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ECG of the month

Article  in  Journal of the American Veterinary Medical Association · March 2016

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ECG of the Month

A 5-year-old 30-kg (66-lb) spayed female Labrador Re-

triever was referred to the emergency service at a
veterinary teaching hospital because of a 2-week history
of progressive lethargy and hyporexia. On initial evalu-
ation, the dog was quiet but responsive, with a rectal
temperature of 40°C (104°F) and a respiratory rate of 45
breaths/min. The mucous membranes were pale pink,
and the dog’s capillary refill time was 2 seconds. Muffled
heart sounds were ausculted bilaterally, and there was
bilateral jugular venous distension. There was no perti-
nent previous medical history, and the dog was not cur-
rently receiving any medications.
Results of a CBC indicated mild normocytic normochro-
mic nonregenerative anemia (Hct, 28%; reference interval,
40% to 55%) and marked leukocytosis (29,300 WBCs/mL;
reference interval, 6,000 to 13,000 WBCs/mL) characterized
by neutrophilia (21,000 neutrophils/mL; reference interval,
3,000 to 10,500 neutrophils/mL) and monocytosis (4,185
monocytes/µL; reference interval, 150 to 1,200 monocytes/
µL). Serum biochemical analysis revealed metabolic acidosis
with high anion gap (27 mmol/L; reference interval, 12 to 20
mmol/L), low albumin concentration (1.7 g/dL; reference in-
terval, 3.4 to 4.3 g/dL), high globulin concentration (4.0 g/
dL; reference interval, 1.7 to 3.1 g/dL), and minor electrolyte
This report was submitted by Minu Im, DVM, and Joshua A. Stern, DVM,
PhD; from the Department of Medicine & Epidemiology, School of Vet-
erinary Medicine, University of California-Davis, Davis, CA 95616.
Address correspondence to Dr. Stern (jstern@ucdavis.edu).
abnormalities including high phosphorus concentration (5.7
mg/dL; reference interval, 2.6 to 5.2 mg/dL) and low concen-
trations of sodium (138 mmol/L; reference interval, 143 to
151 mmol/L), chloride (102 mmol/L; reference interval, 108
to 116 mmol/L),calcium (9.4 mg/dL;reference interval,9.6 to
11.2 mg/dL), and bicarbonate (13 mmol/L; reference interval,
20 to 29 mmol/L). Plasma cardiac troponin I concentration
was high (0.23 ng/mL; reference interval, 0.09 to 0.17 ng/
mL).The dog was negative for circulating antibodies against
Anaplasma phagocytophilum, Borrelia burgdorferi,
Ehrlichia canis, and Dirofilaria immitis.
A brief echocardiographic examination revealed
moderate-volume pericardial effusion (PE) with cardiac
tamponade.There was focal pericardial thickening with
an associated hyperechoic region of epicardium on the
left ventricular free wall. The cardiac base and right au-
ricle appeared normal, and there was no evidence of
cardiac neoplasia. Once the dog was sedated, pericar-
diocentesis was performed. Approximately 625 mL of
blood-tinged opaque effusion was evacuated. The dog
was monitored by ECG during the pericardiocentesis
(Figure 1).
ECG Interpretation
The 3-lead ECG recording obtained during pericar-
diocentesis revealed a regular sinus rhythm with a mean
heart rate of 140 beats/min and a normal mean electrical
axis of +60°. In lead II, the amplitude of the R wave was

Figure 1—Three-lead ECG recording obtained from a dog that was evaluated because of a 2-week history of progressive lethargy and
hyporexia. The dog was subsequently found to have pericardial effusion. This recording was obtained during pericardiocentesis while
the dog was in right lateral recumbency.There is predominantly a sinus rhythm with a mean heart rate of 140 beats/min. Notice the ST-
segment elevation, notched QRS morphology, greater-than-normal T-wave amplitude, and a couplet of ventricular premature complexes
with right bundle branch block morphology followed by a compensatory pause. Paper speed = 50 mm/s; 1 cm = 1 mV.

JAVMA • Vol 248 • No. 5 • March 1, 2016 497

1.0 mV; there was a step in the ascending limb of the R
wave that may have been notching of the QRS complex.
The ST segment (J-point) was greater than baseline (ie,
relative to the TP segment) by 0.3 mV, and the T waves
were prominent, comprising 70% to 80% of the QRS com-
plex amplitude. All findings were consistent with PE and
possible myocardial ischemia or infarction.
After pericardiocentesis, a full echocardiographic
examination was performed, and a well-circumscribed
mass lesion measuring 4 X 2.5 cm was identified within
the left side of the pericardium.This lesion compressed
the underlying epicardium adjacent to the hyperechoic
epicardial region previously observed, and relative dys-
kinesia (compared with interventricular septal motion)
was noted in this region of the left ventricular free wall.
A second ECG recording was obtained 7 minutes after
completion of pericardiocentesis (Figure 2).The dog’s
initial relative tachycardia, compared with subsequent
findings, was likely attributable to cardiac tamponade,
in which reduced aortic pressure stimulated the baro-
receptor reflex to subsequently increase heart rate and
improve cardiac output. This second recording pro-
vided evidence of successful resolution of cardiac tam-
ponade. The mean heart rate had slowed to 100 beats/
min. Additionally, the R-wave amplitude in the lead II
tracing increased by 50% to 1.5 mV. The ST-segment el-
evation, notching of the QRS complex, and abnormally
high T-wave amplitude (60% to 80% of the QRS com-
plex amplitude) remained. Although the QRS complex
amplitude varied slightly during the acquisition of the
second tracing, notably absent from this tracing was
the presence of distinct electrical alternans, which is
frequently associated with PE. Perhaps this finding was
absent because the moderate-volume PE was not suf-
ficient to facilitate a rocking motion of the heart within
the fluid. Two ventricular premature complexes were
present on the initial recording tracing (Figure 1); they
Figure 2—Three-lead ECG recording obtained from the dog in Figure 1 at 7 minutes after pericardiocentesis. This recording
was obtained while the dog remained in right lateral recumbency. At this time, there is a sinus rhythm with a mean heart rate of
100 beats/min. Notice the persistent ST-segment elevation, notched QRS complex morphology, and greater-than-normal T-wave
amplitude. Paper speed = 50 mm/s; 1 cm = 1 mV.
498 JAVMA • Vol 248 • No. 5 • March 1, 2016
occurred as a couplet of left-sided origin or right bun-
dle branch block morphology and were followed by a
compensatory pause.
The decreased R-wave amplitude in the initial
ECG recording and subsequent increase after peri-
cardiocentesis were likely a direct consequence of
incomplete diastolic filling associated with cardiac
tamponade. There are several physiologic explana-
tions for the small QRS complexes observed. The
Brody effect describes the impact that a larger vol-
ume of highly conductive, intracardiac blood has on
the surface ECG tracings. Smaller intracardiac vol-
umes, such as those expected with PE, result in di-
minutive QRS complexes on surface ECG tracings.1
This effect is minor and does not entirely explain
the voltage change observed on the surface ECG
recording in dogs with PE.2 The area of transmural
left ventricular activation is smaller than normal
in instances of cardiac tamponade because of the
changes in heart size, which directly further reduc-
es the QRS complex voltage. Moreover, the composi-
tion of PE has an important impact on its conductiv-
ity, and effusions of higher or lower conductance
than a dog’s blood reduce QRS complex voltages
as measured by surface ECG.2 The effusion in the
dog of this report, although somewhat hemorrhagic
in appearance, was indeed different from blood and
ultimately classified as a septic exudate on the basis
of cytologic examination findings. Interestingly, the
P and T waves and ST segment are generally spared
from the aforementioned complex-diminishing phe-
nomenon.1 This sparing of the P and T waves as well
as the ST segment is secondary to differences in
cancellation potentials, but is not well documented
for dogs. These cancellation potential differences
are secondary to a difference in the degree to which
the dipole theory applies to these ECG segments
or possibly occur because the center of electrical
activity differs for these complexes.3
In both ECG recordings for the dog of this report,
there was a small step in the ascending limb of the R
wave that is referred to as notching of the QRS com-
plex. This was suggestive of considerable myocardial
ischemia.4–6 Other ECG findings that further supported
the presence of myocardial ischemia included greater-
than-normal T-wave amplitude and ST-segment eleva-
tion,7 as seen in the lead II, III, and V3 tracings (Figures
1 and 2). Although ST-segment elevation is usually at-
tributed to myocardial (and epicardial) ischemia, it can
also be associated with epicarditis and pericarditis.8
The observed ventricular ectopy in the dog’s initial
ECG recording may have been the result of direct irrita-
tion of the epicardium by the pericardial catheter. However,
some ectopy was observed prior to pericardiocentesis, and
the complexes appeared to be of left ventricular origin, de-
spite a right thoracic approach for pericardiocentesis. It is
possible that the pericardial mass observed to be in direct
contact with the left ventricular epicardium after pericar-
diocentesis was contributing to generation of this ectopy.
Ultimately, an ECG diagnosis of myocardial ischemia and
possible pericarditis was made for the dog of this report
on the basis of ST-segment elevation, notching of the QRS
complex, and greater-than-normal T-wave amplitude.
Discussion
Cardiac tamponade refers to a state of impaired
ventricular filling and low cardiac output resulting from
increased intrapericardial pressure associated with PE.
In a dog with PE and cardiac tamponade, pericardiocen-
tesis is typically performed, often in conjunction with
rapid IV infusion of fluids to improve cardiac output
in the face of cardiogenic shock.9 Unfortunately, results
of cytologic analysis of PE samples seldom identifiy the
cause of PE (with the exception of exudative effusions)
because hemangiosarcoma often does not exfoliate and
both benign and malignant effusions have similar cel-
lular characteristics.10,11 Although relief of cardiac tam-
ponade is immediately lifesaving, the most common
cause of PE with cardiac tamponade in dogs is heman-
giosarcoma, which has a grave prognosis and an antici-
pated survival time of days to weeks.12 Other neoplas-
tic causes of PE are chemodectoma, lymphoma, ectopic
thyroid carcinoma, and mesothelioma.13 The second
most common form of PE is idiopathic.14 In most cases
of hemangiosarcoma, a mass lesion is visible via echo-
cardiography, usually around the right atrium or right
auricle; however, an absence of an obvious mass cannot
rule out cardiac neoplasia.
Recently, plasma or serum cardiac troponin I con-
centration has become a valuable biomarker in dogs
for myocardial ischemia and necrosis. Dogs with cardi-
ac hemangiosarcoma have significantly higher plasma
or serum concentrations of cardiac troponin I, com-
pared with findings in dogs with idiopathic PE, and
marked increases in plasma or serum cardiac troponin
I concentration may be helpful in determining wheth-
er a cardiac mass is present but not easily detected.15
Unfortunately, to the authors’ knowledge, there is no
current published value for plasma or serum cardiac
JAVMA • Vol 248 • No. 5 • March 1, 2016 499
troponin I concentration in dogs that can clearly es-
tablish a definitive diagnosis of hemangiosarcoma over
other causes of myocardial ischemia or necrosis.
Although ECG is not a sensitive test for PE, ECG
monitoring during pericardiocentesis is paramount.
Early detection of potentially life-threatening arrhyth-
mias as a result of myocardial irritation or even inadver-
tent puncture of the myocardium allows for immedi-
ate administration of antiarrhythmic agents or careful
repositioning of the pericardial catheter.16 Another use
of ECG monitoring during pericardiocentesis is assess-
ment of QRS complex morphology. Because PE is re-
duced after pericardiocentesis, an increase in R-wave
amplitude (taller QRS complexes) and a decrease in
heart rate (longer R-R intervals) would be expected.17
These changes were evident in the dog of this report
(Figures 1 and 2).
For the dog of the present report, multiple ECG
changes supported the diagnosis of myocardial ischemia,
including ST-segment elevation, notched R waves, and
greater-than-normal T-wave amplitude. Myocardial isch-
emia with PE and cardiac tamponade is often a direct
result of increased intrapericardial pressure that prevents
effective diastole and oxygenation of the epicardium. Ad-
ditionally, dogs with cardiac tamponade are often tachy-
cardic to compensate for decreased cardiac output, which
further decreases the duration of diastole and increases
myocardial oxygen demand because of an increased heart
rate.
Elevation of the ST segment can also be associated
with acute pericarditis or epicarditis, but it is often dif-
ficult to differentiate ST-segment elevation induced by
acute pericarditis or epicarditis from that induced by
myocardial ischemia.18 Recent research in humans has
shown that changes in QRS complex duration and QT
intervals may help differentiate the 2 etiologies, but
many of these changes may be difficult to detect via
conventional ECG and there is still much more research
to be done in this area for companion animals. In the
case described in the present report, the contribution
of subepicardial ischemia to J-point elevation was sup-
ported by the dyskinesia of the left ventricular free wall
and the constellation of ECG findings. However, the
modest increase in plasma cardiac troponin I concen-
tration and normal QT interval were more supportive
of a nonischemic cause for the J-point elevation. There
was no doubt that pericarditis and likely epicarditis
were present in the dog of the present report. Ultimate-
ly, the distinction of whether this dog’s ECG findings
represented ischemic or nonischemic effects (or some
combination thereof) cannot be discerned.
The proposed ischemic mechanism of ST-segment el-
evation can be explained by the current of injury theory,
which suggests that a region of ischemic myocardium has
sufficient blood flow to prevent death and fibrosis of car-
diomyocytes, but insufficient blood flow to promote effec-
tive, synchronous repolarization of the ventricular cardio-
myocytes.19 This injured region of ventricular myocardium
may continue to conduct negative impulses, even after
the surrounding ventricular cardiomyocytes have fully re-
polarized.20 Because this site of injury conducts negative
current, the perceived ECG baseline becomes more nega-
tive, creating a depression of the TP segment.This shift in
 baseline creates what is perceived to be an ST-segment
elevation, when in reality, the true change is TP segment
depression.21 This distinction has no clinical importance,
and conventionally, the ECG change is described in terms
of ST-segment or J-point positioning.
The case described in the present report also illus-
trates notching of the R waves indicative of ischemic
heart disease. When present in the terminal third of
the QRS complex, these notches are often referred to
as microscopic intramural myocardial infarction, where
small patchy areas of myocardial infarction often lead to
subsequent myocardial death and fibrosis. In this situa-
tion, the notching occurs in the initial segment of the
ECG complex and would not be characteristic of mi-
croscopic intramural myocardial infarction, but rather
nonspecific myocardial ischemia or perhaps past infarc-
tion in humans.6 The physiologic explanation for this
phenomenon is that areas of necrosis and fibrosis inter-
rupt the normal ventricular depolarization, leading to
interruptions and fragmentations of electrical conduc-
tion that are evident as a notched R wave.6,22
Lastly, T waves of greater-than-normal amplitude are
another ECG change associated with myocardial isch-
emia.22 However, because of the wide variation in T-wave
morphology, this finding should be interpreted in conjunc-
tion with other findings, such as high plasma or serum
cardiac troponin I concentration and the aforementioned
ECG changes. For the dog of this report, a tentative diagno-
sis of myocardial ischemia with pericarditis was made on
the basis of clinical findings and ECG changes.
Initially, echocardiography revealed a focal pericardial
mass in the region of the left ventricular free wall of the
dog of the present report. Although PE is not a common
sequela of pericardial disease in dogs, the exception is peri-
cardial mesothelioma. Pericardectomy was once a poten-
tial treatment of pericardial mesothelioma, but it is now
believed to promote intrathoracic dissemination of the
disease.23 Prior to the cytologic examination of PE samples
from the dog of this report, pericardial mesothelioma was
a top differential diagnosis given the presence of PE along
with a focal pericardial mass. However, the cytologic find-
ings were consistent with septic exudate, a relatively un-
common cause of PE in dogs. Septic exudates in relation
to PE most often develop secondary to systemic coccidio-
mycosis or migrating foreign bodies. Microbial culture of
samples of this dog’s PE yielded growth of Pasteurella ca-
nis and Actinomyces sp.The dog immediately underwent
pericardectomy, and histologic examination of pericardial
tissue samples revealed severe pyogranulomatous inflam-
mation and granulation. Grass material was identified at
the center of the pericardial mass lesion, and the diagnosis
of septic pericarditis secondary to a migrating grass awn
was made. The dog recovered fully after pericardectomy
and treatment with antimicrobials (selected on the basis of
culture results and antimicrobial susceptibility testing) and
was doing well at home 6 months after surgery. No further
follow-up ECG examinations were performed.
Acknowledgments
No external funding was used in this study. The authors declare
that there were no conflicts of interest.
500 JAVMA • Vol 248 • No. 5 • March 1, 2016
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