30 SURGICAL SHOCK 



shows that when the abdominal viscera are exposed 

 to a current of air, they rapidly exhale COa. The 

 rate of loss is about forty times as great as that from 

 the skin. Consequently there is both a local and 

 a general reduction of the carbon dioxide. The 

 vessels of the peritoneum become dilated, peristalsis 

 is reduced or inhibited altogether, and the systemic 

 lack of COa results in apnoea and, finally, the vascular 

 phenomena of shock. It is well known that in 

 partial asphyxia the intestinal movements are 

 exaggerated. If the peritoneal cavity is filled with 

 CO2 gas, peristalsis is very active, like that seen with 

 the x-Ta.ys in a normal animal, and quite unUke the 

 quiescence which we are accustomed to observe even 

 under light anaesthesia. Saline fluid saturated with 

 CO2 also produces peristalsis, avoids that paralytic 

 condition of the bowel which is a bugbear of 

 abdominal surgery, and prevents the redness and 

 congestion of the vessels induced by the local acapnia. 

 Whilst the handling and pulling are actually going 

 on, the painful stimuli are sufficient to avert fatal 

 respiratory failure. It is well known that any pain 

 increases the rate and depth of breathing. If death 

 from shock occurs at this stage, it wiU be by failure 

 of the circulation. But as soon as the painful im- 

 pulses cease, neither pain nor CO2 is present to stir 

 the respiratory centre into activity, and death by 

 failure of respiration soon ensues. It is a common- 

 place that patients usually survive the operation 

 itself, but may die of shock a few hours afterwards. 

 Henderson found that even a few minutes' cessation 

 of the stimuli would allow the animals to lapse into 



