At higher altitudes, our bodies make adjustments: creating more red blood cells to carry oxygen

through the bloodstream, High altitude also triggers an increase in our heartbeat, breathing and
urination. The low humidity and low air pressure at high altitudes causes moisture from your
skin and lungs to evaporate at a faster pace -- and your body's increased exertion requires even
more water to keep it hydrated.

When your body loses fluid through its blood vessels, it tries to counteract the effect by holding
water and sodium in its kidneys. As a result, even more fluid builds up in your body -- and more
trickles out of your blood vessels [source: Mayo Clinic]. This fluid can get into body tissue and
cause edema (swelling of the face, legs and feet). Edema is more common in women. There's no
clear reason why, but researchers suspect it has something to do with their hormones and
menstrual cycles. The condition isn't always an indicator of altitude sickness (it can occur from
malnutrition and other illnesses at low altitudes), so it can be discounted as a precursor of
altitude sickness if no other symptoms are present. While swelling may worsen with ascent, it
usually resolves after descent.

As your sleeping body attempts to strike some balance between oxygen and carbon dioxide
levels, it falls into periodic breathing. Periodic breathing is a cycle of decreased breathing,
followed by a complete absence of breathing (from three to 15 seconds). Breathing resumes once
carbon dioxide has sufficiently built up in your bloodstream to prompt your brain. Periodic
breathing is fairly common at higher altitudes and is not itself a sign of altitude sickness, but it
often leaves afflicted individuals feeling worn out upon waking

Changes in oxygen transport

At sea level, the PO2 available in the atmosphere and the oxygen demands of mitochondria are
large. At each stage of the oxygen transport system, PO2 decreases; this phenomenon is
figuratively called the oxygen cascade.

At high altitudes, the decrease in barometric pressure reduces the amount of oxygen initially
available in the environment, making the slope of the cascade considerably less steep than it
otherwise is. Mechanisms that compensate for the decreased availability of oxygen in the
environment include changes in the intracellular enzyme systems to allow them to function at
low levels of oxygen and changes in the oxygen transport system to increase the amount of
oxygen delivered. The latter is the primary compensatory mechanism. [5]

Changes occur at all levels of the oxygen transport system, namely, ventilation, pulmonary
diffusion, circulation, and tissue diffusion.

A slight increase in ventilation is first noted on ascent above 1524 m (5000 ft). At rest, this
increase is manifested primarily as an increased tidal volume. With exercise, both the tidal
volume and the respiratory rate increase. The effect of hyperventilation is to decrease PaCO2,
increasing PAO2. This is the most important form of early acclimatization to high altitude. The
hypoxia-induced increase in minute ventilation occurs shortly after arrival at altitude and
increases during week 1. Minute ventilation decreases later but remains above sea-level values.
An increased hypoxic ventilatory response is an important means of acclimatization for a sea-
level resident who aspires to participate in activities at high altitude. Mountain climbers with an
increased hypoxic ventilatory response are better able to climb to great heights, presumably
because of the increased availability of alveolar oxygen; this capacity may also have a downside.
A low hypoxic ventilatory response has been implicated in acute mountain sickness, excessive
polycythemia, and low birth weight.

Stimulation of the carotid bodies mediates hyperventilation. With acute exposure, ventilation
does not notably increase below 3000 m (9840 ft). This situation corresponds to a PAO2 of 60
mm Hg. However, after 4 days of exposure to even modest increases in altitude, ventilation is
consistently greater than normal ventilation at sea level.

After a person acclimatizes, hyperventilation may occur at a PaO2 as high as 90 mm Hg. The
hypoxic ventilatory response persists for the sea-level resident who continues to remain at high
altitude. At extreme altitudes, marked respiratory alkalosis develops to maintain a PAO2 of more
than 35 mm Hg. In a decompression chamber with conditions equal to those at Mount Everest,
PaCO2 is 8 mm Hg.

In contrast, the native high-altitude resident has a blunted hypoxic ventilatory response (ie, is
desensitized) to hypoxia. Improved oxygen usage in the peripheral tissues with decreased
ventilatory effort has been postulated as an explanation for this phenomenon. Studies of high-
altitude residents showed that for desensitization to occur, exposure to high altitude must occur
in early childhood and last for several years. The decrease in hypoxic ventilatory response is first
noted after 8 years of age. At the same time, vital capacity increases correspondingly.

After desensitization to hypoxia has occurred in the high-altitude resident, it persists for years,
even if the person returns to sea level. Offspring of lowlanders born and raised at high altitude
have the same phenomenon as that of native highlanders. The native highlander hyperventilates
compared with the lowlander, and the high-altitude resident hypoventilates compared with the
newcomer to altitude.

Therefore, native high-altitude residents can perform a given physical activity with a relatively
small ventilatory requirement; hence, they have less dyspnea than others do. This advantage
increases their capacity to perform work at high altitude.

A patient with cyanotic congenital heart disease also has a blunted hypoxic ventilatory response.
This effect develops as early as age 7 or 8 years. The most blunted ventilatory responses have
been noted in patients with the highest degree of desaturation. After arterial saturations are
brought back to normal by surgical correction and normalized, the ventilatory response to
hypoxia returns to normal.

This outcome is unlike that observed in the native highlander, whose response remains blunted
for years. An important distinction between the native highlander and the patient with cyanotic
congenital heart disease (CHD) may be that although they both have arterial hypoxemia, the
highlander has a lowered PAO2, whereas the patient with cyanotic CHD has a normal PAO2.
At sea level, the alveolar-arterial (A-a) gradient is 6-17 mm Hg. This gradient may limit exercise
by the newcomer to high altitude even if he or she hyperventilates. The development of notable
arterial desaturation during exercise suggests this possibility. The native high-altitude resident
has a pulmonary diffusion capacity 20-30% higher than that of a sea-level resident. This capacity
helps maximize gas exchange in the alveoli.

Configurational changes of the chest, anatomic changes of the lungs to increase the surface area
of the alveoli, and an improved ventilation-perfusion ratio owing to pulmonary hypertension
have been offered as possible explanations for this finding. Animal studies in chronically
hypoxic newborn rats have shown structural changes that appear to optimize the structure and
function of the lungs.

Exposure to high altitude has important implications for the cardiovascular system. On initial
ascent, sympathetic activity markedly increases, resulting in an initial increase in heart rate and
cardiac output. However, after prolonged exposure, maximal oxygen uptake decreases, stroke
volume is lowered, and cardiac output falls below sea-level values. The reduction in stroke
volume is thought to be secondary to decreased ventricular filling. Exercise markedly reduces
maximum cardiac output; this effect is more pronounced in visitors than in natives.

A 32% decrease in coronary blood flow has been observed after 10 days at 3100 m (10,200 ft). [6]
However, no evidence of myocardial ischemia is observed. This finding is presumably due to
increased extraction of oxygen from coronary arterial blood and reduced oxygen requirements
secondary to decreased cardiac work. Left ventricular (LV) dysfunction has been suggested;
however, echocardiographic indices of LV contractility are normal and chamber sizes are
reduced at altitude.

In one study, Bernheim et al found that increased pulmonary arterial pressure in association with
exercise and altitude hypoxia did not cause LV diastolic dysfunction. [7] The authors concluded,
“Ventricular interaction seems not to be of hemodynamic relevance in this setting.” Significant
increase in right ventricular (RV) wall thickness and decreased ejection fraction are observed on
magnetic resonance imaging (MRI) scans in children with high-altitude pulmonary hypertension.
[8]

With increasing hypoxia, the maximum heart rate decreases by 1 beat/min for every 130 m
(about 430 ft) above 3100 m (10,200 ft). The decreased cardiac output, stroke volume, and
exercise capacity noted at high altitude may be due to decreased preload secondary to a reduction
in plasma volume associated with arrival at high altitude.

Electrocardiographic (ECG) changes after ascent to high altitude have also been described.
Right-axis deviation, right precordial T-wave inversion from a normally upright adult T wave,
and T-wave changes in the left precordial leads have been described in mountaineers. ECGs of
immigrants to high altitude demonstrate an increase in RV hypertrophy with increased duration
of high-altitude residence. Loss of normal circadian rhythm and QTc prolongation have been
described in both infants and adults.
In general, systemic blood pressure is slightly lower at high altitude than it is at sea level. This
difference is thought to be secondary to the vasodilatory effects of hypoxia on the systemic
vascular smooth muscle. The incidence of hypertension at high altitude has been reported to be
less than that the rate at sea level.

The final step in the oxygen cascade is the diffusion of oxygen from the capillaries to the
mitochondria. For understandable reasons, this step has not been extensively studied at high
altitude. Increases in the capillary density and decreases in the size of muscle fibers combine to
shorten the distance over which oxygen must diffuse. In several species of animals, this response
appears to help them adapt to high altitude, but it does not appear in humans until after 40 days
of marked hypobaric exposure.

Oxygen-hemoglobin dissociation curve

Tissue PO2 (tPO2) varies little over a PAO2 range of 70-100 mm Hg. As might be expected at
high altitude, a PAO2 of 40-70 mm Hg is associated with rapid unloading of oxygen for small
changes in oxygen tension. Some suggest that increased oxygen affinity or left-shifting of the
oxygen-hemoglobin dissociation curve may be beneficial at high altitude. As with fetal
hemoglobin, a leftward shift facilitates oxygen loading in a hypoxic environment. Others suggest
that a rightward shift may increase the ability of the blood to unload oxygen at the tissue level.

Studies at 4520 m (14,830 ft) have demonstrated that the curve shifts to the right under standard
laboratory conditions (pH, 7.40; partial pressure of carbon dioxide [PCO2], 40 mm Hg) because
of an increase in 2,3-diphosphoglycerate. [9] However, in vivo, the respiratory alkalosis associated
with high-altitude hyperventilation results in a leftward shift on the curve. Therefore, the actual
PO2 for 50% oxygen saturation (P50) at altitude is not significantly different from that at sea
level.

The Mount Everest Medical Expedition revealed a progressive leftward shift at high altitudes as
the respiratory alkalosis increased. This effect improves oxygen loading in the lungs.

In summary, at each stage of the oxygen transport system, considerable changes occur to
facilitate oxygen delivery. The extent to which the patient with cyanosis makes use of these or
similar mechanisms can be a focus of future research.

Hematologic changes

No less important than the transport system is the transport vehicle—namely, the red blood cell
(RBC). During the first 1-2 weeks at high altitude, plasma volume decreases, raising the
hemoglobin concentration by 1-2 g/dL. In addition, within hours of exposure to altitude, RBC
production increases because production of erythropoietin is heightened. However, the overall
response is slow, taking months to reach equilibrium.

The degree of polycythemia is directly related to the altitude, up to an elevation of 3660 m

(12,000 ft). Above this altitude, the hemoglobin concentration increases rapidly. However, if the
systemic arterial saturation falls below 60%, erythropoietic activity decreases. In subjects living
at 4540 m (14,900 ft), total blood volume gradually rises from 80 to nearly 100 mL/kg, a change
that represents an increase in RBC volume as plasma volume decreases. Monge disease (chronic
mountain sickness) is associated with excessive erythropoiesis.

Polycythemia is associated with hyperviscosity and declining oxygen transport. A further rise in
hemoglobin is observed with age at high altitude. At altitude, climbers with polycythemia exhibit
reduced maximal oxygen consumption, even on 100% oxygen. This observation suggests that
peripheral extraction of oxygen from blood is limited by its reduced flow. Phlebotomy and
hemodilution experiments in mountain climbers and autologous RBC transfusions in athletes
have not yielded information about the ideal hematocrit for any given altitude.

The platelet count decreases by 7% after 2 days at 2990 m (9800 ft) and by 25% after 2 days at
5370 m (17,600 ft). Some suggest that exposure to high altitude induces a hypercoagulable state
in humans.

Increased fibrinogen levels and a decreased clot lysis time were noted in 38 soldiers living at
high altitude for 2 years, as compared with control subjects at sea level. [9] Soldiers with clinical
evidence of pulmonary arterial hypertension had somewhat low levels of fibrinogen, high levels
of platelet factor III, and increased platelet adhesiveness. This evidence suggests that conversion
to fibrin, and possibly platelet deposition, were occurring in these subjects.

Similar studies of the coagulation status of patients with cyanotic congenital heart disease have
been conducted. The Operation Everest II project performed in a hypobaric chamber showed no
changes in coagulation factors.

Metabolic changes

Most visitors to high altitude notice initial weight loss, which has been attributed to reduced
dietary intake, enhanced water loss, and loss of stored body fat. Anorexia is a common complaint
of visitors to even moderate altitude. At high altitude, appetite and caloric intake decrease
dramatically in unacclimatized persons, who generally find fat distasteful and prefer sweets.
Fluid losses result from the insensible water losses associated with hyperventilation and low
humidity, as well as diuresis induced by hypoxia and the cold environment.

Changes in sensory, motor, and mental function

Because the retina of the eye has a great requirement for oxygen, vision is the first sense altered
with the lack of oxygen. This phenomenon is demonstrated by diminished night vision even at
altitudes below 3000 m (about 9600 ft). At 3048 m (10,000 ft), people require more time to learn
a new task than they do at low elevations. At 6100 m (20,000 ft), impairments in sensory,
perceptual, and motor performance have been demonstrated. [10]

In acute hypoxia, reduction of arterial oxygen saturation to 85% decreases a person’s capacity
for mental concentration and abolishes fine motor coordination. Reduction of saturation to 75%
leads to faulty judgment and impaired muscular function.
One year after the American Medical Research Expedition to Everest, reductions in finger-
tapping speed persisted. Also observed were declines in visual long-term memory and verbal
learning, along with increased aphasic errors during neuropsychological testing after climbs to
high altitude. This finding prompted some to surmise whether climbs to extreme altitude cause
brain damage.

On initial exposure to altitude, cerebral blood flow (CBF) decreases because of vasoconstriction
associated with hypocarbia. However, when PaO2 decreases to 50-60 mm Hg, CBF increases.
Blood flow appears to be regionally uneven, increasing at the brainstem level at the expense of
cortical flow. This mechanism may possibly explain the increased vulnerability of the cortex to
hypoxia.

A surprising observation is that the climbers with a high ventilatory response to hypoxia have the
most impairment. The hypocapnia associated with hyperventilation possibly causes a marked
decrease in CBF that offsets any beneficial effects of increased oxygenation.

Vital Signs Increase

Both heart rate and respiratory rate increases as altitude increases. Respiratory rate is how many
breaths an individual takes per minute. During initial exposure to altitude the body must increase
respiratory rate in order to get more oxygen to the body and expel carbon dioxide. Heart rate
increases as respiratory rate increases to help pump oxygen through the body.

Red Blood Cells

One way the body acclimatizes to high altitude is by increasing the amount of red blood cells
produced. It takes the body about four to five days to create new red blood cells and after an
individual has been exposed to altitude for long periods of time, they will have 30 percent to 50
percent more red blood cells than an individual at sea level, according to Rick Curtis, director of
the Outdoor Action Program at Princeton University. The body also creates more capillaries to
match the production of new red blood cells. Extra capillaries decrease the distance between the
cell and capillary, making it easier to transport oxygen throughout the body.

Dehydration

Low humidity, dry air and increased respiratory rate are all factors that contribute to dehydration
at high altitude. Above 6,000 feet, the body exhales and perspires twice as much moisture than at
sea level. Also as a result of lower air pressure moisture from the skin is evaporated at faster
rates that can cause dehydration. With lower levels of oxygen available and less body moisture,
the body is more sensitive to diuretics, such as alcohol and caffeine at high altitudes.

Fluid Shifts

The body knows it needs to sustain vital organs with oxygen and because the amount of oxygen
available decreases at higher altitudes, the body redistributes blood throughout the body. It
decreases the amount of blood flowing to digestive organs and increases blood to the brain, heart
and lungs. As a result of more blood being pumped through the arteries to the brain, headaches
are common. Lack of blood flow to the digestive organs can cause nausea, vomiting and loss of
appetite.

Acclimatization is the beneficial physiological adaptations that occur during repeated exposure
to a hot environment. These physiological adaptations include:

 Increased sweating efficiency (earlier onset of sweating, greater sweat production, and
reduced electrolyte loss in sweat).
 Stabilization of the circulation.
 The ability to perform work with lower core temperature and heart rate.
 Increased skin blood flow at a given core temperature.

To acclimatize workers, gradually increase their exposure time in hot environmental conditions
over a 7-14 day period. New workers will need more time to acclimatize than workers who have
already had some exposure.

Adaptation is a generic phrase encompassing all changes undertaken by an organism to reduce

the negative effects of unfamiliar and undesirable external environment. This includes both
acclimatization and acclimation.
Adaptation describes a spectrum of changes that follow acute and repeated exposure
incorporating genotypic (changes within the genome) and phenotypic (within an organism’s
physiology) adaptations. It may also include behavioural responses including reduced activity
levels.

Acclimatization describes adaptive physiological or behavioural changes within an organism in

response to their natural climate or environment.

Acclimation differs from acclimatization in that rather than adaptive characteristics being
augmented in a natural climate or environment, the stimuli for adaptation is artificially induced,
typically within an enclosed chamber within which ambient conditions (temperature/oxygen
content) are altered.

Acclimatization schedule

 For new workers, the schedule should be no more than a 20% exposure on day 1 and an
increase of no more than 20% on each additional day.
 For workers who have had previous experience with the job, the acclimatization regimen
should be no more than a 50% exposure on day 1, 60% on day 2, 80% on day 3, and
100% on day 4.

In addition, the level of acclimatization each worker reaches is relative to the initial level of
physical fitness and the total heat stress experienced by the individual.
Maintaining acclimatization

Workers can maintain their acclimatization even if they are away from the job for a few days,
such as when they go home for the weekend. However, if they are absent for a week or more
then there may be a significant loss in the beneficial adaptations leading to an increased
likelihood of heat-related illness and a need to gradually reacclimate to the hot environment.

Some additional information on maintaining acclimatization:

 It can often be regained in 2 to 3 days upon returning to a hot job.

 It appears to be better maintained by those who are physically fit.
 Seasonal shifts in temperatures may result in difficulties.
 Working in hot, humid environments provides adaptive benefits which also apply in hot,
desert environments, and vice versa.
 Air conditioning will not affect acclimatization.

Heat Stroke

Heat stroke is the most serious heat-related illness. It occurs when the body becomes unable to
control its temperature: the body's temperature rises rapidly, the sweating mechanism fails, and
the body is unable to cool down. When heat stroke occurs, the body temperature can rise to
106°F or higher within 10 to 15 minutes. Heat stroke can cause death or permanent disability if
emergency treatment is not given.

Symptoms

Symptoms of heat stroke include:

 Confusion, altered mental status, slurred speech

 Loss of consciousness (coma)
 Hot, dry skin or profuse sweating
 Seizures
 Very high body temperature
 Fatal if treatment delayed

First Aid

Take the following steps to treat a worker with heat stroke:

 Call 911 for emergency medical care.

 Stay with worker until emergency medical services arrive.
 Move the worker to a shaded, cool area and remove outer clothing.
 Cool the worker quickly with a cold water or ice bath if possible; wet the skin, place cold
wet cloths on skin, or soak clothing with cool water.
 Circulate the air around the worker to speed cooling.
  Place cold wet cloths or ice on head, neck, armpits, and groin; or soak the clothing with
cool water.

Heat Exhaustion

Heat exhaustion is the body's response to an excessive loss of the water and salt, usually through
excessive sweating. Workers most prone to heat exhaustion are those that are elderly, have high
blood pressure, and those working in a hot environment.

Symptoms

Symptoms of heat exhaustion include:

 Headache
 Nausea
 Dizziness
 Weakness
 Irritability
 Thirst
 Heavy sweating
 Elevated body temperature
 Decreased urine output

First Aid

Treat a worker suffering from heat exhaustion with the following:

 Take worker to a clinic or emergency room for medical evaluation and treatment.
 If medical care is unavailable, call 911.
 Someone should stay with worker until help arrives.
 Remove worker from hot area and give liquids to drink.
 Remove unnecessary clothing, including shoes and socks.
 Cool the worker with cold compresses or have the worker wash head, face, and neck
with cold water.
 Encourage frequent sips of cool water.

Rhabdomyolysis

Rhabdomyolysis is a medical condition associated with heat stress and prolonged physical
exertion, resulting in the rapid breakdown, rupture, and death of muscle. When muscle tissue
dies, electrolytes and large proteins are released into the bloodstream that can cause irregular
heart rhythms and seizures, and damage the kidneys.

Symptoms
Symptoms of rhabdomyolysis include:

 Muscle cramps/pain
 Abnormally dark (tea or cola colored) urine
 Weakness
 Exercise intolerance
 Asymptomatic

First Aid

Workers with symptoms of rhabdomyolysis should:

 Stop activity.
 Increase oral hydration (water preferred).
 Seek immediate care at the nearest medical facility.
 Ask to be checked for rhabdomyolysis (i.e., blood sample analyzed for creatine kinase).

Heat Syncope

Heat syncope is a fainting (syncope) episode or dizziness that usually occurs with prolonged
standing or sudden rising from a sitting or lying position. Factors that may contribute to heat
syncope include dehydration and lack of acclimatization.

Symptoms

Symptoms of heat syncope include:

 Fainting (short duration)

 Dizziness
 Light-headedness during prolonged standing or suddenly rising from a sitting or lying
position

First Aid

Workers with heat syncope should:

 Sit or lie down in a cool place.

 Slowly drink water, clear juice, or a sports drink.

Heat Cramps

Heat cramps usually affect workers who sweat a lot during strenuous activity. This sweating
depletes the body's salt and moisture levels. Low salt levels in muscles causes painful cramps.
Heat cramps may also be a symptom of heat exhaustion.
Symptoms

 Muscle cramps, pain, or spasms in the abdomen, arms, or legs

First Aid

Workers with heat cramps should:

 Drink water and have a snack and/or carbohydrate-electrolyte replacement liquid (e.g.,
sports drinks) every 15 to 20 minutes.
 Avoid salt tablets.
 Get medical help if the worker has heart problems, is on a low sodium diet, or if cramps
do not subside within 1 hour.

Heat Rash

Heat rash is a skin irritation caused by excessive sweating during hot, humid weather.

Symptoms

Symptoms of heat rash include:

 Looks like red cluster of pimples or small blisters

 Usually appears on the neck, upper chest, groin, under the breasts, and in elbow creases

First Aid

Workers experiencing heat rash should:

 When possible, a cooler, less humid work environment is best treatment.

 Keep rash area dry.
 Powder may be applied to increase comfort.
 Ointments and creams should not be used.

Hypothermia

When exposed to cold temperatures, your body begins to lose heat faster than it can be produced.
Prolonged exposure to cold will eventually use up your body's stored energy. The result is
hypothermia, or abnormally low body temperature. A body temperature that is too low affects
the brain, making the victim unable to think clearly or move well. This makes hypothermia
particularly dangerous because a person may not know it is happening and will not be able to do
anything about it.

Symptoms
Symptoms of hypothermia can vary depending on how long you have been exposed to the cold
temperatures.

Early Symptoms

 Shivering
 Fatigue
 Loss of coordination
 Confusion and disorientation

Late Symptoms

 No shivering
 Blue skin
 Dilated pupils
 Slowed pulse and breathing
 Loss of consciousness

First Aid

Take the following steps to treat a worker with hypothermia:

 Alert the supervisor and request medical assistance.

 Move the victim into a warm room or shelter.
 Remove their wet clothing.
 Warm the center of their body first-chest, neck, head, and groin-using an electric
blanket, if available; or use skin-to-skin contact under loose, dry layers of blankets,
clothing, towels, or sheets.
 Warm beverages may help increase the body temperature, but do not give alcoholic
beverages. Do not try to give beverages to an unconscious person.
 After their body temperature has increased, keep the victim dry and wrapped in a warm
blanket, including the head and neck.
 If victim has no pulse, begin cardiopulmonary resuscitation (CPR).

Frostbite

Frostbite is an injury to the body that is caused by freezing. Frostbite causes a loss of feeling and
color in the affected areas. It most often affects the nose, ears, cheeks, chin, fingers, or toes.
Frostbite can permanently damage body tissues, and severe cases can lead to amputation. In
extremely cold temperatures, the risk of frostbite is increased in workers with reduced blood
circulation and among workers who are not dressed properly.

Symptoms

Symptoms of frostbite include:

  Reduced blood flow to hands and feet (fingers or toes can freeze)
 Numbness
 Tingling or stinging
 Aching
 Bluish or pail, waxy skin

First Aid

Workers suffering from frostbite should:

 Get into a warm room as soon as possible.

 Unless absolutely necessary, do not walk on frostbitten feet or toes-this increases the
damage.
 Immerse the affected area in warm-not hot-water (the temperature should be
comfortable to the touch for unaffected parts of the body).
 Warm the affected area using body heat; for example, the heat of an armpit can be used
to warm frostbitten fingers.
 Do not rub or massage the frostbitten area; doing so may cause more damage.
 Do not use a heating pad, heat lamp, or the heat of a stove, fireplace, or radiator for
warming. Affected areas are numb and can be easily burned.

Trench Foot

Trench foot, also known as immersion foot, is an injury of the feet resulting from prolonged
exposure to wet and cold conditions. Trench foot can occur at temperatures as high as 60 degrees
F if the feet are constantly wet. Injury occurs because wet feet lose heat 25-times faster than dry
feet. Therefore, to prevent heat loss, the body constricts blood vessels to shut down circulation in
the feet. Skin tissue begins to die because of lack of oxygen and nutrients and due to the buildup
of toxic products.

Symptoms

Symptoms of trench foot include:

 Reddening of the skin

 Numbness
 Leg cramps
 Swelling
 Tingling pain
 Blisters or ulcers
 Bleeding under the skin
 Gangrene (the foot may turn dark purple, blue, or gray)

First Aid
Workers suffering from trench foot should:

 Remove shoes/boots and wet socks.

 Dry their feet.
 Avoid walking on feet, as this may cause tissue damage.

Chilblains

Chilblains are caused by the repeated exposure of skin to temperatures just above freezing to as
high as 60 degrees F. The cold exposure causes damage to the capillary beds (groups of small
blood vessels) in the skin. This damage is permanent and the redness and itching will return with
additional exposure. The redness and itching typically occurs on cheeks, ears, fingers, and toes.

Symptoms

Symptoms of chilblains include:

 Redness
 Itching
 Possible blistering
 Inflammation
 Possible ulceration in severe cases

First Aid

Workers suffering from chilblains should:

 Avoid scratching
 Slowly warm the skin
 Use corticosteroid creams to relieve itching and swelling
 Keep blisters and ulcers clean and covered

Atmospheric pressure

Variations in atmospheric pressure can present special problems for the respiratory systems of
animals because atmospheric pressure affects the exchange of oxygen and carbon dioxide that
occurs during animal respiration. Normal atmospheric pressure at sea level is the total pressure
that a column of air above the surface of the Earth exerts (760 millimetres of mercury, or 1
atmosphere). The total pressure is the sum of the pressures that each gas—mainly nitrogen,
oxygen, and carbon dioxide—would exert alone (the partial pressure of that gas; see respiration:
The gases in the environment). As an animal breathes, oxygen moves from the environment
across the respiratory surfaces into the blood; carbon dioxide moves in the reverse direction. This
process occurs primarily by passive diffusion; each gas moves from an area of greater to lesser
partial pressure, driven by the differential that exists across the respiratory surface. At higher
altitudes, where the atmospheric pressure is lower, the partial pressure of oxygen is also lower.
The partial pressure differential of oxygen, therefore, is also lower, and the organism effectively
receives less oxygen when it breathes, even though the percentage of oxygen in the air remains
constant. This lack of oxygen is why humans carry oxygen when ascending to high altitudes.
Humans who live in mountainous regions, however, can become acclimatized to the lowered
availability of oxygen, and certain animals such as llamas have adaptations of the blood that
allow them to live at high altitudes. Birds have very efficient lungs, and many apparently have no
problems flying to high altitudes, even for extended flights (

G force

‘G’ is the ratio between a given acceleration and the acceleration due to gravity. The term ‘G force’
is used sometimes to describe a force, which produced acceleration, which is a multiple of the
acceleration due to gravity (9.81 m/sq sec). Thus, an acceleration of 98.1 m/sq sec would be 10 G.
High sustained G, that the modern day combat aircraft are capable of, is G forces of 7G or more
sustained for 15 seconds or more.

Conventionally there are three axes of acceleration, as per the inertial forces acting acting on the
human body:-

 Gx : acceleration acting in antero-posterior axis.

o + Gx = when inertial force acts from front to back
o – Gx = when inertial force acts from back to front
 Gy : acceleration acting in side to side axis
o + Gy = when inertial force acts from left to right
o – Gy = when inertial force acts from right to left
 Gz : acceleration acting in head to feet axis
o +Gz = when inertial force acts from head to feet
o -Gz = when inertial force acts from feet to head

Effects of acceleration on the human body depends on the following factors:–

 Magnitude: Higher the magnitude, more the effects.

 Duration: Shorter the duration, lesser the effects
 Rate of onset/offset:
o Gradual onset – circulatory reflexes are effective;
o Rapid onset – circulatory reflexes bypassed;
o Slow offset – longer to recover; and
o Faster offset – shorter time to recover.
 Site of application: if force is dissipated over larger area, there is less distortion of tissue.
 Direction: Human tolerance is poor in Gz axis but best in Gx axes.
 Acceleration stress, physiological changes that occur in the human body in motion as a
result of rapid increase of speed. Rapid acceleration and surges in acceleration are felt
more critically than are gradual shifts. Pilots are especially subject to the effects of
 acceleration because of the high speeds at which they travel. Acceleration forces are
measured in units of gravitational acceleration, or g. A force of 3 g, for example, is
equivalent to an acceleration three times that of a body falling near Earth.
 Three kinds of acceleration stress are distinguished—positive, negative, and transverse—
according to the position of the body with relation to the direction of acceleration.
 Positive acceleration stress
 Positive acceleration stress occurs when the direction of acceleration is along the long
axis of the body from head to foot. As acceleration increases the force exerted on the
pilot from 1 g to 2 g, there is an awareness of increased pressure and a general feeling of
heaviness in the seat, hands, and feet. Three and 4 g further increase this sensation, and
movement of the extremities becomes difficult; unless the trunk and head are supported,
it may be difficult to keep them erect. The internal organs are pulled down in the body
cavity, and blood pressure falls. Eyesight may become limited, or there may be total
blackout. The legs may feel congested and may have muscle cramps. Breathing may
become difficult. If the acceleration is uneven or if the pilot is inexperienced, there may
be mental confusion and disorientation. Unconsciousness can occur when the force
exerted is from 3 to 5 g.
 When acceleration is in the direction from head to feet, the blood is forced to the lower
part of the body, and unconsciousness occurs when the brain fails to receive enough
oxygen. Increased pressure in the extremities can cause rupture of the small blood vessels
of the skin. The more gradual the acceleration, the less will be the fall in blood pressure,
since the circulatory system is capable of making adjustments; however, it takes about
five seconds before this mechanism becomes fully activated.
 There are seldom any aftereffects of acceleration in the direction from head to feet except
for a few moments of mental confusion. There is usually no pain, though there may be
some discomfort. Repeated exposures to such acceleration do not usually have permanent
effects.
 Negative acceleration stress
 Negative acceleration stress occurs when the direction of acceleration is from feet to
head. This causes a slight displacement of the internal organs in the abdomen and chest
and a rush of blood to the face accompanied by the feeling of congestion. As the
acceleration increases, the congestion increases and throbbing pains are felt throughout
the head. When the force is from 3 to 4.5 g, the eyes feel as though they are protruding,
and there is a gritty feeling under the eyelids because of swelling in the small blood
vessels. There may be temporary loss of vision, or all objects may appear red; this latter
condition is known as “red-out.” The mental confusion that develops at high
accelerations may lead to unconsciousness.
 In acceleration in the direction from feet to head, the blood pressure in the skull rises. In
order to relieve the pressure in the skull, the velocity of the blood flow to the rest of the
body must be increased. Temporary cardiac arrest may occur at around 5 g. Respiration is
also impaired because of the pressure upon the lungs from the abdominal contents and the
muscular diaphragm (the wall between the chest and the abdomen). Bleeding can occur
under the skin of the face; weak arteries or veins in the head region can rupture while
under such stress. The average endurable times for negative stress are a few seconds at 5
g, 15 seconds for 4.5 g, and around 30 seconds for 3 g. Stunt fliers and pilots experienced
 with accelerations in the direction from feet to head seem to tolerate its effects better than
new or inexperienced fliers.
 Transverse acceleration stress
 Transverse acceleration stress occurs when the direction of acceleration is sideways with
relation to the long axis of the body. The effects of transverse acceleration are not as
great as those of equivalent forces in the previous two cases. Thus, the position in which
a pilot lies on his back at right angles to the direction of flight seems to be best for the
high accelerations required to reach orbital velocity and reentry decelerations in manned
space flight. (Space shuttle launches typically have a maximum acceleration of 3 g.)
Accelerations up to 6 g directed across the body produce only the sensations of increased
pressure on that part of the body that supports the weight. As the force increases toward 8
g, breathing may become difficult because of the compression of the abdomen and chest.
Accelerations of up to 12 g can be tolerated in transverse acceleration without undue
discomfort or visual disorders. There may, however, be a slight increase in heart rate and
blood pressure, and the blood oxygenation level seems to decrease with pressure.
 As you may expect, our body’s physiology will both be affected by and respond to this
novel variability in G forces. When an aircraft is traveling towards the earth and exerting
thrust in that path of motion, it is accelerating at that rate plus 1G (9.82 m/s2). When the
same aircraft is accelerating away from the Earth’s surface, the sum of accelerative forces
will be the difference from the thrust and 1G. Newton’s First Law of Motion explains
why the occupant of the aircraft will attempt to remain in motion at a constant direction
and velocity during changes in direction and accelerative forces during flight. Though
they will be prevented from doing so by the seat restraints. These safety restraints will
exert an equal (almost) and opposite force on the occupant’s body as Newton’s Third
Law of Motion predicts. A detailed discussion on the physics behind G-forces and the gas
laws of aerospace physiology can be found elsewhere. But it is important to note that on
Earth we are always under 1G of force, but that in flight vertical accelerations increase or
decrease this value depending on the direction.

It depends on the direction. An upwards acceleration of about 5g is enough to overwhelm the

ability of your heart to pump blood to your brain. This causes oxygen starvation and you will
black out within a few seconds.

Downward, or negative, g-force is even worse. The blood pools in your head, your face swells up
and your lower eyelids are forced over your eyes. This is called ‘redout’ because all you see is
the light shining through your eyelids. At negative 3g, the blood can’t get back to your lungs to
re-oxygenate, so you pass out.

G-forces act on the human body in different axes (or directions). These are usually described as
the x, y, z axes. Each has a positive (+) or negative (-) direction. When standing upright, the
force of gravity acts along the longitudinal or Gz axis parallel to the spinal cord. +Gz acts
downward in the same direction as Earth’s gravity. Negative Gz‘s act in a direction opposite to
gravity. Common notation identifies the axis acting through the front and back of the body as Gx
and the axis acting laterally as Gy. These different axes correspond to yaw (Gz), roll (Gx), and
pitch (Gy) of the aircraft.
HUMAN PHYSIOLOGY IN RESPONSE TO GRAVITY

The circulatory system is most significantly affected by increased G-forces during flight. Even at
1G, blood pressure in an upright person is highest in the lower extremities (the legs) and lowest
intracerebrally (in the cranium) due to gravity. Because our bodies have adapted in a 1G
environment, we have built in mechanisms to compensate for this discrepancy. Experiencing
higher magnitudes of gravity presents unique problems to circulatory regulation. At larger +G
forces, the above physiologic phenomenon is magnified and a larger discrepancy of blood
pressures between cranium and the lower body occurs. At some point, intracranial perfusion
cannot be maintained and significant cerebral hypoxia (no blood = no oxygen) follows. The end
result is unconsciousness. In the world of aviation this is called a G-LOC, aka G-induced loss of
consciousness, and remains a significant cause of loss of aircraft and pilot in both military fighter
aviation and civilian acrobatic aviation. Throughout the 1990’s, for example, the USAF lost
approximately one aircraft per year due to G-LOC.

In addition to circulatory effects, increased +Gz disrupts respiration by shifting blood to the lung
bases, which collapses the small sacs of air (called alveoli) and creates a general
ventilation/perfusion mismatch as air remains in the upper lung where there is little blood flow.
As +Gz forces increase less blood flow combined with poorly oxygenated blood compound the
cerebral (brain) hypoxia described above. Other less serious effects of large G forces are
musculoskeletal pain (usually confined to the back and neck) and small punctate bruises called
petechiae from overwhelmed capillaries that rupture. This usually occurs in gravity-dependent
areas of the body and are affectionately known as G-measles, or Geasles.
THE G-LOC

As stated above, the most significant physiologic effect from G-forces are related to tissue
ischemia (insufficient blood flow), specifically intracerebral (brain) ischemia. Because of the
high sensitivity that the eye’s retina has to hypoxia, symptoms are usually first experienced
visually. As the retinal blood pressure decreases below the eye’s globe pressure (usually 10-21
mm Hg), blood flow begins to cease to the light sensing receptors in the retina, first affecting
perfusion (and therefore vision) farthest from the optic disc with progression of central vision
loss. Therefore visual symptoms in response to increased G’s usually progresses from increasing
tunnel vision to ‘graying out’ to full ‘black out’ – a phenomenon in which a person retains
consciousness, but full retinal ischemia causes absolute blindness.

The final submission to G-forces produces a G-induced loss of consciouness (aka G-LOC),
which is usually divided into a relative and absolute component. Absolute incapacitation is the
period of time when the aircrew member is physically unconscious and averages about 12
seconds. Relative incapacitation is the period in which the consciousness has been regained,
but the person is confused and remains unable to perform simple tasks (obviously cannot fly an
aircraft). This period averages about 15 seconds. Upon regaining cerebral blood flow, the G-
LOC victim usually experiences myoclonic convulsions (a seizure-like episode often called the
‘funky chicken’) and oftentimes full amnesia of the event is experienced.

Many militaries train their aircrew about G-forces and the anti-G straining maneuver (AGSM)
using a centrifuge. See the youtube video below for an anthology of centrifuge-induced G-
LOC’s. The AGSM has two components – isometric muscle contraction and a particular
respiratory sequence, which attempts to maximize cerebral blood flow and cardiac output, while
maintaining an adequate level of oxygenation. A separate post written for pilots describing the
AGSM technique with recommendations on how to improve G-tolerance can be found here.

When the AGSM is combined with an inflatable G-suit, one’s tolerance to high G’s increases
markedly. Studies performed in the 1940’s and 1950’s by the U.S. DoD found that without any
strain or G-suit, average G’s prior to G-LOC was dependent on the rate of G onset. G-LOC
occurred at an average of 5.4 G’s at 1 G/sec rate and 4.5 G’s at 2 G/sec rate. An effective AGSM
is thought to increase one’s G tolerance by 3 full G’s. Most legacy G-suits like the CSU 13B/P
used by the USAF and CSU 15 A/P used by the USN/USMC can increase G tolerance for an
additional 1 to 1.5 G’s. Newer G-suits such as the ATAGS provides even greater
protection. When using this important life support equipment, a modern fighter pilot can be
expected to remain conscious and continue to fly tactically at up to +9Gz. For a demonstration of
G-LOC and AGSM (though in this case, inadequate AGSM), see the youtube video below.