The Lungs in Special

Environments
Aviation and High Altitude
Physiology
Composition of Atmospheric
Gases
Barometric Pressures
Barometric pressure at sea level is 760
mm Hg
As altitude increases, barometric pressure
drops while partial pressure of oxygen
remains at 21%
PO
2
at sea level is about 159 mm Hg while at
50,000 feet is only 18 mm Hg
Partial Pressures of O2 and
CO2
0
20
40
60
80
100
120
140
160
180
Air Trachea Alveoli Tissues Cells
Oxygen Carbon Dioxide
Alveolar PO
2
at Different Elevations
CO
2
and water vapor decrease alveolar
oxygen
Vapor pressure in the alveoli remain at 47 mm
Hg regardless of altitude
CO
2
decreases in higher altitudes due to
hyperventilation, more so in the acclimatized
individual
Alveolar PO
2
at Different Altitudes
Effect on high altitude on O2
saturation
0 10 20 30 40 50
50
60
70
80
90
100
Altitude (thousands of feet)
A
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a
l

o
x
y
g
e
n

s
a
t
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r
a
t
i
o
n

(
p
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)

Pure oxygen
Breathing air
Effect of Breathing Pure O
2

Individual can achieve greater altitudes
when breathing pure oxygen
Person remains conscious when oxygen
saturation remains above 50%
Ceiling for breathing air is 23,000 feet, while it
is 47,000 feet when breathing pure oxygen
Acute Effects of Hypoxia
At 12,000 feet drowsiness, lassitude,
mental and muscle fatigue, headache,
nausea, sometime euphoria
At 18,000 feet twitching or seizures
At 23,000 feet coma followed shortly by
death
Acclimatization
Hypoxia is the primary physiological insult
on ascent to high altitude
The response to hypoxia depends on both
the magnitude and the rate of onset of
hypoxia
The process of adjusting to hypoxia,
termed acclimatization, is a series of
compensatory changes in multiple organ
systems over differing time courses from
minutes to weeks
Acclimatization
Most important immediate response of the
body to hypoxia is an increase in minute
ventilation
Increased ventilation = higher alveolar PO
2

Lowered alveolar PCO
2
= respiratory alkalosis
Renal compensation, through excretion of
bicarbonate ion, gradually brings the blood pH
back toward normal and allows further
increase in ventilation
Acclimatization
Ventilatory acclimatization requires 4 days
Enhanced by acetazolamide
Acclimatization
Circulatory changes increase delivery of
O2 to tissues
Increase HR, CO, BP
Pulmonary vasoconstriction to improve VQ
Increase in cerebral blood flow
Increase in RBC and Hgb concentration
Alkalosis causes left shift of O2-Hgb curve
Natural Acclimatization
Acclimatization begins at infancy
Chest size is increased, body size somewhat
decreased, larger right heart
Delivery of oxygen is also greatly facilitated
Work Capacity at High Altitudes
Capacity of all muscles is greatly
depressed in hypoxia, including cardiac
muscle
Acclimatized individuals can perform more
work at high altitudes
Acute Mountain Sickness
Nonspecific symptoms with a broad
spectrum of severity
Occurs in non-acclimatized persons in the
first 48 h after ascent to altitudes above
2500 m, especially after rapid ascent (1 d
or less)
Exact cause is unknown but cerebral
edema may play a role
Acute Mountain Sickness
Headache is the principal symptom,
typically frontal and throbbing
Gastrointestinal symptoms (anorexia,
nausea, or vomiting), and constitutional
symptoms (weakness, lightheadedness, or
lassitude) are common
Similar to an alcohol hangover, or to a
nonspecific viral infection, but without
fever or myalgias
Acute Mountain Sickness
Defined as: in the setting of a recent gain
in altitude, the presence of headache and
at least one of the following symptoms:
Gastrointestinal (anorexia, nausea or
vomiting)
Fatigue or weakness
Dizziness or lightheadedness
Difficulty sleeping
Acute Mountain Sickness
High altitude cerebral edema (HACE)
Local vasodilatation of cerebral blood vessels
caused by hypoxia cerebral edema
High altitude pulmonary edema (HAPE)
Cause is unknown but probably due to
intense vasoconstriction diversion of blood
capillary pressure becomes high and edema
develops
Chronic Mountain Sickness
RC mass and hct become very high
Blood becomes very viscous
Pulmonary arterial pressure becomes
elevated
Alveolar hypoxia
Chronic Mountain Sickness
Right side of the heart becomes greatly
enlarged
Peripheral arterial pressure begins to fall
Congestive heart failure
Death ensues unless moved to lower
altitude
Physiology of Deep Sea Diving
and Other Hyperbaric Conditions
Hyperbarism exposure of blood in the
lungs to extremely high alveolar gas
pressures
Sea Depth to Pressure
Depth (feet)

Sea Level
33
66
100
133
166
200
300
400
500
Atmosphere(s)

1
2
3
4
5
6
7
10
13
16
Effect on Depth on Volume
Boyles Law
Henrys Law
The Henry law states that the solubility of
a gas in a liquid is directly proportional to
the pressure exerted upon the gas and
liquid
Effect on High Partial Pressures on
Gases on Body
Gases which a diver breathes is nitrogen,
oxygen, and carbon dioxide
Nitrogen narcosis at high nitrogen
pressures
Varying degrees of narcosis at high pressures
1
st
symptoms of mild narcosis appear at 120
feet for 1 hour exhibits joviality
At 150 to 200 feet, diver becomes drowsy
At 200 to 250 feet, too clumsy
Effect on High Partial Pressures
on Gases on Body
Nitrogen narcosis at high nitrogen
pressures
Characteristics similar to alcohol intoxication
Narcotic effect is same as gas anesthetics
Nitrogen dissolves freely in the fats of the
body
Oxygen Toxicity at High Pressures
Effect of extremely high PO
2
on blood
oxygen transport
Effect of high alveolar PO
2
on tissue PO
2

Acute oxygen poisoning
Brain mostly affected cause seizures
followed by coma at 4 atm within 30 to 60
minutes
Nausea, muscle twitching, dizziness,
disturbance of vision, irritability and
disorientation
Oxygen Toxicity at High Pressures
Excessive intracellular oxidation as the
cause of nervous system oxygen toxicity
oxidizing free radicals
O
2
has little capability oxidizing other chemical
compounds must be active
Oxygen free radicals (superoxide O
2
-
)
Tissues contain enzymes that remove free
radicals (peroxidases, catalases, superoxide
dismutases)
Oxygen Toxicity at High
Pressures
Oxidizing free radicals
At 2 atm Hgb-O2 buffering mechanisms fail
Oxidizes polyunsaturated fatty acids
Oxidizes cellular enzymes
Nervous system specially susceptible due to
high lipid content
Carbon Dioxide Toxicity
Normally not a problem with ordinary
diving gear
Production of CO
2
not increased at great
depths
Diving helmet and rebreathing apparatus
CO
2
builds up since air is rebreathed
Beyond 80mmHg of CO
2
develops acidosis
lethargy, narcosis, anesthesia
Decompression After Exposure to
High Pressures
Amount of nitrogen dissolved in body
becomes great after a person breathes air
under high pressure
Blood flowing thru capillaries becomes
saturated with nitrogen saturate tissues
not metabolized
When pressure in the lungs normalizes,
nitrogen is removed but slowly
Decompression After Exposure to
High Pressures
Volume of nitrogen dissolved in body fluids
at different depths
At sea level 1L of nitrogen is dissolved in the
body (half in water, half in fat)
At 33 feet 2L of N
2
are dissolved, at 100 feet,
4L are dissolved
Water equilibrates in 1 hour while fat takes
several hours to equilibrate
Decompression sickness (Bends,
Caisson Disease)
If a diver has been beneath the sea long
enough and ascends rapidly,
decompression sickness develops
Gas forms bubbles due to sudden
decompression of gasses
Symptoms depend on where bubbles
dislodge (joints, nervous system,
pulmonary capillaries)
Nitrogen Elimination
Decompression tables
Tank decompression
Treatment
Decompression tank
Helium Oxygen in Deep Dives
Divers working at deep levels between
250 to 1000 feet use helium-oxygen
mixtures
Helium used due to:
One fifth narcotic effects of nitrogen
One half as much volume dissolves in tissues
Low density of helium
Use 1 percent oxygen mixtures
Hyperbaric Oxygen Therapy
Oxidizing free radicals responsible for
oxygen toxicity are also responsible for
therapeutic benefits
Treatment of gas gangrene
leprosy