Johnson Jake, Bowden Seth, Fitzgerald Alyson H, Enders Brittany D, Pierce Kursten V
Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, Raleigh, NC, United States.
Front Vet Sci. 2025 Aug 18;12:1622850. doi: 10.3389/fvets.2025.1622850. eCollection 2025.
Common cocaine-induced arrhythmias include tachyarrhythmias such as sinus tachycardia, supraventricular tachycardia, and atrial fibrillation. Most studies evaluating cocaine toxicosis in canines have been performed in an experimental setting, using intravenous administration of the drug. Though helpful, these studies cannot be directly extrapolated in a clinical setting given the different routes of administration.
A 2-year-old male-neutered Chihuahua presented for further management of acute onset of lethargy and a transient episode of unresponsiveness. Initial point of care ECG was consistent with an underlying sinus bradycardia with concurrent first-degree AV block and intermittent high-grade second-degree AV block. No murmur was noted on thoracic auscultation. Normal sinus rhythm returned after administration of atropine and epinephrine. Upon referral to a different facility for pacemaker implantation, sinus tachycardia was appreciated on point of care ECG without evidence of supraventricular or ventricular ectopy. On cardiac focused point of care ultrasound there was normal heart function and structure with no evidence of congenital heart defects. Both cardiac troponin and NT-proBNP were within normal limits. Urine toxicology was positive for cocaine, cocaine metabolites, norfentanyl and trace amounts of fentanyl. The patient was hospitalized overnight on telemetry, during which time infrequent ventricular premature complexes were the only abnormalities noted. The patient was discharged the following day.
Cocaine-induced AV block in canines is an unusual presentation in a clinical setting, given the sympathetic stimulation this drug commonly causes. Emergency veterinary clinicians should be aware of this rare but important electrocardiographic abnormality following cocaine toxicosis.
常见的可卡因诱发的心律失常包括快速性心律失常,如窦性心动过速、室上性心动过速和心房颤动。大多数评估犬类可卡因中毒的研究是在实验环境中进行的,采用静脉给药。尽管这些研究有帮助,但鉴于给药途径不同,不能直接将其推断到临床环境中。
一只2岁去势雄性吉娃娃犬因嗜睡急性发作和短暂无反应发作前来进一步治疗。初始床旁心电图显示为潜在的窦性心动过缓,并发一度房室传导阻滞和间歇性高度二度房室传导阻滞。胸部听诊未闻及杂音。给予阿托品和肾上腺素后恢复正常窦性心律。转诊至另一家机构进行起搏器植入时,床旁心电图显示窦性心动过速,无室上性或室性早搏证据。心脏床旁超声检查显示心脏功能和结构正常,无先天性心脏缺陷证据。心肌肌钙蛋白和N末端脑钠肽前体均在正常范围内。尿液毒理学检测显示可卡因、可卡因代谢物、去甲芬太尼和微量芬太尼呈阳性。患者通过遥测进行了一夜住院观察,在此期间仅发现偶发室性早搏。患者于次日出院。
鉴于可卡因通常引起交感神经兴奋,可卡因诱发的犬类房室传导阻滞在临床环境中是一种不寻常的表现。急诊兽医临床医生应意识到可卡因中毒后这种罕见但重要的心电图异常。