Circulatory failure after anesthesia induction in a patient with severe primary pulmonary hypertension.

Abstract

probe were placed, and arterial and pulmonary artery catheters were inserted during local anesthesia for continuous monitoring of mean arterial pressure (MAP), mean pulmonary arterial pressure (MPAP) and central venous pressure. After a 3-min oxygenation period, arterial oxygen saturation (SpO2 ) and SmvO2 increased (SpO2 from 91 to 95% and SmvO2 from 72 to 78%), with no change in systemic and pulmonary artery pressures (150/100 mmHg and 130/62 mmHg, respectively). General anesthesia was induced with incremental doses of fentanyl (250 mg) and midazolam (3.5 mg). Succinylcholine (75 mg) was given to facilitate airway intubation with a double-lumen tracheobronchial tube, and controlled mechanical ventilation was initiated using low tidal volumes (5‐7 ml/kg). Anesthesia was maintained with 0.5‐1% isoflurane in oxygen. As shown in figure 1, anesthesia induction was associated with a marked decrease in MAP (from 125 to 85 mmHg). A large increase in MPAP (from 80 to 115 mmHg) occurred in response to tracheal intubation, with MPAP exceeding the level of MAP. Within 2 min after the start of positive-pressure ventilation, right ventricular failure developed, as indicated by high end-expiratory central venous pressure, a dramatic decrease in cardiac output (from 3.9 to 1.2 l/min) and by low SpO2 (, 85%), SmvO2 (30%), and expired carbon dioxide values (, 2%). Hemodynamics and gas exchange improved transiently with the administration of epinephrine (two repeated doses of 50 mg followed by an infusion of 0.01 mg z kg 21 z min 21 ). At that time, transesophageal echocardiography (TEE) showed marked dilatation of the right cardiac chambers, with massive tricuspid dilatation and underfilling of the left cardiac cavities caused by a leftward shift of the interatrial and interventricular septa (fig. 2A). Shortly after thoracotomy (10 min after the start of positive-pressure ventilation), hemodynamics dramatically deteriorated (MAP of 50 mmHg with sinus rhythm at 50 beats/min); therefore, heparin (300 IU/kg) was administered and cardiac arrest ensued; open-chest cardiac massage was initiated while the femoral vessels were cannulated. Immediately after the institution of partial cardiopulmonary bypass (3.5 l/min, pump flow), MAP increased, rightsided cardiac pressures (MPAP and central venous pressure) decreased, and arterial oxygenation recovered to normal values. Bilateral sequential lung transplantation was uneventful and adequate gas exchange was easily achieved. Temporary inotropic support was necessary during weaning from cardiopulmonary bypass. At the end of surgery, transesophageal echocardiography showed marked improvement of cardiac function, with normalization of right ventricular size and interventricular septum position (fig. 2B). Postoperatively, the patient slowly emerged from anesthesia. Pressure support ventilation was necessary for 10 days, and the patient was discharged, fully ambulant and self-caring, from the hospital 70 days after undergoing transplantation. At the 2-yr follow-up, the patient’s lung function volumes and arterial gas exchange are within normal values (forced vital capacity of 85%, and forced expiratory volume i n1so f 75% of