Case Studies In Small Animal

Cardiovascular Medicine

Home Up

Case 19

Follow-Up

After cardiac evaluation,  Axel had a syncopal episode in ICU at 18:36. Within 4 minutes respiratory arrest occurred. He was intubated, ventilated, and 2 ml epinephrine was administered along with a total of 6 mls atropine IV. A slow heart rate and minimal pulses were obtained. Ventricular fibrillation occurred at 18:53. 2 ml epinephrine was administered and chest compressions started. He was defibrillated twice. Faint pulses were detected. 4 ml epinephrine and 3 ml atropine were injected. 500ml Dextran 70 was bolused IV. Defibrillation was repeated. At 19:03 no pulses were present and electromechanical dissociation was identified. CPR was discontinued. The owner claimed Axel's body. No necropsy was permitted.

Case Discussion

Axel had a large mass in his right ventricular outflow tract. It was so large that it extended into his main pulmonary artery and even into the right caudal lobar pulmonary artery branch. Although a thrombus is one potential rule-out for this mass, it was most likely a large tumor. On his ECG he had a complete right bundle branch block. The terminal forces (last portion of the QRS complexes) all point to the right and cranially, the location of the right ventricle in the chest. In a right bundle branch block, the left ventricle is activated normally by the left bundle branch. Normal activation is rapid since conduction velocity through the conduction system is approximately 3 times faster than conduction through myocardium. The right ventricle cannot be activated normally and so must be activated slowly, from muscle cell to muscle cell. This widens the QRS complex and pulls the last portion of the QRS complex rightward since the right ventricle is depolarized last. Presumably, the tumor invaded Axel's right bundle branch and disrupted it.

Tumors in the right ventricular outflow tract have been described before (Bright JM, et al: Right ventricular outflow tract obstruction caused by primary cardiac neoplasia. J Vet Intern Med 4:12-16, 1990). In the reference, one tumor was an ectopic thyroid carcinoma and the other was a myxoma. In Axel's case, the tumor had attained a very large size such that it partially occluded flow resulting in a low cardiac output. Upon entry to our hospital his blood lactate concentration was very high indicating that his oxygen delivery was inadequate for his tissue oxygen demands because of poor blood flow. In addition he had collapsing episodes. These episodes may have occurred when the tumor shifted slightly and completely or almost completely occluded flow. The alternate explanation is that when he tried to exercise his right ventricular pressure increased as it tried to increase flow. The increase in right ventricular pressure could have stimulated right ventricular mechanoreceptors resulting in a reflex increase in vagal tone causing bradycardia and systemic vasodilation. Whichever occurred, the final result was cardiac arrest that was unresponsive to CPR. One can imagine what chest compressions might have done to the mass and why resuscitation efforts weren't successful. Surgery was successfully performed on one of the dogs in the reference. Although this was contemplated in Axel, nature intervened before the surgeons could.

The following is a demonstration of a right bundle branch block. On the left are complexes from another dog with a right bundle branch block. On the right one can see the depolarization wave as it traverses the ventricular myocardium (right ventricle is on top and left ventricle is on the bottom as seen in the frontal plane which is the same as a right parasternal cross-sectional view on an echocardiogram). Normally the right ventricular myocardium is completely depolarized long before the left ventricle because of its lesser mass. As you watch, you should be able to see in this example that the right ventricular free wall is depolarized last because the right bundle branch has been disrupted and so normal high velocity conduction to that region has been lost. Note that the terminal (i.e., last phase) depolarization heads toward the negative pole of lead II (opposite of the label "II"). (Figures courtesy of Dr. Mark Rishniw, College of Veterinary Medicine, Cornell University)

                                       

 

Mark D. Kittleson, D.V.M., Ph.D. All rights reserved.