Assessment of extravascular lung water and cardiac function in trimix SCUBA diving.

UNLABELLED: An increasing number of recreational self-contained underwater breathing apparatus (SCUBA) divers use trimix of oxygen, helium, and nitrogen for dives deeper than 60 m of sea water. Although it was seldom linked to the development of pulmonary edema, whether SCUBA diving affects the extravascular lung water (EVLW) accumulation is largely unexplored. METHODS: Seven divers performed six dives on consecutive days using compressed gas mixture of oxygen, helium, and nitrogen (trimix), with diving depths ranging from 55 to 80 m. The echocardiographic parameters (bubble grade, lung comets, mean pulmonary arterial pressure (PAP), and left ventricular function) and the blood levels of the N-terminal part of pro-brain natriuretic peptide (NT-proBNP) were assessed before and after each dive. RESULTS: Venous gas bubbling was detected after each dive with mean probability of decompression sickness ranging from 1.77% to 3.12%. After each dive, several ultrasonographically detected lung comets rose significantly, which was paralleled by increased pulmonary artery pressure (PAP) and decreased left ventricular contractility (reduced ejection fraction at higher end-systolic and end-diastolic volumes) as well as the elevated NT-proBNP. The number of ultrasound lung comets and mean PAP did not return to baseline values after each dive. CONCLUSIONS: This is the first report that asymptomatic SCUBA dives are associated with accumulation of EVLW with concomitant increase in PAP, diminished left ventricular contractility, and increased release of NT-proBNP, suggesting a significant cardiopulmonary strain. EVLW and PAP did not return to baseline during repetitive dives, indicating possible cumulative effect with increasing the risk for pulmonary edema.

Heliox in airway management.

Helium-oxygen ("heliox") mixtures have been used for decades in the treatment of various respiratory problems ranging from acute upper airway obstructions to lower airway derangements, such as asthma and exacerbations of chronic bronchitis. This review presents a brief history of helium and helium-oxygen mixtures and their potential clinical uses, summarizes the results of past research into heliox in respiratory applications, explains the physiology of heliox, and presents more recent literature relating to heliox in the clinical setting.

Effect of hypobaric air, oxygen, heliox (50:50), or heliox (80:20) breathing on air bubbles in adipose tissue.

The fate of bubbles formed in tissues during decompression to altitude after diving or due to accidental loss of cabin pressure during flight has only been indirectly inferred from theoretical modeling and clinical observations with noninvasive bubble-measuring techniques of intravascular bubbles. In this report we visually followed the in vivo resolution of micro-air bubbles injected into adipose tissue of anesthetized rats decompressed from 101.3 kPa to and held at 71 kPa corresponding to approximately 2.750 m above sea level, while the rats breathed air, oxygen, heliox (50:50), or heliox (80:20). During air breathing, bubbles initially grew for 30-80 min, after which they remained stable or began to shrink slowly. Oxygen breathing caused an initial growth of all bubbles for 15-85 min, after which they shrank until they disappeared from view. Bubble growth was significantly greater during breathing of oxygen compared with air and heliox breathing mixtures. During heliox (50:50) breathing, bubbles initially grew for 5-30 min, from which point they shrank until they disappeared from view. After a shift to heliox (80:20) breathing, some bubbles grew slightly for 20-30 min, then shrank until they disappeared from view. Bubble disappearance was significantly faster during breathing of oxygen and heliox mixtures compared with air. In conclusion, the present results show that oxygen breathing at 71 kPa promotes bubble growth in lipid tissue, and it is possible that breathing of heliox may be beneficial in treating decompression sickness during flight.

The ratio of the alveolar ventilations of SF6 and He in patients with lung emphysema and in healthy subjects.

This study assess the possible impact of changes in the morphometry of acinar airways and air spaces on the efficacy of intrapulmonary gas mixing for sulphur hexafluoride (SF6) relative to that for helium (He). To that end the alveolar ventilations of He and SF6 were determined in patients with macroscopic lung emphysema and in healthy subjects. He-SF6 washout tests were performed in 17 patients (15 emphysema, 2 chronic bronchitis) and 21 healthy subjects. Using a three-compartment model, the data obtained were used to estimate the overall, effective, alveolar ventilations of SF6 and He, and their ratio VAASF6/VAHe. Mean VAASF6/VAHe (+/- S.D.) for patients (0.80 +/- 0.06) was significantly smaller (P < 0.001) than the value for the group of age-matched healthy subjects (0.90 +/- 0.05) which was non-significantly smaller than the result for the group of young, healthy subjects (0.93 +/- 0.03). In our patients, we also determined a score for emphysema using high resolution computed tomography, and this score correlated inversely with VAASF6/VAHe (r = -0.56, P = 0.018). We have interpreted our observations to mean that in patients with lung emphysema, the efficacy of intrapulmonary gas mixing for SF6 as compared with that for He reflected by VAASF6/VAHe is diminished due to increased diffusive path-lengths within the enlarged air spaces of their lungs which impair diffusive gas mixing for SF6 more than for He.

Anomalous behavior of helium and sulfur hexafluoride during single-breath tests in sustained microgravity.

We performed single-breath wash-in tests for He and SF6 in four subjects exposed to 14 days of microgravity (microG) during the Spacelab flight Spacelab Life Sciences-2. Subjects inspired a vital capacity breath of 5% He-1.25% SF6-balance O2 and then exhaled to residual volume at 0.5l/s. The tests were also performed with a 10-s breath hold at the end of inspiration. Measurements were also made with the subjects standing and supine in 1 G. Phase III slope was measured after the dead-space washout and before the onset of airway closure. In all subjects in 1 G, whether standing or supine, phase III slope for SF6 was significantly steeper than that for He. However, in microG, the slopes became the same. Furthermore, after breath holding in microG, the SF6 slopes were significantly flatter than those for He. On return to 1 G, the changes were reversed, and there was no difference between preflight and postflight values. Because most of the phase III slope reflects events occurring in the acinar regions of the lung, the results suggest that microG causes conformational changes in the acini or changes in cardiogenic mixing in the lung periphery, but in either case the mechanism is unclear.

Hypoxic helium breathing does not reduce alveolar-arterial PO2 difference in the horse.

In a previous study we evaluated the mechanism of alveolar-arterial PO2 (AaPO2) reduction when nitrogen is replaced with helium in normoxia (FIO2 = 0.21). The reduction in AaPO2 was not due to changes in VA/Q inequality, pulmonary O2 diffusing capacity, or cardiac output, but to more complete diffusion equilibration as a consequence of the higher ventilation and thus PAO2 (which reduced the average slope of the hemoglobin O2 dissociation curve (ODC), and thus enhanced diffusive equilibration). We hypothesized that hypoxic He/O2 breathing in contrast would not reduce the AaPO2 because PAO2 and PaO2, although higher with He than N2, would remain constrained to the linear region of the ODC. Breathing hypoxic gas mixtures did constrain the PAO2 to the linear region of the ODC, even when PAO2 was increased by He/O2 breathing. Thus, the average slope of the ODC did not change when He replaced N2 and this explains the lack of change in AaPO2, as hypothesized.

Theoretical validation of the respiratory benefits of helium-oxygen mixtures.

A theoretical analysis of convective gas transport validates the clinically demonstrated advantage of using helium-oxygen mixtures in treating patients with respiratory problems. Previous studies have attributed that advantage to the ability of helium-oxygen to stay laminar at higher velocities than nitrogen-oxygen. The present work shows that helium-oxygen does not need to be laminar to provide higher flow rates and that its benefits persist under turbulent conditions. The analysis is applied to steady flow through the lungs and through a circular airway obstruction. A simplified model of the lungs gives pressure-flow relations that show a significant increase in oxygen flow rate when nitrogen is substituted by helium. A similar improvement is found for flow through an obstruction. For a given pressure difference across the lungs or across an obstruction, the turbulent flow rate of oxygen increases by approximately 50% when nitrogen is replaced by helium in a mixture containing 20% oxygen.

Collateral ventilation and gas exchange in emphysema.

Resistance to collateral flow of gas is high in the normal human lung but may be lower in emphysema. However, the contribution of collateral ventilation to gas exchange in emphysema remains unclear. This study evaluates the role and magnitude of collateral ventilation between bronchopulmonary segments in six patients with clinical, functional, and computed tomographic evidence of emphysema, compared with our previous findings in 12 normal subjects. To assess collateral flow, a balloon-tipped catheter with a lumen that opened distal to the balloon was inflated in segmental bronchi during fiberoptic bronchoscopy. Respiratory gas tensions were sampled by mass spectrometer from beyond the occlusion via the catheter lumen. Subjects breathed air until occlusion was established and then switched to 79% helium/21% oxygen. The rate of rise of helium concentration was measured within occluded segments and used as an index of collateral ventilation. The mean (+/- SEM) rate of rise of helium concentration was ten times greater in emphysema patients (9.5 +/- 2.7%/min) compared with normal subjects (0.8 +/- 0.3%/min) (p = 0.009). The mean PO2 within occluded segments was similar in normal subjects and emphysema patients: 45.4 +/- 1.8 mm Hg and 44.8 +/- 3.6 mm Hg, respectively. Mean PCO2 within occluded segments was lower in patients (40.1 +/- 1.9 mm Hg) than in normal subjects (46.4 +/- 1.3 mm Hg), probably due to higher regional ventilation-perfusion ratios in emphysema patients rather than collateral ventilation. In emphysema patients there was a positive correlation between rate of rise of helium concentration and final PO2 within an occluded segment (r = 0.73; p = 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)

[Cerebral blood flow dynamics in monkeys breathing a helium-oxygen mixture under high pressure]. / Dinamika mozgovogo krovotoka u obez'ian pri dykhanii geliokislorodnoi smes'iu pod vysokim davleniem.

Breathing with normoxic helium-oxygen mixture under high pressure successively induced tremor, myoclonia, seizures. Blood flow and the pO2 during the motor disorders increased, depending in the pressure, in the cortex, caudate nucleus, black substance and reticular formation.

P300 latency indexes nitrogen narcosis.

This experiment investigated the effects of nitrogen narcosis on reaction time (RT) and P300 latency and amplitude. Ten subjects breathed either air or a non-narcotic 20% oxygen-80% helium (heliox) mixture in a hyperbaric chamber at 6.5, 8.3 and 10 atmospheres absolute (ATA). The subjects responded under controlled accuracy conditions to visually presented male or female names in an oddball paradigm. Single-trial analysis revealed a strong relationship between RT and P300 latency, both of which were slowed in a dose-related manner by hyperbaric air but not by heliox. A clear-cut dose-response relationship could not be established for P300 amplitude. These results indicate that P300 latency indexes nitrogen narcosis and are interpreted as support for the slowed processing model of inert gas narcosis.

Detection of venous air embolism in dogs by emission spectrometry.

Emission spectrometers provide alternative, relatively inexpensive methods for detecting the concentration of respiratory gas nitrogen. Mass spectrometers are accepted as reliable monitors of end-tidal nitrogen for detection of venous air embolisms. We evaluated an inexpensive emission spectrometer for detecting changes in nitrogen levels and compared it with a mass spectrometer for detecting increased end-tidal nitrogen levels in dogs with venous air embolisms. During in vitro gas flow studies (helium; oxygen; helium/oxygen mixtures; or 70% nitrous oxide/30% oxygen with 0, 1, 2, or 3% isoflurane), air boluses (0.01 to 5.0 ml) were injected into a gas flow circuit and outlet nitrogen levels were measured by a Collins 21232 emission spectrometer. Responses were greater after each bolus when helium rather than oxygen was the major diluent gas. During in vivo studies, 5 dogs were anesthetized, ventilated, denitrogenated, and given venous air embolisms (0.1, 0.5, and 1.0 ml.kg-1) during oxygen and then during Heliox (20% oxygen:80% helium) breathing. End-tidal nitrogen increased approximately two-fold after venous air embolisms given during Heliox as compared with oxygen ventilation. In all 0.1-ml.kg-1 venous air embolisms end-tidal nitrogen increased when the emission spectrometer was used, but venous air embolisms less than 1.0 ml.kg-1 were not consistently detected by mass spectrometry. Emission spectrometry can be used to detect increased end-tidal nitrogen levels indicative of venous air embolism and may be a more sensitive detector than mass spectrometry.

The contribution of heart beat to gas mixing in the lungs of dogs.

The mixing efficiency for two gases of different gaseous diffusivity, helium (He) and sulphur hexafluoride (SF6) have been studied in anaesthetised dogs, closed and open chested, with and without the heart beating. Equilibration of He and SF6 was studied during rebreathing at frequency of 0.5 Hz and a tidal volume of either 0.3 or 0.5 L. Circulation and gas exchange were taken over by a complete heart and lung bypass circuit during the periods when the heart was stopped. The number of breaths required to reach 99% equilibration (n99) ranged from 4 to 14 for He and from 6 to 17 for SF6. There was no significant change in mixing efficiency in any situation. Stopping the heart increased the n99 for He by only 0.4 +/- 11% (1 SD) (n = 21). Opening the chest increased n99 by 1.4 +/- 13% with the heart beating and 2.5 +/- 19% with the heart stopped. The n99 for SF6 was 30 +/- 22% higher than that for He with the chest closed with or without the heart beating. This increased to 37% with the chest opened but was not altered by stopping the heart. The findings for the final phase equilibration rate constant were similar. We conclude that the beating action of the heart does not affect gas mixing in the lungs in the tidal breathing range.

Synergism of hyperoxia and high helium pressures in the causation of convulsions.

Hyperoxia beyond 1.8 ATA results in a striking reduction of high-pressure neurological syndrome (HPNS) type I convulsion threshold pressures but is without measurable effect on type II convulsions. The synergism is partially or completely reversed by increasing alveolar or tissue CO2 levels. High total pressures (PI) result in striking reductions in the duration of hyperoxic exposure preceding seizure onset (tc). The interaction of hyperoxia and high pressure gives rise to three zones on the PO2-Pt plane. In zone I, Pt less than 30 ATA, the duration of hyperoxia prior to convulsion onset is given by the equation PO2 -- PO2 lim = K/(tc -- tc lim), where PO2 lim and tc lim both decrease with increasing total pressure. Zone II, Pt = 30-50 ATA and PO2 1.8-2.3 ATA, is characterized by a sharp drop in tc, as Pt is increased beyond 30 ATA, to a value near 15 min that is constant within the PO2 limits given. In zone III, Pt greater than 50 ATA and PO2 greater than 0.2 ATA, tc is of the order of 2 min, and the seizures are essentially HPNS seizures only slightly modified by hyperoxia. The data are interpreted as suggesting that zone I represents hyperoxic seizures facilitated by high pressures, whereas zone II represents HPNS type I seizures facilitated by hyperoxia.

Postinspiratory mixing in the lung and cardiogenic oscillations.

Subjects inspired a 300-ml bolus of indicator gas cocktail (5% each of SF6, Ar, Ne, and He) form residual volume (RV), then inspired air to functional residual capacity (FRC). There was no evidence that a 10-s breath hold changed the relative concentrations or amounts of indicator gases in phases III and IV of expiration or allowed additional gas to mix into the RV, but the breath hold caused cardiogenic oscillations (CO) in expired gas to decrease in height. The units responsible for cardiogenic troughs and peaks are different from the units responsible for phases III and IV, respectively, in that the oscillation troughs had a lower He/SF6 ratio than the peaks whereas phase III had a higher He/SF6 than phase IV. We explain the CO as due to variation in mechanical properties, leading to variation in response to the pressure wave caused by the heart, in units that are relatively near to each other. We conclude that there is little or no postinspiratory mixing between distant lung units, but the dampening of CO suggests that units that are close to each other can mix if time is allowed.