A STUDY OF CYCLOPROPANE ANESTHESIA WITH ESPECIAL REFERENCE TO GAS CONCENTRATIONS, RESPIRATORY AND ELECTROCARDIOGRAPHIC CHANGES

¹ From the Departments of Pharmacology, Physiology and Anesthesia of the University of Wisconsin Medical School

A study of cyclopropane anesthesia in the dog is presented. This gas compares favorably with other common agents and lies in an intermediate position between ethylene and ether as regards induction, maintenance and recovery from anesthesia. Surgical anesthesia may be maintained for long periods of time without immediate or late untoward effects. Complete muscular relaxation can be obtained with safe concentrations as with ether. The signs of anesthesia in the dog vary somewhat from ether, the outstanding difference being the persistence of the wink reflex into the middle of the third stage. The concentration of the gas required to maintain deep surgical anesthesia varies considerably with the individual but averages about 25 per cent. Premedication with morphine diminishes by about 12 volumes per cent the concentration of cyclopropane required to maintain a given level of anesthesia.

Respiration invariably fails before the circulation, paralysis occurring at an average concentration of 39 per cent in this series. Respiration throughout the third stage is quiet, regular, with little depression of rate. Minute volume respiration is seriously diminished only when intercostal paralysis occurs. The rather slow establishment of equilibrium between alveolar and tissue tensions, and the loss of cyclopropane from the respiratory system, as described, suggest a gradual saturation of the body lipoids with the gas.

Cardiac arhythmias occur with high concentrations of cyclopropane. The concentration required to initiate these irregularities is in the same range as that required to produce respiratory paralysis, which usually occurs a few minutes prior to or following the arhythmia. These arhythmias usually disappear as artificial respiration is instituted or the concentration lowered by adding oxygen. This agent, like ether, is sufficiently toxic to produce cardiac paralysis even under artificial respiration in the presence of an adequate alveolar tension of oxygen. These concentrations are, however, far above the anesthetic range (above 60 per cent). The initial irregularities seen are probably of vagal origin since they are abolished by atropine. It is quite evident that these arhythmias are not indicative of permanent cardiac change since a normal rhythm invariably returns and remains regular as the concentration is diminished by adding oxygen.

The many examples of respiratory failure and cardiac irregularity noted in table 4 need not be interpreted to the disadvantage of cyclopropane as a satisfactory anesthetic since the experiments were purposely designed to bring out all the potential toxicity of the agent.

More diligence is required in the use of this gas than with other agents. Being a gas and labile, like ethylene, the passage through the various stages can be exceedingly rapid. On the other hand, it possesses a potential toxicity like ether and can paralyze vital mechanisms while the alveolar oxygen tension remains high.

The evidence indicates that this agent is worthy of extended laboratory and clinical trial. We believe that cyclopropane may fulfill a long felt need of the experienced gas anesthetist.

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