Test 3: Wk 11: 9 High Altitude, Exercise, and Deep Sea Adaptations - Puri Flashcards

1
Q

Owles Point represents

A

ventilation increase above the predicted by an extrapolation of the linear part of the ventilation/ oxygen consumption relationship

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2
Q

Anaerobic Threshold

A

point where alveolar ventilation increase is disproportionate to O2 consumption

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3
Q

any increase in O2 consumption beyond owles point leads to

A

greater increase in alveolar ventilation that what is required

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4
Q

disproportionate — occurs after the anaerobic threshold

A

hyperventialtion

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5
Q

PaCO2 =

A

PaCO2 = VCO2 / VA

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6
Q

before anaerobic threshold is reached, VA increases proportional to

A

VCO2

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7
Q

at normal work loads PaCO2, PaO2 and pH are — than anaerobic threshold

A

less than

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8
Q

Exercise Hyperpnea

A

not hyperventilation, metabolic rate has increased and so has ventilation

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9
Q

— most likely drives surplus alveolar ventilation during exercise

A

lactic acid

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10
Q

lactate — and blood pH — once anaerobic threshold is met

A

incerase; decrease

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11
Q

metabolic acidosis stimulates

A

peripheral chemoreceptors to increase ventilation

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12
Q

inspiration increase disproportionately greater than

A

CO2 production

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13
Q

PaCO2 — and PaO2 — at high workloads due to alveolar ventilation

A

decreases; increases

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14
Q

Anaerobic threshold

A

point where alveolar ventilation increase is disproportionate to O2 consumption

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15
Q

any increase in O2 consumption beyond Owles point leads to

A

greater increase in alveolar ventilation that what is required

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16
Q

Surplus alveolar ventilation is most likely driven by

A

lactic acid

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17
Q

PaCO2 =

A

PaCO2 = VCO2 / VA

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18
Q

before Anaerobic threshold is reached

A

VA increases proportional to VCO2

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19
Q

at normal workloads PaCO2, PaPO2, and pH are — than anaerobic threshold

A

less than

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20
Q

Exercise Hyperpnea

A

not hyperventilation

metabolic rate has increased and so has ventilation

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21
Q

lactate — and blood pH — once anaerobic threshold is met

A

metabolic acidosis stimulates

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22
Q

metabolic acidosis stimulates

A

peripheral chemoreceptors to increase ventilation

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23
Q

ventilation increases disproportionately greater than

A

CO2 production

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24
Q

PaCO2 — and PaO2 — at high workloads due to alveolar ventilation

A

decreases; increases

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25
Q

— will not be effected until ventilation changes

A

PaCO2

26
Q

Impaired mental function from hypoxia is due to

A

direct effect of hypoxia on brain tissue and from cerebral vasoconstriction from hypocapnia

27
Q

cerebral vasoconstriction is causes by

A

hypocapnia

28
Q

Acute exposure altitude sickness 5km sx

A

amnesia, dizziness, breathless at rest, insomnia, anorexia

29
Q

Acute exposure altitude sickness 10km sx

A

loss of consciousness

30
Q

Acute exposure altitude sickness ~20km sx

A

body fluids boil

31
Q

why does hyperventilation occur during acclimation to high altitude

A

increased sensitivity of peripheral chemoreceptors

32
Q

PAO2 =

A

PAO2 = PIO2 - PACO2

33
Q

PIO2 at high altitudes

A

decreases

34
Q

Hypercapnia

A

higher than normal PaCO@ >45

35
Q

Hypocapnia

A

lower than normal PaCO2 <40

36
Q

Hypocapnia can result only from an alveolar ventilation that is

A

excessive in relation

to carbon dioxide production

37
Q

— is a common cause of hypocapnia

A

Hypoxemia

38
Q

Hypoxemia occurs in

A

congenital heart disease

with right- to-left shunting, residence at high altitude, Po2 below about 60mmHg.

39
Q

Hypocapnia secondary to hypoxaemia opposes the

A

ventilatory response to the

hypoxemia.

40
Q

Metabolic acidosis produces a compensatory

A

hyperventilation

41
Q

Neurological disorders may result in — and —

A

hyperventilation and hypocapnia

42
Q

Hypercapnia is most commonly caused by

A

ventilatory failure due to acute or chronic conditions

43
Q

ARDS is an example of

A

acute ventilatory failure

44
Q

COPD is an example of

A

chronic ventilatory failure

45
Q

every 10m of seawater is — atm

A

1 additional atm

46
Q

10m below surface of sea atm =

A

2 atm

47
Q

N2 is highly lipid soluble and

high N2 interferes with

A

ion channels and slows ion conductance

48
Q

Mild nitrogen narcosis resembles

A

alcohol

intoxication

49
Q

“Martini’s law”

A

each 15 m of depth has the effects of drinking an additional martini.

50
Q

Solution to nitrogen necrosis in scuba diving

A

replace nitrogen with helium in the SCUBA tanks. Helium is more inert than
nitrogen and has less side effects.

51
Q

Mild oxygen toxicity

A

disorientation and headaches

52
Q

Severe oxygen toxicity

A

damage to the airways, pulmonary edema, coma, and death.

53
Q

solution to oxygen toxicity in scuba diving

A

scuba tank mixture is typically 98% helium and inly 2% oxygen. This is enough
to achieve PaO2 similar to sea levels due to high barometric pressures

54
Q

Decompression sickness (DCS or bends) is caused by

A

local bubble formation,

either in tissues or in venous blood

55
Q

DCS Bubbles in veins cause

A

obstruction, leading to capillary leaks

56
Q

Mild or type I DCS

A

mild pains (“niggles”), pruritus, a skin rash, and deep throbbing pain (bends),

57
Q

Serious or type II DCS

A

CNS, lungs, and circulatory system.

58
Q

CNS disorder in dysbarism

A

most commonly involving the spinal cord—reflects bubble formation in the myelin sheath of axons, which compromises nerve conduction

dizziness—the staggers—to paralysis.

59
Q

Pulmonary symptoms in dysbarism

A

the chokes—
result from bubbles that originate in the systemic veins and travel as gas emboli to
lodge in the pulmonary circulation, and include burning pain on inspiration

60
Q

circulatory system dysbarism

A

bubbles not only can
obstruct blood flow but also can trigger the coagulation cascade, leading to the
release of vasoactive substance

61
Q

Arterial gas embolization (AGE) is caused by

A

bubbles that enter the systemic arterial blood via either tears in the alveoli or right-to-left shunts and then become wedged in the brain or other organs.

62
Q

Best treatment of dysbarism is

A

recompression