However the pathophysiology of hypoxaemia and consequent decrease in SpO2 differs between the two anaesthetic techniques.
The normal physiological response to massive atelectasis is an increase in pulmonary vascualr resistance (hypoxic pulmonary vasoconstriction) with re-routing of blood to well ventilated lung zones and consequent improvement of in PaO2. However, during endobronchial anaesthesia for thoracic sympathectomy there is an apparent failure of this compensatory mechanism. When more than 70% of the lung is atelectatic, compensation by hypoxic pulmonary vasonstriction appears to be ineffective. Furthermore, in in vitro and animal studies, inhalation anaesthetic agent have been shown to depress hypoxic pulmonary vasoconstriction.
In a study by Hartrey and colleagues, SpO2<95%>20 mm Hg in 21% of patients. Similarly, we have reported sudden hypotension and bradycardia after injudicious carbon dioxide insufflation.
In an interesting study of the delayed cardiac effects of T2-4 sympathectomy, Drott and colleagues demmonstrated significantly reduced heart rate at rest, and during both exercise and the recovery phase of the exercise.
Changes in the electrical axis and shortening of the QT interval have also been reported.
B. Fredman, D. Olsfanger, R. Jedeikin
British Journal of Anaesthesia 1997; 79: 113-119
