Junctional bradycardia masking compensatory tachycardia leading to refractory hemodynamic instability during massive intraoperative bleeding: a case report

Background Junctional bradycardia during general anesthesia may obscure the expected compensatory tachycardic response to acute hypovolemia, delaying recognition of severe intraoperative hemorrhage. Case presentation We report a case of a woman in her 50s with intraperitoneal leiomyomatosis who underwent total abdominal hysterectomy and developed persistent hypotension during surgery. Despite repeated vasopressor administration, aggressive fluid resuscitation, and blood transfusion, hemodynamic instability remained refractory. A slow junctional rhythm with a heart rate of approximately 50 beats/min masked the physiological tachycardic response to massive blood loss. Following atropine administration, junctional rhythm converted to sinus tachycardia, and the heart rate abruptly increased to more than 130 beats/min while blood pressure transiently declined, unmasking the severity of the underlying hypovolemic shock. Guided by repeated laboratory testing and point-of-care thromboelastography, additional red blood cell transfusion and targeted correction of coagulopathy with fresh frozen plasma were administered, after which hemodynamic status gradually stabilized. The patient was admitted to the intensive care unit for 2 days, transferred to the general ward in stable condition, and discharged uneventfully on postoperative day 8. Postoperative transthoracic echocardiography and 24-hour Holter monitoring showed no clinically significant abnormalities. Conclusions This case highlights that a slow junctional rhythm under general anesthesia may conceal an important sign of acute blood loss and reduce the reliability of heart rate as an indicator of circulatory compromise. Following atropine administration, sinus tachycardia emerged, and the severity of ongoing hemorrhagic hypovolemia became clinically apparent. Clinical trial number Not applicable.