Case Studies In Small Animal

Cardiovascular Medicine

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Case 21

Case Discussion

Freckles was a 10-year-old cat that presented with signs of caudal aortic thromboembolism (rear limb paralysis, cold limbs, cyanotic nail beds and pads, lack of femoral pulses). He was in left heart failure at presentation. The left heart failure was producing pulmonary edema, which could be identified most readily caudal to his heart and ventral to his caudal vena cava. The left heart failure was also producing a small amount of pleural effusion which could be identified ventral to the last thoracic vertebrae. The pulmonary edema, although it was not severe on radiographs, was bad enough to cause respiratory distress when Freckles was physically stressed during examinations. Thoracic radiographs revealed cardiomegaly. The left auricle was so large it touched the lateral chest wall. The massive enlargement resulted in a marked increase in left auricular (and left atrial) blood volume, so much so that the left auricle stood out as a structure that was more dense than the rest of the cardiac structures on the lateral radiograph. The marked increase in left atrial size was confirmed on echocardiography.

Because the left atrium was so markedly enlarged, blood flow velocity through it was severely slowed. This is similar to water flow velocity in a river that flows through a pond. Flow velocity in the river on either side of the pond is normal while flow velocity in the pond is much slower. When red cells slow to a certain velocity, they clump together. Red cell clumping could be seen in Freckles' left atrium on the echocardiogram. This is called spontaneous contrast or echocardiographic smoke and is seen in humans predisposed to thrombus formation. It is thought that spontaneous contrast also predisposes cats to left atrial thrombus formation and in the presentations on subsequent pages you will see that this appeared to be true for Freckles. It was presumed in Freckles' case that he had previously formed a left atrial thrombus that broke loose and was carried by blood flow to his terminal aorta.

Why was Freckles left atrium so large? Because he had hypertrophic cardiomyopathy (HCM). The HCM in Freckles was evident only in his free wall and papillary muscles. Although this is a variant form of HCM, it is a relatively common variant. Presumably left ventricular diastolic function was severely compromised in Freckles because of the HCM. The increased stiffness of the left ventricular chamber resulted in an increase in left ventricular diastolic pressure. Because the mitral valve is open in diastole, whatever pressure is present in the left ventricle in diastole is also present in the left atrium. It is this increase in left atrial pressure that results in the left atrium blowing up like a balloon. It is also this pressure that causes pulmonary edema (fluid weeping from the pulmonary capillaries into the lung tissue) and pleural effusion (fluid weeping from the visceral pleural capillaries into the pleural space).

What else did the severe left atrial enlargement produce in this cat? It also produced one of his rhythm disturbances. The ECG revealed that the heart rate was approximately 240 beats/minute. Although the rate was fast, it was irregular. All of the QRS complexes appeared to have a normal configuration which means that each impulse must have originated from a supraventricular focus (sinus node, atrial myocardium, or AV junctional tissue). When an impulse originates from a supraventricular focus, the wave of depolarization must travel through the AV node, bundle of His, and bundle branches to the ventricles. If all these regions are normal, depolarization travels quickly (conduction through the conduction system is about three times as fast as from muscle cell to muscle cell) to and through the ventricles normally and so produces QRS complexes that are normal (narrow and oriented toward the left ventricle). From what we have seen so far, we are dealing with a rhythm that is fast, irregular, and supraventricular in origin. Whenever this combination is present, atrial fibrillation is a good rule-out. Examination of the baseline in this cat reveals no consistent P waves (although the eleventh and 19nth complexes in the second ECG look like they have a P wave, they are only baseline artifacts). Consequently, the diagnosis is atrial fibrillation. A large atrial surface area is required for atrial fibrillation to form and become sustained. Consequently, it is easy for a horse to develop atrial fibrillation but difficult for it to develop in a cat. Only cats with severe left atrial enlargement develop atrial fibrillation. In addition to atrial fibrillation, premature ventricular complexes (PVCs) were also present due to the presence of the severe left ventricular disease. PVCs originate in a ventricle and so cannot take advantage of the normal conduction system. Instead they must travel through the ventricles slowly, by depolarizing from muscle cell to muscle cell. This results in wide, bizarre QRS complexes followed by wide bizarre T waves. Often the orientation of the QRS complexes is also abnormal.

Lastly, Freckles had pericardial effusion and a mass in his pericardial space on the echocardiogram. This could be a neoplastic mass with a subsequent effusion but this scenario is rare in cats and would constitute a separate problem. It is more likely that the mass is related to his other problems. The only possible scenario here is that his markedly enlarged left atrium ruptured and bled into his pericardial space, and some of that blood clotted. Although this scenario is also rare in cats, it is at least plausible and because the mass appeared to be associated with his left auricle it is the one we assumed occurred. This, along with everything else we saw, prompted us to tell the owner that the prognosis was very poor.

Freckles was started on Lasix therapy (10 mg IV initially followed by 10 mg IM q 6 hours) and heparin administration (1400 U heparin SQ TID).

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