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Re: Lung ventilation rates

In article <199609172336.SAA17807@juliet.ucs.indiana.edu>, Nathan
Myhrvold <nathanm@MICROSOFT.com> writes
> From:         John Ruben[SMTP:rubenj@BCC.ORST.EDU]
>>Re the notion that high Mesozoic atmospheric oxygen concentration would
>>alter mammal/reptile lung ventilation rates.  This is broadly incorrect: 
>>  ALL tetrapod lung ventilation rates are governed primarily by lung
>>CARBON DIOXIDE pressures, not by oxygen pressures. Regardless of lung
>>oxygen pressure, at any given metabolic rate significant reduction of lung
>>ventilation rate would result in unacceptably high lung carbon dioxide
>>levels.  The result would be chronic systemic hypercapnia and acidosis -
>>physiologically unacceptable at any level of oxygen availability. 
>>It is also worth noting that, given the respiratory physiology of all 
>>extant tetrapods, upward alteration of Mesozoic atmospheric 
>>concentration to 30% oxygen would have had little significant effect on 
>>oxygen consumption levels in Mesozoic tetrapods, either ecto- OR 
>>endothermic.  Tetrapod blood hemoglobin affinity for oxygen is such that 
>>blood oxygen loading is virtually 100% at oxygen pressures well below 
>>those of current levels of atmosperic oxygen. Thus, even doubling of 
>>atmospheric oxygen would only increase oxygen available to tissues by 
>>a small fraction.  
>This is interesting, however it does beg the question of why 100% oxygen
>is used for humans in medical situations (and in some veternary cases) .
>I have naively assumed that this is done because the (approximately)
>five fold increase in oxygen partial pressure allows better oxygenation
>in individuals with impared ventilation.  
>Granted, pure oxygen is a LONG way from having a 32% enhancement.
>Still, I am curious about why folks would bother with pure oxygen if in
>fact the blood loading is already nearly maxed out, and carbon dioxide
>exhalation is the gaiting factor.   

        Ambient oxygen level do have a bearing on the breathing of
the  animals with four chambered heart. Though the primary drive for
respiration is the partial pressure of carbon dioxide in blood (not in the
alveoli of the lungs) it is not the only one. Hypoxia (low oxygen level in
blood) is actually a stronger driving force. Chronic retention of carbon
dioxide (hypercapnia) is compatible with life and occurs in human
patients with congenital cyanotic heart disease and chronic
obstructive lung disease. These people do not develop life
threatening acidosis because kidneys are perfectly capable for 
controlling the acid-base balance. In such a condition hypercapnia
loses its effect and hypoxia alone drives the respiration.

        The rate of gas exchange depends on the difference of the
partial pressures of the gasses in the blood and in the alveolar air
across the alveolar membrane. Greater the difference, quicker the
gas exchange. When a person develops a shallow breathing problem
(low tidal volume, as occurs in  emphysema) increasing the oxygen
level in the inhaled air improves the blood oxygen level. Usually a
small increase in the oxygen level (24 - 28%) in the inhaled air is quite
sufficient for correcting hypoxia and very rarely anything higher than
that is required in clinical practice in such conditions. Carbon dioxide
level is of very little importance here because this gas is much more
diffusible than oxygen and the difference of the partial pressure is
also much bigger. Patients with emphysema do not turn blue with
retained carbon dioxide, they become short of breath due to low
oxygen level in blood. Thus low volume breathing could be
compatible with a good life if there is more oxygen in the inhaled air.

        The rate of oxygen saturation of haemoglobin is not a factor
here. Haemoglobin can pick up oxygen only after the gas has diffused
across the alveolar membrane. Neither haemoglobin nor red blood
cells come in direct contact with alveolar oxygen - they come in
contact with the alveolar membrane only. 

Gautam Majumdar                 gautam@majumdar.demon.co.uk