The lung's response to decompression was studied in dogs anesthetized with pentobarbital sodium. Arterial pressure, hematocrit, right ventricular pressure, left ventricular end-diastolic pressure (LVEDP), dynamic compliance (CL), pulmonary resistance (RL), and arterial PO2, PCO2, and pH were measured prior to and for 3 h after a simulated air dive to 300 feet of seawater. Bronchoscopy was performed predive and at 3 h postdive. At 3 h animals were killed, and sections of lung were excised for histological examination. The decompression profile used regularly produced pulmonary hypertension, systemic hypotension, hemoconcentration, and arterial hypoxemia. CL fell in all but one dived animal. RL was more variable but remained unchanged postdive in most animals. The decompression stress did not alter the bronchoscopic and histological appearance of the airway mucosa. Pulmonary edema was regularly observed in histological sections and occurred without elevations of LVEDP. We concluded that noncardiac pulmonary edema is the principal response of the lung to decompression stress.

The mechanical properties of the lungs were measured in 10 men before and after a simulated air dive to 285 ft of seawater (87 m). The objective was to determine whether a dive likely to produce pulmonary bubble emboli would alter lung mechanics. Lung function was measured predive and at 1, 2, 3, 6, 7, and 23 h postdive. Measurements of lung function were also made at identical times on a control day when no dive was made. Each set of measurements included precordial Doppler signals, pulmonary resistance, quasistatic lung compliance, forced vital capacity (FVC), forced expired volume after 1.0 s (FEV 1.0), the ratio of FEV 1.0 to FVC (FEV 1.0/FVC%), and maximal airflow after 50 and 75% of the vital capacity had been expired (Vmax50 and Vmax75, respectively). Base-line measurements of pulmonary resistance and quasistatic compliance were normal in all subjects. FVC and FEV 1.0 were greater than predicted for most subjects and were increased proportionately so that the FEV 1.0/FVC% was normal. Following the dive, bubble signals were heard in four subjects, and two subjects had mild symptoms of decompression sickness. No subject demonstrated any alteration in lung function that could be attributed to the dive. We concluded that stressful decompressions capable of producing "silent" pulmonary bubble emboli do not alter lung mechanics.

SummaryDivers face problems during their work due t o s t r e s s e s p l a c e d upon t h e r e s p i r a t o r y s y s t e m by t h e hyperbaric environment. In addition, both the r e s p i r a t o r y and cardiovascular systems may be injured during the course of decompression sickness. Work a t the Naval Medical Research Institute ( W I ) i s directed toward solving problems in both these areas. A system of magnetometers allows evaluation of the impact of s t r e s s e s from the underwater environment on t h e d i v e r ' s r e s p i r a t o r y s y s t e m w i t h o u t i n t e r f e r i n g w i t h h i s b r e a t h i n g . O t h e r r e s e a r c h d e s c r i b e d h e r e i n is e x p l o r i n g h i g h -f r e q u e n c y o s c i l l a t i o n (HFO) of a d i v e r ' s b r e a t h i n g g a s a s a means of l e s s e n i n g l i m i t a t i o n s imposed by increased gas density. F i n a l l y , r e c e n t a n d o n g o i n g r e s e a r c h d e s c r i b e d i n t h i s paper i s aimed a t u n d e r s t a n d i n g t h e n a t u r e and mechanisms of i n j u r y t o t h e h e a r t and lungs during decompression sickness, with the goal of improving prevention and treatment of this disorder.Divers working a t d e p t h i n c u r a l i m i t a t i o n on t h e i r e x e r c i s e p e r f o r m a n c e t h a t i s imposed by t h e respiratory system. This limitation can be magnified by breathing equipment designed without regard to the u n i q u e s t r e s s e s p l a c e d upon t h e r e s p i r a t o r y s y s t e m by the diver's environment.To s t u d y t h e e f f e c t s of t h e h y p e r b a r i c environment on t h e r e s p i r a t o r y s y s t e m , a system of magnetometers has been developed that allows monitoring of t h e d i v e r ' s v e n t i l a t i o n w i t h o u t i n t e r f e r i n g w i t h h i s b r e a t h i n g , and without concern for the dependence on d e n s i t y of standard flow measuring devices.A magnetometer consists of a p a i r o f w i r e C o i l s .A l t e r n a t i n g c u r r e n t i s passed through one of the c o i l s . This induces a c u r r e n t i n t h e s e c o n d c o i l t h a t i s p r o p o r t i o n a l t o t h e d i s t a n c e b e t w e e n t h e c o i l s . Using magnetometers t o measure the anteroposterior (AP) and l a t e r a l (L) dimensions of t h e abdomen (ab)and r i b c a g e ( r c ) , R o b e r t s o n e t a l . were a b l e t o c a l c u l a t e r e s p i r a t o r y v o l u m e . ' The method was automated off-line using a d i g i t a l computer and the following model f o r c a l c u l a t i n g pulmonary volume (V): (1) where (Arc) i s the area of the rib cage and (Aab) i s t h e a r e a o f t h e abdomen c a l c u l a t e d by assuming a h o r i z o n t a l o v a l t h r o u g h t h e r i b c a g e and another h o r i z o n t a l o v a l t h r o u g h t h e abdomen. The l e n g t h O f t h e a x i s of each oval i s measured by t h e a p p r o p r i a t e AP and L magnetometer p a i r , and the area is c a l c u l a t e d as fo...