Case Studies In Small Animal
The heart was markedly enlarged on the thoracic radiographs and the left atrium was noticeably larger than all other chambers. On his ECG, he had occasional premature complexes (fourth and 25th complexes). These QRS complexes were abnormally oriented, wider than the sinus QRS complexes, and had abnormal T waves following them that were opposite in polarity to the QRS complexes. These features are consistent with premature ventricular complexes (PVCs). Note that each of these had a P wave in front which may make one tend to think they are supraventricular in origin. Note also, however, that the PR interval is very short, especially when compared to the normal PR intervals in other complexes. These leads one to surmise that the P waves and the QRS complexes are not associated. Rather, an ectopic focus in a ventricle depolarizes before the sinus depolarization can make it through the AV node to the ventricles. The premature complexes come in 7 mm (7/25th of a second or 0.28 seconds) after the sinus QRS complexes and so are depolarizing at a rate of 215 beats/minute (60 beats/minute divided by 0.28 seconds per beat).
On the echocardiogram, Joey had severe mitral regurgitation due to myxomatous degeneration of his mitral valve leaflets and chordae tendineae. The latter resulted in rupture of at least one minor chord if not more. The ruptured chord was evident on the two-dimensional echocardiograms (the arrow). The force of the jet against the interatrial septum and/or the high left atrial pressure resulted in an endocardial tear and perforation of the interatrial septum. This resulted in an acquired atrial septal defect. Joey was lucky. A perforation in any other part of its septum would have resulted in hemorrhage into the pericardial sac and acute cardiac tamponade. This most commonly results in acute death. The picture below is from another dog with an endocardial tear (thick vertical arrow). The tear in this dog did not perforate the atrial wall. However, the primary chord to the septal leaflet (thin horizontal arrow) in this dog ruptured resulting in acute death.
Joey most likely went into right heart failure because of the acquired atrial septal defect coupled with the existing tricuspid regurgitation. The increase in right heart volume brought about by the left-to-right shunting of blood at the atrial level would increase right atrial and right ventricular diastolic pressures. This would increase systemic venous and capillary pressures resulting in transudation of fluid, in this case, into the abdomen (i.e., ascites).
The continuous wave Doppler velocity tracing of the systolic jet in the left atrium showed that the pressure gradient across the mitral valve was 115 mm Hg. The dog's systolic systemic arterial blood pressure was approximately 170 mm Hg. What is the systolic pressure in this dog's left atrium using this jet velocity? To determine this subtract 115 mm Hg from 170 mm Hg to get 65 mm Hg. This is a tremendous increase in the systolic left atrial pressure. This tremendous increase may explain why the left atrial wall tore and then ruptured.
The continuous wave Doppler beam of the blood flow jet that was flowing from the left atrium to the right atrium showed a pressure gradient across the interatrial septum of 47 mm Hg. Since this dog was in right heart failure (i.e., has ascites), its right atrial pressure must have been between 10 and 15 mm Hg. If we assume that it is 13 mm Hg, then this dogs calculated systolic left atrial pressure using this jet velocity (note that it is slightly different from what you calculated above) must have been 60 mmHg.
This dog also had a cardiac arrhythmia (fifth beat on the ECG trace of the spectral Doppler recording). It was a premature ventricular complex (PVC).
Joey was sent home on furosemide 50mg 1 tab TID and enalapril 10mg 1/2 tab SID. This
level of furosemide should help to decrease the ascites and alleviate the volume overload
this dog has. The enalapril should also help to relieve the volume overload.
One week later
Two weeks later
©Mark D. Kittleson, D.V.M., Ph.D. All rights reserved.