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Deranged Physiology » CICM Primary Exam » Required Reading » Respiratory system
Physiological effects of high and low barometric pressure
is chapter is not relevant to any specific Section from the 2017 CICM Primary Syllabus, because
there is no specific entry for "describe the physiology of being sucked out of an airlock".
However, estion 10 from the second paper of 2009 specifically asked for "the respiratory
physiological responses to altitude". e examiners also wanted a discussion of "the changes in
inspired and alveolar oxygen partial pressure with increasing altitude", which allows for some
fascinating digressions. So that the reader can avoid these, a brief exam-focused summary follows:
With altitude:
Barometric pressure decreases and is ~ 200 mmHg at 10,000m altitude
Saturated vapour pressure remains stable at 37 ºC (47 mmHg)
Alveolar PO2 decreases, and is ~ 30 mmHg at 8,000m altitude
PaCO2 decreases due to hypoxic drive, and is ~ 10mmHg at 8,000m
e physiological responses to altitude are:
Acute:
Respiratory:
Minute volume increases due to hypoxic reaspiratory drive, mediated by
peripheral chemoreceptors
Cardiovacular:
Tachycardia and increased cardiac output due to increased sympathetic drive
ere is also a mild blood pressure increase
Neurological:
Decreased cognitive function
With profound hypoxia, delirium can develop
Renal and electrolyte:
Diuresis
Decreased serum bicarbonate (due to hypcapnia)
Chronic:
Respiratory:
Minute volume remains the same
Tidal volume may gradually increase due to thoracic remodelling
Cardiovascular:
Heart rate and stroke volume return to normal values as the haematocrit
adapts
Haematological:
Haematocrit increases over days/weeks, largely due to haemopoiesis and
haemoconcentration
ough the term "altitude" of course implies "great height", barometric pressure is a continuum which
spans in both directions from the impossibly narrow range of physiologically normal values. In this
chapter, some effort will be spent to cover both the highs and the lows, as they are equally interesting.
Some discussion of the more practical aspects of this is also discussed in a chapter concerning critical
illness due to high altitude. A good single reference for adaptation to low barometric pressure is Martin
& Windsor (2009), which would be enough for anybody preparing for CICM exams.
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Atmospheric and alveolar gas content at depth and altitude
Atmospheric pressure drops with increasing altitude, such that at around 8000m altitude we encounter
what is lovingly known as the "death zone" in mountaineering circles, where survival without
supplemental oxygen is impossible. If one were to plug a progression of altitude values into a simple
formula, a graph like this could be generated, which appears to agree with empirically measured
values.
What puts the "death" into "death zone" is, of course, the fall in the concentration of oxygen which
occurs with decreasing barometric pressure. To borrow some data from Ortiz-Prado et al (2019), a
handy chart can be generated to represent the thin 10km sliver of lowermost troposphere:
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e gas mixture at this lowish altitude remains relatively stable in its proportion of partial pressures. In
other words, at an altitude of 10,000m where the atmospheric pressure is 200mmHg, oxygen still makes
up 21% of the gas mixture, which gives it a partial pressure of 42 mmHg. For this reason, "high altitude"
for purposes of medical discussion is defined at about 2,700m above sea level, where the partial
pressure of oxygen is 60 mmHg, enough to bring about all those interesting physiological phenomena
so beloved by CICM examiners.
Beyond the relatively thin layer of troposphere, the composition of which is recognisable as a humanbreathable gas mixture, there is a huge diffuse layer which has a very different composition. Here is a
graphic borrowed from mrreid.org which is based on the NASA MSIS-90 atmosphere model:
As one can see, by the time we reach an altitude of 800-900 km, the dominant gases in the mixture are
now helium and hydrogen. e physiological implications of breathing this sort of gas mixture will not
be discussed here any further, as the barometric pressure at 100km is already 0.0008 mmHg, and
therefore resembles interplanetary vacuum for the intents and purposes of respiratory physiology.
Changes in alveolar gas composition with altitude
With altitude, the temperature of the gas mixture also changes, plateauing at around -57 ºC from
around 40,000m onwards. Fortunately, the human upper respiratory tract has excellent efficiency as a
heater and humidifier, which means that even at such temperatures the gas mixture reaching the lungs
would be heated to body temperature and maximally humidified. us, the saturated vapour pressure
of water remains a constant 47 mmHg, at least until you hit the Armstrong limit.
is is a problem, as the constant partial pressure of water vapour reduces the potential space for
oxygen in the gas mixture. e other gas in the alveolar mixture is CO2, which fortunately does not
stay at sea level values, mainly because hypoxia produces vigorous hyperventilation. Healthy young
anaesthetists at the summit of Everest had PaCO2 values of around 10-15 mmHg as the result of this.
So, what are the implications of this for alveolar oxygen? If one were to plot the results of the alveolar
gas equation, estimating a relatively linear progression of CO2 decrease (down to a minimum of 10
mmHg) it would look like this:
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In summary, without supplemental oxygen, the alveolar oxygen content would be zero by about
15,000m altitude (at a total atmospheric pressure of around 86 mmHg). At the summit of Everest, the
aforementioned splendid examples of courage were able to survive with a PaO2 of around 30 mmHg on
average (an arterial pO2 of ~ 25 mmHg, giving peripheral sats in a range of 34-69%), mainly because
they were fit, healthy, and preceded their ascent with a period of acclimatisation.
Acute physiological responses to low barometric pressure
At risk of trespassing out of respiratory territory and into cardiovascular, the following acute changes
occur with a sudden exposure to hypobaric pressure:
Respiratory changes:
Increased resting minute ventilation due to hypoxic drive (via peripheral chemoreceptors),
which is moderated by the response to hypocapnia from central chemoreceptors.
Decreased PaCO2 which results from this increased ventilation; the drop can be quite
substantial, as illustrated abundantly by the much-quoted example of the Everest mountaineers.
Cardiovascular changes:
Increased resting heart rate and cardiac output occurs almost immediately, and takes a few days
to subside. Vogel & Harris (1967) locked a bunch of healthy young people in a hypobaric
chamber and then made them pedal endlessly on cycle ergometers. ey found that total cardiac
output increases substantially with increasing altitude:
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is all appears to be the consequence of increased sympathetic nervous system activity, and
tends to return to near-normal levels the end of the first week.
Increased blood pressure is modest, and occurs as the result of increased cardiac output; total
peripheral resistance is actually decreased.
Neurological changes:
Decreased cognitive function and delirium are the consequences of acute hypobaric hypoxia.
is is a well-known phenomenon, and with an abrupt exposure, it is only a maer of time.
Specifically, that time is known as TUC, "Time of Useful Consciousness", the brief panic-filled
period of scrambling for your oxygen mask as the cabin suddenly depressurises. Wikipedia
produces this helpful table:
Altitude
TUC (normal ascent)
TUC (rapid decompression)
5,500 m
20 to 30 minutes
10 to 15 minutes
6,700 m
10 minutes
5 minutes
7,600 m
3 to 5 minutes
1.5 to 3.5 minutes
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8,550 m
2.5 to 3 minutes
1.25 to 1.5 minutes
9,150 m
1 to 2 minutes
30 to 60 seconds
10,650 m
30 secs to 1 minute
15 to 30 seconds
12,200 m
15 to 20 seconds
7 to 10 seconds
13,100 m
9 to 12 seconds
5 seconds
15,250 m
9 to 12 seconds
5 seconds
Hall (1949), trying to investigate this, asked healthy subjects to perform simple tasks (eg. react to
changing images by clicking a selector switch)
Presumably, the period of useful consciousness is followed by a period of useless consciousness,
during which the subject performs various disorganised tasks which do not appear to have
his/her survival as the goal. Beyond that, coma ensues aer several seconds. As one's organ of
remembering is the first to starve of oxygen, the descent into purposeless fidgeting oen goes
unnoticed, and Hall reports that "most of the subjects disclaimed knowledge of loss of
consciousness".
Chronic adaptation to low barometric pressure
Respiratory changes:
Increased resting minute ventilation persists during one's stay at altitude
Decreased PaCO2 which results from this increased ventilation; the drop can be quite
substantial, as illustrated abundantly by the much-quoted example of the Everest mountaineers.
Increased pulmonary arterial pressure and vascular density, which allows for improved
pulmonary perfusion, is apparently mild: Naeije (2010) reports a mean PA pressure of only 25
mmHg. e total pulmonary diffusing capacity increases, partly due to increased alveolar
surface area and partly due to an increase in pulmonary blood volume associated with larger
tidal volumes.
Oxygen carrying capacity of the blood changes: increased erythrocyte 2,3-DPG shis the oxygen
dissociation curve to the right, facilitating the release of oxygen to the tissues. ere is also an
increase in skeletal muscle vascularity and muscle tissue myoglobin
Cardiovascular changes:
Heart rate remains increased: Naeije (2010), quoting a study of adaptation to an altitude of
3800m, produces this trend of the first eight days:
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"This situation then remains stable over time", he says. Mountain natives all seem to have a
higher resting heart rate as compared to lowlander controls, but the cardiac output in both
groups is prey much the same.
Increased blood pressure remains increased due to systemic vascular resistance from increased
catecholamine secretion at any given workload, and due to increased blood viscosity resulting
from increased haematocrit.
Electrolyte changes:
Serum bicarbonate decreases, which is a totally predictable consequence of chronic
hypocapnia. Hannon et al (1971) marched nine healthy young soldiers up to Pikes Peak and
found that on average, their serum HCO3- levels decreased by 7 mmol/L.
Fluid balance and haematological changes:
Haematocrit increases, in part due to a loss of extracellular water, and in part due to the
erythropoiesis stimulated by hypoxia. is graph from Zubieta-Calleja et al (2007) demonstrates
the sort of timeframe we are talking about:
e plasma volume is reduced and the fluid balance is negative, when compared to preacclimatisation values. is "high-altitude diuresis" is thought to be the product of the net action
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of BNP, renin, aldosterone and decreased circulating levels of vasopressin (Goldfarb-Rumyantzev
et al, 2014).
Physiological consequences of explosive decompression
Unfortunately, in some circumstances, there may be no time to undergo physiological adaptation in
any meaningful sense, as hypobaric conditions may arrive suddenly. If this happens and you happen to
have a ready supply of 100% oxygen, ongoing (unhappy) survival can be assured at minimum
barometric pressures of around 190 mmHg, which corresponds to an altitude of about 10,000m.
To go higher than that for any extended period of time would require the use of a pressurised suit.
Harry Armstrong, aer whom the Armstrong Limit is named, described the upper limits of even shortterm survival as being around the territory of 18,000-19,000m above sea level, where the boiling point
of body fluids is below the boiling point of water at that pressure (47 mmHg). e partial pressure of
atmospheric oxygen at this altitude is so low that total anoxia should be assumed, and the conditions
are assumed to be rapidly lethal.
At this stage, and beyond, survival is unlikely unless urgent repressurisation takes place. As if anoxia
were not enough, as pressure drops even more disturbing phenomena take place. For instance, as blood
in arteries and veins is relatively pressurised in comparison to the external environment, it is not
expected to boil at the Armstrong limit, but in complete vacuum that is exactly what might happen. In
the so tissues, the extracellular fluid evaporates, creating painful pockets of vapour ("ebullism"); in the
intravascular volume the evolution of bubbles produces "vapour lock" of the cardiac chambers,
producing a cessation of circulation within 10-15 seconds. As the intrathoracic air content expands, the
pressure on mediastinal structures also produces a profound vagal bradycardia."Some degree of
consciousness will probably be retained for 9 to 11 seconds", the Bioastronautics Data Book helpfully
remarks. Presumably, it would be acceptable to perform compression-only CPR in this scenario. In
short, the immediate consequences of explosive decompression are:
Pneumothorax and pneumomediastinum, because of the rapid expansion of intrathoracic gas
Gas embolism, because of the same
Decreased lung volumes because of the displacement of the diaphragm upwards by expanding
gas in the abdominal contents
Vagally mediated bradycardia, also due to the relative increase in intrathoracic pressure
Shock, from multiple mechanisms, not the least of which being:
Vapour lock by air emboli
Decreased blood pressure and heart rate due to vagal stimulation
Decreased venous return due to intrathoracic gas expansion
Decreased level of consciousness due to a combination of poor perfusion and poor oxygenation,
as well as microscopic gas emboli
Expulsion of intestinal contents
Most of these data are derived from cruel animal experiments performed by well-meaning villains such
as Bancro & Dunn (1965). "A generalized muscle spasticity, a few gasps, momentary convulsive
seizures, apnea, and gross swelling of the body and extremities" were reported; in spite of these
phenomena all dogs exposed for less than 120 seconds survived, albeit usually with some neurological
sequelae (eg. blindness).
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Human experience of sudden vacuum exposure seems to be thankfully limited; or at least, most of the
time the subject is in no position to be rescued and studied. One oen-quoted case is described by
Emanuel Roth (1968). A vacuum chamber technician was the victim. At an equivalent altitude of
around 40,000m, "the subject decompressed his pressure suit in a vacuum chamber by disrupting a
connection on his chamber umbilical hose", the narrative went.
"The subject lost consciousness in 12 to 15 seconds after decompression. Clonic and tonic
movements of the feet were noted. After only 20 seconds in a vacuum, the suit was
recompressed to 3.7 psia. Within a period of 27 seconds the chamber was at 6 psia. He
regained consciousness at this time. There was no recollection of chest or abdominal pain in
the accident report."
Extraterrestrial cases of accidental suit failure are poorly reported. An event oen quoted as "Landis,
G.A. Personal communication, 1999" records the recollection of the astronaut Gregory Benne, which
was apparently reported via a post he had made on the sci.space Usenet group:
"Incidentally, we have had one experience with a suit puncture on the Shuttle flights. On
STS-37, during one of my flight experiments, the palm restraint in one of the astronaut’s
gloves came loose and migrated until it punched a hole in the pressure bladder between his
thumb and forefinger. It was not an explosive decompression, just a little 1/8 inch hole, but
it was exciting down here in the swamp because it was the first injury we’ve ever had from
a suit incident. Amazingly, the astronaut in question didn’t even know the puncture had
occurred; he was so hopped on adrenaline it wasn’t until after he got back in that he even
noticed there was a painful red mark on his hand. He figured his glove was chafing and
didn’t worry about it…. What happened: when the metal bar punctured the glove, the skin
of the astronaut’s hand partially sealed the opening. He bled into space, and at the same
time his coagulating blood sealed the opening enough that the bar was retained inside the
hole."
Any list of poorly reported space accidents must also mention the Soyuz 11 catastrophe, where the
return capsule depressurised on reentry, killing the three crew members inside. Georgy Dobrovolskiy,
Vladislav Volkov and Viktor Patsaev died as the consequence of what appears to be a valve
leak. Communication was lost shortly aer the capsule undocked from the space station, and
communication was lost with the crew, who were found lifeless upon their descent. It appeared that at
an altitude of approximately 168 km, the cabin depressurised to a barometric pressure of 0 mmHg over
approximately 100 seconds. An inspection of the ship's interior revealed that the shoulder straps of all
the cosmonauts were unfastened, and the commander was tangled in his straps. Telemetery recording
of these final moments observed that the respiratory rate of the crew increased to 40-50 in the four
seconds following seal failure; death occurred aer 48-49 seconds. Onboard voice tapes reveal that the
crew were able to identify the source of the leak within a few seconds, but the remaining TUC was too
short.
Changes in alveolar and atmospheric gas far below sea level
e discussion of atmospheric and alveolar gas in free-range humans are far less informed, because
there are more heights on earth than depths, and the depths are less thoroughly plumbed. Tan et al
(2008), on trying to create some sort of overview for this topic, found themselves without anything to
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overview:
"the authors emphasise that detailed pressure and density measurements within deep mines
could not be found in the literature despite an intensive search, and probably do not exist".
However, the change in temperature with depth is known - on average, for every kilometre of crust,
the minesha heats up by 10-25 ºC. e deepest mine (currently, the Mponeng gold mine) has a
rockface temperature of 66 ºC, and management ends up having to pump thousands of litres of ice
slurry down there purely as a means of keeping the miners alive. Unfortunately, nobody seems to care
about those miners' alveolar gas content (or their lives in general), and sexy British anaesthetists have
never descended into that sha with an ABG machine, so we have no direct data to inform our
discussion. Using the same formulae as above, it is possible to construct some intelligent speculations
regarding atmospheric pressure, at least:
us, theoretically at least, at the boom of a mine sha which penetrates 10km into the Earth's crust,
you would be enjoying an atmospheric pressure of 2200 mmHg (2.8 atm), with an atmospheric PO2 of
466mmHg on room air. So; would you be …healthier… down there? Unlikely, given that the
temperature would be around 150 ºC. But, let's consider a more plausible scenario, where hyperbaric
conditions are experienced occupationally or therapeutically, i.e. with conditions made as pleasant and
survivable as possible.
Physiological effects of increased barometric gas pressure
e most commonly encountered hyperbaric situation in CICM past papers is hyperbaric oxygen and
this is discussed in some detail elsewhere. e effects and complications of high oxygen concentrations
are described best in the chapter on the pharmacology of oxygen. To summarise here:
Hyperbaric hyperoxia has significant toxicity, which manifests as:
Tracheobronchitis
Acute lung injury
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Hypertension
Seizures
If the inspired fraction of oxygen remains unchanged, raised barometric pressure still has undesirable
effects, except now the nitrogen becomes harmful. A classic example of this is nitrogen narcosis,
which manifests as "certain changes in personality and performance in men subjected to increased
pressures of air" It is mainly seen in deep divers breathing compressed nitrogen/oxygen mixtures.
ough most authors report "proper" party-level narcotic effects at 10-15 atmospheres of pressure
(Pastena et al, 2005, and omas et al, 1976), there is clearly some psychomotor slowing even at 3
atmospheres of air pressure (Kiessling & Maag, 1962). Hyperbaric nitrogen toxicity manifests as:
Muscular tremors
Loss of coordination
Memory deficits
Confusion and psychosis
So, with seizures on oxygen and delirium on nitrogen, a trend seems to emerge which might suggest
that hyperbaric gases cause neurological complications. D'Agostino et al (2009) evolved this concept
further in a discussion of hyperbaric gas effects on nervous system function, which can be summarised
effectively by borrowing one of their concluding statements:
"The neurological consequences of breathing hyperbaric gases are directly related to the
gas' partial pressure, lipid solubility, and capacity to alter the physicochemical properties
of adjoining membrane nanostructures through oxidation and mechanical perturbation"
Following from this, one might surmise that gases which have low lipid solubility would be well
tolerated under high pressures. is is probably true; helium has the lowest solubility in lipid
membranes compared with other gases, and truly insane pressures of helium can be tolerated with
apparently lile physiological effect.
Effect of barometric pressure aside from gas toxicities
Enough of the effects of gases, what about the pressure itsel? Dean & D'Agostino also have an
excellent chapter on this topic in Neuman & om's Physiology and Medicine of Hyperbaric Oxygen
Therapy which is somehow available online. In short, the effects of pressure itself are as far-reaching
as one might expect from something which governs the very properties of maer and the rate of
chemical reactions which maintain life. At any given constant temperature, the equilibrium constant of
all chemical relationships is affected by the pressure variable, causing reactions to go faster or
slower. Indeed, deep-sea organisms which live at extreme pressures (eg. 1100 atmospheres, at the
boom of the Challenger Deep) have had to make major molecular modifications to their enzymes and
lipid bilayers in order to function (Macdonald, 1997). For example, the tidepool snailfish Liparis
florae has a version of lactate dehydrogenase which functions optimally at a pressure of around 60
MPa, where the LDH of surface-dwellers suffers from a greatly decreased activity (Gerringer et al,
2017).
So, what is the uppermost limit of pressure for the sustained survival of complex organisms? Pradillon
& Gaill have an excellent article outlining the challenges of survival at great depth. Under high
pressure, delicate protein structures tend to unfold and denature. Deep sea fish have met the need to
keep proteins stable under pressure by producing copious amounts of trimethylamine oxide (TMAO),
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but this is something limited by hyperosomolarity: it is an "idiogenic osmole", and beyond a certain
intracellular concentration of this substance, intracellular osmolarity would increase to the point
where much ATP would be used to pump water out of the cells. Given the extreme scarcity of
metabolic substrate down in the oceanic trenches, this is unlikely to be viewed as a satisfactory
solution by the locals. As the result of this, there may be a real biochemical constraint to the survival of
vertebrates under extreme pressure, which Yancy et al (2014) put at 8400m, or approximately 840
atmospheres of pressure. at's fragile vertebrates, mind you. Supergiant amphipods look quite healthy
as they scurry around in the Mariana Trench, and we have no clear idea as to how much deeper they
could get.
What about life in general? ere are solid chemical limits to what can be expected from unmodified
carbon-based molecules under great pressure. Elo et al (2000) determined that the tertiary strurure of
proteins begins to self-dismantle at a pressure of around 5000 atmospheres. At around the same
pressure, the DNA strand loses its helical properties. Ultimately, at 15,000 atmospheres, the primary
structure of proteins unravels, and they disintegrate into individual amino acids. In case anybody is
interested, that's probably the pressure range one encounters under the lowermost cloud layer of
Jupiter.
One might at this stage point out that human beings are in fact adapted to life at sea level, and the
discussion of Hadal crustaceans and gas giants is probably pointless to anyone who might be mainly
interested in human physiology. What, then, is the limit of human survival at high pressure? e exact
number is unknown, as to test it would require the nonsurvival of some of the subjects. We do know
however that trained professionals can tolerate extreme pressure for short periods safely. e current
record is held by eo Mavrostomos, who spent about 7 hours at a pressure of 70 atmospheres,
equivalent to a depth of 701 metres. He was pressurised over about 18 days, and depressurised over 24
days (Gardee et al, 1992). e gas mixture he was breathing consisted of 99.5% helium and hydrogen
in approximately 2:1 fractions. ere was only 0.5% oxygen, to maintain a PAO2 of less than 200
mmHg. No complex biochemical monitoring was undertaken, but the following signs and symptoms
were observed, aributed mainly to the pressure effects themselves rather than to helium:
Tremor
Mild myoclonus
Psychometric and intellectual performance were decreased
Dyskinesia with mainly proprioceptive problems
Decrease in appetite
Mild shortness of breath
General fatigue (which resolved with depressurisation to 65 atmospheres)
Physiological effects of such massively increased barometric pressure include:
Increased airway resistance due to increased viscosity of the gas mixture
Increased work of breathing due to this, as well as due to the added weight of the gas being
moved
Hypoventilation results probably from
Bradycardia: at pressures of around 5 atmospheres, heart rate decreases, albeit slightly
(Linnarsson et al, in 1999, found the heart rate of their divers dropped by about 6 bpm on
average).
Diuresis is experienced during “exposure to moderate pressure (15 to 50 atmospheres), and is
associated with a decrease in urine osmolality from reduced water reabsorption. A decrease in
ADH secretion is thought to be the cause.
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So, 70 atmospheres is the record, and humans have gone no deeper. However, at even higher pressures,
on the basis of animal studies, it is theorised that even helium will have a neurotoxic effect. It is not the
fault of helium, which is inert as inert can be, but rather the effect of the pressure itself, exerted by
aforementioned mechanisms of changing lipid membrane properties and chemical reaction rates. is
was elegantly demonstrated by Brauer et al (1982). Rats exposed to helium at pressures in excess of 200
atmospheres were observed to develop incoordination followed by seizures; rats breathing a
perfluorocarbon liquid mixture at a similar pressure developed exactly the same clinical features,
suggesting that hydrostatic pressure itself was to blame. is probably represents some sort of
maximum for multicellular organisms adapted to Earth surface pressures.
Previous chapter: Abnormal capnography
waveforms and their interpretation
Next chapter: Age-related changes in respiratory
physiology
References
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