Site shows some of the common clinical situations associated with ventricular arrhythmias. As can be seen, many cardiac and extracardiac conditions which compromise oxygen supply to cardiac muscle leading to ischaemia, or which increase sympathetic stimulation to the heart or generate factors which are toxic to the myocardium, commonly give rise to ventricular arrhythmias. If cardiac muscle is abnormal or diseased in some way the chances of arrhythmias developing and being sustained are greater when compared to animals with a normal myocardium. It is important to distinguish between ventricular escape beats which occur due to failure of generation and or conduction of impulses from the sinoatrial node (which are preceded by a pause) and ventricular premature contractions () which occur prematurely after the preceding sinus beat. Escape complexes should never be suppressed by the use of antidysrhythmic drugs.
Having diagnosed the presence of ventricular premature contractions (VPCs) or bouts of ventricular tachycardia, the next decision to make is whether or not drug treatment is indicated to suppress that arrhythmia. Obviously, where there is an underlying predisposing condition for which there is appropriate treatment then this should be administered (for example fluid therapy to treat hypovolaemic shock and / or to correct acid-base and electrolyte disturbances, oxygen therapy to treat hypoxia, blood transfusion to increase oxygen-carrying capacity in severe anaemia). It is important that plasma electrolytes are measured in animals with cardiac arrhythmias since not only can abnormalities contribute to arrhythmogenesis but the efficacy and toxicity of antiarrhythmic drugs will be affected by electrolyte disturbances, particularly of potassium ion concentration. The danger with ventricular arrhythmias is that they may progress to ventricular fibrillation which leads to death very rapidly.
When should a ventricular arrhythmia be treated?
It is not possible to predict which patterns of ventricular arrhythmia are most likely to progress to ventricular fibrillation. The recommendations for treating or not treating a specific ventricular arrhythmia are therefore not based on controlled scientific studies but more on intuition. The importance of this decision is that many of the antidysrhythmic drugs used to treat ventricular arrhythmias have pro-arrhythmogenic potential and so could make the situation worse.
The decision to give drugs to suppress a ventricular arrhythmia is probably best made by assessing whether or not the rhythm disturbance is resulting in haemodynamic abnormalities. Those animals with weak pulses, poor peripheral perfusion and signs of muscle weakness and mental depression which can be attributed to the arrhythmia, should be treated. In addition, it is thought that frequent ventricular premature contractions (more than 20 per minute), particularly if they are multiform and are characterized by beats which occur immediately after the previous repolarization phase (the so called Vulnerable period) are more likely to progress to ventricular fibrillation.