8.1 Breathing and Respiration in special circumstances - ALTITUDE and DIVING Flashcards

1
Q

ALTITUDE
how is the AIR

A

% Composition does NOT change

ASCENT: PARTIAL PRESSURES DECREASE with Decreasing Atmospheric/Barometric Pressure (climbing up)

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2
Q

ALTITUDE
PO2 at sea level vs at peak of Everest

A

sea level: 760 mm Hg

peak Everest: 43 mm Hg

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3
Q

ALTITUDE
PAO2 (ARTERIAL) in comparison to in DRY AIR and why

A

LOWER THAN IN DRY AIR

  • Airways ADD WATER during Inspiration
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4
Q

ALTITUDE
effect of FALLING PAO2 on PARTIAL PRESSURE GRADIENT and what effect does this have

A

REDUCES PARTIAL PRESSURE GRADIENT

driving O2 UPTAKE

  • causes HYPOXIA (low O2 in tissues)
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5
Q

ALTITUDE
effect of HYPOXIA

A

SENSORY and COGNITIVE Functions DECLINE

  • CNS DEPENDENT on O2
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6
Q

ALTITUDE
HYPOXIA sensed by..

A

PERIPHERAL CHEMORECEPTORS

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7
Q

ALTITUDE
3 EFFECTS of HYPOXIA

A
  1. detected by Peripheral Chemoreceptors.
    RESPIRATORY CENTRE responds by INCREASING VENTILATORY DRIVE
    - Increase O2, Decrease CO2
    - ACTIVATES CENTRAL CHEMORECEPTORS
    -> BLUNTS RESPIRATORY DRIVE (decreases rate and depth)
  2. Respiratory Centre INHIBITS CARDIOINHIBITORY CENTRE
    - Increases HEART RATE, CARDIAC OUTPUT, O2 UPTAKE by PULMONARY PERFUSION
  3. Hypoxia causes PULMONARY VASOCONSTRICTION
    - Increases PULMONARY VASCULAR RESISTANT (blood flow resistance from pulmonary artery to left atrium)
    - RIGHT HEART forced to generate HIGHER PRESSURE to MAINTAIN CARDIAC OUTPUT
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8
Q

ALTITUDE
effects of HYPOXIA on HEART

A
  • RESPIRATORY CENTRE INHIBITS CARDIOINHIBITORY CENTRE
    so INCREASES HEART RATE, CARDIAC OUTPUT, and O2 uptake by Pulmonary Perfusion
  • Pulmonary Vasoconstriction (pulmonary vascular resistance) causes RIGHT HEART to generate HIGHER PRESSURE to MAINTAIN CARDIAC OUTPUT
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9
Q

ALTITUDE
how does HYPOXIA affect VENTILATION

A

PERIPHERAL CHEMORECEPTORS: INCREASED VENTILATORY DRIVE (more O2)

LOW CO2 detected by CENTRAL CHEMORECEPTORS
- BLUNTS VENTILATORY DRIVE

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10
Q

ALTITUDE
ADAPTIVE RESPONSES (DAYS TO WEEKS)

A
  1. CENTRAL CHEMORECEPTORS adapt slowly over 8-24 HOURS so allow INCREASED VENTILATION
  • LOW PaCO2 causes RESPIRATORY ALKALOSIS
  1. KIDNEY COMPENSATES for alkalosis: LESS H+ SECRETION so blood pH renormalises
  2. ALKALOSIS stimulates 2,3-DPG PRODUCTION
    - LOWERS Hb O2 AFFINITY, dissociation curve shifts to RIGHT
    - MORE O2 UNLOADING to tissues
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11
Q

ALTITUDE
how do you develop ALKALOSIS over few days/weeks

A

CENTRAL CHEMORECEPTORS ADAPT (8-24 hours)

  • allow INCREASED VENTILATION

-> LOW CO2 (PaCO2) causes respiratory alkalosis

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12
Q

ALTITUDE
how do KIDNEYS compensate for ALKALOSIS development over few days/weeks

A

LESS H+ SECRETION

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13
Q

ALTITUDE
how does the ALKALOSIS Help

A

STIMULATES PRODUCTION of 2,3-DPG

  • LOWERS Hb AFFINITY for OXYGEN (shift RIGHT)
  • more O2 UNLOADING
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14
Q

ALTITUDE
ACCLIMATION: how do these people ADAPT LONG-TERM (over MONTHS/YEARS)

A
  1. Hypoxia stimulate ERYTHROPOIETIN from KIDNEYS
    - Increase RBC
    - INCREASE Hb CONC
    - Increased BLOOD VOLUME

-> Blood’s OXYGEN-CARRYING CAPACITY INCREASES
by 50%

  1. Hypoxia stimulates ANGIONEOGENESIS (Production NEW CAPILLARIES)
    - Increased CAPILLARY DENSITY
    - Increased Tissue PERFUSION

-> INCREASED PULMONARY ARTERY PRESSURE promotes VASCULAR and VENTRICULAR REMODELLING (change shape to cope with pressure)

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15
Q

ALTITUDE
adverse EFFECTS of ACUTE (Short term) altitude sickness

A
  • Headache
  • Irritability
  • Insomnia
  • Dyspnoea (struggling to breathe)
  • Dizziness
  • Nausea and Vomiting
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16
Q

ALTITUDE
adverse EFFECTS of CHRONIC (Long term) altitude sickness

A

BRONCHOCONSTRICTION
-> stresses RIGHT side of heard
can cause
- PULMONARY OEDEMA
- RIGHT HEART FAILURE
- DEATH

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17
Q

ALTITUDE
how do KIDNEYS help LONG-TERM ADAPTATION (ACCLIMATION)

A

produce ERYTHROPOEITIN which increases RBC, INCREASEs Hb,
blood carries 50% MORE OXYGEN

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18
Q

ALTITUDE
LONG-TERM adaptation of HEART

A

VASCULAR and VENTRICULAR REMODELLING

due to ANGIONEOGENESIS
- increased CAPILLARY DENSITY, tissue perfusion
- increased PULMOANRY ARTERIAL PRESSURE causes change in shape

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19
Q

DIVING
how is the PRESSURE

A

EXTERNAL HYDROSTATIC PRESSURE

  • pressure INCREASES quickly with INCREASED DEPTH

water SQUEEZES and COMPRESSES from all sides

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20
Q

DIVING
a COLUMN of WATER OF 10m exerts a PRESSURE EQUIVELENT to…

A

ATMOSPHERIC PRESSURE

21
Q

DIVING
at DEPTH 30 m a diver subject to PRESSURE of approximately..

A

4 ATMOSPHERES

(10 m Equivalent to atmospheric pressure)

22
Q

DIVING
EFFECTS of DEPTH on ALVEOLI

A

COMPRESSES GAS within the ALVEOLI
- INCREASES PARTIAL PRESSURES of all gases
- DECREASES ALVEOLAR VOLUME

23
Q

DIVING
INCREASED PARTIAL PRESSURE of gases in ALVEOLI and DECREASED ALVEOLAR VOLUME causes 2 issues:

A
  1. at sea level, ONLY O2 and CO2 can dissolve in blood.
    diving increases partial pressures of all gases so
    ALL GASES DISSOLVE IN BLOOD (potentially lethal effects)
  2. PRESSURISING a GAS DECREASES its VOLUME
    - at 30m 1L of gas (sea level volume) SHRINKS down to occupy250ml
  • surfacing above 30m 1L of gas EXPANDS to fill 4L

-> can cause SEVERE DAMAGE

24
Q

DIVING
at SEA LEVEL which GASES can DISSOLVE in BLOOD

A

ONLY O2 and CO2

diving: all dissolve

25
Q

DIVING
PRESSURISING a GAS has what effect

A

DECREASES its VOLUME

deeper - gas occupies less volume (shrinks down)

26
Q

DIVING
which GASES are TOXIC when INHALED UNDER PRESSURE

A

N2 and O2

(air 78% N2, 21% O2)

(CO2 only of concern if breathing apparatus traps exhaled air causing CO2 to rise)

27
Q

DIVING
why does NITROGEN (N2) have no effect on body function at SEA LEVEL

A

DOES NOT DISSOLVE in tissues

28
Q

DIVING
when can N2 CAUSE HARM

A

DEPTH 40m OR MORE

29
Q

DIVING
what HARM does N2 CAUSE at Depth 40m or More

A

PARTIAL PRESSURE (PN2) RISES
- DISSOLVES in CELL MEMBRANES
DISRUPTS ION CHANNEL FUNCTION

-> NARCOTIC EFFECTS similar to of ETHANOL
(severity of effects related to depth and pressure, worsen further down)

30
Q

DIVING
N2 NARCOTIC EFFECTS INITIALLY and ULTIMATELY at 80M or BELOW

A

Initially: feeling of WELLBEING (jolly)

Ultimately: cause LOSS OF FUNCTION at 80m or below

31
Q

DIVING
when can N2 cause LOSS OF FUNCTION

A

80m or Below

32
Q

DIVING
why can O2 be TOXIC

A

FORMS FREE RADICALS

33
Q

DIVING
why is O2 SAFE at SEA LEVEL

A

amount O2 being delivered to tissues is CLOSELY REGULATED by Hb
- acts as a vehicle for Transport and a BUFFER

Hb HIGHLY SATURATED under normal circumstances

34
Q

DIVING
how is Hb at SEA LEVEL (normal circumstances)

A

acts as a vehicle for TRANSPORT

and a BUFFER

CLOSELY REGULATES O2 delivered to tissues

  • HIGHLY SATURATED
35
Q

DIVING
why can breathing O2 at HIGH PRESSURE be harmful

A

DISSOLVE in BLOOD in HIGH AMOUNTS that EXCEED BUFFERING CAPACITY of Hb

  • TISSUES exposed to PO2 that EXCEEDS NORMAL SAFE RANGE (20-60 mm Hg)
36
Q

DIVING
EFFECTS of BREATHING O2 at HIGH PRESSURE

A

NEUROLOGICAL EFFECTS
- VISUAL disturbances
-SEIZURES
- COMA

37
Q

DIVING
why do Divers who work at Depth breathe a HELIUM/OXYGEN MIX (HELIOX)

A
  • O2 CAREFULLY TAILORED to yield PARTIAL PRESSURE that is SUPPORTIVE not harmful
  • HELIUM REPLACES N2 because it DISSOLVES in body tissues LESS READILY
    -> LESS NARCOTIC
  • HELIUM LESS DENSE than N2
  • HELIOX REDUCES AIRWAYS RESISTANCE (smaller molecule)
    and DECREASES the WORK OF BREATHING
38
Q

DIVING
why is HELIUM used to REPLACE N2 in HELIOX

A
  • LESS DENSE
  • DISSOLVES LESS READILY
    -> LESS NARCOTIC
  • HELIOX LESS AIRWAYS RESISTANCE (smaller)
    and less work of breathing
39
Q

DIVING
what is DECOMPRESSION SICKNESS / ‘THE BENDS’

A

presence of N2 BUBBLES in the BLOODSTREAM
(can block blood vessels)

from ASCENT / coming back up to surface (too QUICKLY)

and N2 loses pressure and solubility

40
Q

DIVING
what is the AVERAGE AMOUNT of N2 contained in the body at SEA LEVEL

A

approx 1L

41
Q

DIVING
AVERAGE AMOUNT of N2 in the body INCREASES to …. at PROLONGED DIVE at 30 m

A

as much as 4L

(N2 accumulates in tissues at high pressure and so increased solubility - DISSOLVES)

42
Q

DIVING
how is N2 in the body at PRESSURE

A

DISSOLVES

  • DIFFUSES across BLOOD-GAS INTERFACE and then DISTRUBUTED by CIRCULATION to ALL TISSUES
  • PREFENTIALLY partitions (stays) in FAT TISSUE
43
Q

DIVING
what happens to divers N2 as they ASCEND BACK to the SURFACE (after N2 dissolved at high pressure)

A

N2 no longer subject to PRESSURE

DECREASED PARTIAL PRESSURE & SOLUBILITY

-> COMES OUT of SOLUTION and FORMS N2 BUBBLES (IF ASCEND TOO QUICKLY)
(DECOMPRESSION SICKNESS/’THE BENDS’)

44
Q

DIVING
Why are N2 BUBBLES in the BLOODSTREAM HARMFUL (decompression sickness/’the bends’)

A

BLOCK BLOOD VESSELS
as small bubbles form larger bubbles, progressively LARGER VESSELS Affected

-> Tissues dependent on these vessels become ISCHAEMIC (LACK BLOOD SUPPLY)

cause PAIN in JOINTS and LIMB MUSCLES

45
Q

DIVING
SYMPTOMS of DECOMPRESSION SICKNESS / ‘THE BENDS’ (N2 bubbles)

A
  • JOINT and LIMB MUSCLES PAIN

more severe:
- NEUROLOGICAL DEFICITS
- DYSPNOEA
- DEATH

46
Q

DIVING
how can you PREVENT DECOMPRESSION SICKNESS

A

SLOWING RATE of ASCENT
- allows MORE TIME for excess Gas to DISSUFE OUT of tissues and INTO LUNGS for EXHALATION

47
Q

DIVING
what SLOWS the RATE at which N2 can be REMOVED

A

FAT is AVASCULAR (no blood supply)
(N2 mostly in FAT tissues)

  • INCREASES DISTANCE of N2 DIFFUSION to be carried away by circulation
48
Q

DIVING
how long can COMPLETE RENORMALISATION of N2 LEVELS take after ASCENT

A

SEVERAL HOURS

49
Q

DIVING
what is the TREATMENT for DECOMPRESSION SICKNESS

A

DECOMPRESSION CHAMBER for HYPERBARIC TREATMENT

  • in a sealed vessel with PRESSURE EQUAL to PRESSURE AT DEPTH that they were diving at before ascent
    -> N2 DISSOLVES AGAIN (driven back into solution) to RELIEVE SYMPTOMS
  • PRESSURE in chamber SLOWLY DECREASED over a period of several HOURS
    so N2 can come out of solution SLOWLY and Diffuse back into Blood WITHOUT FORMING BUBBLES