7.8.8 Ventricular premature complexes
Clinical examination and electrocardiography
VPCs are caused by abnormal impulses originating in the ventricular myoBecause they are premature they disturb the R-R interval, resulting in an irregular rhythm. Auscultation will reveal an early beat, usually followed by a longer than normal (compensatory) diastolic pause. The intensity of S1 may be greater than normal, and S2 may be relatively quiet, depending on the duration of diastole. Often a pulse deficit will be palpated.
VPCs are ectopic and do not follow the normal conduction pathways; therefore, the resultant QRS complex differs from normal. However, the normal range of QRS complex duration is quite variable in horses (0.08-0.14 sec) and the duration of a VPC may not exceed this value. VPCs may therefore have to be distinguished from sinus beats on the grounds that they have an abnormal configuration QRS complex (Figure 7.10). If the ventricular origin QRS morvaries, the condition is described as multiform. This may mean that there are multiple ectopic foci (multifocal VPCs) or that conduction from one ectopic focus is variable. Two other features can also be useful to identify VPCs. The T wave is widened, larger and of opposite polarity to the QRS complex. In addition, a VPC is almost always followed by a full compensatory pause. The sinus beat which occurs fractionally after the VPC is not conducted because the ventricles are refractory, but the following sinus beat is conducted in the usual way. This means that the short diastolic interval which indicates a premature beat is followed by a longer diastolic interval, with an R'-R interval which is greater than the normal R-R interval. This can be a useful guide when a prebeat is auscultated because APCs are seldom followed by a compensapause. However, an ECG is always required to make a definitive diagnosis. Occasionally a VPC occurs between two normal QRS complexes without disrupting the R-R interval, in which case it is called an interpolated beat.
The significance of VPCs
VPCs are relatively uncommon in horses in comparison with other species. However, the presence of an occasional, isolated VPC is not necessarily abnormal and is found in a few apparently normal individuals during a 24-hour ECG recording. If no other abnormalities are detected, the abnormal beat may be of no significance. However, detection of even a single VPC should alert the clinician to the possibility of myocardial disease and a thorough investigation should be performed. In some animals, the frequency of the VPCs may increase during exercise. This may be associated with poor athletic performance or even collapse. However, in a few cases, a normal increase in the sinus rate during exercise will result in abolition of the VPCs, if they have a slow intrinsic rate which is overridden by a raised sinus rate. In this instance, the VPCs are unlikely to limit performance. Radiotelemetry and 24-hour ECG recording may be useful to assess the significance of the arrhythmia.
Ectopic foci which cause VPCs can result from primary myocardial disease or from the effects of systemic disease on a normal myocardium. Investigation should be aimed at detecting underlying cardiac or systemic disease. If myodisease is the cause this may involve just a small focal lesion or the whole of the myocardium may be involved. Echocardiography may be required in order to identify underlying heart disease. Systemic disease may be evident on clinical examination. Routine biochemistry and haematology may also be helpful.
Management and treatment of horses with VPCs
Treatment is aimed at reversing the underlying condition in the first instance; only if clinical signs at rest are severe should antidysrhythmic drugs be used. However, specific treatment is seldom possible; the principal treatment is rest. A period of 1-2 months may be sufficient. The horse should then be re-evaluated and, if VPCs are still present, a further period of rest or treatment may be required. If a moderate number of VPCs are occurring (e.g. 1-6 per minute), and an inflammatory myocarditis is suspected, then corticosteroid treatment (as described for treatment of APCs) may be helpful (see Appendix). On some occasions corticosteroids have helped when the VPCs are more frequent or even if they dominate the rhythm.
If VPCs are frequent and constitute a ventricular tachycardia (see below), antidysrhythmic treatment may be required in some cases. Treatment may also be required if there are multiform VPCs, or if R-on-T phenomenon is observed (when the QRS complex of the VPC coincides with the T wave of the previous complex). The judgement of whether to treat or not is primarily dependent on the clinical condition of the horse. If the animal is weak then treatment is more likely to be required.
The drug of choice is quinidine gluconate given intravenously. Quinidine sulcan be given by stomach tube if this is not available. Lignocaine can also be used to treat ventricular tachycardias, although it has the potential to cause neurological side-effects including seizures. In fact, this problem is seldom encountered and, if quinidine gluconate is not available, lignocaine (without adrenaline) can be used, particularly if the arrhythmia occurs during general anaesthesia. Monitoring of the ECG is advisable during the course of treatment of ventricular tachydysrhythmias.
In the majority of horses with VPCs, antidysrhythmic drugs are not required. If treatment is needed, great caution should be used because these drugs are negative inotropes. If widespread cardiac disease with poor myocardial conis detected, lignocaine may be preferable to quinidine because it is less likely to precipitate a profound fall in blood pressure. If the condition can be managed by box rest and reversal of underlying disease, this is preferable.