Sedative and electrocardiographic effects of low dose dexmedetomidine in healthy cats

Abstract

In feline veterinary practice sedation is often needed to perform diagnostic or minimally invasive procedures, minimize stress, and facilitate handling. The mortality rate of cats undergoing sedation is significantly higher than dogs, so it is fundamental that the sedatives provide good cardiovascular stability. Dexmedetomidine (DEX) is an α2-adrenergic receptor agonist utilized in cats to provide sedation and analgesia, although studies have been utilized high doses, and markedly hemodynamic impairments were reported. The aim of this study was to prospectively investigate how the sedative and electrocardiographic effects of a low dose of DEX performing in cats. Eleven healthy cats were recruited; baseline sedative score, systolic arterial pressure, electrocardiography, and vasovagal tonus index (VVTI) were assessed, and repeated after ten minutes of DEX 5μg/kg intramuscularly (IM). A smooth sedation was noticed, and emesis and sialorrhea were common adverse effects, observed on average seven minutes after IM injection. Furthermore, electrocardiographic effects of a low dose of DEX mainly include decreases on heart rate, and increases on T-wave amplitude. The augmentation on VVTI and appearance of respiratory sinus arrhythmia, as well as sinus bradycardia in some cats, suggesting that DEX enhances parasympathetic tonus in healthy cats, and therefore will be best avoid in patients at risk for bradycardia.

Effects of intranasal and intramuscular dexmedetomidine in cats receiving total intravenous propofol anesthesia

“…The present study revealed that vomiting occurred more in the IN group (62.5%) than in the IM group (37.5%). Contrastingly, the previous study in children [5] revealed IN dexmedetomidine as an effective for sedation and reduce the incidence Available at www.veterinaryworld.org/Vol.15/July-2022/14.pdf of nasal irritation and post-operative nausea and vomiting compared with opioids. This result may support the suggestion that nose-to-brain delivery is an effective route for targeting the central nervous system [20].…”

“…During the anesthetic maintenance, the respiratory and HR after receiving IV propofol anesthesia did not differ between the two groups and likely reflected the dexmedetomidine effects (HR = 98 ± 15 bpm in the IN group and HR = 88 ± 10 bpm in the IM group). Dexmedetomidine is known to cause bradycardia by vasopressor action that increases arterial and pulmonary pressures [5]. In addition, this drug decreases sympathetic nervous system activity within the central nervous system, thereby decreasing both GABAergic and glycinergic inhibitory input into the cardiac vagal neurons, which may worsen bradycardia [31].…”

“…Dexmedetomidine mediates its effects by stimulating the presynaptic alpha-2 adrenoreceptor, inhibiting norepinephrine release [1,2], and stimulating postsynaptic alpha-2 adrenoreceptors on the vascular smooth muscle [3]. Dexmedetomidine is used for physical examinations of aggressive pets, minor clinical procedures, and as a pre-anesthetic medication [4][5][6].…”

“…Dexmedetomidine provides a strong sedative effect and significantly reduces the required dosage of anesthetic induction drugs, including propofol [7], as well as the dosage of anesthetic maintenance gas [1,4,7,8]. However, dexmedetomidine can cause decreased heart rate (HR) and body temperature [1], respiratory depression [7], transient hypertension to hypotension [5], and vomiting [1,4].…”

“…This represents a convenient, simple, and noninvasive administration approach [8,10]. Recently, IN dexmedetomidine has been applied in children [5,[11][12][13]. The drug delivery effectiveness through the IN route that targets the brain has been previously shown in humans [14,15] and dogs [6,8,10].…”