Today's Veterinary Practice

SEP-OCT 2018

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FEATURES todaysveterinarypractice.com SEPTEMBER/OCTOBER 2018 21 myocardium is performing more work, is prone to arrhythmias, and is sensitive to fluid challenges or overload. 11 While cats are in a hospital setting, their increased stress level is reflected by clinically significant increases in heart rate, respiratory rate, and blood pressure. 12 Although these changes did not seem detrimental to healthy cats studied, these changes may cause complications in cats with cardiomyopathy. DRUGS FOR SEDATION OF CATS WITH CARDIAC DISEASE The ideal sedative or anesthetic agent for cats with cardiac disease would be one that causes sedation or anesthesia without cardiorespiratory depression. Unfortunately, for cats, no single drug provides the optimal balance of sedation without cardiorespiratory depression; therefore, the clinician must select a drug combination that produces the least amount of cardiorespiratory depression with the best quality of sedation. The drugs commonly used to produce sedation or anesthesia in cats are opioids, benzodiazepines, antiepileptics (gabapentin), phenothiazines, alpha-2 agonists, and injectable anesthetics (e.g., ketamine, alfaxalone, propofol, etomidate). Opioids Opioids have minimal negative cardiovascular effects and are thus desirable drugs for sedating or anesthetizing cats with cardiac disease. The most common cardiac side effect of opioids is vagally mediated bradycardia, which may be negligible in cats because of their propensity for increased sympathetic tone while in the hospital and because opioids can also stimulate their sympathetic nervous system. 13-15 The vagally mediated bradycardia can be offset with anticholinergic drugs (e.g., atropine or glycopyrrolate); however, these drugs will increase heart rate, myocardial work, and oxygen consumption, none of which are desirable in cats with hypertrophic heart disease. Therefore, anticholinergics should be considered only if the opioid produces severe bradycardia (i.e., heart rate <120 beats/min). The activation of the sympathetic nervous system has led to the association of opioids and excitement in cats. Morphine and other pure mu opioid agonists have been reported to cause excitation in cats; however, the studies demonstrating this effect used supra clinical doses in cats not experiencing pain. 16,17 Although sedative effects in cats are also minimal when pure mu opioid agonists are administered, the cats often become euphoric, as demonstrated by rubbing, purring, rolling, and kneading with the front paws. An opioid alone provides mild sedation that is usually enhanced by concurrently administering a sedative or low dose of an injectable anesthetic drug. Butorphanol, a mu antagonist and kappa agonist, usually produces good-quality sedation in cats with minimal untoward effects, such as ptyalism or dysphoria. 18,19 Benzodiazepines Midazolam and diazepam are benzodiazepines commonly used as anesthetic and sedative adjuncts because they augment the effects of other sedatives and anesthetics without producing cardiorespiratory depression. These drugs produce centrally mediated muscle relaxation and anxiolysis by potentiating the neurotransmitter gamma aminobutyric acid (GABA). Despite this mechanism of action, sedation is often mild or may not observed, particularly when one of these drugs is administered alone. Paradoxical responses (e.g., resisting restraint, growling, hissing, attempting to escape) have been observed in cats that initially appear sedate after being given benzodiazepines. 20,21 This potential response is especially noteworthy when the drug is used to facilitate procedures necessitating restraint (e.g., echocardiography, radiography). Although benzodiazepines have a wide therapeutic index and are very effective muscle relaxants when co-administered with other sedatives or injectable anesthetics, supratherapeutic doses (>0.5 mg/kg) can produce muscle rigidity and poor-quality sedation or anesthesia. 22 Phenothiazines Acepromazine is a phenothiazine sedative that antagonizes the effects of dopaminergic neurotransmission in the limbic and hypothalamic systems. It produces sedative and anxiolytic effects without producing analgesia. Compared with the response in dogs, equal doses in cats produce less profound sedation but adequate tranquilization. Acepromazine produces vasodilation mediated through alpha-1 adrenergic blockade on vascular smooth muscles. This effect might be particularly detrimental in cats with obstructive hypertrophic cardiomyopathy because reducing afterload exacerbates the pressure gradient across the left ventricular outflow tract. In addition, hypotension resulting from alpha-1 blockade could also decrease coronary perfusion pressure. Acepromazine has antiarrhythmic properties, which

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