Hemodynamic effects of carbon dioxide insufflation during thoracoscopy.

Bhavani Shankar Kodali MD

Capnothorax

As more complex thoracoscopic procedures are performed, adequate exposure becomes increasingly more important. The insufflation of CO2 has been demonstrated to aid in the compression of lung parenchyma and the effacement of subpleural lesions, and to act as a retractor when combined with changes in patient position. However, a recent study demonstrated that CO2 insufflation during thoracoscopy in the pig had adverse hemodynamic consequences. Thirty two patients undergoing thoracoscopy were studied to evaluate the effects of CO2 insufflation in the clinical setting.1 The end-tidal CO2 pressure, arterial oxygen saturation, mean arterial pressure, heart rate, and central venous pressure were monitored. Measurements were determined at baseline, at the initiation of one-lung ventilation, and at intrapleural pressures of 2 to 14 mm Hg. The authors found that the insufflation of CO2 of 2 to 14 mm Hg had no significant effect on the end-tidal CO2 pressure, arterial oxygen saturation, heart rate, or mean arterial pressure, but the central venous pressure did rise from 7.00 +/- 1.5 mm Hg to 17.30 +/- 2.53 mm Hg (p < 0.05). It is concluded from this that the insufflation of CO2 during thoracoscopy does not have adverse hemodynamic effects in the clinical setting. Therefore, a low-pressure (< 10 mm Hg) insufflation is a safe adjunct to the conduct of routine thoracoscopic surgical procedures.

Peden and Prys-Roberts2 studied 10 patients undergoing laparoscopic surgical technique for thoracic and cervical dissection of the esophagus during esophagogastrectomy. Right lung was collapsed using a double-lumen bronchial tube and carbon dioxide was insufflated into the right pleural cavity to compress the lung. Changes in hemodynamic and respiratory variables occurred. In the majority of patients airway pressure and end-tidal CO2 increased, despite alterations in ventilation. If five patients, systolic blood pressure decreased suddenly by between 15 and 35 mm Hg. In four patients, SPO2 decreased to 91% or less despite an FIO2 of 1.0. If CO2 was insufflated too fast, or the lung failed to deflate adequately, the clinical picture was that of a tension pneumothorax. One patient developed surgical emphysema and contralateral pneumothorax.

Hemodynamic instability and hypoxia can be caused by the increase in intrathoracic pressure resulting from rapid or excessive insufflation of CO2, or failure of the lung to deflate adequately in response to compression by CO2. The clinical picture which can result is that of tension pneumothorax. If this occurs the endoscope should be withdrawn immediately, the CO2 released and the patient stabilized before further cautious reinsufflation of CO2. To avoid this occurrence the CO2 should be insufflated by the surgeons at as slow rate as possible to produce the desired compression of the lung. Peden and Prys-Roberts2 suggest to ventilate lungs with 100% oxygen before deflation of the lung, and another source of oxygen is available to insufflate at 1 l.min-1 into the deflated lung, should unacceptable desaturation still occur. The lumen of the bronchial tube must be opened to air before CO2 insufflation, to allow the lung to deflate as it is compressed.

1. Wolfer RS Krasna MJ, Hasnain JU, McLaughlin JS. Hemodynamic effects of carbon dioxide insufflation during thoracoscopy. Ann Thorac Surg 1994;58(2):404-7.

2. peden CJ, Prys-Roberts C. Capnothorax: Implications for the anaesthetist. Anaesthesia 1991;48(8):664-6.