Unit 5 Asma Hyperbaric Physiology

Front 1

Describe the relationship between depth (in sea water) and ambient pressure.

Back 1

A column of sea water 33 feet deep exerts the same pressure at its bottom as the entire atmosphere above the earth. Therefore, a person 33 feet beneath the ocean surface is exposed to a pressure of 2 atmospheres, 1 atmosphere of pressure caused by the air above the water and the second atmosphere by the weight of the water itself. At 66 feet the pressure is 3 atmospheres and so forth.
Depth (feet) Atmosphere(s)
Sea Level 1
33 2
66 3
100 4
133 5
166 6
200 7

Front 2

Calculate volumetric changes in gas as a function of change in sea water depth.

Back 2

An important effect of depth is the compression of gases to smaller and smaller volumes. A volume of 1 liter of air when brought to the depth of 33 feet beneath the sea, 2 atmospheres, would be compressed to only ½ liter. At 8 atmospheres (233 feet) the original volume of 1 liter at sea level would be compressed to 1/8 liter.

Front 3

Describe the relationship between hyperbaric exposure and hypobaric exposure.

Back 3

Boyle’s law holds true for both descent from altitude to sea-level and descent in water to depth from sea level. Gas will be compressed to smaller and smaller volumes, thus the volume to which a given quantity of gas is compressed is inversely proportional to the pressure. Physiologically we need to compensate for the increase in pressure in both hyperbaric and hypobaric exposure by using the Valsalva maneuver to force air into the middle ear and sinuses as the volume of gas decreases in these spaces.

Front 4

Describe the physiological mechanism that causes nitrogen narcosis.

Back 4

The mechanism of the narcotic effect of delivered nitrogen at high pressures is believed to be the same as that of essentially all the gas anesthetics. That is, nitrogen dissolves freely in the fats of the body, and it is presumed that it, like most of the anesthetic gases, dissolves in the membranes of the neurons and because of its physiological effects on altering ionic conductance through the membranes reduces neuronal excitability.

Front 5

State the depth in sea water at which nitrogen narcosis can become a physiological concern.

Back 5

About four fifths of the air is nitrogen. At sea level pressure the nitrogen has no known effects on bodily function, but at high pressures it can cause varying degrees of narcosis. When a diver remains beneath the sea for an hour or more and is breathing compressed air, the depth at which the first symptoms of mild narcosis appear is about 120 feet. At this level the individual begins to exhibit joviality and to lose many of his cares.

Front 6

Describe the symptoms of nitrogen narcosis

Back 6

Nitrogen narcosis has characteristics similar to those of alcohol intoxication.
120 Feet Joviality and euphoria
150-200 feet drowsy
200-250 feet strength wanes considerably, often becomes too clumsy to work
250 feet beyond- Diver becomes useless

Front 7

What (that have evolved over centuries of adaptation to the earth’s atmospheric oxygen tensions) are among the most vital and basic of all biological functions?

Back 7

Cellular antioxidant defense mechanisms.

Front 8

In the absence of cellular antioxidant defense mechanisms, oxygen pressures required to sustain life would cause what?

Back 8

Lethal poisoning due to cellular damaged caused by oxygen free radicals that are by-products of cellular metabolism.

Front 9

The severityof oxygen poisoning increases with what?

Back 9

The severity of oxygen poisoning increases progressively with elevation of the inspired PO2 and with greater duration of exposure. At sufficient pressure and exposure duration, oxygen will cause initial functional impairment and ultimate chemical destruction of any living cell due to the antioxidant defense mechanisms not being able to keep up with the production of oxygen free radicals.

Front 10

Does molecular oxygen (O2) have the capability of oxidizing other compounds?

Back 10

Molecular oxygen (O2) has little capability of oxidizing other compounds.

Front 11

What must moleculr oxygen be converted into before it can oxidize other compounds?

Back 11

It must first be converted into an “active” form of oxygen.

Front 12

What are the forms of active oxygen called?

Back 12

Oxygen free radicals

Front 13

Name two oxygen free radicals.

Back 13

Superoxide free radical O2 and the peroxide radical in the form of hydrogen peroxide

Front 14

How are oxygen free radicals removed from the tissues?

Back 14

The tissues also contain multiple enzymes that rapidly remove these free radicals, including especially, peroxidases, catalases, and superoxide dismutases. Therefore, so long as the hemoglobin-oxygen buffering mechanism functions properly and maintains a normal tissue PO2, the oxidizing free radicals are removed so rapidly that they have little or no effect in the tissues.

Front 15

Are oxygen free radicals still being formed even when tissue PO2 is normal at the level of 40 mmHg

Back 15

Yes, are continually being formed from the dissolved molecular oxygen.

Front 16

A person can be exposed to how many atmospheres of pressure of oxygen almost indefinitely without developing acute oxygen toxicity?

Back 16

1

Front 17

After only 12 or so hours at 1 atmosphere of exposure the amount of oxidizing free radicals do what?

Back 17

Literally overwhelm the enzyme system for removing them.

Front 18

Describe the physiological mechanisms that cause pulmonary oxygen toxicity.

Back 18

The oxidizing free radicals oxidize the polyunsaturated fatty acids that are essential components of many of the membranous structures of the cells as well as oxidize some of the cellular enzymes damaging the cellular metabolic systems. These slow effects have serious destructive and even lethal effects on the cells of the linings of the bronchi and alveoli.

Front 19

What is the reason for the effect in the lungs and not the other tissues caused by oxidizing free radicals?

Back 19

The reason for this effect in the lungs and not in the other tissues is that the air spaces of the lungs are directly exposed to the high oxygen pressure, whereas oxygen is delivered to the other tissues at almost normal PO2 b/c of the hemoglobin-oxygen buffer system, as long as the air PO2 remains less than about 2 atmospheres.

Front 20

Why are nervous tissues especially susceptible to oxygen toxicity?

Back 20

Because of their high lipid content.

Front 21

Describe the symptoms of pulmonary oxygen toxicity.

Back 21

Known as the “Lorraine Smith Effect” the symptoms of pulmonary oxygen toxicity appear to be caused by a tracheobronchitis (lung passageway congestion), pulmonary edema and atelectasis.
Symptoms begin with a mild tickling sensation that is accentuated by inspiration and occasionally induces a cough.
Tracheal irritation becomes progressively more intense and widespread in parallel with more frequent coughing.
When extreme the tracheal symptoms are characterized by a constant burning sensation, exacerbated by inspiration, accompanied by an uncontrollable coughing.
The most severe symptoms are associated with dyspnoea (difficulty breathing) on exertion or even at rest.

Front 22

Describe the physiological mechanisms that cause neural oxygen toxicity.

Back 22

Above a critical alveolar PO2 (about 2 atmospheres PO2) the hemoglobin-oxygen buffering mechanism fails, and the tissue PO2 can then rise to hundreds or thousands of millimeters of mercury. Then, the amounts of oxidizing free radicals literally overwhelm the enzyme systems for removing them, and now they do have serious destructive and lethal effects on the cells. Membranous structures of the cell are disrupted by oxidation of polyunsaturated fatty acids. Cellular enzymes are oxidized, thus severely damaging cellular metabolic systems.

Front 23

Most of the acute lethal effects of acute oxygen toxicity are related to what?

Back 23

Brain dysfunction.

Front 24

What are the symptoms of neural oxygen toxicity also known as?

Back 24

The “Paul Bert Effect”

Front 25

Describe the symptoms of neural oxygen toxicity

Back 25

The manifestations of neural oxygen toxicity range from localized muscle twitching to grand mal seizures, and with continued exposures past the onset of these signs progressive neural destruction, permanent paralysis and death. Effects elsewhere include retinal separation, destruction of visual cells and blindness. There is considerable variability in the effects of neural oxygen toxicity symptoms seen in individuals.

Front 26

What is the culmination of neural oxygen toxicity symptoms?

Back 26

A convulsive seizure.

Front 27

List some of the signs and symptoms of neural oxygen toxicity.

Back 27

Facial Pallor, Acoustic symptoms, sweating, respiratory changes, bradychardia, severe nausea, choking sensation, spasmodic vomiting, sleepiness, vertigo, depression, fibrillation of lips, euphoria, lip twitching, apprehension, twitching of cheeks and nose, changes in behavior, palpitations, visual symptoms, epigastic tensions, syncope, convulsions.

Front 28

Hyperbaric therapy is achieved how?

Back 28

Hyperbaric therapy is achieved by applying two physical factors related to the pressure environment.

Front 29

What are the two physical factors that are applied to achieve hyperbaric therpy?

Back 29

The first factor is the mechanical compression of gas-filled entities such as bubbles. The second factor is the elevation of the partial pressure of inspired gases and the subsequent increase in the amount of various gases that enter into physical solution in body fluids.

Front 30

Describe the physical and physiological explanation for the use of recompression therapy in the management of DCS.

Back 30

The use of hyperbaric oxygen therapy for treating decompression sickness results in bubble size reduction, a positive nitrogen gradient to reduce the size of bubbles and resolve them, perfusion in ischemic tissues, and correction of local tissue hypoxia.

Front 31

During recompression therapy the surrounding barometric pressure is ____ producing what?

Back 31

Increased producing a reduction in bubble volume in accordance with Boyle’s Law. During compression, the bubble becomes smaller and the surface tension increases. Below a certain critical diameter, the surface tension becomes so great that the bubble collapses and the gas within it dissolves.

Front 32

Breathing 100% oxygen at incerased pressure during hyperbaric therepy provides what?

Back 32

An increased gradient for eliminating nitrogen from evolved bubbles and aids in their resorption. The increased gradient also speeds the elimination of nitrogen from supersaturated tissues and thus helps prevent further bubble formation.

Front 33

Hyperbaric oxygenation results in _____oxygen tension in the capillaries surrounding ischemic tissue causing what?

Back 33

Increased. The increased oxygen tension extends the oxygen diffusion distance from functioning capillaries and corrects the local tissue hypoxia. Overcoming the tissue hypoxia tends to disrupt the vicious cycle of hypoxia-induced tissue damage that causes tissue edema and interferes with circulation and oxygenation.

Front 34

Why are aero-embolisms (gas embolisms) dangerous?

Back 34

The onset of gas embolism is sudden, dramatic, and life-threatening. Bubbles obstruct the systemic or pulmonary arterial circulation. As decompression continues, they expand to produce local endothelial cell damage and herniation into the vessel wall which produces immediate hypoxia symptoms that may appear as neurological deficits.

Front 35

Describe the physical and physiological explanation for the use of recompression therapy in the management of aero-embolism (gas embolism).

Back 35

The rational for hyperbaric therapy for decompression sickness also applies to the management of gas embolism; mechanical compression of bubbles and hyperbaric oxygenation of tissue. Because of the massive amounts of air that are often introduced into the cerebral circulation, it is usually necessary to mechanically compress the entrapped air maximally. The volume of air can be reduced by 83% by compressing to 6 atm. 100% oxygen cannot be administered at 6 atm due to the extremely short time to CNS oxygen toxicity. Elevated oxygen percentages can be administered in the form of 50/50 Nitrox (50% O2, 50% nitrogen). This mixture will assist in correcting tissue hypoxia and ischemia because of improved oxygen diffusion distance. Hyperbaric therapy is the only definitive treatment for arterial gas embolism.

Front 36

What is the only definitive treatment for arterial gas embolism?

Back 36

Hyperbaric Therapy

Front 37

How is hyperbaric oxygen therepy conducted?

Back 37

It has been learned that the intense oxidizing properties of high-pressure (hyperbaric oxygen) can have valuable therapeutic effects in several important clinical conditions. The oxygen is usually administered at PO2s of 2 to 3 atmospheres of pressure through a mask or intratracheal tube, while the gas around the body is normal air compressed to the same high-pressure level. It is believed that the same oxidizing free radicals responsible for oxygen toxicity are also responsible for the therapeutic benefits.

Front 38

List (non-pressure related) medical conditions that may be treated with hyperbaric oxygen therapy.

Back 38

Gas gangrene (clostridial organisms)
Leprosy (leprosy bacillus)
Carbon monoxide poisoning (smoke inhalation)
Osteomyelitis (bone infection)
Clostridal myonecrosis (bacterial caused muscle tissue death)
Crush Injury, compartment syndrome and other acute traumatic ischaemias.
Exceptional blood loss, anemia
Radiation tissue damage
Skin grafts and flaps
Thermal Burns

Front 39

Describe the physiological basis for using HBO for the treatment of carbon monoxide poisoning.

Back 39

At atmospheric pressure and breathing air, the normal half-life of CO in blood is approximately 5 h 20 min, although this may be dependent on metabolic rate and other factors. Breathing 100% O2 at one atmosphere, the half-life is shortened to 1h 20 min. At 3 atm and breathing 100% O2 in the chamber, the half-life is shortened to 23 min. As enough oxygen can be dissolved in plasma at 3 atm to meet all the patients’ metabolic needs, the deleterious effects of carboxyhaemoglobin per se are ended immediately the patient reaches full pressure in the chamber.

Front 40

What is the cause of the fatal outcome seen in severe carbon monoxide poisoning and why?

Back 40

Simple carboxyhaemoglobinaemia is not the cause of the fatal outcome seen in severe CO poisoning, but that there is a vital metabolic intracellular component. Lipid peroxidation in the brain and probably also the heart is seen as being a possible mechanism for the severe morbidity and mortality. Lipid peroxidation is terminated by exposure to 3 atm of oxygen. Even though HBO quickly removes CO from the hemoglobin and possibly from the organelles, and immediately restores full oxygenation, it is conceivable that termination of lipid peroxidation is its most important function.

Front 41

Describe the physiological basis for using HBO therapy for wound healing

Back 41

Hyperbaric oxygenation results in increase oxygen tension in capillaries surrounding ischemic tissue. The increased oxygen tension extends the oxygen diffusion distance from functioning capillaries and corrects local tissue hypoxia. Overcoming the tissue hypoxia tends to disrupt the vicious cycle of hypoxia-induced tissue damage that causes tissue edema and interferes with circulation and oxygenation.
The higher tissue oxygen tensions achieved under hyperbaric conditions result in an increased oxygen diffusion distance that permits fibroblast division and the production of collagen. For capillaries to arborize and advance, they must invade a collagen matrix. Collagen formation can precede some three times further away from capillary buds under hyper baric condition because of the increase PO2. Increased vascularization speeds tissue healing through the delivery of O2 and nutrients and the removal of cellular metabolic by products.

Front 42

Describe the physiological basis for using HBO therapy for treating radial osteonecrosis (Osteoradionecrosis ORN)

Back 42

Osteoradionecrosis (ORN) is basically an ischemic disorder following radiation therapy. The ischemic disorder results from blocked vessels of the irradiated tissue that gradually sclerose. The tissues are rendered hypoxic and hyocellular in addition to being hypovascular.
The mechanism of action of HBO begins by raising the PO2 in the radiated area. Functioning capillaries are very sparse and the tissues may have oxygen tension considerably below the 30 mmHg necessary for fibroblast division, collagen production and neoangiogenesis. Generalized hypoxia present in these wounds would be sufficient to stimulate capillary budding; capillaries cannot advance unless they can arborize into a soft collagen matrix.
HBO appears to produce the necessary collagen and facilitates capillary growth to establish tissue (bone) vascularization and promote healing.

Front 43

Describe the physiological basis for using HBO therapy for treating gas gangrene.

Back 43

Probably the most successful use of hyperbaric oxygen has been in the treatment of gas gangrene. The bacteria that cause this condition, clostridial organisms, grow best under anaerobic conditions and stop growing at oxygen pressures greater than about 70mmHg. Therefore, hyperbaric oxygenation of the tissues can frequently stop the infectious process entirely and thus convert a condition that formerly was almost 100% fatal into one that is cured in the most instances