Case Studies In Small Animal

Cardiovascular Medicine

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Case 15

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The ECG above was recorded from an 11-year-old male standard poodle that was examined after it experienced two syncopal episodes. The first episode occurred three days and the second 6 hours prior to presentation. In each instance the recovery was prolonged. On physical examination the dog had a grade IV/VI left apical holosystolic heart murmur that was characteristic of mitral regurgitation. The heart was generally enlarged on thoracic radiographs. Pericardial effusion, left atrial enlargement, left ventricular enlargement, and normal myocardial function were identified on an echocardiogram (not shown). What would be the most likely cause of pericardial effusion in a dog with this signalment, history, and physical examination findings?

The top trace of the above ECG was recorded at presentation. It is lead II recorded at 50 mm/second and a calibration of 1 cm = 1 mV.  There are 12 mm in between the QRS complexes which means there is 12/50 of a second or 0.24 seconds between them. This translates into a heart rate of 250 beats/minute. The QRS complexes are normal in appearance. No P waves can be identified. The rhythm is extremely regular ("like a quartz crystal"). The diagnosis is supraventricular tachycardia. Based on this dog's left atrial size and his suspected disease, the arrhythmia most likely originates from the left atrium and so this is probably an atrial tachycardia. Without any P waves evident, however, the correct term is supraventricular tachycardia.

In the second tracing, carotid sinus massage was performed. Stimulation of the carotid sinus results in a reflex increase in vagal tone to the heart. In this dog it resulted in a "break" in the cardiac rhythm after the fourth complex. The fifth and sixth complexes come in at a rate of 150 beats/minute (60 seconds/minute divided by 0.4 seconds/beat). These are too fast to be junctional or nodal escape beats (these should depolarize at a rate of 40 to 65 beats/minute). They do not appear to be sinus beats since there is no P wave in front of each one and their configuration is not normally oriented. They may be junctional premature complexes that are conducted aberrantly. A normal sinus complex occurs on the last beat on this strip.

The third trace was recorded after verapamil, a calcium channel blocker, was administered intravenously (0.1 mg/kg over 5 minutes). The SVT slowed after the fourth complex allowing a P wave and a normal QRS complex to break through. A premature ventricular complex was then formed followed by the same junctional appearing rhythm seen in the second trace. These are followed by two sinus beats that have aberrant conduction (i.e., sinus beats with a left bundle branch block). This continues for a short while.

Sinus rhythm is restored in the fourth trace. This occurred about 10 minutes after the drug was administered. First degree AV block is now apparent. This is almost certainly secondary to the drug effect since the AV node depolarizes via slow calcium channels and verapamil is known to slow conduction through the AV node.

This dog improved clinically following the conversion of his rhythm. However, he continued to deteriorate after that. Pericardiocentesis resulted in withdrawal of a very bloody fluid with a PCV of 28%. The owners were told that the dog probably had a tear in the wall of his left atrium. Surgical options were discussed. The owners were told that these types of tears had been treated surgically in other dogs but that the tissue is often so friable that suturing often creates more holes than it closes and that surgery has often been unsuccessful in these dogs. They opted for euthanasia. A 5 mm tear in the left atrial wall was identified at necropsy. The arrhythmia most likely originated from this site. Whether the dogs clinical signs (e.g., "syncope") were primarily due to its arrhythmia or cardiac tamponade are unknown.

 

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