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Flashcards in Hypoxia Deck (24)
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1
Q

What parameter defines hypoxaemia?

A

PO2 < 8 kPa

2
Q

Describe how the partial pressure of oxygen changes from inspired air to the tissues.

A

21.3 —> 20 (conducting airways) —> 13.5 (alveoli) —> 13.5 (PaO2 immediately past exchange surface) —> 13.3 (diluted by return of bronchial circulation) —> 5.3 (mixed venous blood)

3
Q

How does PAO2 and PaO2 change with age?

A

DECREASES

4
Q

How can the partial pressure of oxygen in the alveoli (after mixing) be changed?

A

It’ll continue to move down its concentration into the blood until it reaches equilibrium.

5
Q

What percentage of cardiac output goes to perfuse the bronchial tree?

A

1%

6
Q

State the normal arterial and venous PO2.

A

Arterial = 13.3
Venous = 5.3
NOTE: only 25% of haemoglobin desaturates when going from arteries to veins

7
Q

How does dissolved oxygen affect the oxygen that is bound to haemoglobin?

A

The PO2 (dissolved oxygen) only counts for a small part of oxygen transport in the blood (the rest is bound to haemoglobin) but it is like the conductor of an orchestra. Uptake of dissolved oxygen into tissues is NOT keeping you alive directly, but it is accompanied by a LARGE unloading of oxygen from haemoglobin, which provides a sufficient supply of oxygen to the tissues.

8
Q

State four factors affecting the oxygen cascade.

A

V/Q mismatch
Alveolar Ventilation
Diffusion Capacity
Cardiac Output

9
Q

State the different energy sources for different durations of exercise.

A
(in order of increasing duration of exercise - longest at the bottom)
Intramuscular ATP
Phosphocreatine
Lactic Acid 
Aerobic
10
Q

Describe how ventilation changes with submaximal exercise.

A

If we initiate submaximal exercise we increase the oxygen demand. Ventilation takes a little bit of time to meet these demands.
So, once exercise is finished, ventilation will remain higher for a little while longer to repay the oxygen debt from the start.

11
Q

Describe and explain the ventilatory response to exercise.

A

When exercise begins, respiratory rate rapidly increases from around 12-20 then it remains stable for a long time.
Tidal volume then increases considerably (more efficient at increasing ventilation than increasing respiratory rate).
Eventually you get to a point where increasing tidal volume any further is energy inefficient.
Then respiratory rate increases further.

12
Q

State the five challenges of altitude.

A
Hypoxia
Solar Radiation
Thermal
Hydration
Dangerous
13
Q

What’s the difference between accommodation and acclimatisation.

A
Accommodation = ACUTE response to this kind of change - rapid physiological change in response to a change in oxygen in the oxygen environment 
Acclimatisation = physiology becomes more efficient so that you can get more out of the environment
14
Q

What have the benefits of increased ventilation and PaO2 been attributed to?

A

Renal compensation for the respiratory alkalaemia

Increased sensitivity to hypoxia

15
Q

Where is erythropoietin produced?

A

Renal cortex

16
Q

What does low PaO2 stimulate and what is the name given to this response?

A

Hypobaric Hyperventilation

Decreased PaO2 –> Increase Ventilation –> Increase PAO2 –> Increase PaO2

17
Q

State four innate adaptations of native highlanders.

A

Barrel Chest
Increased Haematocrit
Large Heart
Increased Mitochondrial Density

18
Q

What causes chronic mountain sickness and what are the consequences of CMS?

A

CMS is thought to be due to secondary polycythaemia in response to hypoxia - RBCs are overproduced to the point where they are no longer beneficial
Consequences - heart failure, eventual death

19
Q

What causes acute mountain sickness and what are the consequences?

A

Maladaptation to the high altitude environment

Consequences: HACE + HAPE

20
Q

What causes High Altitude Cerebral Oedema (HACE)?

A

Vasodilation of vessels in response to hypoxaemia

More blood going to the capillary beds and so more leakage —> cerebral oedema —> rise in ICP —> herniation

21
Q

What causes High Altitude Pulmonary Oedema (HAPE)?

A

Pulmonary arteries VASOCONSTRICT in response to hypoxaemia - leading to pulmonary hypertension.
This means that hydrostatic pressure in the capillaries is increased so more fluid moves out of the capillaries and into the tissue.

22
Q

What are the two main types of respiratory failure? State the parameters that define them.

A

Type 1 = Hypoxaemic (PO2 < 8 kPa)
Type 2 = Hypercapnic (PCO2 > 6.7 kPa)
There is also a third type: Mixed = PO2 < 8kPa AND PCO2 > 6.7 kPa

23
Q

What causes type 1 and type 2 respiratory failure?

A

Type 1 = V/Q mismatch

Type 2 = Hypoventilation

24
Q

How do the kidneys control blood pH?

A

By secretion and retention of weak acids

They can eliminate or replenish H+ by altering the plasma bicarbonate concentration