THE EFFECT ON RESPIRATORY DEAD SPACE OF PROLONGED EXPOSURE TO A SUBMARINE ENVIRONMENT by

Measurements were made of arterialized capillary carbon dioxide tension and mixed expired carbon dioxide as well as respiratory minute volume, tidal volume and respiratory frequency on 10 subjects during control periods and following 20 days of exposure to submarine atmosphere on two patrols. The physiological dead space was found increased by 60% on the first patrol, and 61 % on the second patrol, in which the average C02 concentrations were, 0.8% and 0.9%, respectively. These findings correspond with previous observations obtained under laboratory conditions, showing a 62% increase in physiological dead space, following 40 days of exposure to 1.5% C02. Six of the same ten subjects on the second patrol had also served on the first patrol. Their physiological dead space returned to control values after the patrol showing that the effect is reversible. Smoking habits and length of service on submarines did not change either control values of physiological dead space or the values obtained during the patrols. The significance of these findings for the evaluation of the health hazards of prolonged exposure to the submarine atmosphere is discussed. THE EFFECT ON RESPIRATORY DEAD SPACE OF PROLONGED EXPOSURE TO A SUBMARINE ENVIRONMENT INTRODUCTION Respiratory adaptation to carbon dioxide (C02) has been shown in laboratory tests to include, among other effects, an increase of 62% in respiratory dead space after 40 days of exposure to 1.5% CO2. During the subsequent recovery period on air, the physiological dead space returned to control values. This report concerns a study made aboard an operating nuclear submarine to determine whether similar results would be found. The concentrations of carbon dioxide found in such a submarine are in the neighborhood of one per cent-. Ten subjects were studied prior to and during two patrols, to determine whether changes in physiological dead space would occur. MATERIALS AND METHODS The following measurements were made, first under normal conditions, and then at sea after about 20 days of continuous exposure to average daily carbon dioxide levels of 0.91% during the. first patrol, and 0.79% C02 during the second patrol: breathing frequency in breaths/minute, tidal volume, minute volume, mixed expired percentage of COo, arterialized venous partial pressure of C02 and blood pH. The experimental protocol was as follows: In the control period prior to first patrol, measurements were taken with the subjects supine, whereas on patrol in rough seas and with limited space in the sick bay, the measurements were taken in a sitting position. A correction factor used for converting the supine control measurements to equivalent sitting values was based on studies of Larson and Severinghaus*. After the subject accustomed himself to a two-way inspiration/ expiration valve with a pliable rubber mouthpiece, a 100-liter Douglas bag was attached so as to collect any expired air over a ten minute period during which the average respirations per minute were noted. The volume of the expired air was measured with a dry gas meter and the expired CO2 concentration was determined with an infrared CO2 analyzer (Beekman LBL 1) on three occasions, except during the first patrol, where measurements were made with a Harvard Series 2000 C02 analyzer. Blood Pco2 and pH was measured with an Ultra-Micro pH/Blood Gas Analyzer, 113 SI (Instrumentation Laboratories, Inc.). During the first patrol a Radiometer Micro Blood Gas Analyzer and Tonometer were used. The ten minute volume of collected expired air was corrected to Body Temperature Pressure Saturated (BTPS), and the average tidal volume was determined by dividing the ten-minute corrected expired volume by the total number of respirations over the 10minute period. The investigations were repeated during a second patrol and, in this case, both control and patrol measurements were made in a sitting position. Moreover, six subjects participated in both studies, allowing an evaluation of recovery between patrols. The actual blood pH values and the blood Pc02 values were determined on arterialized capillary blood samples. Gambino, et al.,, have shown that arterialized capillary blood can be substituted for the arterial blood sample, giving equivalent results. The physiological dead space (VDrHy) was calculated according to Enghoff, as follows: Vn T "Pur — VB (Pae002 — PEC02) Pacnn9 Plr C02 ■C02 where: VDPHT = physiological dead space VE = tidal volume (expiratory) PacC02 = arterialized capillary C02 pressure ^oo2 == mixed expired C02 pressure Pco2 —■ inspired C02 pressure RESULTS Table I presents the data on respiratory functions collected on 10 subjects during control periods and during 20-day exposure to submarine atmosphere. Respiratory minute volume, tidal volume and respiratory frequency did not exhibit consistent changes, however, the blood PC02 tension and physiological dead space were found significantly increased during the patrols. Six of the subjects participated in both patrols. Their data are shown in Table II. The second set of control measurements actually represent data obtained after two months of recovery following the first patrol. It is therefore possible to evaluate whether the physiological dead space returned to normal during the period between two patrols which it does, as indicated in Table II. Since the length of submarine service might produce some differences in the changes in physiological dead space, a group of three submariners, with average submerged time of 19.3 months, was compared with the other seven submariners having an average submerged time of 4.9 months. As can be seen in Table III, control, as well as patrol values, were nearly the same in both groups. Smokers and non-smokers do not show any differences in their control values as well as in their response to the exposure to the submarine environment, as shown in Table IV. DISCUSSION The blood PC02 control values for the first and the second patrol are rather low, particularly the supine control data which should be higher. Both sets of control data probably reflect some hyperventilation of the submariners carrying out a test in the unfamiliar laboratory setting. This means that the dead space measurements during control condition are most likely too low. However, since they are still in the range of normal values, they cannot be too far off. On the other hand, the data obtained during the patrols show a consistent increase in PC02 as well as physiological dead space. The physiological dead space data during patrol are significantly higher and out of normal range. If the subjects had hyperventilated during patrol, the dead space should be lower. In spite of the obvious limitation of this study, consisting of only one measurement during the patrol and the hyperventilation problem during the control period, the consistency of the findings demonstrating abnormally higher physiological dead space values makes them significant, particularly since they represent the first data obtained under these conditions. It is obviously necessary to expand this work and to include far more frequent measurements during patrol.