Study
Objectives
· To define the law of ideal gasses, Boyle-Mariotte´s law and Newton’s law of universal
gravitation.
· To describe essential topics related to flying, space life and diving, hyperbaric
oxygenation and recompression therapy, inert gas narcosis and oxygen toxicity.
· To calculate one variable from relevant variables given.
· To explain decompression sickness, hypobarotrauma (squeeze), and alveolar rupture in the
hypo- and hyperbaric environment.
· To use the above concepts in problem solving and in case histories.
Principles
· Newton’s
law of universal gravitation: Every particle in the universe attracts every
other particle with a force directly proportional to the product of the two
masses and inversely proportional to the square of the distance between them.
· Haldane’s
law: Any saturation dive to less than 10 m does not cause decompression
sickness and allows ascent without decompression stops.
· Flight
decompression. Fast ascent during flight rarely causes decompression problems
at altitudes below 10 km (30 000 feet).
Definitions
· Absolute
atmospheric pressure is the
pressure measured in atmospheres
absolute (ie, one atm.abs. at
the surface of earth, and 2-3-4 atm abs at 10-20-30 m of seawater depth).
· Decompression is the gradual fall in ambient pressure during ascent both in air and in
water.
· Decompression
sickness refers to the
formation of growing bubbles during decompression causing tissue ischaemia and
necrosis.
· Gravity
units (G) refers to the
gravity of the earth (G = 9.807 or approximately 10 m s-2).
· Hyperbarotrauma or air embolism is a major problem
of submarine escape. As the submariner escapes and ascends from the vehicle,
the gas volume of the lungs expands and ruptures pulmonary vessels. Air enters
the tissues, the thoracic cavity and the circulatory system. This causes air
embolism and death.
· Inert
gas narcosis describes an
intoxication syndrome with euphoria or anxiety, gross errors in performance
and eventually unconsciousness. Nitrogen starts to be narcotic at depths of 40
m or more.
· Pressure is measured as force per area unit. The pressure of a 10 m high sea
water column resting on 1 m2 is 1
atmosphere equal to 101.3 kPa or 760 mmHg.
· Recompression
therapy of decompression
sickness takes place in a pressure chamber, where sufficient pressure can be
established to eliminate the bubbles causing the disease.
· Squeeze or hypobarotrauma is caused by
a negative pressure difference across the wall of a non-collapsible air space
(middle ear, sinuses, compressed lungs, hollow teeth etc.).
Essentials
High-altitude
flight, space flight, and diving encounters disorders due to change of total
pressure (cf. barotrauma, decompression sickness), forces of acceleration and
weightlessness, fall in oxygen pressure (oxygen deficiency), fall in ambient
temperature, and increased radiation.
This
paragraph deals with 1. Commercial aircraft flying, 2. Satellite flying, and 3. Diving.
1.
Commercial aircraft flying
Commercial
aeroplanes fly at an altitude of approximately 33 000 ft or 10 300 m, where
the ambient pressure is 26 kPa or 195 mm Hg and the oxygen tension in the
outside cold air is around 40 mmHg - less than on Mt. Everest. The aeroplanes
have cabins pressurised to 80 kPa (corresponding to an altitude of 2000 m or
6000 ft) or sometimes only to an altitude of 2750 m. These levels cause hypoxic
dyspnoea only in cardiorespiratory patients. The main problem for the
average traveller is squeeze (hypobarotrauma) of sinuses and teeth during landing.
In case of depressurisation of an aircraft, PAO2 is rapidly reduced, and oxygen delivery must be sustained with an oxygen mask.
Hypoxia is the acute danger; decompression sickness (see below) is avoided by
fast descent to lower altitudes (higher pressures).
The rhythmicity of
human organ functions is coupled to the daily periodicity of the earth’s
rotation. The unknown endogenous periodicities, correspond approximately
(Latin: Circa) to the duration of a day (Latin: Dies), so they are called circadian
rhythms. Many circadian rhythms are synchronised to the 24-hour cycle (the
biological clock) by external signals such
as light and darkness or social habits.
The most important
diurnal rhythm is the waking-sleeping cycle, with a fall in body temperature,
respiratory rate and heart rate at the onset of sleep. Flight across time
zones causes jet lag, which is a discrepancy between the circadian rhythms and
the external signals. An eastward flight causes greater jet lag than westward
flights. The adjustment of circadian rhythms takes one day for every two hours
of time shift when flying east.
Parachuting: The accelerator force of
gravity has the same size at a
given latitude. Consider a body falling freely in an environment without air
molecules along a straight line perpendicular to the surface of the earth. In
the absence of air resistance, all bodies fall towards the earth with the same
acceleration regardless of the size and composition of the body. The magnitude
of this accelleration, which is represented by the gravity unit (G), is 9.8 or
approximately 10 m s-2. If a
parachuter was only exposed to gravity he would fall towards the earth with the acceleration 10 m s-2.
Following the first 10 s, the velocity is approximately (G* t) = (10 m s-2 *10 s) or 100 m per s.
In real life there
is no such thing as a free fall from an aeroplane, because the air resistance
soon reduces the velocity and outbalance the acceleration. Here, the
parachuter reaches the terminal velocity determined by the relation between G and air resistance. As the parachute
opens, the parachuter experiences an opening
shock load of 500-600 kg. The area of the standard parachute reduces the
terminal velocity to 1/9. The force of impact at landing is (1/9)2 = 1/81 of the landing force without parachute. This is equal to a jump from a
height of 2-3 m.
2. Satellite
flying
Space flight
requires pressure suits or cabins ensuring adequate oxygenation and
pressurisation to protect against hypoxia and decompression sickness. More
than 20 km out in the stratosphere (Fig.
16-9), the barometric pressure is
less than the water vapour tension in alveolar air (47 mmHg or 6.3 kPa), and
the oxygen tension is rapidly approaching zero. Without pressurised cabins the
blood of the astronaut would boil. In the stratosphere, instantaneous
decompression by pressure equalisation with the environment causes a monstrous
form of decompression sickness with air emboli all over the body. The body
volume of humans increases by a factor of at least three by air expansion in
tissues and blood.
Recycling
techniques have been developed for the reuse of O2. The spacecraft - just as submarines - must carry along enough carbon
dioxide absorbent to prevent death from carbon
dioxide poisoning.
Lethal
radiation dose is rapidly
reached when flying around the earth in the Van
Allen radiation belts, consisting of high-energy level protons and electrons. Therefore, commercial flying take places
essentially below the inner belt (500 km). Start and landing of long distance
space flights take place as close to the magnetic poles - with minimum
radiation energy exposure - as possible.
Forces
of acceleration (G) cause
pooling of blood in the lower extremities, a critical drop in arterial blood
pressure with orthostatic hypotension or collapse due to reduced
venous return, but also cause nausea, vomiting, and spatial disorientation.
The start
acceleration of a spacecraft is approximately linear, and the astronaut is
exposed to a tremendous acceleration - often close to 8 times the gravity of
the earth (8 G) at the first stage of a 3-stage blast-off. The space shuttle
implies a 3 G start and a 1.2 G landing.
The body of the
astronaut is located transverse to the axis of acceleration in order to
prevent pooling of blood in the legs. The astronaut often carries an anti-G
suit with the same purpose.
Gravity acts on
both the astronaut and the spacecraft in space, so astronauts are floating
inside the satellite. Weightlessness, caused by the absence of gravitational forces, produces diverse reactions. The
space pilot experience space sickness (nausea and vomiting over the first days), falling total blood volume,
muscular atrophy, Ca2+ loss from the bones, and obstipation,
brought about by the lack of stimuli. After living in outer space for weeks, adaptive
difficulties develop upon return to the life on earth. These difficulties
are low working capacity and a tendency to faint while standing. The bone loss
continues long after the return to earth, because stimulation of bone
formation requires physical activity in a gravity field.
3. Diving
This paragraph
deals with 3a. Senses in
water, 3b.
Inactive gasses, and 3c. Gas stores of man.
3a. Senses
in water
The light intensity
decreases rapidly with depth, and 100 m below sea level, it is permanently
dark.
The ratio of the
speed of light in free space to its speed in a medium is called the index
of refraction of the medium. The power of a lens is proportional to the
change in index of refraction and inversely proportional to the radius of its
curvature.
Fig.
19-1: Light refraction in the reduced eye in air and in water. The effect of goggles is remarkable and shown below.
The light
refraction is shown in a schematised eye, where the air-cornea interface
contributes 43 Diopters and the lens 15 to the focusing of parallel light rays
upon the retina (Fig. 19-1). Normally, it is the difference in index of
refraction between the air (1.00) and the cornea (1.38), which accounts for
the major refraction at the air - cornea interface (Fig. 19-1). When water
(1.33) is substituted for air, this difference becomes so small that parallel
light rays are now focused behind the retina. Only maximal accommodation of
the lens can refract parallel light rays but not enough to focus them on the
retina. Under water the unprotected eye becomes farsighted (hypermetropic) and
the image is distorted.
Goggles restore the
air-cornea interface. In spite of the high index of refraction of glass (1.5),
the parallel light rays are not refracted, because the radius of a glass plate
is infinite. Light rays not
falling perpendicular to the glass are refracted, which explains why objects
look larger under water.
Sound propagates
more rapidly in soft tissue and water than in air (1540 m s-1 as
opposed to 340 m s-1 in air). In air the detectable phase- or time
lag between the two ears helps us to determine the direction of the sound
source. Therefore underwater sound
sources appear much nearer than they actually are. Because of the
shortened delay between the two ears, localisation of sound sources becomes
extremely difficult.
The voice of a
diver speaking in a helium-oxygen atmosphere resembles the voice of Disney's
Donald Duck, because the high tones dominate in this light medium.
3b. Inactive
gasses
Inactive gasses
are eliminated by diffusion to the peripheral blood and by convection with the blood
to the lungs. During diving the ambient pressure will rise by one
atmosphere for every 10 m of
seawater depth you pass.
Fig.
19-2: Desaturation curves showing elimination of nitrogen from tissues with
different half-life. – The depth and bottom time for stage decompression is
shown to the right.
Inactive gasses
(ie, N2, H2, He, Ne, Ar etc) contribute with aa alveolar
partial pressure when present in the breathing medium, and the blood of the
lung capillaries is in immediate equilibrium with the partial pressure in the
alveolar air. Atmospheric air is the commonly used breathing gas for diving.
The solubility coefficient for N2 in blood is low (ie, 0.012 - see Table 13-1), but five times larger in fat
tissue, which has a modest perfusion rate. A large cardiac output is necessary
to transport substantial amounts of N2 to the tissues. During
saturation dives it takes a long tome before the nitrogen tension of fat
tissue reaches equilibrium with PaN2.
The human body is a
complex of tissue types, each with an individual, exponential uptake rate or
half-life for saturation (Fig. 19-2). Often a model with half-life tissues of 5-, 10-, 20-, 40-, 80-, 120-, 240-, 480-
minutes (of half-life) is used.
No
decompression diving
limits (cf. decompression tables) are limits of depth and time spend at the
depth. A work period of one hour at 60 m of depth requires a decompression
period of three hours on the steps scheduled in the decompression tables
during ascent.
Any saturation dive
to less than 10 m allows ascent without decompression stops (Haldane's law).
Fast ascent during flight rarely causes problems at altitudes below 10 km (30
000 feet). At altitudes above 20 km (where the ambient pressure is less than
6.3 kPa or 47 mmHg) the blood of a space traveller with normal body
temperature will boil, if the pressure within his suit is lost. This is
because the partial pressure of saturated water vapour at body temperature is
6.3 kPa or 47 mmHg.
3c. Gas
stores
The gas stores of
the human body are easy to calculate from standard values, and the
calculations are shown in Fig. 19-3.
The resting person
has a lung volume of 2700 ml STPD (standard Expiratory Reserve Volume added to
Residual Volume), and the blood volume consists of 2 l of arterial and 3 l of
venous blood. The extracellular fluid volume (ECV) and intracellular fluid
volume is 13 and 26 l, respectively. The oxygen content of the arterial and
venous blood is 200 and 150 ml STPD per l, respectively. The bicarbonate
concentration extra- and intra-cellularly is 24 and 10 mM, respectively. The
carbon dioxide content of the arterial and venous blood is 500 and 550 ml
STPD, respectively.
Oxygen stores
The oxygen stores
of the lungs are 18 mmol, and of the blood 38 mmol (Fig. 19-3).
We also have small
O2 stores (7 mmol) in myoglobin and in the tissues, a total of
(18+38+7) = 63 mmol.
Hypoxic brain
damage can occur after 5 min of apnoea and after 5 s of cardiac arrest (black
out and grey out).
Fig.
19-3: Comparison of the small oxygen stores to the large exchangeable carbon
dioxide stores of man.
Carbon dioxide stores
The CO2 stores of the lungs are 8 mmol, and those of the blood 118 mmol. The ECV of an
adult person contains 312 mmol bicarbonate. Intracellularly there is 260 mmol
mobile bicarbonate. These exchangeable CO2 stores comprises (8
+118+312+260) = 698 or 700 mmol in total (Fig. 19-3). The size is subject to
changes by alterations of ventilation or acid-base-status. Besides, there are
large amounts of CO2 fixed in bones.
Nitrogen stores
The human tissue
stores of nitrogen (N2) are calculated in Fig.
19-4. A normal
weight person contains 15 kg of fat and 42 litres of water (total water).
Nitrogen is five times as soluble in lipid tissue (solubility coefficient
0.065, see Chapter 13, Table 13-1) as in water (0.013). The blood of the
pulmonary capillaries is saturated with the nitrogen at the pressure
prevailing in the alveolar air.
Fig.
19-4: Partial pressures and bubble formation. The nitrogen content of a diver
at sea level before diving (left) is compared to that depth being saturated
with N2 (middle), and to the content following sudden ascent
(right).
At sea level before
diving, the diver contains about 400 ml of N2 in the total water
phase and 725 ml in the fat tissue (Fig. 19-4, left). The partial pressure of
nitrogen is 566 mmHg in all tissues.
When the diver
reaches the bottom, there is a rise in ambient pressure to 3040 mmHg, and the
new N2-gradient (2504 - 566 mmHg) will increase the uptake of N2 by the
pulmonary blood. It takes hours before all fat-containing body tissues are
saturated with dissolved N2 at the new pressure, because of the low
bloodflow and poor capillary network of fat tissue. The total water phase is
in equilibrium within an hour. The amount of nitrogen is now 1800 ml in the
total water phase and about 3200 ml in the fat tissue (Fig. 19-4, middle). At
depth the compression of the external pressure keeps all gasses dissolved in
the body.
When the diver
suddenly surfaces (sudden decompression to sea level), the total pressure is
suddenly only 1 atm.abs. or 760 mmHg, whereas the pressure inside the body
tissues approaches that of the alveolar air, when he left the bottom (3040 out
of which 2504 mmHg was nitrogen). Obviously, most of the total pressure in the
tissues is due to dissolved nitrogen, and without counter-pressure the N2 -molecules are released from the dissolved state in the form of bubbles. In
the case shown in Fig. 19-4, the diver is supposed to eliminate a large
surplus of N2 (5000 - 1133 ml) during the rapid ascent to the
surface. This is not possible for the circulation to cope with and bubbles are
formed in blood and other tissues (see decompression sickness below).
Pathophysiology
This paragraph
deals with 1.Drowning, 2. Skin diving
and disorders, 3. Disorders from hard hat and SCUBA diving, and 4. Hyperbaric
oxygenation therapy.
1. Drowning.
In more than 90% of
drowning and near drowning the lungs
are flooded with water.
Fresh
water is hypotonic and rapidly absorbed, diluting plasma to become hypotonic
and causing bursting of the red cells (haemolysis).
The victim often dies within 3 min.
Seawater is hypertonic and draws fluid from the blood plasma into the lung
alveoli and interstitial fluid, so that plasma volume decreases. This causes haemoconcentration and shock. The victim often dies within 6 min.
The rational
therapy, if early enough, is immediate resuscitation and treatment of the
respiratory and circulatory disorders including haemolysis or
haemoconcentration.
2. Skin
diving and disorders
The simplest type
of diving is breath-hold diving or naked
skin diving. This is performed without equipment or with only a snorkel
and a mask. This is the most popular form of diving performed as underwater
sports, fishing, photography, archaeology etc, and involving diving tribes as
the Amas of Japan and Korea, and the Polynesian pearl divers.
Breathing through a
snorkel has limitations. The maximum distance between the water surface and
the middle of the immersed thorax, is 0.35 m (Fig.
19-5).
Fig.
19-5: Swimming and skin diving with snorkel just below the surface.
This
is because the water pressure creates a pressure
gradient in the pulmonary vascular system, which is a low-pressure
system. The intra-alveolar pressure is equal to the atmospheric pressure,
so the thoracic vessels are distended with blood, and the high extra-thoracic
pressure restrains the respiration. Thus, the length of the snorkel cannot be
extended beyond that range. The snorkel is sometimes provided with a ball
valve that closes automatically at diving.
Snorkel breathing
implies a dead space problem. This is because the sum of the snorkel- and
person- dead space (here 400 ml) is comparable in size to the normal tidal
volume of 500 ml. Thus it is necessary to increase the tidal volume.
Breath-hold
diving is dangerous for several
reasons: 2a.
Hypoxia, 2b. Cardiac arrhythmias, 2c. Air
embolism, 2d. Squeeze.
2a. Hypoxia
Prior
hyperventilation with only three deep inspirations increases PAO2 to 17.3 kPa (130 mmHg), whereas PACO2 is only 2.6 kPa (20 mmHg). A well-trained swimmer can use up the oxygen
stores during forceful underwater swimming, before sufficient carbon dioxide
is produced to awake the desire for breathing. Hypoxia in itself is
insufficient to trigger inspiration. Cerebral PO2 can fall below 4 kPa or 30 mmHg (zone of unconsciousness or grey out) without
a sufficient PaCO2 is
build up to force the swimmer to the surface. Drowning is likely, if this
occurs underwater. This sequence of events has sometimes been called shallow
water blackout.
Underwater swimming record attempts should be
discouraged, as they are dangerous.
Unconsciousness
from hypoxia and subsequent drowning has occurred among expert pool swimmers
trying to set distance records in underwater swimming (Fig. 19-6).
Fig.
19-6: Record attempts in apnoea underwater swimming is life threatening (+).
Point I is the normal inspiratory point.
Hyperventilation prior to the dive can cause acute
respiratory alkalosis with dizziness and convulsions even before the dive.
The
initial hyperventilation to the point A1 (hyperventilation) eliminates the CO2 drive to respire, so while exercising
underwater they slide into hypoxic unconsciousness (point A2 in
Fig. 19-6) and death. The data for the alveolar points are obtained from a
medical student, who tried to keep his breath for as long as possible (191 s)
lying supine in air - and fainted. He was immediately rescued by neck
extension, whereby he expired and started spontaneous breathing again - making
artificial ventilation unnecessary.
Deep diving with
long bottom time results in anoxia
during ascent. The PAO2 falls
so drastically during ascent that oxygen transport is reversed in the alveoli.
2b. Cardiac
arrhythmias
In cold water
especially, a cutaneo-visceral reflex from cold receptors of the skin seem able to elicit malignant cardiac arrhythmia’s or a
slow heart rate termed diving
bradycardia or both. The latter can be beneficial to the breath-hold diver
by reduction of the oxygen demand of the myocardium, but the slow heart rate
may develop into a vasovagal syncope, which
is lethal under water. Heart rates around 30 beats per min have been observed
in small children, who have been victims of cold water near drowning for
periods up to 40 min. Such heart rates are similar to those found during
hypothermic surgery. These arrhythmias and bradycardias are triggered from
cold receptors in the skin and from general hypothermia.
The human
diving response is a natural vagal reduction of heart rate occurring
during breath holding on land as well as under water (diving
bradycardia). Individuals with a high vagal excitability can experience
sino-atrial blockage, which may develop into a severe Adam Stokes syndrome.
This is fatal under water.
2c.
Submarine escape training and emergency escape
Escape from a
submerged submarine is accomplished from more than 100 m depth without the use
of equipment. The submariner ascends through the water, while exhaling
continuously in a controlled manner. He is trained to follow the ascent rate
of his own exhaled air bubbles. The art of the procedure is to exhale in such
a way that the pulmonary pressure is only slightly elevated when surfacing.
Fig.
19-7: Principal features of breath-hold diving in a submarine-escape training
tank.
At 90 m of depth
the ambient pressure is 10 atm.abs., so with a total
lung capacity of 6 l, the lungs of the submariner contain the same number
of air molecules as those in 60 l of air at 1 atm.abs. according to
Boyle-Mariotte´s law. If the
submariner panics and try to keep all air in his lungs, the gas will expand
the lungs until they rupture, and the air enters the surrounding tissues,
pleural cavity and blood vessels. The air
embolism can kill the
submariners even before they reach the surface. When training such a
controlled procedure in submarine escape training facilities (Fig. 19-7), it
is important to have a recompression
tank close to the surface, and means to place a victim of air embolism at
high pressure within seconds.
Air
embolism is a hyperbarotrauma or barotrauma of ascent (Fig. 19-7). This danger is present whenever a
person breathes compressed air at depth. An emergency escape even from 3 m of
depth may lead to death, if the subject does not exhale. The lung volume
increases during ascent according to Boyle-Mariotte´s law. The low-pressure
vessels of the thoracic cavity are thin-walled. They are compressed and the
alveoli dilatate until they burst, whereby the air dissects its way into the
tissues (subcutaneous emphysema) and into the pleural cavity (pneumothorax).
Alveolar air enters the blood through damaged vessel walls. The blood stream
to the brain, heart and lungs are blocked by air (air embolism), and death
ensues within minutes due to the blocked bloodflow to brain and heart.
2d. Squeeze or
hypobarotrauma
is a function of Boyle-Mariotte´s
law: For a certain amount of gas the product of pressure and volume is
constant at constant temperature.
The hypobarotrauma
is caused by a negative pressure difference across the wall of a
non-collapsible air space in the body (middle ear, sinuses, hollow teeth,
compressed lungs etc). A breath-hold diver who dives too deep will eventually
bleed into his alveoli, and the presence of lung
squeeze is evident, when he surfaces with bloodstained froth around the mouth.
When a healthy
person, with a total lung capacity (TLC) of 6 l and a residual volume (RV) of
1.5 l at the surface, breath-hold dive to 30 m or 4 atm.abs., his TLC is
compressed to 1/4 or 1.5 l, which is equal to his RV at the surface. By
calculation this depth is assumed to be the maximal diving depth. In such a
calculation is implied that the RV at the surface is equal to the RV at the bottom.
However, this is not true.
The world
record is beyond 105 m, which is unbelievable, when compared to the
maximum calculated above. The following two phenomena explain this world
record. RV decreases with increasing
diving depth, because the diaphragm is pushed upwards as the piston in a
syringe, and blood is pushed into
the pulmonary circulation. At some further depth, the capillaries will rupture
and blood/oedema fluid reaches the alveoli (alveolar squeeze). This is a hypobarotrauma or barotrauma of descent, and it has been observed in some of the record
holders.
A diver who has
caught a cold, will descend with sinus openings closed, and develop pain with
depth as the pressure in the occluded sinuses becomes more negative compared
to the surroundings (ie, sinus squeeze).
3. Disorders
from hard hat and SCUBA diving
Use of a diving
helmet with a hose, through which atmospheric air is pumped to the diver at
depth, is the classical form of diving. The depth
limit is around 50 m for air
breathing, because of the danger of gas narcosis and of decompression sickness
at prolonged dives (Fig. 19-8). With
a hose-and-pump system the inspired
air is pressurised to match the surrounding pressure, and the expired air is
given off to the water. Such a device is of no use in secret operations
underwater.
Fig.
19-8: SCUBA and hard hat diving from ship or from personal transfer vehicles.
Pathophysiological barriers of diving depth are given.
Self-Contained underwater
breathing apparatus (SCUBA) is an
open circuit system with a demand valve at the mouth. Usually the diver receives compressed air from 2 tanks carried
on his back (Fig. 19-8). First the pressure of the air stream is reduced from
the initial value of 100-200 atm.abs. inside the tank, to a pressure somewhat
higher than the ambient water pressure. Then the air passes an inhalation
demand valve due to the negative pulmonary pressure during inspiration, and
finally the expired air is exhaled into the water at a positive pressure from
the expiratory muscles. Most SCUBA dives are performed to depths of 30-40 m
(Fig. 19-8). SCUBA divers release bubbles in the water when breathing, so they
are useless for secret tasks.
The problems
related to these types of diving are 3a.
Decompression sickness, 3b. Inert gas
narcosis, 3c. Body
squeeze, 3d. Oxygen
toxicity, and 3e. Carbon dioxide toxicity.
3a.
Decompression sickness
If the diver
ascents from the bottom to the surface too rapidly, inert gases stored in the
tissue form bubbles in the blood and tissues, just as bubbles are formed when
a bottle of soda water is opened. The intravascular bubbles cause tissue
ischaemia and necrosis. Besides there is also serious extravascular damage.
The formation of bubbles is increased by exercise, just as more bubbles are
formed when the bottle of soda water is shaken up. These phenomena are
gathered in the concept decompression
sickness.
Symptoms and signs
can be present in all tissues of the body. The main problems are caused by
bobbles blocking the blood supply. Pains occur in the muscles and in the
joints (bends). Life-threatening bubbles may block the pulmonary capillaries, which trigger thoracic pain called chokes with alarming dyspnoea, pulmonary oedema and often death. The CNS symptoms and signs are dizziness, paralysis, collapse and unconsciousness.
The ascent from deep dives must be slow and systematically in stages.
Stage
decompression, according to
decompression tables, prevents decompression sickness in the majority of
seemingly healthy persons. Stage decompression with a rate below 18 m per min
between stages, allows most people to ascent without decompression sickness
(bends, caisson disease). All dives no deeper than 10 m allows the diver to
emerge without stage stop (Haldane’s law). The limit for compressed air
diving should be 50 m (150 feet).
Rational
therapy requires immediate
recompression in a pressure chamber, where sufficient pressure can be
established to eliminate the bubbles causing the disease.
The nitrogen
gradient from the divers body to the air in the decompression tank is
preferably increased (with oxygen enriched air) for rapid removal of nitrogen
from the body. Recompression can be succesful even hours after the dive.
Diving
at great depth (80-300 m)
makes it necessary to live in large habitats at depth for longer periods.
These divers are saturated with the inert gas (He, Ar etc) to which they are
exposed, and this type of diving is termed saturation
diving. Helium is used together with a small O2 fraction, in
order to avoid acute O2 poisoning (see below). At 200 m of depth
only 1% O2 is necessary in the helium-oxygen mixture (so-called heli-ox-mixture).
The oxygen pressure in the inspired air is (21 atm.abs. * 0.01) = 0.21
atm.abs. or 160 mmHg.
Dives deeper than
50 m are performed with helium instead of nitrogen as the inert gas. The
advantages of helium is a low solubility coefficient in the tissues, a low
narcotic-toxic effect, a rapid diffusion rate out of the tissues, and a
minimal airway resistance due to its low density. The breathing resistance due
to the high density of nitrogen at great depth makes it almost impossible to
perform manual work with nitrogen as the inert gas.
Cases of
decompression sickness have occurred as a result of breath-hold diving in
submarine escape training tanks and among the skin-diving pearl divers of the Tuamotu
Archipelago in the South Pacific. When severe it comprises loss of
consciousness and paralysis of one or more limbs, and is often fatal.
Repetitive skin diving to great depths for prolonged periods in warm and ideal
waters must be avoided.
3b. Inert
gas narcosis
Rapture
of the depth - or nitrogen
narcosis - appears at 40 m when breathing compressed air. The diver
becomes euphoric with behaviour similar to alcoholic intoxication (ie, lack of
judgement and concentration, incoordination, anxiety). The inert gas narcosis
increases in intensity with depth according to Martini’s law: Each 10 m of diving depth changes the behaviour as
much as one drink. Therefore, the limit for compressed air diving should be 50
m (Fig. 19-8). At a depth of 90 m
or more a typical narcotic condition develops (anaesthesia and
unconsciousness). Inert (inactive) gases are lipid-soluble and dissolve easily
in fatty tissues, cell membranes and intracellular structures, where they bind
to active sites or receptors. The gases modify neuronal activity and nerve
conduction velocity as well as ionic transport across cell membranes. Argon
has a larger narcotic effect than nitrogen (larger lipid-solubility, larger
energy content or van der Waal-forces), and nitrogen is a much stronger
anaesthetic than helium.
3c. Whole
body squeeze
was a dramatic
event of the hard hat diving period. Accidental disrupture of the air hose to
the diver working at depth suddenly exposed the diver to an internal pressure
of 1 atm.abs. while the ambient water pressure could be 6 atm.abs or more
(Fig. 19-8). Before the diver was rescued the soft tissues of his body was
virtually compressed into the helmet. Such accidents lead to the development
of contra-valves in the helmet.
3d. Oxygen
poisoning
Active
oxygen or oxygen free radicals (such as the superoxide O2- and hydrogen peroxide) are
continuously produced in the mitochondria from the dissolved oxygen. As long
as the oxygen tension of the tissues is normal, the production equals the
removal by tissue enzymes. These enzymes can be inactivated following
breathing of 100% oxygen above 2 atm.abs for longer periods. Therefore oxygen
free radicals accumulate to a degree that is lethal for cells in
particular brain neurons.
The acute
cerebral oxygen intoxication is presented with fasciculation of the mimic
face muscles, vertigo, universal cramps and coma. The retinal cells of the eye
are actually brain cells. Acute oxygen intoxication in premature babies may
cause retinal vasoconstriction, vessel wall proliferation and retinolysis -
so-called retrolental fibroplasia.
Closed or
recirculation systems with pure oxygen are used by frogmen for secret tasks underwater. The acute oxygen toxicity
limits the O2 diver to dives not deeper than 7 m (Fig.
19-8),
and duration less than 75 min. This depth is equal to a total pressure of (1.7
* 760) or 1292 mmHg (= 172 kPa). The PIO2 of the saturated tracheal air is (1292 - 47)= 1245 mmHg, implying a PAO2 which is toxic to the CNS. Recirculation systems with pure oxygen are so
hazardous that they should be prohibited for sport divers.
Chronic
oxygen toxicity frequently
develops when a patient has been breathing 80% oxygen or more at one atm.abs.
for more than 12 h.
Firstly, the
patient develops pulmonary hypertension with typical retrosternal pain, dyspnoea, coughing, and pulmonary oedema with
bloodstained frothy sputum.
Secondly, the
patient develops atelectasis, because the surfactant is inactivated by the
toxic free radicals. The exposure of lung tissue to high oxygen tension is
direct and total without the protection of the haemoglobin or any other oxygen
buffer system.
Some patients
actually die of hypoxia in spite of the high oxygen tension!
3e. Carbon
dioxide poisoning
Equipment with a
large dead space permits accumulation of carbon dioxide with rebreathing. This
is a problem with hard hat diving and SCUBA diving with large facemasks (Fig. 19-8).
The highest
permissible FICO2 is
0.005 or 0.5%. Slightly higher concentrations are harmful. Firstly, the diver
increases ventilation, but soon after exposure to 5% or more, the respiratory
centre of the medulla is suppressed and ventilation becomes insufficient. An acute
respiratory acidosis develops, and finally carbon
dioxide narcosis (anaesthesia and unconsciousness) is present.
4.
Hyperbaric oxygenation therapy
Hyperbaric
oxygenation therapy is used
for disorders with either local or global oxygen deficiency with oxygen at
approximately 2 atm.abs. These conditions are accomplished in pressure tanks
with atmospheric air, such as those used for recompression treatment of
decompression sickness. Oxygen is administered through a mask at ambient
pressure. Acute O2 poisoning is the risk.
Anaerobic
bacilli cause Clostridial
infections. Clostridium botulinum causing botulism, and clostridium tetani
causing tetanus, both produce neurotoxins, whereas clostridium perfringens and septicum - causing gas gangrene -
produce enzymes. The clostridia
bacilli are spore forming and survive for years in our surroundings. The
bacilli require anaerobic conditions to grow. See infectious disorders in Chapter 33.
The botulism-
neurotoxins cause cholinergic and neuromuscular blockade leading to strabismus
and respiratory insufficiency (mortality rate: 70%). - The tetanus-neurotoxins are tetanospasmin causes
muscle spasms ending in neuromuscular blockade and death. - Gas
gangrene in lacerated wounds is a life-threatening condition.
The treatment of
these three Clostridial disorders with antitoxins is sometimes supported by hyperbaric
oxygenation. The oxygen
free radicals are supposed to inhibit the growth of the clostridia. The
therapeutic results - often some benefit in moribund patients - are
controversial.
Air embolism,
decompression sickness, CO-poisoning and leprosy have been treated with some
benefit with hyperbaric oxygen.
Equations
(See Chapter 13: Eq. 13-3 to
13-6)
Self-Assessment
Multiple Choice Questions
I.
Each of the following five statements have True/False options:
A: The normal length of a snorkel is 0.6 m.
B: A PAO2 below 30 mmHg is the usual threshold for
unconsciousness.
C: Air embolism is always easy to separate from decompression sickness.
D: The botulism- neurotoxins cause adrenergic and neuromuscular blockade.
E: The acute oxygen toxicity limits the O2 diver to dives not
deeper than 7 m.
II.
Each of the following five statements have True/False options:
A. The cornea-air interface becomes a cornea-water interface, when in water
without goggles. The refractive index for water and for cornea itself is much
the same, eliminating most of the refractive power in air. A skin diver
without goggles is hypermetropic under water.
B. Sound propagates more rapidly in soft tissue and water than in air (440
m s-1 as opposed to 340 m s-1). Therefore underwater
sound sources appear much nearer than they actually are.
C. The solubility
coefficient for nitrogen in fat is 10 times larger than in blood.
D. Slightly higher
concentrations of carbon dioxide than 0.5% in the inspired air are harmful to
humans.
E. Lethal radiation
dose is rapidly reached, when flying around the earth in the Van Allen
radiation belts, consisting of high-energy level protons and electrons.
Therefore, commercial flying takes place essentially below the inner belt (500
km).
Case History A
A
male farmer, 18 years of age, is stabbed through the left foot while working
as a stableman. He develops a fulminate infection with clostridium tetani,
which only grows under anaerobic conditions and produce a potent toxin causing
permanent depolarisation of the motor end plate. He is brought to hospital in
a moribund condition, which is not improved by antitoxin and antibiotics. The
farmer is transferred to a pressure chamber, where hyperbaric oxygen therapy
is provided at 3-atmosphere pressure for 20 min. The haemoglobin concentration
of the patient is 170 g per l. PB is one atmosphere (760 mmHg), PACO2 is 5.3 kPa (40 mmHg), and the alveolar water vapour tension (Pwater ) is 6.5 kPa (47 mmHg). The Bunsen solubility coefficient (a)
for oxygen in the blood is 0.022 ml STPD per ml and per mmHg. One mmHg equals
133.3 Pascal.
1. Calculate
the concentration of physically dissolved O2 in the blood leaving
the lung capillaries of the patient.
2. Calculate
the concentration of chemically bound O2 in the blood.
3. Does
excessive oxygenation lead to gas transport problems?
Case History B
A
tall, lean diver, with a body weight of 80 kg, is working 30 m below the
surface of the sea
in
a standard divers suit for one hour. The relative density of seawater is 1033
kg m-3. The diver is
breathing atmospheric air at the environmental pressure, delivered by a pump
system to his helmet. The ventilation is effective, and the diver has normal
alveolar gas tensions (PaO2 is 100 mmHg and PaCO2 40 mmHg). The pressure at the surface of the sea is 1 atmospheres
absolute (atm abs) or 101.3 kPa or 760 mmHg and the water vapour pressure of
body warm alveolar air is 47 mmHg or 6.25 kPa.
1. Calculate the total pressure in kPa and in atm abs at 30 m of depth.
2. Calculate the partial pressure of nitrogen in the alveolar air of the
diver at the surface and at the bottom.
3. Is it advisable to drag the diver to the surface without step
decompression?
Try
to solve the problems before looking up the answers.
Highlights
· Fast
ascent during flight rarely cause problems at altitudes below 10 km (30 000
feet).
· The
aeroplanes have cabins pressurised to 80 kPa (ie an altitude of 2000 m or 6000
ft) or sometimes only to an altitude of 2750 m. These levels cause hypoxic
dyspnoea only in cardiorespiratory patients.
· The
main problem for the average traveller is jet lag, squeeze (hypobarotrauma)
during take-off or Hyperbarotrauma during landing.
· The
area of the parachute reduces the terminal velocity to 1/9. The force of
impact at landing is (1/9)2 = 1/81 of the landing force without
parachute. This is equal to a jump from a height of 2-3 m.
· The
space pilot experience space sickness (nausea and vomiting), falling total
blood volume, muscular atrophy, Ca2+ loss from the bones, and after
living in outer space for weeks, adaptive difficulties to life on earth upon
return. These difficulties are low working capacity and a tendency to faint.
The bone loss continues long after the return to earth, because stimulation of
bone formation requires physical activity in a gravity field.
· At
altitudes above 20 km, where the ambient pressure is less than 47 mmHg or 6.5
kPa, the blood of the space traveller will boil, if he is suddenly exposed
because the pressure within his suit is lost.
· Any
saturation dive to less than 10 m allows ascent without decompression stops
(Haldane’s law).
· If
decompression is too rapid, inert gasses stored in the tissues form bubbles in
the blood and tissues (decompression sickness).
· Drowning.
Fresh water drowning kills the victim rapidly following haemolysis. Seawater
is hypertonic and draws blood from plasma to the alveoli causing
haemoconcentration and shock.
· Shallow
water blackout is a condition where the oxygen stores are used up during
forceful underwater swimming before sufficient carbon dioxide is produced.
· Carbon
dioxide poisoning results in acute respiratory acidosis and finally in carbon
dioxide narcosis.
· Oxygen
poisoning is caused by active oxygen or oxygen free radicals (such as the
superoxide O2- and hydrogen peroxide).
· Rapture
of the depth - or nitrogen narcosis - appears at 40 m when breathing
compressed air. The diver becomes euphoric with behaviour similar to alcoholic
intoxication (ie, lack of judgement and concentration, incoordination,
anxiety).
· Hypobarotrauma
(squeeze) is a barotrauma of descent and a function of Boyle-Mariottes law.
· Hyperbarotrauma
(air embolism) is a barotrauma of ascent during emergency escape. The danger
is present whenever a person breathes compressed air at depth.
· Clostridial
infections are treated with antitoxins and sometimes supplied with hyperbaric
oxygenation. Accumulation of oxygen free radicals kills the microorganisms.
Some cases of air embolism, decompression sickness, CO-poisoning and leprosy
have been treated.
Further
Reading
Bennett,
PB, and Elliott, DH (2004) The Physiology and Medicine of Diving.
5th Ed. Philadelphia: WB Saunders Co.
Paulev,
P-E, Pokorski, M, Honda, Y, Ahn, B, Masuda, A, Kobayashi, T, Nishibayashi, Y,
Sakakibara, Y, Tanaka, M, and Nakamura,
W. Facial Cold Receptors and the Survival Reflex "Diving
Bradycardia" in Man. Jpn. J. Physiol.40: 701-712, 1990.
Undersea
& Hyperbaric Medicine. Journal published by the Underwater and Hyperbaric Medical Society, 10531
Metropolitan Av., Kensington MD 20895, USA.
West JB. Respiratory
Physiology – the essentials. 8th Ed. Williams & Wilkins, Baltimore, USA,
2008.
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