FRANK J. MILNE STATE-OF-THE-ART LECTURE


Fig. 55. Simultaneous ECG rhythm strips obtained with continuous ECG monitoring demonstrating a multiform ventricular couplet. The first VPC is widened and bizarre and occurs just a little early, after the P-wave on the ECG (left larger arrows). The second VPC has a different configuration and is wider and more premature (right smaller arrows). 25 mm/sec paper speed. VE, ventricular extrasystole.


overexertion; anesthesia; hypoxia; significant blood loss; and sepsis; similar to the situation in horses with VPCs. These should be thoroughly investigated, sim- ilar to horses with VPCs, looking for possible revers- ible causes of VT. However, sustained, recurrent, or multiform VT in horses is often associated with pri- mary myocardial disease involving the ventricle. A run or a continuous stream of large, rapidly occurring QRS complexes with their T-waves ori- ented in the opposite direction of the QRS complexes


that are not associated with the P-wave is consistent with VT. The atrial rates (P-waves) occur at a slower rate than the QRS and T complexes and are buried in these complexes (Fig. 57). The QRS is usually widened, in addition to appearing bizarre (different from the normal QRS complexes), but nar- row QRS complex VT does occur in horses (Fig. 58).310 A wide VT can also occur (Fig. 59), the most severe of which is torsades de pointes (Fig. 60), when one QRS merges into the next with a sine wave configuration. VT can be uniform (with all the QRS and T complexes looking alike) or multiform (Fig. 57). An echocardiogram should be performed for all


Fig. 56. Simultaneous ECG rhythm strips obtained with contin- uous ECG monitoring demonstrating a very early VPC (large arrows) originating in the preceding T-wave creating an R on T (small arrows). This VPC is followed by a compensatory pause. Notice the widened and bizarre QRS and T morphology when compared with the normal sinus complexes. 25 mm/sec paper speed.


130 2018  Vol. 64  AAEP PROCEEDINGS


horses with VT to look for evidence of underlying structural heart disease. As with horses with VPCs, the myocardium should be carefully evalu- ated, looking for echoic areas consistent with fibro- fatty infiltrate or a scar that could act as a substrate for reentrant arrhythmias. Changes in myocardial thickness and chamber size should be evaluated, along with evaluation of myocardial function and synergy. Tachycardia-induced cardiomyopa- thy is a possible development in affected horses.39 Horses should also be carefully assessed for any aortic root abnormalities (aneurysm, calcification, or rupture), particularly for an ACF, as these horses often present with colic and VT. The car- diac valves, particularly the aortic valve, should be carefully evaluated for any vegetative lesion of bacterial endocarditis. Once the VT has con- verted to a normal sinus rhythm, the echocardio- gram should be repeated regardless of the etiology of the VT.39 TDI evaluation of myocardial func- tion following conversion may prove to be very


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