A 4-year-old Dachshund was referred for management of a mandibular fracture. The dog underwent cardiopulmonary arrest after sedation for skull radiography. Cardiopulmonary resuscitation was started immediately, and return of spontaneous circulation was rapidly obtained. However, after resuscitation, the dog was hemodynamically unstable. Additionally, global left ventricular systolic dysfunction and a focal hyperechoic myocardial lesion were found echocardiographically, and serum cardiac troponin I was severely elevated (82.80 ng/mL, upper hospital limit <0.7 ng/mL). The dog remained hospitalized in the intensive care unit and received supportive medical therapies, including intravenous inotropes (pimobendan, dobutamine). Over the following days, progressive hemodynamic and echocardiographic improvement was achieved in response to treatment. Moreover, after 72 h, a significant reduction of serum cardiac troponin I (9.80 ng/mL) was documented. On recheck, 3 weeks after discharge, the dog was clinically stable, and both left ventricular systolic function and serum cardiac troponin I (0.10 ng/mL) were normal. Based on clinical and instrumental findings after cardiopulmonary resuscitation, a probable diagnosis of reversible postresuscitation myocardial dysfunction associated with transient myocardial injury was made.
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