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

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
DIVING PRESSURISING a GAS has what effect
DECREASES its VOLUME deeper - gas occupies less volume (shrinks down)
26
DIVING which GASES are TOXIC when INHALED UNDER PRESSURE
N2 and O2 (air 78% N2, 21% O2) (CO2 only of concern if breathing apparatus traps exhaled air causing CO2 to rise)
27
DIVING why does NITROGEN (N2) have no effect on body function at SEA LEVEL
DOES NOT DISSOLVE in tissues
28
DIVING when can N2 CAUSE HARM
DEPTH 40m OR MORE
29
DIVING what HARM does N2 CAUSE at Depth 40m or More
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
DIVING N2 NARCOTIC EFFECTS INITIALLY and ULTIMATELY at 80M or BELOW
Initially: feeling of WELLBEING (jolly) Ultimately: cause LOSS OF FUNCTION at 80m or below
31
DIVING when can N2 cause LOSS OF FUNCTION
80m or Below
32
DIVING why can O2 be TOXIC
FORMS FREE RADICALS
33
DIVING why is O2 SAFE at SEA LEVEL
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
DIVING how is Hb at SEA LEVEL (normal circumstances)
acts as a vehicle for TRANSPORT and a BUFFER CLOSELY REGULATES O2 delivered to tissues - HIGHLY SATURATED
35
DIVING why can breathing O2 at HIGH PRESSURE be harmful
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
DIVING EFFECTS of BREATHING O2 at HIGH PRESSURE
NEUROLOGICAL EFFECTS - VISUAL disturbances -SEIZURES - COMA
37
DIVING why do Divers who work at Depth breathe a HELIUM/OXYGEN MIX (HELIOX)
- 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
DIVING why is HELIUM used to REPLACE N2 in HELIOX
- LESS DENSE - DISSOLVES LESS READILY -> LESS NARCOTIC - HELIOX LESS AIRWAYS RESISTANCE (smaller) and less work of breathing
39
DIVING what is DECOMPRESSION SICKNESS / 'THE BENDS'
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
DIVING what is the AVERAGE AMOUNT of N2 contained in the body at SEA LEVEL
approx 1L
41
DIVING AVERAGE AMOUNT of N2 in the body INCREASES to .... at PROLONGED DIVE at 30 m
as much as 4L (N2 accumulates in tissues at high pressure and so increased solubility - DISSOLVES)
42
DIVING how is N2 in the body at PRESSURE
DISSOLVES - DIFFUSES across BLOOD-GAS INTERFACE and then DISTRUBUTED by CIRCULATION to ALL TISSUES - PREFENTIALLY partitions (stays) in FAT TISSUE
43
DIVING what happens to divers N2 as they ASCEND BACK to the SURFACE (after N2 dissolved at high pressure)
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
DIVING Why are N2 BUBBLES in the BLOODSTREAM HARMFUL (decompression sickness/'the bends')
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
DIVING SYMPTOMS of DECOMPRESSION SICKNESS / 'THE BENDS' (N2 bubbles)
- JOINT and LIMB MUSCLES PAIN more severe: - NEUROLOGICAL DEFICITS - DYSPNOEA - DEATH
46
DIVING how can you PREVENT DECOMPRESSION SICKNESS
SLOWING RATE of ASCENT - allows MORE TIME for excess Gas to DISSUFE OUT of tissues and INTO LUNGS for EXHALATION
47
DIVING what SLOWS the RATE at which N2 can be REMOVED
FAT is AVASCULAR (no blood supply) (N2 mostly in FAT tissues) - INCREASES DISTANCE of N2 DIFFUSION to be carried away by circulation
48
DIVING how long can COMPLETE RENORMALISATION of N2 LEVELS take after ASCENT
SEVERAL HOURS
49
DIVING what is the TREATMENT for DECOMPRESSION SICKNESS
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

Respiratory (16 decks)

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