Respiratory Physiology Flashcards

1
Q

Issues with respiratory physiology in aviation

A
Toxic gases and fumes
Hypoxia
Life support systems
Accident investigation
Vibration
G
Lung diseases
Trapped gases
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2
Q

Partial pressure of gas at sea level

A

Nitrogen 593mmHg
Oxygen 160 mmHg
Other 7mmHg
Total 760mmHg

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3
Q

Partial pressure of the gases in Tracheal and why there is a difference

A

Nitrogen 538mmHg
Oxygen 149mmHg
CO2 26mmHg
Water vapour 47 mmHg

Change is due too water vapour

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4
Q

Partial pressure of gas at the Aveolar and why the change

A

Oxygen 103mmHg

Due to metabolic effect (CO2 dilutes gases)

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5
Q

Describe Oxygen Cascade

A

Atmosphere to trachea - Humidification (47mmHg water vapour. O2 149mmHg
Trachea to alveolus - Alveolar gas equation
- metabolic effect = O2 103mmHg, CO2 40mmHg
Alveolus to pulmonary capillary - Difusion - O2 95 mmHg?
Pulmonary capillary to artery - physiological shunt

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6
Q

Function of respiratory system

A
Gas exchange
Heat exchange
Blood reservior
Immunological functions
Hormonal/enzyme function
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7
Q

Function of Upper respiratory tract

A

Warming
Humidification
Filtration

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8
Q

Mechanics of respiration

A

Inspiration is active - overcome both elastic recoil and viscous forces

Expiration is passive at rest - Accessory muscle use when exercising. Utilise stored energy to overcome airways resistance

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9
Q

What is the work of breathing and what compounds can increase or decrease it

A

Respiratory work 1-2% of BMR
Component
- Resistance
— airways
— Inertial load of gas - related to density
- Compliance
—Parenchyma - effected by eg oedema
— Chest wall - effected by eg obesity or kidneys
Vital importance of surfactant - hold aveola open

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10
Q

Control of minute ventilation

A

Central - in brain stem. Centres in medulla, inputs from other centres to pons. Higher control eg emotional and pain.

Chemoreceptors - homeostatic control
- central - predominantly CO2
—- located in medulla on floor of 4th ventricle detect H+ in CSF
- peripheral: in aorta and carotid bulb. PaO2 threshold in <55mmHg. Results in sympathy-adrenal activation

Lung receptors

  • irritant receptors - initiate cough response
  • stretch receptors- prevents over inflation
  • J receptors - responds to Pul HTN

Peripheral receptors

  • muscle spindles - signal = increase resp rate
  • pain, temperature

Hormonal

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11
Q

Describe hypoxic ventilators response

A

Peripheral chemoreceptors cause an increase in minute ventilation irrespective of PaCO2
Hyperventilation always occurs with hypoxia

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12
Q

The law of gaseous diffusion

A

A gas will move down a pressure gradient from an area of higher pressure to an area of lower pressure.
It’s a passive process with no transporters
No carriers/receptors
Moves based on concentration and solubility

Oxygen is very insoluble and needs high pressure gradient to move it.

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13
Q

Explain Fick’s law of diffusion

A

Diffusion is proportion to SA and Pressure. Inversely to thickness.

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14
Q

Describe the A-a gradient and what it means and what effects it

A

A-a Gap = PAO2-PaO2
Is a marker of oxygen exchange
Measure V/Q scatter

Occurs due to 
- Shunts - pathological (eg pneumonia) and anatomical
- Dead space - air without blood
- Diffusion limitation
V/Q mismatch

A-a gradient 5-15mmHg with mean ~8. Increases with age.
Hypoxemia with normal gradient = hyperventilation
Hypoxemia with widened gradient = V/Q mismatch, diffusion limitation (response to O2) or shunt (poor response to O2)

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15
Q

Vascular tone in response to O2

A

Skeletal - reduced O2 = vasodilation

Lung - reduce O2 = vasoconstriction (about 50%) can result in pul HTN if enough

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16
Q

Explain V/Q mismatching and west zones

A

V/Q mismatching is a difference between vascular flow and air flow.

Zone 1: PA>Pa>Pv
Zone 2. Pa>PA>Pv. Ideal
Zone 3: Pa>Pv>PA

Majority are zone 2.
More alveolus in the bases of the lung and gravity means more blood in the bases as well.

17
Q

Effects of VQ mismatch on gas exchange

A

PaCO2 - no effect. Increased ventilation due to increasing PaCO2 dissociation curve
PaO2 - hypoxemia with widen A-a gap. Inability to compensate with increase ventilation as blood already saturated. Need supplemental oxygen

18
Q

Explained diffusion limitation vs perfusion limited

A

At rest at sea level movement of Oxygen from aveolar to blood is limited by perfusion due to high concentration gradient of O2 from aveolar of 103 to blood at 40mmHg that the 02 moves in to blood and saturation is affect at 1/3 of the distance across capillary. This means the rate of O2 saturation is based on the speed of perfusion through the capillaries. Curve is steep and then plateaus

At Altitude the concentration of the alveolar O2 is reduced = reduced pressure gradient from alveolar to blood which reduces the movement of Oxygen combined with the insolubility of 02. This means that oxygen becomes diffusion limited and requires more time to diffuse into the blood which flattens the curve.

19
Q

Explain the oxygen- haemoglobin Dissociation curve

A

Hb bind 4x02
- the first is bound tight and the last is bound loose
At the tissue there is low partial pressure of 02 which causes disassociation for 02 from Hb.
In certain conditions eg increase H+, ^ temp, ^2,3 DPG, increase CO2, increase Altitude = right shift due to the increase in O2 offloading = lower saturation at tissues
In certain conditions eg reduce H+, reduced CO2, reduced temp, reduced 2,3 DPG, reduce altitude, HbF and Met Hb. Shifts the curve Left as less O2 is unloaded at tissues.

Called the Bohr effect is the right shift

20
Q

How is CO2 carried in the blood

A

Dissolved, 5% in arterial
Bicarbonate 90%
carb amino 5%

21
Q

Haldane effect

A

Describes how with offloading of O2 a the tissues, deoxygenated blood is a better carrier of CO2 as deoxygenated-haemoglobin.
Has increase affinity for CO2
Is a better a buffer

22
Q

Partial pressure of O2 at tissue and mitochondria

A

Tissue ~30mmHg

Mitochondria ~1-3mmHg (5mmHg)

23
Q

Pasteur point

A

Is the cellular PO2 below which aerobic metabolism cannot occur.

~ 1mmHg