histo-
pathological fndings is considered challenging: there are no
standardized criteria that distinguish microscopic fndings
leading to clinical disease from those that do not. On the
other hand, infammatory lesions of the pancreas are often
localized and can easily be missed (6). Abdominal ultraso-
nography, a non-invasive procedure, is considered relatively
sensitive (70%) and highly specifc when performed by an
imaging specialist (1, 6, 7), as was done in this reported case.
Pancreas specifc blood tests including pancreas-specifc
lipase (cPLI), and serum amylase and lipase levels, all have
relatively low sensitivities (1, 7). Among these, cPLI is con-
sidered to have the highest sensitivity and specifcity (78%
and 81% respectively). Unfortunately, in the reported case,
due to fnancial constraints, no specifc blood tests were
undertaken.
Pre-renal azotemia is often seen due to dehydration
or shock, or due to direct renal damage resulting in AKI
(1) secondary to hypovolemia, ischemia, or intravascular
coagulopathy, or due to peritonitis secondary to the local
infammatory process resulting from the pancreatic proteo-
lytic activity (8). In the present case the combination of an
elevated serum creatinine level, minimal dehydration upon
admission, normal kidney structure in abdominal ultraso-
nography, and urinary hyaline and granular casts, indicated
the presence of AKI. It is important to note that AKI can
also cause metabolic changes such as metabolic acidosis
and elevated potassium levels that can infuence cardiac
activity and electrophysiology, however in the reported case
AKI resolved within 24 hours of treatment and cardiac ar-
rhythmias persisted for the next few days.
Cardiovascular efects associated with human AP include
cardiac rhythm abnormalities, decreased ventricular contrac-
tility, and changes in the vasomotor tone of peripheral vessels
(2, 9, 10). Te reported occurrence of ECG abnormalities in
human AP patients is as high as 55% (10). Tachyarrhythmia
such as supraventricular premature complexes, atrial futter
or atrial fbrillation, bradyarrhythmia, and bundle branch
block, have all been reported in human patients with AP (2).
However, in only 3.9% of the patients more than one of such
abnormalities was documented upon admission (10). Te
dog reported here demonstrated several ECG abnormalities
(e.g. ST-segment depression, AV block, atrial standstill) in
the course of its 4 day long hospitalization period, none of
which was a tachyarrhythmia. Acute pancreatitis in human
beings is commonly associated with nonspecifc changes of
repolarization, mainly T-wave inversion and ST-segment
depression or elevation (11, 12). In the present case there
was an ST-segment depression of 0.3 mV, possibly caused
by transient myocardial hypoxia, or by hyperkalemia (12).
Te pathogenesis and clinical relevance of ECG abnor-
malities observed in patients with AP are unclear (2, 10).
Several mechanisms have been proposed, including a direct
toxic efect of the pancreatic proteolytic enzymes on the heart
causing myocardial infarction (11), pancreatitis induced coag-
ulopathy, increased platelet adhesiveness (13), and electrolyte
disturbances (2, 9, 10), all of which are common complica-
tions of AP. A high occurrence of metabolic disturbances,
including electrolyte imbalances, is also reported in veterinary
patients with AP (1). In a study describing the occurrence
of cardiac arrhythmia in human AP patients there was no
correlation between pancreatic enzyme levels (lipase, amylase
and pancreatic amylase) and ECG abnormalities. However,
there was a correlation between ECG abnormalities and
phosphorus, calcium and potassium imbalances (10). Tese
results, combined with the rapid onset of ECG changes in
AP patients, suggest that electrolyte imbalances, rather than
direct myocardial damage due to enzymatic changes, may play
a major role in the pathogenesis of ECG abnormalities in AP
(10). Hypocalcemia and hyperkalemia were indeed existing
in the presently reported case. However, ECG abnormalities
continued after the resolution of these electrical imbalances,
rendering them less likely to be the main contributors to the
documented ECG changes.
Cardiac Tropoin (cTn), a myofbrillar protein that is
released from injured myocardiocytes, is considered the gold
standard biomarker to assess myocardial injury in humans
regardless of the overlying etiology. It was also found efective
in detecting, monitoring and quantifying ongoing cardiac
injury in veterinary medicine (14). No serum samples were
available to measure troponin levels retrospectively, which is
a limitation of the reported case.
Regardless of the cause, in most human patients with AP
there is a complete resolution of ECG abnormalities once the
patient recovers from AP (2, 15-17), as was also seen in the
presently reported case. Terefore, in cases of severe bradyar-
Case Reports
Israel Journal of Veterinary Medicine  Vol. 70 (3)  September 2015 63 Atrioventricular block and Acute Pancreatitis
rhythmia (e.g. 3
rd
degree AV block, atrial standstill) associated
with acute AP, permanent pacemaker implantation as well
as decisions about possible euthanasia should be postponed
or avoided altogether in the acute phase of the disease (as
long as hemodynamic stability can be maintained), due to
the typically transient nature of the bradyarrhythmia, as also
seen in the present case.
Te presently reported patient experienced a single sei-
zure episode. AP can trigger seizure activity by causing severe
electrolyte imbalances or by inducing brain thromboembo-
lism. However, since the dog had clinically improved, intra-
cranial clot embolization appeared less likely to have caused
a seizure. Other possible causes include drug induced CNS
excitability. Teophylline administration has been reportedly
associated with seizure activity in both dogs and humans (18,
19), while terbutaline has been reported to induce tremors in
dogs (20) as has isoproterenol in humans (21).
In summary, although AP has been widely associated
with ECG abnormalities in human beings, specifc anomalies
have not yet been reported in the veterinary literature. In the
present case, a previously healthy dog with AP demonstrated
severe bradyarrhythmia and ST-segment depression, all of
which proved to be transient. As the development of severe
bradyarrhythmia such as a 3
rd
degree AV-block can some-
times lead to euthanasia, it is important that veterinarians be
aware of the possible transient nature of such bradyarrhyth-
mia in patients with acute pancreatitis. Further prospective
and larger scale studies are indicated to establish whether
ECG abnormalities are in correlation with clinical signs,
healing time, systemic complications, and prognosis, as well
as to better assess the required treatment and its efect on
ECG changes in pets with AP.
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Case Reports