Effects of pulmonary gas embolism on circulation and respiration in the dog

Mongrel dogs weighing 15–25 kg and anesthetized with thiopental-gamma-hydroxybutyric acid were used to investigate the effects of pulmonary gas embolism on pulmonary arterial pressure (P _ap ), systemic arterial pressure (P _a ) and cardiac output ( $\dot Q$ ). Pulmonary gas embolism was produced either by venous injection or by venous infusion. The most marked effect of pulmonary gas embolism on circulation was an increase inP _ap which returned to the original level after stopping the gas administration. After gas injectionP _ap rose to a maximum within 30\2-60 s. The extent of this rise inP _ap showed a positive correlation with the volume of the injected gas. The kind of gas (oxygen, helium, neon, nitrogen, air), however, did not influence the extent of the rise inP _ap , but did influence the time of return ofP _ap to the original level. Carbon dioxide showed an exceptional behavior in that it had almost no effect onP _ap at all.P _a hardly changed with the volume of the gas injections (20\2-60 ml injected within 1 s); $\dot Q$ was not measured after gas injections (the direct Fick method is not usable in this situation). Gas infusion caused a slow rise ofP _ap , its steep-ness and extent depending on the rate of infusion and on the physical properties of the infused gas. When the right ventricle was able to maintain its output, a constant level ofP _ap was reached after 10\2-15 min. In this circulatory steady stateP _ap appeared to be a measure of the degree of embolization. However, this relationship no longer held when the right ventricle failed as evidenced by a fall inP _ap ,P _a and $\dot Q$ . It may be concluded that pulmonary gas embolism produces a transient partial obstruction in the pulmonary circulation and that the performance of the right ventricle determines the maximum degree of embolization compatible with a sufficient circulation.