MAY THE

FORCE BE
WITH
YOU
HIGH ALTITUDE
 ASCENSION TO HIGH ALTITUDES

• Aviation

• Mountain climbing

• Space vehicles
 ASCENSION TO HIGH ALTITUDES
EFFECTS ON THE HUMAN BODY

• Altitude

• Low gas pressures

• Acceleratory forces

• Weightlessness
 HIGH ALTITUDE
EFFECTS OF LOW OXYGEN PRESSURE ON THE BODY
 ALVEOLAR PO2 AT DIFFERENT ELEVATIONS
C ARBON DIOXIDE AND WATER VAPOR DECREASE THE
ALVEOL AR OXYGEN .

• Gases that dilute theoxygen in the alveoli, thus reducing the

oxygen concentration:

• Carbon dioxide

• Water

• Water vapor pressure in the alveoli remains 47 mm Hg as long as

the body temperature is normal, regardless of altitude.
 HIGH ALTITUDE
EFFECTS OF LOW OXYGEN PRESSURE ON THE BODY
 HIGH ALTITUDE
ALVEOL AR PO2 AT DIFFERENT ALTITUDES

• the difference between these two alveolar ventilation increases much more in
the acclimatized person than in the unacclimatized person
 HIGH ALTITUDE
SATURATION OF HEMOGLOBIN WITH OXYGEN AT DIFFERENT
ALTITUDES

PAO2 REMAINS ATLEAST 90%

PAO2 FALLS RAPIDLY

 HIGH ALTITUDE
EFFECT OF BREATHING PURE OXYGEN ON ALVEOL AR PO2 AT DIFFERENT ALTITUDES

• When a person breathes pure oxygen instead of air, most of the space in the
alveoli formerly occupied by nitrogen becomes occupied by oxygen.
 HIGH ALTITUDE
SATURATION OF HEMOGLOBIN WITH OXYGEN AT DIFFERENT
ALTITUDES

PAO2 SATURATION
REMAINS ABOVE
90%

PAO2 FALLS RAPIDLY

TO 50%
 HIGH ALTITUDE
THE "CEILING" WHEN BREATHING AIR AND WHEN BREATHING
OXYGEN IN AN UNPRESSURIZED AIRPL ANE
 ACUTE EFFECTS OF HYPOXIA

• drowsiness • twitchings or seizures**

• lassitude

• mental and muscle • coma***

fatigue
• death
• headache

• nausea

• euphoria
 ACUTE EFFECTS OF HYPOXIA

• decreased mental proficiency

• decreases judgment

• decreased memory

• decreased performance of discrete motor movements

 ACCLIMATIZATION TO LOW PO2

• A person remaining at high altitudes for days, weeks, or years

• becomes more and more acclimatized to the low PO2

• causes fewer deleterious effects on the body

 ACCLIMATIZATION TO LOW PO2

• The principal means by which acclimatization comes about are:

• increase in pulmonary ventilation

• increased numbers of red blood cells

• increased diffusing capacity of the lungs

• increased vascularity of the peripheral tissues

• increased ability of the tissue cells to use oxygen despite low

PO2
 INCREASED PULMONARY VENTILATION
ROLE OF ARTERIAL C HEMORECEPTORS

INCREASED
EXPOSURE TO STIMULATES ARTERIAL ALVEOLAR
LOW PO2 CHEMORECEPTORS VENTILATION
(1.65X)

PERSON
REMAINS AT FURTHER STIMULATES INCREASES
HIGH ALTITUDE ARTERIAL VENTILATION
FOR SEVERAL CHEMORECEPTORS (5X)
DAYS
 INCREASED PULMONARY VENTILATION
ROLE OF ARTERIAL C HEMORECEPTORS

• Blows off large quantities of carbon dioxide

• Reducing the PCO2

• Increasing the pH of the body fluids

• Inhibit the brainstem respiratory center

• Opposes effect of low PO2

 INCREASED PULMONARY VENTILATION
ROLE OF ARTERIAL C HEMORECEPTORS

• But during the ensuing 2 to 5 days,

• inhibition fades away

• allowing the respiratory center to respond with full force to the

peripheral chemoreceptor stimulus from hypoxia

• ventilation increases to about five times normal

• Cause of fading inhibition

• reduction of HCO3 ion concentration in the CSF/nervous tissue

• decreases the pH in the fluids surrounding the chemosensitive

neurons of the respiratory center

• increasing the respiratory stimulatory activity of the center

 RENAL COMPENSATORY MECHANISM
RESPIRATORY ALKALOSIS

• kidneys respond to decreased PCO2 by:

• reducing hydrogen ion secretion

• increasing bicarbonate excretion

• reduces plasma and cerebrospinal fluid bicarbonate concentration

• reduces pH toward normal

• removes part of the inhibitory effect on respiration of low hydrogen ion

concentration.

• Thus, the respiratory centers are much more responsive to the peripheral
chemoreceptor stimulus caused by the hypoxia after the kidneys compensate
for the alkalosis.
 INCREASE IN RED BLOOD CELLS AND HEMOGLOBIN
CONCENTRATION DURING ACCLIMATIZATION

• Hypoxia

• principal stimulus for causing an increase in red blood cell production.

• Ordinarily, when a person remains exposed to low oxygen for weeks

at a time:

• hematocrit rises slowly from a normal value of 40 - 45 to an

average of about 60,

• average increase in whole blood hemoglobin concentration from

normal of 15 - 20 g/dl

• blood volume also increases, often by 20 - 30 %

INCREASED DIFFUSING CAPACITY AFTER ACCLIMATIZATION

• Normal diffusing capacity for oxygen through the pulmonary

membrane = 21 ml/mm Hg/min

• Diffusing capacity can increase as much as 3X during exercise.

• A similar increase in diffusing capacity occurs at high altitude.

INCREASED DIFFUSING CAPACITY AFTER ACCLIMATIZATION

RESULTS FROM:

• increased pulmonary capillary blood volume

• which expands the capillaries and increases the surface area through which
oxygen can diffuse into the blood.

• increase in lung air volume

• which expands the surface area of the alveolar-capillary interface still more.

• increase in pulmonary arterial blood pressure

• this forces blood into greater numbers of alveolar capillaries than normally —
especially in the upper parts of the lungs, which are poorly perfused under
usual conditions.
 PERIPHERAL CIRCULATORY SYSTEM CHANGES
DURING ACCLIMATIZATION
• Cardiac output often increases as much as 30% immediately after
a person ascends to high altitude

• Increased tissue capillarity (or angiogenesis)

• Growth of increased numbers of systemic circulatory capillaries

in the nonpulmonary tissues
 CELLULAR ACCLIMATIZATION

• Increase in cell mitochondria and cellular oxidative enzyme

systems
 NATURAL ACCLIMATIZATION OF NATIVE HUMAN BEINGS
LIVING AT HIGH ALTITUDES

• Acclimatization of the natives begins in infancy

• chest size is greatly increased

• body size is somewhat decreased

• high ratio of ventilatory capacity to body mass

• enlarged hearts
OXYGEN-HEMOGLOBIN DISSOCIATION CURVES OF BLOOD
HIGH- ALTITUDE RESIDENTS VS. SEA -LEVEL RESIDENTS
 REDUCED WORK CAPACITY AT HIGH ALTITUDES AND
POSITIVE EFFECT OF ACCLIMATIZATION

• Work capacity of all (skeletal/cardiac) muscles is greatly

DECREASED in hypoxia

• Work capacity is reduced in direct proportion to the decrease in

maximum rate of oxygen uptake that the body can achieve
 REDUCED WORK CAPACITY AT HIGH ALTITUDES AND
POSITIVE EFFECT OF ACCLIMATIZATION

• The work capacities as percent of normal for unacclimatized and

acclimatized people at an altitude of 17,000 feet are as follows:
 ACUTE MOUNTAIN SICKNESS

• A small percentage of people who ascend rapidly to high altitudes

become acutely sick and can die if not given oxygen or removed
to a low altitude.

• The sickness begins from a few hours up to about 2 days after

ascent.
 ACUTE MOUNTAIN SICKNESS

• Two events frequently occur:

• Acute cerebral edema

• Acute pulmonary edema

 ACUTE MOUNTAIN SICKNESS
ACUTE CEREBRAL EDEMA

• Hypoxia causes local vasodilation of the cerebral blood vessels,

• Dilation of the arterioles -> increases blood flow into the

capillaries -> increasing capillary pressure ->causes fluid to leak
into the cerebral tissues.

• Effects:

• severe disorientation

• cerebral dysfunction
 ACUTE MOUNTAIN SICKNESS
ACUTE PULMONARY EDEMA

• unknown cause

• Theories:

• constriction of pulmonary arterioles (much greater in some parts of the lungs)

• pulmonary blood flow is forced through fewer and fewer still unconstricted
pulmonary vessels

• increased capillary pressure -> local edema

• severe pulmonary dysfunction

 CHRONIC MOUNTAIN SICKNESS

EFFECTS:

• high red cell mass and hematocrit

• elevated pulmonary arterial pressure

• enlarged right side of the heart

• decrease in peripheral arterial pressure

• congestive heart failure

• death
 CHRONIC MOUNTAIN SICKNESS

HYPOXIA

INCREASED RED CELL MASS

INCREASED BLOOD VISCOSITY

DECREASED TISSUE DECREASED OXYGEN

BLOOD FLOW DELIVERY
CHRONIC MOUNTAIN SICKNESS

HYPOXIA

PULMONARY ARTERIOLES VASOCONSTRICT*

INCREASED PULMONARY ARTERIAL PRESSURE

RIGHT-SIDED HEART FAILURE

CHRONIC MOUNTAIN SICKNESS

HYPOXIA

SPASM OF ALVEOLAR ARTERIOLES

EXCESS OF PULMONARY SHUNT BLOOD FLOW

POOR BLOOD OXYGENATION

EFFECTS OF ACCELERATORY
FORCES ON THE BODY IN
AVIATION AND
SPACE PHYSIOLOGY
 ACCELERATORY FORCES THAT AFFECT THE
BODY DURING FLIGHT

1. LINEAR ACCELERATION

2. DECELERATION

3. CENTRIFUGAL ACCELERATION
 CENTRIFUGAL ACCELERATORY FORCES

• When an airplane makes a turn, the force of centrifugal

acceleration is determined by the following relation:

• f = centrifugal acceleratory force

• m = mass of the object

• v = velocity of travel

• r = radius of curvature of the turn

MEASUREMENT OF ACCELERATORY FORCE - “G”

• When an aviator is simply sitting in his seat, the force with which
he is pressing against the seat results from the

• pull of gravity and is equal to his weight

• intensity of this force= +1 G

• because it is equal to the pull of gravity

MEASUREMENT OF ACCELERATORY FORCE - “G”

• If the force with which he presses against the seat becomes five
times his normal weight during pull-out from a dive, the force
acting on the seat is +5 G.
MEASUREMENT OF ACCELERATORY FORCE - “G”

• If the airplane goes through an outside loop so that the person is

held down by his seat belt, negative G is applied to his body

• if the force with which he is held down by his belt is equal to the
weight of his body, the negative force is -1 G.
EFFECTS OF CENTRIFUGAL ACCELERATORY FORCE ON THE BODY

POSITIVE G

• Effects on the Circulatory System

• blood is centrifuged toward the lowermost part of the body

• +5 G

• standing position: pressure in the veins of the feet ~450

mmHg

• sitting position: tpressure becomes ~300 mm Hg

• the greater the pooled blood in the LE, the lesser the cardiac
output
 CHANGES IN SYSTOLIC AND DIASTOLIC ARTERIAL
PRESSURES IN THE UPPER BODY WHEN A CENTRIFUGAL
ACCELERATORY FORCE OF +3.3 G IS SUDDENLY APPLIED
TO A SITTING PERSON

<22 MMHG 55/20 MMHG

activation of the
baroreceptor reflexes
EFFECTS OF CENTRIFUGAL ACCELERATORY FORCE ON THE BODY

POSITIVE G

• Acceleration > 4 to 6 G

• causes "black- out" of vision within a few seconds

• unconsciousness

• death
EFFECTS OF CENTRIFUGAL ACCELERATORY FORCE ON THE BODY

POSITIVE G

• Effects on the Vertebrae.

• ~20G : an average person can withstand in the sitting position

before vertebral fracture occurs
 EFFECTS OF NEGATIVE G ON THE BODY

• less dramatic acutely but possibly more damaging permanently

than the effects of positive G

• centrifugation of the blood into the head

• psychotic disturbances lasting for 15 to 20 minutes occur as a

result of brain edema
 EFFECTS OF NEGATIVE G ON THE BODY

• cerebral blood pressure reaches 300 to 400mmHg

• rupture of small vessels (surface of head/brain)

• cranial vessels has less tendency for rupture

• CSF is centrifuged toward the head at the same time that blood
is centrifuged toward the cranial vessels

• increased pressure of the CSF acts as a cushioning buffer on the

outside of the brain to prevent intracerebral vascular rupture
 EFFECTS OF NEGATIVE G ON THE BODY

• eyes are not protected by the cranium

• eyes often become temporarily blinded with "red-out"

 PROTECTION OF THE BODY AGAINST
CENTRIFUGAL ACCELERATORY FORCES

• tightening abdominal muscles

• special "anti-G" suits

• inflating compression bags as the G increases

• limit of safety <10 G

 EFFECTS OF LINEAR ACCELERATORY FORCES ON THE BODY

• Acceleratory Forces in Space Travel

• Linear Acceleration

• blast-off acceleration +G

• landing deceleration - G

• centrifugal acceleration is of little importance except when the

spacecraft goes into abnormal gyrations.
EFFECTS OF LINEAR ACCELERATORY FORCES ON THE BODY

BL AS T -OFF DECELERATION

• not tolerated in
standing position

• semireclining position
(preferred) seen among
astronauts
EFFECTS OF LINEAR ACCELERATORY FORCES ON THE BODY
L ANDING DECELERATION

• person traveling at Mach 1 (speed of sound and of fast airplanes

• can be safely decelerated in a distance of about 0.12 mile

• person traveling at a speed of Mach 100 (a speed possible in

interplanetary space travel)

• would require a distance of about 10,000 miles for safe

deceleration.

• total amount of energy that must be dispelled during deceleration is

proportional to the square of the velocity, which alone increases the
required distance for decelerations between Mach 1 versus Mach 100
about 10,000-fold.
DECELERATORY FORCES ASSOCIATED WITH PARACHUTE JUMPS

• When the parachuting aviator leaves the airplane, his velocity of

fall is

• at 1 sec : 32 ft/sec

• at 2 secs: 64 ft/sec

• at 3 secs: 92 ft/sec

• As the velocity of fall increases, the air resistance tending to

slow the fall also increases
DECELERATORY FORCES ASSOCIATED WITH PARACHUTE JUMPS

Deceleratory force of the air resistance=acceleratory force of gravity

• after falling for about 12 seconds

• the person will be falling at a "terminal velocity"

• 109 to 119 m/hr (175 ft/sec)

• If the parachutist has already reached terminal velocity before

opening his parachute

• an "opening shock load" of up to 1200 pounds can occur on

the parachute shrouds
DECELERATORY FORCES ASSOCIATED WITH PARACHUTE JUMPS

• The usual-sized parachute slows the fall of the parachutist to:

• about 1/9 the terminal velocity

• speed of landing is about 20 ft/sec

• force of impact against the earth is 1/81 the impact force

without a parachute

• trained parachutist strikes the earth with knees bent but muscles
taut to cushion the shock of landing.
"ARTIFICIAL CLIMATE" IN THE SEALED SPACECRAFT

• Because there is no atmosphere in outer space, an artificial

atmosphere and climate must be produced in a spacecraft.

• high oxygen concentration low

• carbon dioxide concentration low

• Modern space shuttles

• 4x as much nitrogen as oxygen

• total pressure of 760 mm Hg

"ARTIFICIAL CLIMATE" IN THE SEALED SPACECRAFT

• it is impractical to carry along an adequate oxygen supply.

• Use of recycling techniques :

• purely physical procedures

• biological methods
 WEIGHTLESSNESS IN SPACE

• A person in an orbiting satellite or a nonpropelled spacecraft

experiences weightlessness, or a state of near-zero G force,
which is sometimes called micro- gravity.
PHYSIOLOGIC PROBLEMS OF WEIGHTLESSNESS (MICROGRAVITY).

• The physiologic problems of weightlessness have not proved to

be of much significance

• motion sickness during the first few days of travel

• translocation of fluids within the body because of failure of

gravity to cause normal hydrostatic pressures

• diminished physical activity

PHYSIOLOGIC PROBLEMS OF WEIGHTLESSNESS (MICROGRAVITY).

MOTION SIC KNESS

• Almost 50% of astronauts experience motion sickness, with

nausea and sometimes vomiting, during the first 2 to 5 days of
space travel.

• CAUSE:

• unfamiliar pattern of motion signals arriving in the equilibrium

centers of the brain

• lack of gravitational signals

 EFFECTS OF PROLONGED STAY IN SPACE

• decrease in blood volume

• decrease in red blood cell mass

• decrease in muscle strength and work capacity

• decrease in maximum cardiac output

• loss of calcium and phosphate from the bones, as well as loss of bone
mass

• execise programs are carried out by astronauts during prolonged space

missions
PHYSIOLOGY OF DEEP-SEA DIVING
AND OTHER HYPERBARIC
CONDITIONS
 DEEP-SEA DIVING

• pressure around them increases tremendously

• To keep the lungs from collapsing, air must be supplied at very

high pressure to keep them inflated.

• This exposes the blood in the lungs also to extremely high

alveolar gas pressure, a condition called hyperbarism.

• Beyond certain limits, these high pressures can cause tremendous

alterations in body physiology and can be lethal
RELATIONSHIP OF PRESSURE TO SEA DEPTH

• A column of seawater 33 feet deep exerts the same pressure at

its bottom as the pressure of the atmosphere above the sea.

• Therefore, a person 33 feet beneath the ocean surface is

exposed to 2 atmospheres pressure:

• 1 atmosphere of pressure caused by the weight of the air

above the water

• second atmosphere by the weight of the water itself

EFFECT OF SEA DEPTH ON THE VOLUME OF GASES-BOYLE'S LAW

• EFFECT

• compression of gases to smaller

and smaller volumes.

• Gases-Boyle's Law

• volume to which a given quantity

of gas is compressed is inversely
proportional to the pressure.
 EFFECT OF HIGH PARTIAL PRESSURES OF INDIVIDUAL
GASES ON THE BODY

• The individual gases to which a diver is exposed when breathing air are

• nitrogen

• oxygen

• carbon dioxide

• each of these at times can cause significant physiologic effects at high

pressures.
NITROGEN NARCOSIS AT HIGH NITROGEN PRESSURES

• About 4/5 of the air is nitrogen

• At sea-level pressure

• the nitrogen has NO significant effect on bodily function

• At high pressures

• can cause varying degrees of narcosis

NITROGEN NARCOSIS AT HIGH NITROGEN PRESSURES

• When the diver remains beneath the sea for an hour or more and
is breathing compressed air

• 120 ft: first symptoms of mild narcosis/joviality and lose many

of his or her cares.

• 150-200 ff: drowsiness

• 200-250 feet: strength wanes,becomes too clumsy to perform

the work required.

• >250 feet (8.5 atmospheres pressure) diver becomes almost

uesless
 NTIROGEN NARCOSIS

• has characteristics similar to those of alcohol intoxication

• called "raptures of the depths."

• MECHANISM:

• dissolves in the fatty substances in neuronal membranes

• altering ionic conductance through the membranes

• reduces neuronal excitability

 OXYGEN TOXICITY AT HIGH PRESSURES

• When the PO2 in the blood rises >100 mm Hg, the amount of
oxygen dissolved in the water of the blood increases markedly.
OXYGEN TOXICITY AT HIGH PRESSURES
DONEC QUIS NUNC
EFFECT OF HIGH ALVEOLAR PO2 ON TISSUE PO2
DONEC QUIS NUNC

• POINT A = total oxygen content in

each 100 milliliters of blood of about
29 volumes%

• 20% bound w/ Hgb

• 9% dissolve in blood water

• POINT B = As this blood passes

through the tissue capillaries and the
tissues use their normal amount of
oxygen, about 5 milliliters from each
100 milliliters of blood

• oxygen content on leaving the

tissue capillaries is still 24

volumes%

• SAFE RANGE: 20-60 mmHg

 ACUTE OXYGEN POISONING

• The extremely high tissue PO2 that occurs when oxygen is

breathed at very high alveolar oxygen pressure can be detrimental
to many of the body's tissues.

• Example

• breathing oxygen at 4 atmospheres PO2 (PO2 = 3040 mm Hg)

will cause brain seizures followed by coma in most people
within 30 to 60 minutes
 ACUTE OXYGEN POISONING

• Other symptoms

• nausea

• muscle twitchings

• dizziness

• disturbances of vision

• irritability

• disorientation
EXCESSIVE INTRACELLULAR OXIDATION AS A CAUSE OF NERVOUS SYSTEM OXYGEN TOXICITY
OXIDIZING FREE RADIC ALS

• Molecular oxygen (02)

• little capability of oxidizing other chemical compounds

• must first be converted into an "active" form of oxygen

EXCESSIVE INTRACELLULAR OXIDATION AS A CAUSE OF NERVOUS SYSTEM OXYGEN TOXICITY
OXIDIZING FREE RADIC ALS

• There are several forms of active oxygen called oxygen free

radicals:

• superoxide free radical 2

• peroxide radical: hydrogen peroxide

• Even when the tissue Po 2 is normal at the level of 40 mm Hg,

small amounts of free radicals are continually being formed from
the dissolved molecular oxygen.
EXCESSIVE INTRACELLULAR OXIDATION AS A CAUSE OF NERVOUS SYSTEM OXYGEN TOXICITY
OXIDIZING FREE RADIC ALS

• tissues also contain multiple enzymes that rapidly remove these

free radicals

• peroxidases

• catalases

• superoxide dismutases
 OXYGEN TOXICITY
ACUTE BRAIN DYSFUNCTION

• Above a critical alveolar PO2 (>2 atm PO2 )

• hemoglobin-oxygen buffering mechanism fails

• tissue PO2 can then rise to hundreds or thousands of millimeters

of mercury.

• amounts of oxidizing free radicals literally swamp the enzyme

systems designed to remove them -> serious destructive/lethal
effects on the cells:

• oxidize the polyunsaturated fatty acids

• oxidize some of the cellular enzymes

 CHRONIC OXYGEN POISONING
PULMONARY DISABILIT Y

• A person can be exposed to only 1 atmosphere pressure of oxygen

almost indefinitely WITHOUT developing the acute oxygen toxicity of
the nervous system

• However, after only about 12 hours of 1 atmosphere oxygen exposure

• lung passageway congestion

• pulmonary edema

• atelectasis caused by damage to the linings of the bronchi and

alveoli begin to develop.
CARBON DIOXIDE TOXICITY AT GREAT DEPTHS IN THE SEA

• If the diving gear is properly designed and functions properly, the

diver has NO problem due to carbon dioxide toxicity

• depth alone does NOT increase the carbon dioxide partial

pressure in the alveoli.

• depth does NOT increase the rate of carbon dioxide production

in the body
CARBON DIOXIDE TOXICITY AT GREAT DEPTHS IN THE SEA

• Up to an alveolar carbon dioxide pressure (PCO2 ) of about 80

mm Hg, twice that in normal alveoli

• diver usually tolerates this buildup by increasing the minute

respiratory volume a maximum of 8- to 11 -fold to compensate
for the increased carbon dioxide.
CARBON DIOXIDE TOXICITY AT GREAT DEPTHS IN THE SEA

• >80-mm Hg alveolar PCO2

• intolerable

• respiratory center depressed

• failing respiratory mechanism

• severe respiratory acidosis

• varying degrees of lethargy, narcosis

• anesthesia
VOLUME OF NITROGEN DISSOLVED IN THE BODY FLUIDS AT DIFFERENT DEPTHS

• Nitrogen is 5x as soluble in fat as in water.

• At sea level:

• almost exactly 1 liter of nitrogen is dissolved in the entire body.

• Slightly less than one half of this is dissolved in the water of the body

• little more than one half in the fat of the body

VOLUME OF NITROGEN DISSOLVED IN THE BODY FLUIDS AT DIFFERENT DEPTHS

• After the diver has become saturated with nitrogen, the sea-level
volume of nitrogen dissolved in the body at different depths is as
follows:

FEET LITERS

0 1

33 2
100 4
200 7
300 10
 DECOMPRESSION SICKNESS

• Bends

• Compressed Air Sickness

• Caisson Disease

• Diver's Paralysis

• Dysbarism
 DECOMPRESSION SICKNESS

• If a diver has been beneath the sea long enough

• large amounts of nitrogen have dissolved in his or her body

• diver then suddenly comes back to the surface of the sea,

• significant quantities of nitrogen bubbles can develop in the body

fluids either intracellularly or extracellularly

• cause minor or serious damage in almost any area of the body

 SYMPTOMS OF DECOMPRESSION SICKNESS

• caused by gas bubbles blocking many blood vessels in different tissues.

• vascular obstruction

• tissue ischemia

• joint pains (“bends”)

• nervous system dysfunction

• shortness of breath (“chokes”)

• pulmonary edema

• death
 NITROGEN ELIMINATION FROM THE BODY
DECOMPRESSION TABLES

• If a diver is brought to the surface slowly, enough of the dissolved

nitrogen can usually be eliminated by expiration through the lungs
to prevent decompression sickness.

• 2/3 of the total nitrogen is liberated in 1 hour

• ~ 90% in 6 hours

• Decompression tables have been prepared by the U.S. Navy that

detail procedures for safe decompression.
 NITROGEN ELIMINATION FROM THE BODY
DECOMPRESSION TABLES

• A diver who has been breathing air and has been on the sea bottom for 60
minutes at a depth of 190 feet is decompressed according to the following
schedule:

• 10 minutes at 50 feet depth

• 17 minutes at 40 feet depth

• 19 minutes at 30 feet depth

• 50 minutes at 20 feet depth

• 84 minutes at 10 feet depth

• Thus, for a work period on the bottom of only 1 hour, the total time for
decompression is about 3 hours.
TANK DECOMPRESSION AND TREATMENT OF DECOMPRESSION SICKNESS

• Pressurized tank

• same time schedule

"SATURATION DIVING" AND USE OF HELIUM-OXYGEN MIXTURES IN DEEP DIVES

• When divers must work at very deep levels — (250 to 1000 feet)

• live in a large compression tank for days or weeks at a time,

remaining compressed at a pressure level near that at which
they will be working.

• keeps the tissues and fluids of the body saturated with the
gases to which they will be exposed while diving

• when they return to the same tank after working, there are no
significant changes in pressure, so that decompression bubbles
do not occur.
"SATURATION DIVING" AND USE OF HELIUM-OXYGEN MIXTURES IN DEEP DIVES

• HELIUM is usually used in the gas mixture instead of nitrogen for

three reasons:

• it has only about 1/5 the narcotic effect of nitrogen

• only about 1/2 as much volume of helium dissolves in the body

tissues as nitrogen volume*

• the low density of helium (1/7 the density of nitrogen) keeps

the airway resistance for breathing at a minimum**
 SCUBA DIVING
(SELF -CONTAINED UNDERWATER BREATHING APPARATUS)

• Before the 1940s

• almost all diving was

done using a diving
helmet connected to
a hose through which
air was pumped to
the diver from the
surface.
 SCUBA DIVING
(SELF -CONTAINED UNDERWATER BREATHING APPARATUS)

• popularized in 1943 by Jacques Cousteau

• The type of SCUBA apparatus used in more than 99 %of

all sports and commercial diving is the open-circuit
demand system
 SCUBA DIVING
(SELF -CONTAINED UNDERWATER BREATHING APPARATUS)

• Components

1. Tanks of compressed air or some other breathing mixture

2. First-stage "reducing" valve

• reducing the very high pressure from the tanks to a

low pressure level

3. Combined inhalation "demand" valve and exhalation

valve

• allows air to be pulled into the lungs with slight

negative pressure of breathing and then to be exhaled
into the sea at a pressure level slightly positive to the
surrounding water pressure

4. Mask and tube system with small "dead space"

• DISADVANTAGE:

• limited amount of time one can remain beneath the sea surface;

• tremendous airflow from the tanks is required to wash carbon

dioxide out of the lungs

• the greater the depth, the greater the airflow in terms of

quantity of air per minute that is required
SPECIAL PHYSIOLOGIC PROBLEMS IN SUBMARINES

• Escape from Submarines.

• same problems encountered in deep-sea diving

• 300 feet - without using any apparatus

• >600 ft - proper use of rebreathing devices

• continous exhalation prevents air embolism

HEALTH PROBLEMS IN THE SUBMARINE INTERNAL ENVIRONMENT

• radiation hazards

• escape of poisonous gases from the submarine

 HYPERBARIC OXYGEN THERAPY

• The intense oxidizing properties of high-pressure oxygen

(hyperbaric oxygen)

• The oxygen is usually administered at PO2 of 2 to 3 atmospheres

of pressure through a mask or intratracheal tube
 HYPERBARIC OXYGEN THERAPY

• Indications

• decompression sickness

• arterial gas embolism

• carbon monoxide poisoning

• osteomyelitis

• myocardial infarction

• gas gangrene infection

“AVIATION IS PROOF THAT GIVEN,
THE WILL, WE HAVE THE CAPACITY
TO ACHIEVE THE IMPOSSIBLE”

EDDIE RIKENBACKER