Case Report. We present the case of a 74-year-old male with a history of hypertension and smoking who was urgently referred for evaluation after he suffered a cardiac arrest after a transurethral prostate resection (TURP) in a community hospital without coronary intervention capabilities. The patient initially presented to the emergency room with progressively worsening abdominal distension and was found to have a distended urinary bladder and bilateral hydronephrosis due to an enlarged prostate. The patient underwent a TURP without complications. While in the recovery room, he was noted to be hypotensive and suddenly had ventricular tachycardia, which progressed to ventricular fibrillation. Advanced cardiac life support measures were immediately implemented, and the patient underwent multiple electrical cardioversions, received several doses of intravenous epinephrine, lidocaine, and atropine, and was intubated. After 20 minutes of resuscitation, he regained a pulse with a systolic blood pressure of 70 mmHg. His 12-lead electrocardiogram showed sinus tachycardia with diffuse 4 mm ST segment elevation in the anterior and inferior leads. Even with escalating doses of intravenous norephinephrine and neosynephrine, he remained hypotensive with a systolic blood pressure in the 70“80 mmHg. A repeat 12 lead electrocardiogram revealed resolution of the inferior ST segment elevation, however there was persistent 3 mm ST elevation in anterior precordial leads in V3 and V4. Physical examination revealed a blood pressure of 72/40 mmHg, a heart rate of 120 beats/minute, a respiratory rate of 20 breaths/minute, and a temperature of 97.8. He had evidence of fractured ribs with paradoxical motion of his chest with the ventilator. He was tachycardic with a regular rate and rhythm, he had a normal S1 and S2 without an appreciable S3 or S4. He had a 2/6 holosystolic murmur heard loudest in the apex radiating to the axilla. There were no thrills or rubs. He had bilateral rales up to half of his lung fields. He had diminished but equal pulses bilaterally in the extremities without periphral edema. His neurological examination was grossly non-focal. His laboratory examination revealed a BUN of 29 mg/dL and creatinine of 1.6 mg/dL. His complete blood count and coagulation profile was within normal limits. His chest radiograph showed bilateral alveolar infiltrates consistent with pulmonary edema. An intraaortic balloon pump was immediately inserted, and he had an augmented blood pressure of 110 mmHg post-procedure. He was immediately transferred to a tertiary care center with for further management.

At the tertiary medical center, coronary angiography demonstrated the following: the left main had a diffuse 30% lesion, the proximal left anterior descending artery (LAD) had a diffuse 70% lesion, and the mid LAD had a tubular 90% lesion. The distal circumflex had a diffuse 90% stenosis (Figures 1 and 2). The right coronary artery (RCA) had a proximal 70% lesion and a diffuse 90% stenosis in its midportion. A pulmonary artery catheter was placed and the mean right atrial pressure was 9 mmHg, the right ventricular pressure was 31/8 mmHg, the pulmonary artery pressure was 25/15 with a mean of 20 mmHg, and the pulmonary capillary wedge pressure was 9 mmHg. The arterial saturation 99% and the mixed venous saturation was 47%. Left ventriculography revealed normal left ventricular function with an estimated ejection fraction of 47% with mild anterolateral hypokinesis, and severe posterobasal, diaphragmatic, and apical hypokinesis. There was severe (4+/4+) mitral regurgiation (with the intraaortic balloon pump on stand-by).

The patient underwent balloon angioplasty and stenting of the lesions in the proximal and mid RCA. Balloon angioplasty was performed in the lesion in the mid RCA with a Maverick Monorail 2.5 x 30 mm (2 inflations with a maximal inflation pressure of 10 atmospheres), and the lesion was stented with a Penta 3.0 x 38 mm device. Balloon angioplasty was performed on the lesion in the proximal RCA using the same balloon (one inflation with maximal inflation pressure of 10 atmospheres), and a Penta 3.0 x 18 mm was placed across the lesion overlapping the proximal portion of the previously placed stent. Post-intervention angiography revealed no significant residual stenosis in the RCA with TIMI 3 flow (Figure 4). A small molecule glycoprotein IIb/IIIa inhibitor was used during the procedure, however had to be discontinued due to persistent bleeding from the endotracheal tube. The patient was transferred to the coronary care unit, and he subsequently underwent coronary artery bypass graft surgery after three days with a saphenous vein graft to the LAD, and a saphenous vein graft to the circumflex artery, and mitral valve repair with a 26 mm ring. The patient™s post-operative course was uneventful.