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13 Complications of Systemic Analgesic Drugs
Maria Amengual‐Vila DVM, DECVAA, MRCVS1 and Eva Rioja Garcia DVM, DVSc, PhD, DACVAA, DECVAA, MRCVS2
1 Highcroft Veterinary Referrals, Wirchurch, Bristol, UK
2 Optivet Referrals, Havant, Hampshire, UK
Overview
Systemic analgesic medications are commonly used in the horse, and are encouraged for the majority of surgical conditions. There are many different agents available for use in the horse. While they are commonly prescribed, the consequences of extended use are not often considered. This chapter discusses the commonly‐used analgesic agents and the potential complications associated with their use.
List of Complications associated with systemic analgesic drugs
Intra‐op complicationsBradyarrythmiasAnaphylactoid reactionNegative effect on recovery from general anesthesiaAlpha‐2 adrenergic agonistsKetamineLidocaine
Post‐op complicationsOpioids – ExcitementIleusAlpha‐2 adrenergic agonistsOpioids
Intra‐Op Complications
Bradyarrythmias
Definition
Bradycardia in horses is considered to be present when the heart rate is below 24 beats per minute. Atrio‐ventricular conduction blocks (AV blocks) occur when the conduction through the AV node is slower than normal and are classified as first‐, second‐ or third‐degree depending on the degree of conduction abnormality. Bradyarrhythmias are commonly associated to the administration of alpha‐2 adrenergic agonists.
Risk factors
The severity of bradycardia is dependent on the route of administration of the alpha‐2 adrenergic agonist, with a greater degree of bradycardia associated with an intravenous compared to an intramuscular route.
The severity and duration of bradycardic effect is dependent on the drug administered, for example:
Detomidine causes more prolonged cardiovascular effects compared with medetomidine and xylazine [1].
Romifidine causes more prolonged cardiovascular effects compared with detomidine and xylazine [2].
Horses with a pre‐existing high vagal tone may be more prone to severe bradyarrhythmias.
Pathogenesis
Alpha‐2 adrenergic agonists result in sedation, skeletal muscle relaxation and analgesia by activating alpha‐2 adrenergic receptors in the locus coeruleus and the spinal cord. They decrease the central nervous system sympathetic output and peripheral sympathetic tone. Bradycardia is observed within 2 minutes following an intravenous bolus and is initially caused by a baroreceptor reflex in response to vasoconstriction and systemic hypertension caused by alpha‐2b postsynaptic receptor activation in vascular smooth muscle. Bradycardia persists once the hypertension subsides due to the decrease in sympathetic tone. Severe bradycardia due to increased vagal tone and decrease sympathetic outflow predisposes to the development of first‐ and second‐degree AV block, and sometimes third‐degree AV block. Bradycardia contributes to the marked decrease in cardiac output observed following administration of these drugs.
A retrospective evaluation of detomidine infusion for standing chemical restraint in 51 horses did not report any complications associated with cardiovascular compromise [3]. In the authors’ experience, the bradyarrhythmias associated with the use of alpha‐2 adrenergic agonists are not clinically concerning in most horses.
Prevention
The administration of a combination of drugs (i.e. alpha‐2 adrenergic agonist and opioid) reduces the dose required to achieve the same desired effect, sedation and analgesia, and therefore reduces the occurrence or degree of adverse effects. It was observed in horses that the administration of methadone, a pure mu opioid agonist, in combination with detomidine, reduced the duration of the bradycardia and increased and prolonged the hypertension induced by detomidine [4].
The IV administration of an anticholinergic drug, such as atropine, glycopyrrolate or hyoscine‐N‐butylbromide, 5 minutes before the alpha‐2 adrenergic agonist drug, prevents the decrease in heart rate without affecting the degree of sedation/analgesia.
