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Saki Kadotani 1Department of Veterinary Clinical Medicine, College of Veterinary Medicine, University of Illinois, Urbana, IL 61802.

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Ryan C. Fries 1Department of Veterinary Clinical Medicine, College of Veterinary Medicine, University of Illinois, Urbana, IL 61802.

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An 11-year-old 6.2-kg (13.6-lb) neutered male domestic shorthair cat was evaluated on an emergency basis because of sudden-onset hind limb paralysis and vocalization. On physical examination, the cat was quiet and unable to use its hind limbs to walk. An irregularly irregular heart rhythm with a rate of 190 beats/min and a gallop sound was auscultated. No heart murmur was present. The cat was tachypneic (respiratory rate, 50 breaths/min) and had increased bronchovesicular sounds bilaterally. Rectal temperature was 33.7°C (92.7°F). The hind limbs were cold to the touch with no appreciable femoral pulses on palpation or Doppler ultrasonographic examination bilaterally. Systemic blood pressure in the left forelimb measured with a Doppler ultrasonographic method was 170 mm Hg.

Thoracic radiography revealed severe cardiomegaly with a lateral vertebral heart size of 9.8.1 There was a moderate unstructured interstitial lung pattern, which was accentuated in the caudodorsal lung fields, and pulmonary venous congestion consistent with cardiogenic pulmonary edema. Analysis of a blood sample with a blood gas analyzer revealed mild azotemia (BUN concentration, 35 mg/dL [reference range, 9.1 to 24.5 mg/dL]; creatinine concentration, 1.9 mg/dL [reference range, 0.73 to 1.19 mg/dL]) and moderate hyperglycemia (232 mg/dL; reference range, 77.96 to 129.84 mg/dL]).

Echocardiography revealed severe left ventricular free wall and interventricular septal concentric hypertrophy and left ventricular apical thinning with hypokinesis and dyskinesis of the left ventricular free wall. The left atrium appeared severely enlarged on the basis of a measurement made on a right parasternal 2-D short axis view (left atrium-to-aorta ratio, 2.2; reference range,2 < 1.5) with evidence of spontaneous echo contrast and a large thrombus. Longitudinal strain analysis performed by means of speckle tracking echocardiography revealed decreased strain in the apical, mid, and basilar portions of the lateral free wall with strain rates of −9%, −7%, and −5%, respectively (reference range,3 20%). Given the cat's clinical signs and thoracic radiographic and echocardiographic findings, diagnoses of aortic arterial thromboembolism and left-sided congestive heart failure secondary to end-stage (burnt-out) hypertrophic cardiomyopathy and left ventricular free wall myocardial infarction were made.

ECG Interpretation

A 6-lead ECG examination was performed to evaluate the arrhythmia (Figure 1). The recording revealed atrial fibrillation with a ventricular response rate ranging from 136 to 214 beats/min; the calculated mean heart rate was 180 beats/min. The amplitude and duration of the QRS complexes were increased (0.9 mV and 80 milliseconds, respectively), indicative of left ventricular enlargement. The mean electrical axis was +120°, consistent with right axis deviation. Small R waves with deep S waves (rS complexes) were evident in leads I and aVL, and small Q waves with tall R waves (qR complexes) were evident in leads II, III, and aVF. In the absence of right ventricular hypertrophy, these findings were suggestive of atrial fibrillation conducted with a left posterior fascicular block.

Figure 1—
Figure 1—

Six-lead ECG recording obtained from an 11-year-old cat with arterial thromboembolism and left-sided congestive heart failure secondary to end-stage hypertrophic cardiomyopathy. Notice the atrial fibrillation with a mean heart rate of 180 beats/min. The prolonged duration (80 milliseconds) of the QRS complexes, right axis deviation (+120°), rS complexes in leads I and aVL, and qR complexes in leads II, III, and aVF are features consistent with a left posterior fascicular block pattern. Paper speed = 50 mm/s; 2 cm = 1 mV.

Citation: Journal of the American Veterinary Medical Association 255, 9; 10.2460/javma.255.9.1013

The cat was hospitalized and immediately given a fentanyl bolus (3 μg/kg [1.4 μg/lb], IV) followed by a continuous rate infusion (3 μg/kg/min, IV) of the drug. The cat also received furosemide (total of 3 mg/kg over 12 hours, IV), pimobendan (0.2 mg/kg [0.1 mg/lb], PO, q 12 h), clopidogrel (loading dose of 12 mg/kg [5.5 mg/lb], followed by a dosage of 3 mg/kg, PO, q 24 h), and unfractionated heparin (200 U/kg [91 U/lb], SC, q 8 h). Antiarrhythmic medication was not administered for atrial fibrillation because the calculated mean heart rate was 180 beats/min and considered physiologically appropriate.

The following day, the cat's rectal temperature remained low at 34.9°C (94.8°F) with no evidence of palpable femoral pulses. The cat's heart rate had decreased to 50 beats/min, and an ECG examination was repeated (Figure 2). The ECG recording revealed a flat baseline with an absence of P waves, wide QRS complexes (duration, 160 milliseconds), and tall and wide T waves, all of which are consistent with ECG features associated with hyperkalemia. Repeated clinicopathologic analyses revealed severe azotemia (BUN concentration, 104 mg/L; creatinine concentration, 5.5 mg/dL), severe hyperkalemia (10.2 mmol/L; reference range, 3.7 to 4.9 mmol/L]), mild hyperlactatemia (3.4 mmol/L; reference range, 0.4 to 2.9 mmol/L]), and mild hyperglycemia (254 mg/dL). The cat was given calcium gluconate (0.5 mL/kg [0.2 mL/lb], IV, over 10 minutes) and regular insulina (1 U, IV) along with a dextrose bolus (0.5 mL/kg, IV); subsequently, a continuous rate infusion of 5% dextrose (2 mL/h) was started and furosemide administration was discontinued. Initially, the treatments resulted in resolution of bradycardia; however, the cat soon had recurrence of bradycardia and became anuric with scant urine in the urinary bladder detected by abdominal ultrasonography. Administration of calcium gluconate and dextrose was repeated, and infusion of 5% dextrose (2 mL/h) was continued. Repeated clinicopathologic analyses after 4 hours of fluid administration (total volume, 8 mL) revealed worsening of azotemia (BUN concentration, 110 mg/L; creatinine concentration, 6.8 mg/dL). These abnormalities were suspected to be secondary to acute renal failure. On the basis of the cat's declining clinical condition and guarded prognosis, the owners elected euthanasia.

Figure 2—
Figure 2—

Six-lead ECG recording obtained from the cat in Figure 1 twelve hours after treatment of arterial thromboembolism. The rhythm remains irregular with a calculated mean heart rate of 50 beats/min. There is an absence of P waves, widening of the QRS complexes (duration, 160 milliseconds), and tented T waves consistent with criteria for severe hyperkalemia. The rhythm resembled sinoventricular rhythm; however, P waves were never documented after treatment of hyperkalemia. The underlying rhythm is likely atrial fibrillation with disruption of conduction secondary to hyperkalemia leading to bradycardia and widened QRS complexes. Paper speed = 50 mm/s; 1 cm = 1 mV.

Citation: Journal of the American Veterinary Medical Association 255, 9; 10.2460/javma.255.9.1013

Discussion

In cats, arrhythmias most commonly develop in association with congestive heart failure or thromboembolism secondary to cardiomyopathy.4 Atrial fibrillation is detected in 38% of cats with hypertrophic cardiomyopathy involving marked atrial enlargement. In addition, a left anterior fascicular block in particular has been associated with hypertrophic cardiomyopathy.5

In humans, the intraventricular conduction system is composed of right and left bundle branches. The left bundle branch divides into the anterior and posterior fascicles. The anterior division activates the anterior and lateral walls of the left ventricle, and the posterior division activates the inferior and posterior walls of the left ventricle. Although left posterior fascicular block in dogs and baboons has been documented,6 it remains unclear whether cats have a left posterior fascicle.

In humans with left posterior fascicular block, the excitation wave initially travels through the anterior fascicle and then spreads out in an inferior direction. The initial deflection is directed toward the superior aspect and to the left, and the subsequent main QRS force is directed inferiorly toward the posterior aspect and to the right, thereby creating small R waves with deep S waves (rS complexes) in leads I and aVL and small Q waves with tall R waves (qR complexes) in leads II, III, and aVF. Additional ECG criteria for left posterior fascicular block include right axis deviation (> +90°), normal to slightly prolonged QRS duration (80 to 110 milliseconds), prolonged R-wave peak time in aVF tracings, and increased QRS-complex voltage in the limb leads. The probability of left posterior fascicular block being the cause of an abnormal right-axis shift increases in a patient with left ventricular disease but no evidence of right ventricular hypertrophy.7

Left posterior fascicular block in humans is rare because the left posterior fascicle is protected by the thickness of the left posterior division and its abundant blood supply. However, left posterior fascicular block is often detected in patients with acute myocardial ischemia or infarction and coexistent lateral wall myocardial infarction secondary to coronary artery disease.7,8 Although the prognostic importance of left posterior fascicular block is unknown, it is reported to be associated with a high mortality rate (80% to 87%) in humans during the first week after a coronary event.9

For the cat of the present report, the initial ECG pattern was consistent with a left posterior fascicular block on the basis of the criteria used for humans. Echocardiographically, there was evidence of thinning of the left ventricular posterolateral free wall with severely reduced myocardial strain and decreased systolic function, suggesting possible myocardial infarction. Advanced imaging, such as coronary angiography or cardiac MRI, is necessary to confirm an infarction but was not pursued in this case. Unfortunately, the cat developed acute, anuric renal failure and severe hyperkalemia. We suspected that the acute renal failure and subsequent hyperkalemia developed secondary to renal arterial thrombosis given the sudden development of azotemia, concurrent aortic thromboembolism, and minimal treatment with furosemide (total of 3 mg/kg). A necropsy was declined by the owners, and this suspicion could not be confirmed.

To our knowledge, left posterior fascicular block in cats has not been documented, and this case has provided an example of intraventricular conduction delay in this species. Although the cat was euthanized owing to complications of arterial thromboembolism, detection of a left posterior fascicular block pattern on ECG examination was supportive of advanced cardiac disease.

Footnotes

a.

Humulin R 100 U/mL, Lilly USA, Indianapolis, Ind.

References

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  • 8. Surawicz B, Knilans TK, Chou T-C. Other intraventricular conduction disturbances. In: Chou's electrocardiography in clinical practice. 6th ed. Philadelphia: Saunders/Elsevier, 2008;108123.

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