high altitude modefied

8/13/2019 High Altitude Modefied

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Effect of Breathing Pure Oxygen onAlveolar P O2 at Different Altitudes

Note that the saturation remains above 90per cent until the aviator ascends to about39,000 feet;

then it falls rapidly to about 50 per cent atabout 47,000 feet.


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The "Ceiling" When Breathing Air and When BreathingOxygen in an Unpressurized Airplane

one notes that an aviator breathing pureoxygen in an unpressurized airplane canascend to far higher altitudes than one

breathing air.For instance, the arterial saturation at 47,000

feet when one is breathing oxygen is about50 per cent and is equivalent to the arterialoxygen saturation at 23,000 feet when one isbreathing air.


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The "Ceiling" When Breathing Air and When BreathingOxygen in an Unpressurized Airplane

In addition, because an unacclimatized personusually can remain conscious until thearterial oxygen saturation falls to 50 per cent,for short exposure times the ceiling for anaviator in an unpressurized airplane whenbreathing air is about 23,000 feet and when

breathing pure oxygen is about 47,000 feet,provided the oxygen-supplying equipmentoperates perfectly.


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Acute Effects of Hypoxia Some of the important acute effects of hypoxia in

the unacclimatized person breathing air,beginning at an altitude of about 12,000 feet, are

drowsiness, lassitude, mental muscle fatigue, sometimes headache, occasionally nausea, sometimes euphoria.


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Acute Effects of Hypoxia

These effects progress to a stage oftwitchings or seizures above 18,000

feet and end, above 23,000 feet in the

unacclimatized person, in coma, followed shortly thereafter by

death .


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Acute Effects of Hypoxia One of the most important effects of hypoxia is decreased mental proficiency, which

decreases judgment, memory, and performance

of discrete motor movements. For instance, if anunacclimatized aviator stays at 15,000 feet for 1hour,

mental proficiency ordinarily falls to about 50per cent of normal,

and after 18 hours at this level it falls to about20 per cent of normal.


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Acclimatization to Low P O2

A person remaining at high altitudes for days,weeks, or years becomes more and moreacclimatized to the low P O2, so that it causesfewer deleterious effects on the body.

And it becomes possible for the person to workharder without hypoxic effects or to ascend tostill higher altitudes.


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Acclimatization to Low P O2

The principal means by which acclimatizationcomes about are

(1) a great increase in pulmonary ventilation,

(2) increased numbers of red blood cells,

(3) increased diffusing capacity of the lungs,

(4) increased vascularity of the peripheral tissues,

(5) increased ability of the tissue cells to useoxygen despite low P O2.


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Increased Pulmonary Ventilation-Roleof Arterial Chemoreceptors

Immediate exposure to low P O2 stimulates thearterial chemoreceptors, and this increasesalveolar ventilation to a maximum of about 1.65times normal. Therefore, compensation occurswithin seconds for the high altitude, and it aloneallows the person to rise several thousand feethigher than would be possible without theincreased ventilation. Then, if the person remains

at very high altitude for several days, thechemoreceptors increase ventilation still more,up to about five times normal


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Increase in Red Blood Cells and HemoglobinConcentration During Acclimatization

hypoxia is the principal stimulus for causing anincrease in red blood cell production.

Ordinarily, when a person remains exposed to

low oxygen for weeks at a time, thehematocrit rises slowly from a normal value of40 to 45 to an average of about 60, with anaverage increase in whole blood hemoglobinconcentration from normal of 15 g/dl to about20 g/dl.


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Increased Diffusing Capacity AfterAcclimatization.

It will be recalled that the normal diffusing capacity foroxygen through the pulmonary membrane is about 21ml/mm Hg/min, and this diffusing capacity canincrease as much as threefold during exercise.

A similar increase in diffusing capacity occurs at highaltitude.

Part of the increase results from increased pulmonarycapillary blood volume, which expands the capillariesand increases the surface area through which oxygencan diffuse into the blood.


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Peripheral Circulatory System Changes DuringAcclimatization-Increased Tissue Capillarity.

The cardiac output often increases as much as30 per cent immediately after a personascends to high altitude but then decreasesback toward normal over a period of weeks asthe blood hematocrit increases , so that theamount of oxygen transported to the

peripheral body tissues remains about normal.


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Natural Acclimatization of NativeHuman Beings Living at High Altitudes

Many native human beings in the Andes and in theHimalayas live at altitudes above 13,000 feet-one group inthe Peruvian Andes lives at an altitude of 17,500 feet andworks a mine at an altitude of 19,000 feet.

Many of these natives are born at these altitudes and livethere all their lives.

Acclimatization of the natives begins in infancy. The chestsize, especially, is greatly increased, whereas the body sizeis somewhat decreased, giving a high ratio of ventilatorycapacity to body mass. In addition, their hearts, which frombirth onward pump extra amounts of cardiac output, areconsiderably larger than the hearts of lowlanders.


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Reduced Work Capacity at High Altitudes and PositiveEffect of Acclimatization

addition to the mental depression caused by hypoxia,as discussed earlier, the work capacity of all muscles isgreatly decreased in hypoxia. This includes not onlyskeletal muscles but also cardiac muscles.

In general, work capacity is reduced in directproportion to the decrease in maximum rate of oxygenuptake that the body can achieve.

To give an idea of the importance of acclimatization inincreasing work capacity, consider this: The workcapacities as per cent of normal for unacclimatized andacclimatized people at an altitude of 17,000 feet are asfollows:


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Thus, naturally acclimatized native personscan achieve a daily work output even at highaltitude almost equal to that of a lowlander atsea level, but even well-acclimatizedlowlanders can almost never achieve thisresult.


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Acute Mountain Sickness and High-Altitude Pulmonary Edema

small percentage of people who ascend rapidly to highaltitudes become acutely sick and can die if not givenoxygen or removed to a low altitude. The sickness beginsfrom a few hours up to about 2 days after ascent.

Two events frequently occur: Acute cerebral edema . This is believed to result from local

vasodilation of the cerebral blood vessels, caused by thehypoxia. Dilation of the arterioles increases blood flow intothe capillaries, thus increasing capillary pressure, which inturn causes fluid to leak into the cerebral tissues. Thecerebral edema can then lead to severe disorientation andother effects related to cerebral dysfunction.

Acute pulmonary edema . The cause of this is still unknown,


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Chronic Mountain Sickness Occasionally, a person who remains at high altitude too

long develops chronic mountain sickness , in which thefollowing effects occur:

(1) the red cell mass and hematocrit become exceptionallyhigh,

(2) the pulmonary arterial pressure becomes elevated evenmore than the normal elevation that occurs duringacclimatization,

(3) the right side of the heart becomes greatly enlarged,

(4) the peripheral arterial pressure begins to fall, (5) congestive heart failure ensues, and (6) death often follows unless the person is removed to a

lower altitude.


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Physiology of Deep-Sea Diving andOther Hyperbaric Conditions

When human beings descend beneath thesea, the pressure around them increasestremendously. To keep the lungs from

collapsing, air must be supplied at very highpressure to keep them inflated. This exposesthe blood in the lungs also to extremely highalveolar gas pressure, a condition calledhyperbarism . Beyond certain limits, these highpressures can cause tremendous alterations inbody physiology and can be lethal.


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Relationship of Pressure to Sea Depth

A column of seawater 33 feet deep exerts thesame pressure at its bottom as the pressure ofthe atmosphere above the sea. Therefore, aperson 33 feet beneath the ocean surface isexposed to 2 atmospheres pressure, 1atmosphere of pressure caused by the weight ofthe air above the water and the second

atmosphere by the weight of the water itself. At66 feet the pressure is 3 atmospheres, and soforth


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Effect of Sea Depth on the Volume ofGases-Boyle's Law

At 33 feet beneath the sea, where the pressure is 2atmospheres, the volume has been compressed to onlyone-half liter, and at 8 atmospheres (233 feet) to one-eighth liter.

Thus, the volume to which a given quantity of gas iscompressed is inversely proportional to the pressure.

This is a principle of physics called Boyle's law , which isextremely important in diving physiology becauseincreased pressure can collapse the air chambers of thediver's body, especially the lungs, and often causesserious damage.


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Effect of High Partial Pressures ofIndividual Gases on the Body

The individual gases to which a diver isexposed when breathing air are nitrogen ,oxygen , and carbon dioxide; each of these attimes can cause significant physiologic effectsat high pressures.


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Nitrogen Narcosis at High NitrogenPressures

About four fifths of the air is nitrogen. At sea-levelpressure, the nitrogen has no significant effect onbodily function, but at high pressures it can causevarying degrees of narcosis. When the diver remainsbeneath the sea for an hour or more and is breathingcompressed air, the depth at which the first symptomsof mild narcosis appear is about 120 feet. At this levelthe diver begins to exhibit joviality and to lose many ofhis or her cares. At 150 to 200 feet, the diver becomes

drowsy. At 200 to 250 feet, his or her strength wanesconsiderably, and the diver often becomes too clumsyto perform the work required.


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Oxygen Toxicity at High Pressures Effect of Very High P O2 on Blood Oxygen Transport. When the P O2 in the blood rises above 100 mm Hg, the

amount of oxygen dissolved in the water of the bloodincreases markedly.

Note that in the normal range of alveolar P O2 (below120 mm Hg), almost none of the total oxygen in theblood is accounted for by dissolved oxygen, but as theoxygen pressure rises into the thousands of millimetersof mercury, a large portion of the total oxygen is thendissolved in the water of the blood, in addition to thatbound with hemoglobin.


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Acute Oxygen Poisoning The extremely high tissue P O2 that occurs when oxygen is

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

For instance, breathing oxygen at 4 atmospheres pressureof oxygen (P O

2 = 3040 mm Hg) will cause brain seizures

followed by coma in most people within 30 to 60 minutes. symptoms encountered in acute oxygen poisoning include

nausea, muscle twitchings, dizziness, disturbances of vision,irritability, and disorientation. Exercise greatly increases thediver's susceptibility to oxygen toxicity, causing symptomsto appear much earlier and with far greater severity than inthe resting person.


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Decompression of the Diver AfterExcess Exposure to High Pressure

When a person breathes air under high pressure for a long time,the amount of nitrogen dissolved in the body fluids increases.

The reason for this is the following: Blood flowing through thepulmonary capillaries becomes saturated with nitrogen to the samehigh pressure as that in the alveolar breathing mixture. And over

several more hours, enough nitrogen is carried to all the tissues ofthe body to raise their tissue P N2 also to equal the P N2 in thebreathing air.

Because nitrogen is not metabolized by the body, it remainsdissolved in all the body tissues until the nitrogen pressure in thelungs is decreased back to some lower level, at which time the

nitrogen can be removed by the reverse respiratory process;however, this removal often takes hours to occur and is the sourceof multiple problems collectively called decompression sickness .


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Decompression Sickness (Synonyms: Bends,Compressed Air Sickness, Caisson Disease, Diver's

Paralysis, Dysbarism a diver has been beneath the sea long enough

that large amounts of nitrogen have dissolved inhis or her body and the diver then suddenlycomes back to the surface of the sea, significantquantities of nitrogen bubbles can develop in thebody fluids either intracellularly or extracellularlyand can cause minor or serious damage in almost

any area of the body, depending on the numberand sizes of bubbles formed; this is calleddecompression sickness .


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Symptoms of Decompression Sickness("Bends").

The symptoms of decompression sickness are caused by gasbubbles blocking many blood vessels in different tissues.

At first, only the smallest vessels are blocked by minute bubbles,but as the bubbles coalesce, progressively larger vessels areaffected. Tissue ischemia and sometimes tissue death are the

result. In most people with decompression sickness, the symptoms arepain in the joints and muscles of the legs and arms, nervous systemsymptoms occur, ranging from dizziness in about 5 per cent toparalysis or collapse and unconsciousness in as many as 3 per cent.

Finally, about 2 per cent of people with decompression sicknessdevelop "the chokes,"; this is characterized by serious shortness ofbreath, often followed by severe pulmonary edema and,occasionally, death


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Nitrogen Elimination from the Body;Decompression Tables

If a diver is brought to the surface slowly, enoughof the dissolved nitrogen can usually beeliminated by expiration through the lungs toprevent decompression sickness. About twothirds of the total nitrogen is liberated in 1 hourand about 90 per cent in 6 hours. Decompressiontables have been prepared by the U.S. Navy 17minutes at 40 feet depth

19 minutes at 30 feet depth 50 minutes at 20 feet depth 84 minutes at 10 feet depth

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