Alpha-2 (α2) agonists can cause profound sedation and due to their rapid effectiveness following intramuscular administration can be convenient in animals that are difficult to restrain. Due to the profound sedation, usually less inhalant anesthetic is necessary, and induction drug doses can be markedly decreased. Occasionally, animals will respond in less desirable ways from the α2 agonists, such as extreme aggression when touched, or they can become very ataxic (Muir et al. 2000).
Dexmedetomidine, medetomidine, and xylazine are the three most commonly used α2 agonists in small animal medicine. Medetomidine and dexmedetomidine have largely replaced xylazine in small animal medicine due to their higher specificity for the alpha-2 receptor and decreased side effects. All three drugs are listed with much higher doses on the bottle in comparison with what is commonly used in practice (see Table 13.1). Cardiovascular effects include an initial spike in arterial blood pressure due to intense vasoconstriction and increased systemic vascular resistance (SVR) and a reflexive bradycardia. These effects are usually transient, and the arterial blood pressure, in most cases, normalizes. Due to a decrease in the release of norepinephrine, there is usually a decrease in arterial blood pressure over time (Tranquilli 2002).
Dysrhythmias from α2 agonists can include 1st, 2nd, and even 3rd degree atrioventricular block (Muir et al. 2000). Pale mucous membranes may be noted due to the profound peripheral vasoconstriction. Heart rates in the 40s and 50s are commonly encountered after the administration of an α2 agonist. The bradycardia should be tolerated as long as evidence of tissue perfusion is maintained. This is noted by observing the waveform on the pulse oximeter and by monitoring arterial blood pressure. If tissue perfusion is in doubt, the α2 agonists can be antagonized with yohimbine or antipamazole. Treating α2 agonist–induced bradycardia with anticholinergics is controversial because of the added myocardial work induced with anticholinergic administration. If reducing doses of anesthetic concentrations does not improve heart rate and blood pressure, reversal of the drugs may be the next best step.
Dose-dependent respiratory depression is a common side effect of α2 agonists, and in larger doses apnea and cyanosis may occur. However, ventilation is usually well maintained with therapeutic doses. Due to the vasoconstriction, decrease in cardiac output, and respiratory depression, oxygen transport is reduced. Because of the depressive effects on the cardiovascular system, α2 agonists should be avoided in cardio vascularly compromised patients or patients with a systemic illness. An increase in urine production is typically noted after administration of these drugs, so care should be used when administering to animals in renal failure or with obstructed urinary tracts (Blaze et al. 2004). Care should also be used with laryngeal paralysis patients because α2 agonists can depress swallowing reflexes. Hyperglycemia may be induced after α2 agonist administration; this results from a suppression of insulin release (Muir et al. 2000). Unlike tranquilizers, α2 agonists have potent analgesic effects by stimulating the central nervous system α2 receptors (Muir et al. 2000). Most of the positive effects of α2 agonists are enhanced when combined with other drugs such as dissociative drugs or opioids.
Dissociative drugs include ketamine and tiletamine. These drugs are categorized by the cataleptic-like state they cause. Ketamine should be avoided in epileptic animals because it has been found to cause seizures in those patients (Lin 2007). Increased heart rate and blood pressure are due to an indirect stimulation of the cardiovascular system by ketamine. Other effects are an increase in cerebral blood flow, intracranial pressure, and cerebrospinal fluid because of cerebral vasodilation and an increase in blood pressure (Lin 2007). Cats tend to have poor or sometimes even violent recoveries from ketamine alone. Symptoms include an increased sensitivity to touch, ataxia, possible hallucinations (cats may seem extremely jumpy as though they are avoiding something invisible), increased motor activity (as if they can’t sit still), and even hyperreflexia (stiffness) (Lin 2007). When ketamine is combined with other drugs such as tranquilizers, these effects tend to be less extreme, and the cardiovascular effects of ketamine are lessened or negated (Lin 2007).
Historically, it was believed that ketamine provided good somatic analgesia but poor visceral analgesia in most patients. Recently evidence has been brought to light that ketamine may have some additional analgesic qualities when used in the perioperative period such as decreasing opiate requirements (Bilgin et al. 2005). Ketamine works as an NMDA receptor antagonist, blocking the effects of glutamate, which is an excitatory neurotransmitter. In this way, ketamine helps prevent windup pain. Cats receive visceral analgesia similar to the analgesic effects of butorphanol, but it does not last very long and is not sufficient for abdominal surgeries (Lin 2007). Hypersalivation is common following ketamine, especially with oral administration.
Finally, opioid drugs are commonly a key component in preanesthetic protocols. All opioids provide analgesia; however, there are several different receptors on which opioids work and several different categories into which they fall. Most opioids will cause sedation, but the extent is dependent upon the drug, the dosage, and the health of the animal. Nonpainful animals may become nauseous or vomit; an example would be a healthy animal undergoing an ovariohysterectomy. Panting is another common side effect of opioids in many animals. Cats tend to get mydriasis and dogs miosis after opioid administration. Most opioid drugs are reversible, either by an agonist-antagonist opioid (butorphanol) or by an opioid antagonist (naloxone). The different categories of opioids are: partial agonists, agonists, agonist-antagonists, and antagonists.
Buprenorphine is a partial agonist. Buprenorphine works at the mu receptor to provide moderate analgesia and minimal sedation. Because of its strong affinity for the mu receptor, buprenorphine is difficult to antagonize; yet it can partially antagonize some of the effects of pure agonists. The full onset of action for buprenorphine is about 30–45 minutes, so it cannot be titrated to effect (Blaze et al. 2004). Buprenorphine is not commonly used as a premedication drug except perhaps in routine cases such as ovariohysterectomy and neuter patients. It is commonly used for postoperative pain management. Buprenorphine’s duration of action when given intravenously can be up to 6–8 hours.
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