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Minu Im Department of Medicine & Epidemiology, School of Veterinary Medicine, University of California-Davis, Davis, CA 95616.

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Joshua A. Stern Department of Medicine & Epidemiology, School of Veterinary Medicine, University of California-Davis, Davis, CA 95616.

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A 5-year-old 30-kg (66-lb) spayed female Labrador Retriever was referred to the emergency service at a veterinary teaching hospital because of a 2-week history of progressive lethargy and hyporexia. On initial evaluation, 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 pertinent previous medical history, and the dog was not currently receiving any medications.

Results of a CBC indicated mild normocytic normochromic nonregenerative anemia (Hct, 28%; reference interval, 40% to 55%) and marked leukocytosis (29,300 WBCs/μL; reference interval, 6,000 to 13,000 WBCs/μL) characterized by neutrophilia (21,000 neutrophils/μL; reference interval, 3,000 to 10,500 neutrophils/μL) 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 interval, 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 abnormalities including high phosphorus concentration (5.7 mg/dL; reference interval, 2.6 to 5.2 mg/dL) and low concentrations 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 auricle appeared normal, and there was no evidence of cardiac neoplasia. Once the dog was sedated, pericardiocentesis was performed. Approximately 625 mL of blood-tinged opaque effusion was evacuated. The dog was monitored by ECG during the pericardiocentesis (Figure 1).

Figure 1—
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.

Citation: Journal of the American Veterinary Medical Association 248, 5; 10.2460/javma.248.5.497

ECG Interpretation

The 3-lead ECG recording obtained during pericardiocentesis 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 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 complex 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 × 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 dyskinesia (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 provided evidence of successful resolution of cardiac tamponade. 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 elevation, notching of the QRS complex, and abnormally high T-wave amplitude (60% to 80% of the QRS complex 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 sufficient 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 occurred as a couplet of left-sided origin or right bundle branch block morphology and were followed by a compensatory pause.

Figure 2—
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.

Citation: Journal of the American Veterinary Medical Association 248, 5; 10.2460/javma.248.5.497

The decreased R-wave amplitude in the initial ECG recording and subsequent increase after pericardiocentesis were likely a direct consequence of incomplete diastolic filling associated with cardiac tamponade. There are several physiologic explanations for the small QRS complexes observed. The Brody effect describes the impact that a larger volume of highly conductive, intracardiac blood has on the surface ECG tracings. Smaller intracardiac volumes, such as those expected with PE, result in diminutive 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 reduces the QRS complex voltage. Moreover, the composition of PE has an important impact on its conductivity, 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 phenomenon.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 complex. 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 elevation,7 as seen in the lead II, III, and V3 tracings (Figures 1 and 2). Although ST-segment elevation is usually attributed 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 irritation 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, despite 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 pericardiocentesis 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, pericardiocentesis 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 cellular characteristics.10,11 Although relief of cardiac tamponade is immediately lifesaving, the most common cause of PE with cardiac tamponade in dogs is hemangiosarcoma, which has a grave prognosis and an anticipated survival time of days to weeks.12 Other neoplastic 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 echocardiography, 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 concentration has become a valuable biomarker in dogs for myocardial ischemia and necrosis. Dogs with cardiac hemangiosarcoma have significantly higher plasma or serum concentrations of cardiac troponin I, compared with findings in dogs with idiopathic PE, and marked increases in plasma or serum cardiac troponin I concentration may be helpful in determining whether 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 troponin I concentration in dogs that can clearly establish 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 arrhythmias as a result of myocardial irritation or even inadvertent puncture of the myocardium allows for immediate administration of antiarrhythmic agents or careful repositioning of the pericardial catheter.16 Another use of ECG monitoring during pericardiocentesis is assessment of QRS complex morphology. Because PE is reduced 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 ischemia with PE and cardiac tamponade is often a direct result of increased intrapericardial pressure that prevents effective diastole and oxygenation of the epicardium. Additionally, dogs with cardiac tamponade are often tachycardic 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 difficult 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 supported by the dyskinesia of the left ventricular free wall and the constellation of ECG findings. However, the modest increase in plasma cardiac troponin I concentration 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. Ultimately, 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 elevation 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 cardiomyocytes, but insufficient blood flow to promote effective, synchronous repolarization of the ventricular cardiomyocytes.19 This injured region of ventricular myocardium may continue to conduct negative impulses, even after the surrounding ventricular cardiomyocytes have fully repolarized.20 Because this site of injury conducts negative current, the perceived ECG baseline becomes more negative, 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 illustrates 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 situation, the notching occurs in the initial segment of the ECG complex and would not be characteristic of microscopic intramural myocardial infarction, but rather nonspecific myocardial ischemia or perhaps past infarction in humans.6 The physiologic explanation for this phenomenon is that areas of necrosis and fibrosis interrupt the normal ventricular depolarization, leading to interruptions and fragmentations of electrical conduction 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 ischemia.22 However, because of the wide variation in T-wave morphology, this finding should be interpreted in conjunction 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 diagnosis 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 pericardial mesothelioma. Pericardectomy was once a potential 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 findings were consistent with septic exudate, a relatively uncommon 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 canis and Actinomyces sp. The dog immediately underwent pericardectomy, and histologic examination of pericardial tissue samples revealed severe pyogranulomatous inflammation 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.

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