A cardiovascular collapse following vigorous cough during spinal anesthesia

provided the original work is properly cited. CC Violent coughing can trigger symptomatic hypotension and may further lead to a complete loss of consciousness, which is considered a 'cough syncope' in the latter case [1]. We experienced a case of cardiovascular collapse after coughing under spinal anesthesia. We report on the case with a review of the relevant literatures. A 73-year old man was scheduled to undergo an emergency cystoscopic evacuation and transurethral resection of the prostate (TURP) under spinal anesthesia, due to gross hematuria. He weighed 55 kg and was 160 cm tall. He had a history of hypertension lasting for 5 years and received treatment with diuretics. He arrived at the operating room without premedication. His vital signs were a 120/75 mmHg of blood pressure (BP), heart rate (HR) of 75-78 beats/min with normal sinus rhythm and 99% of oxygen saturation (SpO2). With the patient in the sitting position, a 25-gauge Whitacre spinal needle was inserted at the third to fourth lumbar spinal interspace; and 6 mg of 0.5% hyperbaric bupivacaine, mixed with 15 μg of fentanyl, was injected. Sensory block to cold with an alcohol swab was tested bilaterally 5 and 10 minutes after the injection; they were T12 and T10, respectively. At the start of operation, 10 minutes after the subarachnoid block, his vital signs were a 95/60 mmHg of BP, 65-70 beats/min of HR and 99% of SpO2. During the surgery, sedative drug was not administered, and the patient had intermittent conversations with the anesthesiologist. He did not complain of dizziness, nausea or other discomforts. Fifteen minutes after the start of surgery, 25 minutes after the subarachnoid block, the patient had a very loud cough, once. Immediately after the cough, HR decreased abruptly from 65 beats/min to 30 beats/min, with sinus rhythm. Simultaneously the patient lost consciousness and did not breathe at all, and noninvasive blood pressure could not be estimated. An intravenous atropine 1 mg was administered with manual mask ventilation, with 100% O2. His heart rate increased to 100 beats/min, but BP was 55/30 mmHg. A tracheal intubation was performed, and mechanical ventilation was applied with 100% O2. Epinephrine 0.1 mg was administered intravenously with rapid hydration and Trendelenburg position. Invasive arterial BP monitoring through the right radial artery was performed (BP was 60-65/30-32 mmHg; and heart rate increased to 110 beats/min). We inserted central venous catheter in the right internal jugular vein (central venous pressure: 6 mmHg). The transesophageal echocardiography (TEE) demonstrated no evidence of LV systolic dysfunction or RV wall motion abnormality or thrombus at any angle. Hypovolemia was diagnosed; and continuous volume therapy and packed RBSs were administered. Phenylephrine infusion was maintained. Following vital sign stabilization, the surgery proceeded. During the surgery, volume status was evaluated through TEE and central venous pressure. Three units of packed RBCs and 1000 ml of cystralloid were administered. Postoperative brain MRI findings were unremarkable, and the patient recovered consciousness 25 hours after arriving at the intensive care unit and was extubated at postoperative day (POD) 2. The patient was discharged at POD 6 without any complications. Although being widely known to clinicians, the pathophysiology of cough syncope has not been completely understood owing to its uncommon occurrence. Sustained coughing can elicit decreased venous return and reduced cardiac output, fol-