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Environmental physiology > Diving > Flashcards

Diving Flashcards

1
Q

Barometric pressure

A

pressure around us and above us (weight of air pressing down on earth - greatest at sea level)

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2
Q

barometric pressure becomes smaller at altitude just as

A

it gets greater in caves, mines and holes that penetrate crust

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3
Q

hyperbaric

A

greater pressure than normal

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4
Q

1 bar

A

= 260 mmHg

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5
Q

0m=1 atmo/bar

A

10m= 2 bar, 20m= 2 bar, 20m= 3 bar etc

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6
Q

pressure change decrease at greater depth

A

water changes pressure greater than altitude

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7
Q

Boyle’s law

A

pressure and volume in a system always remains constant- p1V1=p2V2- air compressible

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8
Q

main limitation of breath hold diving

A

lungs squeezed further due to pressure which reduces volume of air inside

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9
Q

occupational applications of breath holding

A

pearl collection, sponge collection and spear gun fishing

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10
Q

what happens when lungs compress to a volume that is less than a diver’s residual volume

A

lung capillaries begin to fail and blood floods the alveoli ( as alveoli pressure becomes negative in respect to hydrostatic pressure in capillaries, causing oedema)

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11
Q

Blood shift to avoid lung compression problem

A

translocation of blood away from the periphery (aims to protect O2 supply to vital organs), increase periphery pressure by shifting blood from periphery to central to make more solid and resistant to central pressure changes

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12
Q

presence of increased amount of fluid from blood shift prevents

A

lung collapsing (greater fluid in thoracic cavity)

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13
Q

2 types of scuba diving

A
  • open circuit with 2 regulators (cylinder pressure and regulator-demand)
  • closed circuit (rebreathing), more efficient gas use and deeper dives possible (uses soda limes to remove exhaled CO2)
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14
Q

the increase ambient pressure with descent to greater depths causes gas partial pressure to

A

increase as well

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15
Q

due to greater diffusion of gases into the blood from greater partial pressure increases risk of

A

nitrogen narcosis and decompression sickness and oxygen toxicity (at sea- nitrogen 0.8 bar and O2 0.2 bar, at 30 m depth nitrogen 3.2 bar and O2 0.8bar

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16
Q

Nitrox gas mixture

A

32% O2, 68% N2 or 36%O2 and 64% N2 for up to 30 m depths to prevent risk of nitrogen narcosis and decompression sickness (any deeper risk oxygen toxicity)

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17
Q

Heliox gas mixture

A

10% O2 and 90% helium for bottom dives

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18
Q

why is helium used sometimes

A

can be used for greater depths and less narcotic but expensive and requires longer decompression and can cause hypothermia and high pressure nervous syndrome also hypoxic mixture

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19
Q

Normoxic trimix (30-60m) hypoxic trimix (>60m)

A

trimix contains O2,N2 and He, provides good balance btw cost and effectiveness - trimix at greater depths requires less O2 to prevent oxygen toxicity

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20
Q

lung volume expansion big problem in scuba diving

A

happens in ascent of ascent of scuba dive , holding breath while going up lungs expand as ambient pressure declines - lung tissue injury is unavoidable in this case

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21
Q

lung expansion most dangerous..

A

at ascent near surface as greater pressure difference for given distance travelled

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22
Q

pulmonary barotrauma

A

resulted from lung expansion

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23
Q

Lung barotrauma includes arterial gas embolism (structural alveolar damage)

A

bubbles enter arterial side which causes blockage (embolism) in brain or heart = stroke or mycardial infarction

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24
Q

Lung barotrauma includes emphysema

A

over inflation of alveoli causing shortness of breath

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25
Q

Lung barotrauma includes pneumothorax (lung collapse)

A

air enters pleural sac (no negative pressure in pleural sac to keep lungs inflated) or air released near bronchi filling thoracic near heart and air gets trapped and when expands on ascent causes pressure on heart

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26
Q

ear barotrauma includes

A

outer ear (blockage, vacuum or pressure), middle ear (inability to equalise ), inner ear (stubborn divers who initially fail to equalise )

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27
Q

types of issues that can come from barotrauma

A
  • squeezed sinuses
  • painful expanding sinuses which can cause fracture
  • burst eye capillaries
  • imploding and exploding teeth (tooth barotrauma)
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28
Q

Barotrauma

A

physical damage to tissues caused by pressure difference between gases inside body and surrounding fluid or gas

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29
Q

oxygen toxicity

A

oxygen breathed at high partial pressure (greater depths) can cause serious pulmonary and neurological damage

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30
Q

safe cut off point for inspired pO2

A

1.6 bar (x8 value on surface) achieved by 100% 6m 32% 40m and 21% 65m

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31
Q

neurological symptoms of oxygen toxicity

A

muscle twitching, disturbed vision and hearing, loss of coordination as affects muscles, confusion and convulsions

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32
Q

pulmonary symptoms of oxygen toxicity

A

difficulty breathing and airway damage and inflammation

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33
Q

manifestation of nitrogen narcosis

A

euphoria, intoxication, impaired CNS function (starts mild and gets progressively worse)

34
Q

when does nitrogen narcosis occur

A

when nitrogen reaches very high partial pressure and enters the blood

35
Q

What does nitrogen narcosis do

A

dissolved nitrogen interferes with the synaptic membranes of the CNS and disrupts signalling

36
Q

why is nitrogen narcosis serious during diving

A

it affects judgement and cognitive ability

37
Q

How does helium help prevent nitrogen narcosis and yet presents danger

A

in inspired mixture in prevent NN bc it’s not narcotic yet can cause serious neurological problems -HPNS under acute expose and rate of ascent important on helium (harder to reverse than nitrogen narcosis)

38
Q

helium increases heat loss which

A

can reduce dive times due to increase metabolic demands

39
Q

Cause of O2 toxicity

A

hyperopia doesn’t exist naturally in the environment - ability of human to cope with this condition is extremely limited

40
Q

effects of oxygen toxicity on cardiovascular

A

peripheral vasoconstriction, cardiac output decreases- the aim is to reduce amount of O2 in the blood

41
Q

effects of oxygen toxicity on cellular

A

scavenging of superoxide and related products resulting from oxidative stress ad damage caused on cells (not directly caused by high O2)- aim is to partly restore the damage caused by high level of O2

42
Q

Pulmonary versus CNS effects from oxygen toxicity

A

-pulmonary toxicity symptoms take longer to reverse and symptoms vary (also gradual but is sustained)
-CNS toxicity symptoms are same each time
oxygen toxicity manifests acutely on the CNS whilst pulmonary toxicity manifests chronically and it depends on the frequency of re exposures

43
Q

neurological oxygen toxicity associated with

A

neurotransmitters in CNS

44
Q

How does Vigabatrin (affects GABA and prevents seizures) help neurological oxygen toxicity

A

increase delay of neurological toxicity and at high dosage it prevents seizures completely (not a treatment of O@ toxicity)

45
Q

How does high O2 effect signalling

A

increases sensitivity of neurotransmitters at synapses and increases neurotransmitters release - can cause blockage of signalling synapses and increased sensitivity + blockage cause siezures

46
Q

Oxygen toxicity on neural

A

affects entire nervous system with increased excitability and blockage of impulse conduction - affects most neurotransmitters (GABA, dopamine etc), neuromodulators (nitric oxide) and cellular membrane transport systems

47
Q

what does pulmonary oxygen toxicity affect

A

structure of air sac/alveolus and capillary around it

48
Q

first stage of pulmonary oxygen toxicity

A

exudative- fluid in alveoli (oedema) and interstitial space that happens as membranes replace type 1 cells where gas exchange occurs which increases alveoli permeability so more water/oedema in alveoli (reversible)

49
Q

second stage of pulmonary oxygen toxicity

A

proliferative- type 2 cells increase and take place of type 1 cells -cells become ineffective in gaseous exchange , leaving gaps in btw which allows fibres to enter interstitial space preventing air absorption into blood as no diffusion area cause blockage (irreversible)

50
Q

dehydration in diving

A

divers experience increased diuresis (urge to urinate) cause in water everything in periphery is compress due to translocation of blood in the chest (thoracic cavity) which leads to an increase in central venous pressure - arterial natriuretic peptide hormone then released which acts on kidneys

51
Q

when does decompression sickness occur

A

when dissolved gas in the body is allowed to expand when changing pressure (think champagne)

52
Q

what does the severity of decompression sickness depends on

A

maximum depth reached, time spent in depth, rate of ascent, rapid and multiple ascents, repetitive dives, flying after dives, age weight gender, and alcohol consumption

53
Q

type 1 of decompression sickness

A

bubble formation in tissues but not in the circulation-affects skin and joints, symptoms include skin itchiness, blotched appearance and rashes, inner ear spinning sensation, ringing, deafness or vomiting

54
Q

type 2 of decompression sickness

A

bubble formation in the venous circulation which can cause pulmonary embolism (blockage in vessel) can lead to cerebral or cardiac embolism in some cases

55
Q

symptoms of type 2 decompression sickness

A

numbness and tingling, loss of mat coordination, cognitive impairment and loss of consciousness, loss of autonomic ctrl of key functions (respiratory and cardiac), loss of reflexes, and difficulty breathing, intense cough, increased respiration

56
Q

effect of temperature in diving

A

cold water immersion causes transient hyperventilation but subsides when the thermoreceptors habituate

57
Q

effect on behaviour in diving

A

novice divers tend to hyperventilate due to anxiety/fear causes problem in dive time due to increase in pressure= increase compression of gas cylinder so less air

58
Q

increased oxygen consumption due to

A

increased drag due to density which increases cost of exercise which increases muscular work for given task and so increased oxygen demand, as well as increased demand for temperature regulation and increased shivering thermogenesis and so decreased aerobic efficiency

59
Q

decompression sickness depends on

A

the depth and total duration of the dive

60
Q

what gases are responsible for decompression sickness

A

Nitrogen and helium -gases that aren’t absorbed b the body

61
Q

how are gases responsible for decompression sickness

A

by expanding in volume in blood if there is no adequate time for outgasing

62
Q

No decompression limit (NDL)

A

the depth and duration of a dive that doesn’t require decompression before surfacing

63
Q

continuous decompression

A

slow but specific rate of ascent

64
Q

staged decompression

A

predetermined stop points during an ascent

65
Q

How to reduce NDL

A

with repeated dives

66
Q

dives that fall within boundaries of NDL do not require…

A

stops during ascent

67
Q

Main reasons for recommended safety stop at 3-5 m

A

precautionary measure from possible error in estimation depth and duration of dive, more flexible scheduling of repeat dives, eliminates residual nitrogen at a much faster rate than at the surface when under some compression

68
Q

when does nitrogen elimination happen

A

when the gas diffuses down it’s partial pressure gradient -during ascent from the high partial pressure in the blood to the lower partial pressure in alveoli

69
Q

issue with nitrogen at surface

A

when the pressure decreases abruptly and substantially the gas from bubbles and diffusion is reverted until the bubbles are filtered

70
Q

how does a safety stop allow offgasing of nitrogen more efficiently

A

gas still under pressure and the formation of bubbles limited or prevented as keeps nitrogen under pressure

71
Q

greater nitrogen absorbed at greater depths

A

rapid ascent leads causes nitrogen bubble to form in the blood in capillaries-rather ascent from 40-30 m has a bit of expansion but not much bc nitrogen gets outgased from capillary into the alveoli

72
Q

risidual nitrogen

A

nitrogen that can’t be outgased so stays in body - pulmonary circulation deal with residual nitrogen on the surface

73
Q

what is accepted ascent rate

A

10 m per minute

74
Q

importance of ascent rate

A

too fast can cause decompression sickness by allowing expansion of gas even from relatively shallow dives, too slow can add time to dive

75
Q

what needs to be taken in account in gas supply for dive

A

breathing rate of diver, target depth, descent, bottom time, ascent (including decompression stops) and reserve

76
Q

diving experience affects

A

breathing rates and influences depth and duration of dives

77
Q

deeper dives require greater air because..

A

greater bottom time and air for decompression

78
Q

joint and tissue bubble formation

A

nitrogen expansion in tissue causes localised rash, bruising or internal bleeding in organs. nitrogen bubbles in joints causes stiffness and pain (expands joints)

79
Q

Arterial gas embolism

A

embolism is a blockage in a vessel, AGE occurs when nitrogen bubbles pass into the arterial circulation

80
Q

What can AGE cause

A

cerebral or cardiac ischaemia (lack of blood flow) due to blockage of arteries

81
Q

When can AGE occur

A

During lung expansion- alveolar damage when holding breath during rapid ascent. Patent foramen ovale which allows blood to bypass pulmonary circulation through hole in heart

Environmental physiology (4 decks)

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