Dilative Cardiomyopathy with Paroxysmal Atrial Tachycardia
History. An owner brings his 5-year-old male Saint Bernard to you because of a distended abdomen, weakness, coughing, and difficulty breathing. The owner believes these signs developed gradually over several weeks; however, before the last few weeks, there were occasional episodes when the dog suddenly seemed weak and very listless.
The episodes lasted from a few minutes to about an hour.Clinical Examination. Palpation reveals that the dog has muscle wasting and marked ascites (fluid in the abdominal cavity). The jugular veins are distended. The arterial pulse is rapid and irregular; there are frequent pulse deficits (missing beats). Thoracic radiography reveals an enlarged heart and an accumulation of fluid near the lung hilus.
You record the dog’s ECG for several minutes. You note that P waves usually occur at a rate of 160 to 170 per minute and that each P wave is followed by a QRS-T complex. However, the ECG also shows frequent episodes when there are 210 to 230 P waves per minute. During these episodes, most P waves are followed by QRS-T complexes, but others are not. As a result, the QRS-T complexes occur irregularly, with about 180 per minute.
Echocardiography reveals severe dilation of all four cardiac chambers, particularly the atria. Even though the ventricles are enlarged, the ventricular walls are thinner than normal, a condition called eccentric hypertrophy. Ventricular contractions are weak.
Comment. The ECG indicates that this dog has atrial tachycardia. 'Γhe information presented does not establish whether the atrial pacemaker is located in the SA node or somewhere else in the atria. It is likely that one atrial pacemaker area is initiating depolarizations at a rate of 160 to 170 per minute and that another atrial area intermittently preempts the first pacemaker by initiating depolarizations at the more rapid rate of 210 to 230 per minute.
VXTien the atrial rate is 160 to 170 per minute, the AV node conducts every atrial action potential to the ventricles, so that the ventricles also contract 160 to 170 times/min. However, when the atrial rate is 210 to 230 per minute, some of the atrial action potentials arrive at the AV node when the nodal cells are still refractory from the preceding action potential. These atrial action potentials are not conducted into the ventricles, which is why there are only about 180 ventricular contractions per minute. This is a case in which a second-degree AV node block, created by the relatively long refractory period of AV node cells, is beneficial, because it prevents the ventricles from beating too rapidly. The problem, when an arrhythmia triggers very frequent ventricular contractions, is that the time available between contractions becomes too short for adequate ventricular refilling. As ventricular rate increases, the volume of blood pumped with each beat (stroke volume) decreases, and so does cardiac output. At ventricular rates above 180 per minute, cardiac output could fall to such a low level that the dog would collapse.This dog’s primary problem is probably a chronic, progressive weakening of his heart muscle (cardiomyopathy). All the clinical signs, including atrial tachycardia, can be attributed to a primary cardiomyopathy. Dilative cardiomyopathy is common in giant-breed dogs, especially males, and often (as in this case) there is no discernible cause.
Even though the cause of the cardiomyopathy could not be determined from the evidence available in this case, the sequence of dysfunctions that resulted from the cardiomyopathy can be inferred with near-certainty. Ventricular weakness caused heart failure; the cardiac output fell below normal, especially during exercise. The dogs body attempted to compensate for the heart failure by increasing blood volume, which increased both venous and atrial pressures far above normal. The elevated atrial pressure had the beneficial effect of “supercharging" the ventricles with an extra volume of blood before each contraction, which partially returned the stroke volume toward normal.
However, the excessive volume and pressure of blood in the veins caused pulmonary edema (which led to coughing and difficulty breathing) and systemic edema (which led to fluid in the abdomen). Also, distention of the atria made the atrial cells more excitable electrically, which resulted in the formation of ectopic pacemakers and the onset of atrial tachycardia. The tachycardia limited the ventricular refilling time, causing further compromise in cardiac output. A vicious cycle began in which decreased cardiac output caused further venous congestion and atrial distention, which aggravated the arrhythmia, and so forth. The atrial tachycardia will likely progress to atrial fibrillation. The prognosis is poor without treatment.This case of heart failure provides a good preview for the next several chapters, which deal in detail with the physiological mechanisms of cardiac and vascular control in both normal and heart failure states.
Treatment. A diuretic drug (e.g., furosemide) is administered to promote an increase in urine formation. The goal is to reduce the blood volume and venous and atrial pressures, thereby reducing the signs resulting from congestion and edema. Sometimes the paroxysmal atrial tachycardia resolves after diuretic-induced reductions in atrial size. If it does not, antiarrhythmic drugs (e.g., quinidine or lidocaine, and/or a cardiac glycoside such as digitalis) can be used to try to reduce the electrical excitability of atrial tissue.