ABSTRACT
This is found in many healthy patients (particularly trained athletes), but also in hypothyroidism and hypothermia, and with raised intracranial pressure. When a bradycardia develops anew, it is often the result of excessive vagal stimulation and may resolve on stopping the stimulus (e.g. carotid sinus stimulation in carotid surgery or oculocardiac reflex in eye surgery). Although the prolonged diastole which accompanies a bradycardia aids coronary perfusion, coronary blood flow still depends on an adequate filling pressure in the aortic sinus. This, in turn, demands that the ventricle must be able to compensate for a reduction in rate by an increase in stroke volume. Although easy for a healthy ventricle, this may be impossible for one that is close to failure or that has previously been infarcted. Under these conditions, it is possible that a bradycardia (usually below 50 beats/min) will result in systemic hypotension and poor coronary filling that may be sufficient to demonstrate ischaemia on the ECG. The treatment is small incremental doses of atropine (0.1-mg steps) to return the rate to normal without overshooting to a tachycardia (unless the bradycardia occurs during carotid endarterectomy when lignocaine [lidocaine] on the carotid sinus is the treatment of choice).
