1 Feb 2016
Alessandra Mathis
Job Title
Figure 1. A multiparameter monitor showing second degree atrioventricular blocks.
You are anaesthetising Bullo, a two-year-old Staffordshire bull terrier, for an exploratory laparotomy to remove an intestinal foreign body. Other than this, Bullo is fit and healthy.
Your premedication consisted of acepromazine 0.03mg/kg and methadone 0.3mg/kg, given intramuscularly. The induction of anaesthesia was performed with propofol, the trachea was intubated and anaesthesia maintained with isoflurane in the oxygen.
You are midway through surgery when the nurse draws your attention to the low heart rate and strange ECG. The heart rate has dropped to 36bpm and P waves are not followed by QRS waves, indicative of second degree atrioventricular blocks (2AVB; Figure 1).
So, what are your options in this situation? Do you:
Opioids can cause bradycardia and bradyarrhythmias. These can be exacerbated under general anaesthesia, in patients with high vagal tone or when the vagus nerve is stimulated, such as during gastrointestinal surgery.
In dogs, opioid-induced bradycardia is responsive to atropine, an anticholinergic agent. For treating of excessive vagal tone, the recommended dose is 0.01mg/kg to 0.04mg/kg IV or IM.
The immediate effects of atropine can be more worrying than relieving, especially if given intravenously.
Sometimes, especially at lower doses, atropine can cause the appearance of worsening 2AVB and paradoxical bradycardia. This effect is short-lived and the heart rate will rapidly increase above the pre-atropine value.
The physiological process behind bradyarrhythmia is the presynaptic blockade of muscarinic receptors that normally inhibit acetylcholine release. Once the postsynaptic blockade is established then the desired vagolytic effects of atropine will develop.
In other occasions, atropine can cause severe tachycardia with heart rates over 200bpm. Again, this is usually short-lived and the heart rate will quickly decrease to a more physiological value.
A fast heart rate will cause a rise in cardiac output and the anaesthetic depth may lighten if the vaporiser settings are not increased. Also, before administering atropine, the cardiovascular status of the patient should be taken into consideration. Atropine increases the cardiac oxygen demand and can lead to myocardial damage or arrhythmias in compromised hearts.
In patients receiving an alpha-2 agonist, atropine is not recommended as, in these cases, bradycardia is a reflex response to systemic hypertension and the administration of atropine can lead to severe and prolonged hypertension.
Although the indiscriminate use of atropine is not recommended and its effects can, initially, be paradoxical or dramatic, it is important to remember these are transient and one should not be worried about administering it when conditions demand it.
