ECG Interpretation

The initial ECG recordings revealed that the cria had a heart rate of 136 beats/min with a sinus rhythm (Figure 1). The heart rate was higher than the reported range for this species (range of 50 to 110 beats/min reported¹ for alpacas that were 3 months to 6 years old) and was consistent with a sinus tachycardia; heart rate data for healthy 6-week-old crias have not been published, to our knowledge. Electrical alternans was apparent, characterized by variation in the QRS complex morphology on a beat-to-beat basis, and the amplitude of the QRS complexes was low. Prolonged PQ intervals (200 to 210 milliseconds; reported range for healthy alpacas, 120 to 160 milliseconds¹) were present (indicative of first-degree atrioventricular block). Electrocardiographically, the first-degree atrioventricular block resulted in superposition of the P wave onto the preceding T wave.

With the cria positioned in left lateral recumbency, pericardiocentesis was performed with a 16-gauge, 82.5-mm (3.25-inch) over-the-needle catheter at the right fourth intercostal space. Initial attempts at pericardial evacuation revealed frank blood, which rapidly clotted; this finding was consistent with right ventricular puncture. The catheter was retracted, and 600 mL of serosanguineous fluid containing fibrin clumps was removed from the pericardial space and submitted for cytologic evaluation and assessment of specific gravity and total protein concentration. Samples of effusate were also submitted for aerobic and anaerobic bacterial cultures.

Occasional premature ventricular extrasystoles, which were self-limiting, were detected during the pericardiocentesis. Echocardiography performed immediately after pericardiocentesis revealed trivial pericardial effusion, and the left ventricular internal dimensions were slightly increased (postpericardiocentesis left ventricular end-diastolic dimension, 33 mm [prepericardiocentesis value, 29 mm]; postpericardiocentesis left ventricular end-systolic dimension, 22 mm [prepericardiocentesis value, 18 mm]). Electrocardiography was repeated (Figure 2). The ECG recordings revealed a reduction in heart rate to 115 beats/min. The morphology of the QRS complexes was consistent; the amplitude of the complexes was greater than that recorded previously. The PQ interval remained prolonged (200 milliseconds). In contrast to the prepericardiocentesis ECG findings, mild ST-segment depression was evident in leads II, III, and aVF with slight ST-segment elevation in lead aVR; these findings were consistent with epicardial injury to the right ventricle. The ST-segment deviation was suspected to be secondary to the right ventricular puncture that occurred during pericardiocentesis.

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Six-lead ECG tracings obtained from the alpaca cria in Figure 1 immediately after pericardiocentesis and inadvertent right ventricular puncture. The cria was positioned in left lateral recumbency during the ECG examination. The heart rate is 115 beats/min, and the electrical alternans and low-voltage QRS complexes have resolved, although the first-degree atrioventricular block persists (PQ interval, 200 milliseconds). In contrast to the tracings in Figure 1, slight ST-segment depression in leads II, III, and aVF with slight ST-segment elevation in lead aVR is evident; these changes are consistent with epicardial injury to the right ventricle. Paper speed, 50 mm/s; 2 cm = 1 mV.

Citation: Journal of the American Veterinary Medical Association 238, 5; 10.2460/javma.238.5.572

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Evaluation of the effusate obtained during pericardiocentesis revealed that the specific gravity was 1.026 g/dL and total protein concentration was 3.8 g/dL; the WBC count was 596 cells/μL (neutrophils, 48%; monocytes, 50%; and lymphocytes, 2%). Microscopic evaluation revealed a large number of erythrocytes, neutrophils (nondegenerative), moderate numbers of macrophages and mesothelial cells, and platelets; occasional occurrences of erythrophagia were evident. No evidence of infectious organisms was found. Cytopathologic interpretation was prior hemorrhage with peracute blood contamination. At 48 and 72 hours after submission of samples, the aerobic and anaerobic bacterial cultures of the effusate revealed no growth.

The cria was treated empirically for sepsis with ceftiofur (4 mg/kg [1.8 mg/lb], IV, q 12 h) and IV fluid therapy. The next day, echocardiography revealed mild pericardial effusion. A CBC revealed progressive anemia (Hct, 11%) and neutrophilia (38.2 × 10⁹ cells/L). Antimicrobial treatment was switched to oxytetracycline (10 mg/kg [4.5 mg/lb], IV, q 12 h). Three days after pericardiocentesis, ECG revealed a normal sinus rhythm with resolution of the atrioventricular block (PQ interval, 150 milliseconds). With time, the hematologic abnormalities normalized and the pericardial effusion resolved, and the cria was discharged from the hospital after 10 days. The cria was reevaluated 4 weeks later and was considered clinically normal. Echocardiographically, there was no evident pericardial effusion, mild mitral valve regurgitation, and mild tricuspid valve regurgitation that had apparently normal Doppler velocity (2.54 m/s, corresponding to a right ventricular to right atrial pressure gradient of 25.7 mm Hg). A third ECG recording was obtained and revealed a normal sinus rhythm (heart rate, 90 to 96 beats/min) and resolution of the first-degree atrioventricular block (PQ interval, 140 to 150 milliseconds; Figure 3). The QRS complexes were all of comparable morphology and of higher amplitude than that observed in previous recordings, and the ST segment was considered normal.

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Lead I, II, and III tracings obtained from the alpaca cria in Figure 1 fourweeks after discharge from the hospital following resolution of pericardial effusion. Sinus rhythm is present (heart rate, 90 to 96 beats/min), the morphology of the QRS complexes appears normal, and the electrical alternans is no longer evident. The PQ prolongation and ST-segment changes have resolved. Paper speed, 50 mm/s; 1 cm = 1 mV.

Citation: Journal of the American Veterinary Medical Association 238, 5; 10.2460/javma.238.5.572

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Discussion

Pericardial effusion is defined as excessive fluid accumulation within the pericardial sac. There is little information in the veterinary literature regarding pericarditis and other pericardial disorders in alpacas, to our knowledge. A review² of cardiovascular disorders noted in records of 2,167 llamas in the Veterinary Medical Database at Purdue University revealed 11 cases of pericarditis and epicarditis, and there are 3 case reports^3–5 of pericardial disease in llamas.

In the cria of this report, the auscultatory findings were atypical of pericardial effusion in that heart sounds were normal in intensity and ventral lung sounds were dull. Because of its size, the heart had displaced much of the ventral lung tissue, which we suspect resulted in the pulmonary findings, whereas the narrow thoracic conformation of alpacas apparently allowed transmission of the heart sounds to the thoracic wall despite the insulating effects of the pericardial effusion.

Although not definitive, ECG findings of electrical alternans can support a diagnosis of pericardial effusion or cardiac tamponade; up to 50% of dogs with pericardial effusion may have this phenomenon.⁶ Electrical alternans develops in the presence of large-volume pericardial effusions because of changes in cardiac position and excessive pendular and rotational cardiac motion in relation to the ECG limb leads, which would normally be constrained by the pericardium.⁷ The ratio of the 2 QRS morphologies of the electrical alternans in the cria of this report was not precisely 1:1. However, precise alternans with complexes in a 1:1 pattern occurs when the swinging motion of the heart maintains a 2-beat periodicity, often related to the heart rate.⁸ If the pendular motion of the heart is not rhythmic with alternating heart beats, the ratio of the 2 QRS morphologies may not be precisely 1:1, though electrical alternans may still be diagnosed.⁹

Low-amplitude QRS voltages are often detected in animals with pericardial effusion because of the insulating effects of the pericardial fluid.⁷ Additionally, a decrease in intracardiac blood volume results in lower-amplitude QRS complexes, known as the Brody effect,¹⁰ and this may occur secondary to compression of cardiac chambers during cardiac tamponade. The ventricular activation process of camelids complicates interpretation of the low-voltage QRS complexes. The Purkinje systems of horses, ruminants, and camelids have more complete penetration of the ventricular myocardium than do the Purkinje systems in dogs, cats, and humans, which results in greater cancellation of dipoles and less-prominent QRS complex amplitudes in the standard ECG limb leads.^1,11 However, the increase in R-wave amplitude immediately after pericardiocentesis in the cria of this report supports the contention that abnormally low voltages were present on the initial tracings and is consistent with the low-voltage QRS complexes observed in other species with pericardial effusion. Other causes for low QRS voltages, including hypothyroidism, amyloidosis, and myocardial fibrosis, were considered unlikely in this young animal.⁷

First-degree atrioventricular block is defined as a prolongation of the PQ interval. In camelids, low-grade heart block is commonly caused by vagal influences, which may occur with gastrointestinal tract, neurologic, or respiratory tract disease.¹² The influence of vagal tone on the PQ interval in the cria of this report was uncertain because a vagolytic agent was not administered. It is known that Mobitz type I second-degree atrioventricular block may occur in otherwise normal healthy camelids.¹³ Interestingly, second-degree atrioventricular block in an adult llama with pericardial effusion that ceased with resolution of the pericardial effusion has been reported.⁴ Experimental studies^14–16 have provided evidence that acute cardiac tamponade is associated with an increase in vagal tone, which could lead to atrioventricular block. In the cria of this report, the pericardial effusion was believed to have contributed to the first-degree atrioventricular block because the block subsequently resolved within 72 hours after pericardiocentesis. We cannot exclude the possibility that the cria's underlying systemic inflammatory disease may have resulted in inflammation or injury to the cardiac conduction system, thereby causing the first-degree atrioventricular block.

The cause for the pericardial effusion in this alpaca cria was not determined. A recent review¹² of cardiac disease in camelids identified pericardial effusion in association with congenital heart malformations (ie, ventricular septal defect or pulmonary atresia), pulmonary hypertension, and pleuropneumonia. None of these conditions was evident in the cria of this report, although pleuropneumonia was considered given the respiratory tract signs detected at the initial evaluation. The high right ventricular pressure (as estimated by use of the Doppler velocity of the tricuspid valve re-gurgitation) was presumably related to the animal's age and not a sign of clinically important pulmonary hypertension because it had resolved by the 4-week recheck examination. Similar to the situation for this cria, the underlying cause of pericardial effusion (which resulted in cardiac tamponade) in a pregnant 2-year-old llama was also not determined in another report.⁴ We hypothesized that the pericardial effusion in this cria was related to an underlying systemic inflammatory cause or viral infection, which is suspected in most cases of idiopathic pericarditis in humans.¹⁷