Pulmonary 9: Extreme Conditions

Question 1

What would a water bottle look like at high altitude vs low?

Altitude Andes mountains (4938 m)
Pacific ocean - 0 feet

Answer 1

full/condensation of water at high altitude

collapses on self w cap on at low altitude

slide 4

Question 2

How do barometric pressure and inspired PO2 change with altitude?

Answer 2

barometric pressure and inspired PO2 decrease with altitude

Slide 5

Question 3

The barometric pressure is 255mmHg at Mt Everest. Calculate PO2 and PiO2.

Answer 3

PO2 = .21 x 255 mmHg = 54mmHg

PiO2: .21 (255-47mmHg) =44mmHg

Question 4

Find PAO2 assuming PCO2 = 40mmHg, respiratory ratio = 1.
barometric pressure is 255mmHg

How does this value change with acclimatization? (Also, how does one acclimatize?)

Answer 4

4mmHg

acclimatization occurs through hyperventilation (5 fold increase)

PAO2 = 44 -8 = 35mmHg

unacclimatized persons are unconscious in 45 sec and dead in 4-6 min

Question 5

Describe the lung under extreme conditions.

How do permanent residents at 4600 m adapt?

When are chemoreceptors stimulated? By what? (What type of chemoreceptor?)

Answer 5

Typical PaCO2 in permanent residents at 4600m is about 33mmHg

hypoxic stimulation of peripheral chemoreceptors

Question 6

How does someone adapt when they first arrive at high altitude?

Answer 6

initial respiratory alkalosis (low PaCO2 and high pH) inhibits increase in ventilation but is compensated within 2-3 days, thus further increasing ventilation

Question 7

The barometric pressure in Denver is about 600mmHg. What happens when you first arrive?

Calculate PIO2 and PAO2.

How do you accommodate?

Answer 7

abrupt decrease in PIO2 when first arrive in mountains.

(PIO2= [600-47] x .21= 116mmHg)

and alveolar and arterial O2 decrease

(PAO2= 116 - [40/.8] = 66mmHg; PaO2=61mmHg (assuming AaDO2 is 5mmHg/hasn’t changed)

the decrease in arterial O2 stimulates the peripheral chemoreceptors and thereby increases ventilation

this increase in ventilation decreases arterial PCO2 and elevates arterial pH… result of this increase in ventilation is to minimize the hypoxemia by increasing PAO2.
(if PACO2 decreases to 30mmHg then [(600-47) x .21] - [30/8] = 78mmHg

decrease in arterial PCO2 also decreases PCO2 of CSF… (Bc HCO3- is unchanged, pH of CSF increases… this increase in pH of CSF attenuates the rate of discharge of central chemoreceptors and decreases their contribution to ventilatory drive)

over next 12-36 hours, HCO3- in CSF decreases as acid-base transporter proteins in blood reduce HCO3-

Question 8

What is polycythemia? What effect will it have?

Answer 8

• increase in RBC concentration
• erythropoietin from kidney
• increases Hb/O2 carrying capacity
• normalizes O2 concentration

Question 9

Describe/draw a graph showing PO2 values from inspired air- alveolar gas- arterial blood- mixed venous blood at sea level and at 4600m.

Answer 9

Slide 9

Question 10

At moderate and high altitude how does does the O2 binding curve shift? (why)?

Answer 10

moderate- rightward shift of O2 binding curve due to 2/3 DPG (develops bc of respiratory alkalosis) …assists in unloading O2 in venous blood

-at higher altitudes leftward shift (alkalosis) …this assists in loading of O2 in the pulmonary capillaries

Question 11

Is air more or less dense at high altitude? Will maximal breathing capacity increase or decrease?

Answer 11

maximal breathing capacity increases as air is less dense

Question 12

What does alveolar hypoxia result in?

Answer 12

alveolar hypoxia results in pulmonary vasoconstriction

-right heart hypertrophy and pulmonary edema
(hypertension is exaggerated by polycythemia, which raises the viscosity of the blood

The probable mechanism is that the arteriolar vasoconstriction is uneven, and leakage occurs in unprotected, damaged capillaries. The edema
fluid has a high protein concentration, indicating that the permeability of the
capillaries is increased.

Question 13

Describe acute mountain sickness and chronic mountain disease.

Answer 13

acute mountain sickness: headache, fatigue, dizziness, nausea…can progress to high altitude pulmonary edema, high altitude cerebral edema

chronic mountain disease: polycythemia, fatigue, reduced exercise tolerance, hypoxemia

Question 14

In diving, how do pressures change as you descend deeper?

Answer 14

pressure doubles with every 10m/33ft below water.

So at 0 depth pressure is 1 atm
at 33’ pressure is 2 atm

See slide 11

Question 15

Describe the diving response.

How is it induced?

Will the body respond with peripheral vasoconstriction or dilation? Due to parasympathetic or sympathetic activity?

Initial hypotension or hypertension?

Bradycardia or tachycardia?

Reduction or increase of CO?

Hb changes?

Answer 15

• detectable in all air breathing vertebrates
• induced by apnea
• peripheral vasoconstriction due to sympathetic activity
• initial hypertension
• vagally induced bradycardia and reduction of the cardiac output
• enhancement of hemoglobin concentration of circulating blood by splenic contraction

Question 16

When does hypoxic loss of consciousness occur? At what PO2?

Answer 16

LOC at PO2: 20-25mmHg

Question 17

How does hyperventilation affect divers?

Answer 17

• reduces CO2 drive to breathe
• loss of consciousness without forewarning bc the weak respiratory stimulus from hypoxia is voluntarily overridden

Breath holders die every year due to preventable
pathophysiological mechanisms

Question 18

Describe ascent blackout (hypoxia of ascent).

What is pressure at a depth of 40m?
What is PiO2 and PO2 in the lungs?
(Fraction of oxygen is reduced from .21 to .016)

Answer 18

Breath holders die every year due to preventable
pathophysiological mechanisms

-reduction of water pressure and gas pressure

For example, at a depth of 40m under water, pressure is 5x the pressure at sea level (5 x 760mmHg=3800mmHg) and PO2 in the lungs is 749mmHg.
PiO2= (760x5)-47 x .21 =788mmHg
PO2 of 60mmHg when PAO2 reduced to 1.5%

PO2 is still 60 mmHg when the fraction of O2 in the lung has been reduced from 21% to 1.6%.

Question 19

What happens when the diver ascents to 10m of water? (What is PO2 then?) What may result?

Answer 19

When the diver ascents to 10m under water, PO2 will be 23mmHg, which may result in LOC.

at 10m:
PO2= (760 x 2)-47 mmHg x 0.01 =23mmHg =LOC

Question 20

Hyperventilation and ascent blackout can result in deaths in divers. What else?

Answer 20

carbohydrate depletion (less CO2 production)

Question 21

Discuss diving-barotrauma of descent before the dive. Explain/draw the components of diagram A on slide 20

Does the manometer show overpressure or equilibrium/why?

Answer 21

Before dive: inhalation to TLC before submersion;

vital capacity (VC) represents the portion of TLC that can be used for pressure equilibration. The manometer indicates overpressure in lung air relative to the ambient atmosphere due to inward recoil of chest and lungs

RV represents the “noncollapsable” fraction of TLC

the normal intrathoracic blood volume (ITBV) in the vascular bed and heart) is modest in size; the extrathoracic blood volume is ETBV

Question 22

Describe beginning of descent (equilibrium, etc) (diagram B slide 20)

Answer 22

beginning of descent with pressure equilibrium relative to ambient water maintained as indiciated by manometer, by compression of chest and some translocation of blood from ETBV to ITBV

Question 23

Describe diagram C slide 20.

Answer 23

at greater depth the limits of mechanical compression of chest wall and stretching of diaphragm have been reached, but further compression of lung air and maintenance of pressure equilibrium is achieved by redistribution of large volume of blood from ETBV to ITBV

Question 24

Describe diagram D slide 20.

Answer 24

with further descent, the dispensibility limit of blood containing structures in the chest wall may be reached, an underpressure develops in the lung relative to the ambient water and therefore to the ITBV with possible extravasation of fluid (pulmonary edema) and bleeding due to capillary rupture

Question 25

Describe decompression sickness.

At what level is euphoria experienced? Loss of coordination?

Answer 25

• inert gas narcosis
• caused by formation of N2 bubbles during ascent from a deep dive
• may result in pain (“bends”) and neurological disturbances
• can be prevented by a slow, staged ascent
• treated by recompression in a chamber
• incidence is reduced by breathing a helium-oxygen mixture
• at 50m under water: euphoria
• at deeper levels: loss of coordination, coma

During diving, the high partial pressure of N2 forces this poorly soluble gas
into solution in body tissues. This particularly occurs in fat, which has a relatively
high N2 solubility. However, the blood supply of adipose tissue is meager,
and the blood can carry little N2. In addition, the gas diffuses slowly
because of its low solubility. As a result, equilibration of N2 between the
tissues and the environment takes hours.
During ascent, N2 is slowly removed from the tissues. If decompression is
unduly rapid, bubbles of gaseous N2 form, just as CO2 is released when a bottle
of champagne is opened. Some bubbles can occur without physiological
disturbances, but large numbers of bubbles cause pain, especially in the region
of joints (“bends”). In severe cases, there may be neurological disturbances
such as deafness, impaired vision, and even paralysis caused by bubbles in the
central nervous system (CNS) that obstruct blood flow.
The treatment of decompression sickness is by recompression. This
reduces the volume of the bubbles and forces them back into solution, and
often results in a dramatic reduction of symptoms. Prevention is by careful
decompression in a series of regulated steps.

Question 26

What are some common signs of a diving bend?

Describe for: 
head
spine
knees, elbow, shoulders
fingers and feet
chest and body

Answer 26

head- vertigo, poor balance, confusion, nausea, fatigue, unconsciousness

spine-abdominal pain, loss of bladder function, paralysis

knees, elbows shoulder- joint pain

fingers and feet- tingling, pins and needles,

chest and body- skin rash

Question 27

What are clinical symptoms of oxygen toxicity in the CNS (hyperbaric O2)?

Answer 27

inhalation of 100% O2 at 1 atm can damage the lung.
Another form of O2 toxicity is stimulation of the CNS, leading to convulsions,
when the Po2 considerably exceeds 760 mm Hg.

vomiting
dizziness
vision/hearing impairment
confusion, seizures, coma (4atm/30min)

Question 28

What results in the lung with oxygen toxicity (FiO2 > 0.4-0.5)

Answer 28

• damage of endothelial cells of pulmonary capillaries
• substernal pain during breathing
• impaired gas exchange
• reduction of vital capacity
• atelectasis
• retrolental fibroplasia in premature infants

Question 29

How can a diver reduce the risk of “bends”?

Answer 29

The risk of decompression sickness following very deep dives can be reduced if a helium-O2 mixture is breathed during the dive.

Helium is about one-half as soluble as N2, so less is dissolved in tissues. Helium-O2 mixture is also less dense, which reduces work of breathing. In addition, it has one-seventh
of the molecular weight of N2 and therefore diffuses out more rapidly through tissue (Figure 3-1). Both these factors reduce the risk of bends

Question 30

Describe the likelihood of convulsions at a PO2 of 4atm.

What happens in regards to O2 concentration with increasingly deep dives?

Should a diver fill his or her tanks with O2 before descending underwater?

Answer 30

The likelihood of convulsions depends on the inspired PO2 and the duration of exposure, and it is increased if the subject is exercising.

At a PO2 of 4 atm, convulsions frequently occur within 30 minutes.

For increasingly deep dives, the O2 concentration is progressively reduced to avoid toxic effects and
may eventually be less than 1% for a normal inspired PO2! The amateur scuba
diver should never fill his or her tanks with O2 because of the danger of a convulsion underwater.