Gas Transport and Respiratory Control - L5 Flashcards

1
Q

oxygen transport is in 2 forms what are they and their %?

A

a)1.5 % Dissolved in plasma
So, 3 mlO2.litre-1blood (0.3 mlO2.dl-1) dissolved in plasma
NB: Only dissolved gas contributes to circulating partial pressures
b) 98.5 % Bound to haemoglobin
* Hb binds 1.34 ml O2.g-1 (x 130 – 150 g.litre-1 )
* Provides 175 – 200 ml O2.litre-1blood (17.5 – 20 ml O2.dl-1)

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2
Q

where is Hb - Haemoglobin found?

A

only in RBCs

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3
Q

g.litre ^-1 of Hb in men and women?

A

150 g.litre-1 in men (15 g.dl-1)
130 g.litre-1 in women (13 g.dl-1)

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4
Q

Structure of Hb?

A

Tetrameric globular protein
4 Haem groups (each contain 1 Fe2+ ion)

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5
Q

Hoe much O2 does Hb move?

A

Transports 98.5% of O2 in blood

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6
Q

What function does Hb provide?

A

Greater oxygen carrying capacity

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7
Q

What does the co-operative reversible binding of Hb go up to? in terms of O2+CO2 molecules

A

4 O2 molecules (haem groups)
4 CO2 molecules (globin portion, normally 2 at most in venous blood)

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8
Q

Does Hb change affinity and for who?

A

Yes Hb changes affinity for O2

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9
Q

3 Forms of CO2 transport? and %

A
  1. Dissolved - 10%
  2. Bound to hg - 30%
  3. Bicarbonate (HCO3) - 60% – Mostly in plasma
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10
Q

Dissociation curve of Hb and O2?

A

NOT Linear

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11
Q
A

When arterial blood is 100 and the 95% of O2 is taken by Hb - most of Hb sites takes by O2
veins have a PO2 of 40 on average and saturation of O2 of Hb with veins is 75% even when CO2 drops - gives us a safety zone of O2

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12
Q

What happens the more O2 is bound to Hb?

A

the more O2 bound to Hb the easier it gets to bind to new O2 molecules

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13
Q

What can we not have a PO2 level of?

A

cannot have a PO2 level of 760 mm Hg

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14
Q

PO2 levels when metabolism higher?

A

PO2 levels in vein is higher

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15
Q

Can you change the dissociation curve of Hb for O2?

A

YES due to many factors

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16
Q

What happens if this Hb for O2 curve is shifted to the right? Main thing + 3 things

A

Tissue level unloading: easier to get rid of O2
1. Increased PCO2 Hb + CO2<-> HbCO2 (Eq right)
2. Decreased pH (­ increase H+)
Hb + O2 Hb <->O2 + H+ (Eq left)
3. Increased Temperature and changes conformation of Hb so it is easier to unload Hb from O2

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17
Q

What happens left side of curve?

A

Left shifted
* Lung level loading – ¯ PCO2
– ­ pH (¯ H+)
– ¯ Temperature
easier to load on O2 to Hb

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18
Q

what is the metabolite made in produced of RBC? when is it signficant?

A

when O2 levels are low at high altitude and this induces a change in Hb so it is easier to unload O2 from Hb in tissue
2,3-diphosphoglycerate
- 2,3-DPG → right shift
- Metabolite of rbc glycolysis
- Significant in hypoxia (altitude)
- At lungs: promotes unloading

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19
Q

4 types of hypoxia

A

Hypoxic hypoxia, anaemic hypoxia, circulatory hypoxia and histotoxic hypoxia

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20
Q

what is hypoxia?

A

insufficient cellular O2 - low levels of oxygen in the blood

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21
Q

exam + mqs

A

follow numbers from slide 7 yellow box

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22
Q

What is the Chloride shift?

A

Cl ions moved into RBCs and hydrogen carbonate shifted out and this is how most of CO2 are carried out

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23
Q

Hypoxic Hypoxia?

A

Arterial PO2 levels are low due to high altitude
Lots of O2 sites are not taken on Hb as Hb is not taken by O2 such as when staurtion drops below 70%
Low PaO2 (hypoxemia) → ↓ %Hb Sat – Inadequate gas exchange
– ↓ PB (altitude)
– Cyanosis (skin bluish tint) = <70% Hb Sat

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24
Q

Anaemic hypoxia?

A

Arterial O2 levels can be normal but not enough Hb: ↓ total blood O2 content with normal PaO2
can be induced by ingesting Carbon monoxide as CO has a higher affinity (24 times) for Hb than O2 - so it takes all the sites
receptors don’t detect how much Hb is bound by O2 - silent killer

– ↓ circulating rbc’s; ↓ rbc Hb content
– CO poisoning (no cyanosis – HbCO is pink, pale skin)
* CO: 24 times more affinity with Hb than O2.

25
Q

Circulatory hypoxia?

A

O2 and Hb content normal but there’s a blockage so O2 cannot get into cells
↓ supply of oxygenated blood with normal O2 content and PaO2
– Vessel blockage, congestive heart failure

26
Q

What pathology is associated with circulatory hypoxia?

A

Congestive heart failure

27
Q

Histotoxic hypoxia?

A
  • O2 delivery to tissues normal, but cells unable to use it.
    – Cyanide is an example poisoning (cyanide blocks essential enzymes for cellular
    respiration) and prevent from getting O2 needed in cells
    some cellular mechanisms do not work properly
28
Q

What is hyperoxia?

A

Too much O2 in cells - i.e. O2 toxicity - above normal arterial O2

29
Q

Disease Hyperoxia?

A

(when ↓PaO2 arterial O2):
* can improve gradient but can be dangerous as an ­O2 can damage brain (could cause blindness)
* when O2 is the main driver of ventilation: ­O2 can increase the risk of ↓ peripheral chemoreceptor sensitivity

30
Q

can too much O2 be fatal?

A

YES - can damage brain and rest of body

31
Q

When O2 levels are very low what happens?

A

Becomes main driver of ventilation control and so when CO2 comes in it can mess up this control

32
Q

Is there a big effect of Hyperoxia in a healthy person?

A

no big effect (Hb saturation almost to the max)

33
Q

What is hypercapnia?

A

Too much CO2 in arterial blood

34
Q

What is hypocapnia

A

Not enough CO2 in arterial blood

35
Q

Cause of hypocapnia?

A

Via hyperventilation - over breathing - taking more O2 then needed and losing too much CO2

36
Q

How does hypercapnia occur?

A

Via hypoventilation - under breathing

37
Q

When does hypercapnia occur and what does it occur in conjuction in ?

A

Occurs with most lung diseases
Occurs in conjunction with reduced PaO2

38
Q

When does hypocapnia occur with?

A

Occurs with anxiety and fear

39
Q

Is there an impact on arterial O2: PAO2 with hypocapnia? is there an exception?

A

No impact on PaO2
- Except at low PB (e.g. altitude) where low PaO2 stimulates a hyperventilation

40
Q

What is Hyperpnea?

A

Increased breathing/ventilation to match metabolic demand (e.g. exercise)

41
Q

What is ventilation controlled by?

A

Chemoreceptors

42
Q

What 2 chemoreceptors control ventilation?

A

Peripheral and central

43
Q

Where and are the respiratory controls in the brain?

A

Pons and Medulla respiratory controls
Pons - Pneumoatix and Apneustic centres
Medulla - Dorsal and Ventral respiratory group

44
Q

What does the medulla respiratory control activate and when?

A

dorsal activates respiratory muscles
ventral activated when breathing is more active such as active breathing in exercise when abdominal muscles are being used

45
Q

Hering-Breur reflex - Pulmonary stre

A

prevents an over inflation of lungs when Tv is below 1L they promote a reduction to regulate

46
Q

what do irritant receptors do?

A

Irritants receptors - dust and pollutants they trigger coughing or sneezing when needed

47
Q

Proprioceptors?

A

Joints
Evidence that they influence breathing during exercise just by flexing some muscles you can indcue some increase in ventilation

48
Q

Where are peripheral chemoreceptors located?

A

change to change in arterial PO2 substantitaly not when it just drops slightly
they provide about 20% of respiratory drive
some studies show that these receptoprs might detect Hb content howver it is up for debate
rarely there is evidnce that they can detect total arterial content - how much Hb is bound to O2 and this is important for anaemia and CO poisoning etc

49
Q

Where are central chemoreceptors located?

A

Medulla in brain

50
Q

Can H^+ions cross the BBB? What is the importance of this?

A

important than H^+ions cannot cross BBB
CO2 reacts with H20 -> carbon

51
Q

Function of central chemoreceptors?

A

they don’t react to changes in O2 levels - it is to Hydrogen ions so they indirectly respond to arterial pressure of CO2

52
Q

% respiratory drive of central chemoreceptors?

A

80% of respiratory drive

53
Q

cnetral chemorecpetors for control of cO2 in body what do they do?

A

when co2levels icnrease to a toxic level instead of stimulating the rsportaory centre they depress it

must not icnrease levels to a toxic way above 80/90 then they start inhibiting

54
Q

What is the effects of arterial O2 on ventilation? due to CO2/O2 levels

A
  • Not much of a change until PO2 £ 60 mm Hg
  • Response due to activation of peripheral
    chemoreceptors only (assuming no changes in PCO2 or pH are also occurring)
  • small drop in O2 not really detected
55
Q

when co2 levels are toxic?

A

can lose consciousness

56
Q

What is the effect of hypoventilation on minute ventilation: VE?

A

Negative feedback
arterial co2 increase and arterial oxygen decrease and hydrogen ions go up
chemoreceptors detect and respond
resiratory control centre increases ventilation

57
Q

What is the effect of hyperventilation on minute ventilation: VE?

A

negative feedback
decrease of co2 in blood and decrease of hydrogen ions with an increase in arterial o2 in blood, chemoreceptors detect and respond and the respiratory control centre causes a decrease in ventilation

58
Q

Perspective

A

potentially carotid infection might be responsible for siolent Hypoxemia in COVID 19 patients