The adverse effects of hypoxic hypoxia include acute mountain sickness (AMS), high altitude pulmonary edema, and high altitude cerebral edema. It has long been assumed that those manifestations are directly related to reduction in the inspired partial pressure of oxygen (P(I)O2). This assumption underlies the equivalent air altitude (EAA) model, which holds that combinations of barometric pressure (P(B)) and inspired fraction of O2 (F(I)O2) that produce the same P(I)O2 will result in identical physiological responses. However, a growing body of evidence seems to indicate that different combinations of P(B) and P(I)O2 may produce different responses to the same P(I)O2. To investigate this question with respect to AMS, we conducted a search of the literature using the terms hypobaric hypoxia, normobaric hypoxia, and hypobaric normoxia. The results suggest that the EAA model provides only an approximate description of isohypoxia, and that P(B) has an independent effect on hypoxia and AMS. A historical report from 1956 and 15 reports from 1983 to 2005 compare the same hypoxic P(I)O2 at different P(B) with respect to the development of hypoxia and AMS. These data provide evidence for an independent effect of P(B) on hypoxia and AMS, and thereby invalidate EAA as an ideal model of isohypoxia. Refinement of the EAA model is needed, in particular for applications to high altitude where supplemental O2 is inadequate to prevent hypoxic hypoxia. Adjustment through probabilistic statistical modeling to match the current limited experimental observations is one approach to a better isohypoxic model.

No abstract

The use of a 12 degrees taper criterion did not result in preclinical students achieving the goal of a 12 degrees taper. However, a 12 degrees criterion is more realistic than a 6 degrees criterion for full veneer crown preparations.

It is expedient to use normobaric hypoxia (NH) as a surrogate for hypobaric hypoxia (HH) for training and research. The approach matches inspired oxygen partial pressure (P(I)o₂) at the desired altitude to that at site pressure (PB) by reducing the inspired fraction of oxygen (FIo₂) to <0.21 using the equation: PIo₂= (PB - 47) × FIo₂, where 47 mmHg is the vapor pressure of water at 37°C. The investigator then has at site pressure the equivalent PIo2 as at altitude, i.e., the NH exposure is at an "equivalent air altitude." Some accepted as fact identical signs and symptoms of hypoxia for both conditions. However, those that derived the alveolar air equation showed that the coupled alveolar oxygen (PAo₂) and carbon dioxide partial pressures (PAco₂) for NH and HH are not identical when PIo₂is equivalent. They attribute the difference in alveolar gas composition under equivalent PIo₂to a nitrogen dilution effect or, more generally, to the respiratory exchange effect. Those that use NH as a convenient surrogate for HH must concede that physiological responses to NH cannot be identical to the responses to HH given only equivalent hypoxic PIo₂.

No abstract

Some manufacturers of reduced oxygen (O2) breathing devices claim a comparable hypobaric hypoxia (HH) training experience by providing F1O2 < 0.209 at or near sea level pressure to match the ambient oxygen partial pressure (iso-PO2) of the target altitude. I conclude after a review of literature from investigators and manufacturers that these devices may not properly account for the 47 mmHg of water vapor partial pressure that reduces the inspired partial pressure of oxygen (P1O2), which is substantial at higher altitude relative to sea level. Consequently, some devices claiming an equivalent HH experience under normobaric conditions would significantly overestimate the HH condition, especially when simulating altitudes above 10,000 ft (3048 m). At best, the claim should be that the devices provide an approximate HH experience since they only duplicate the ambient PO2 at sea level as at altitude. An approach to reduce the overestimation and standardize the operation is to at least provide machines that create the same P1O2 conditions at sea level as at the target altitude, a simple software upgrade.

Our hypothesis is that metabolic gases play a role in the initial explosive growth phase of bubble formation during hypobaric exposures. Models that account for optimal internal tensions of dissolved gases to predict the probability of occurrence of venous gas emboli were statistically fitted to 426 hypobaric exposures from National Aeronautics and Space Administration tests. The presence of venous gas emboli in the pulmonary artery was detected with an ultrasound Doppler detector. The model fit and parameter estimation were done by using the statistical method of maximum likelihood. The analysis results were as follows. 1) For the model without an input of noninert dissolved gas tissue tension, the log likelihood (in absolute value) was 255.01. 2) When an additional parameter was added to the model to account for the dissolved noninert gas tissue tension, the log likelihood was 251.70. The significance of the additional parameter was established based on the likelihood ratio test ( P < 0.012). 3) The parameter estimate for the dissolved noninert gas tissue tension participating in bubble formation was 19.1 kPa (143 mmHg). 4) The additional gas tissue tension, supposedly due to noninert gases, did not show an exponential decay as a function of time during denitrogenation, but it remained constant. 5) The positive sign for this parameter term in the model is characteristic of an outward radial pressure of gases in the bubble. This analysis suggests that dissolved gases other than N2in tissues may facilitate the initial explosive bubble-growth phase.

To develop a predictive equation and to test ideas about the mechanisms involved in hypobaric decompression sickness, we performed statistical analyses on published results of 7,023 exercising O2-breathing men subjected to one-step decompressions in altitude chambers. The dependent variable was signs or symptoms so severe that the person's trial was terminated (forced descent). The three independent variables were 1) duration of 100% O2 breathing at ground level (prebreathing), 2) atmospheric pressure after ascent, and 3) exposure duration. The best model, chosen from trial-and-error combinations of premises about bubble behavior, indicates that decompression sickness outcome depends on 1) prebreathing time, but with an unexpectedly long washout half time for N2; 2) time at altitude, as if bubbles grow; and 3) the estimated difference, raised to the fifth power, between the partial pressure of N2 in tissue before and that in bubbles after decompression, perhaps an index of the number of bubbles generated. We expect the model to provide accurate predictions for decompressions matching those of the bulk of the data; the mechanistic cues should be considered hypotheses for further investigation.