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CAM201 Physiology > Introduction to Gas Transport > Flashcards

Introduction to Gas Transport Flashcards

1
Q

PP’s in atmospheric air

A 
PO2 = 159 mmHg
PCO2 = 0.3 mmHg
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2
Q

PP’s in alveolar air

A 
PO2 = 105 mmHg
PCO2 = 40 mmHg
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3
Q

PP’s of arterial blood

A 
PO2 = 100mmHg
PCO2 = 40 mmHg
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4
Q

PP’s of tissues

A 
PO2 = 40 mmHg
PCO2 = 45 mmHg
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5
Q

PP’s of venous blood

A 
PO2 = 40 mmHg
PCO2 = 45 mmHg
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6
Q

At a PO2 of 100mmHg the O2 dissolved in the blood will equal what?

A

3mL O2/L blood

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7
Q

When we are referring to PO2 what are we referring to?

A

Dissolved oxygen.

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8
Q

How much oxygen travels dissolved in the blood?

A

3%

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9
Q

If Hb is fully saturated, 1L of blood carried how much O2?

A

Normal blood carries 150g Hb/L blood.
1g of Hb can bind with up to 1.34 mL of O2.

Therefore, 1L of blood carries 200mL of O2.

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10
Q

What part of Hb does oxygen bind to?

A

The Fe2+ portion of the heme groups.

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11
Q

Oxyhaemoglobin

A

Red arterial blood

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12
Q

Deoxyhaemoglobin

A

Dark venous blood

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13
Q

Cooprative binding

A

When one oxygen molecule binds to Hb, it causes a confirmational change in the molecule which increases its affinity for oxygen, and therefore enhances binding.

This results in a sigmoidal (S) shaped dissociation curve (not linear).

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14
Q

At a PO2 of 100mmHg, how saturated is Hb?

A

97-98%

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15
Q

At a PO2 of 40mmHg, how saturated is Hb?

A

75%

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16
Q

At a PO2 of 27mmHg, how saturated is Hb?

A

50%

P50 for Hb

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17
Q

What is the functional benefit of the sigmoidal shape of the oxygen-Hb dissociation curve?

A

Tissue oxygen concerntration is held constant over a wide range of alveolar PO2 (at higher PO2), but facilitates delivery of oxygen to the tissues at lower PO2.

  • Flat part of the curve means that >90% saturation of Hb over a wide range of higher PPs (ie. from 60-120mmHg).
  • Steep part of the curve means large amounts of oxygen can be released from Hb with only small changes in PO2, facilitating release into the tissue.
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18
Q

Oxygen content/concerntration

A

Oxygen bound to Hb + dissolved oxygen.

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19
Q

Carbon monoxide

A

CO is a colourless, odourless and tasteless gas (no reflex coughing or sneezing), but highly toxic.

CO combines with Hb at the same site as O2 but has a much greater affinity (200x).

CO-Hb = carboxyhaemoglobin

As CO binds to Hb in a similar fashion to O2, Hb remains a red colour - not purple like deoxyhaemoglin (saturation may appear normal - need to use a CO-oximeter).

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20
Q

CO affect on PaO2

A

PaO2 may remain normal while O2 content decreases without cyanosis. Carbon monoxide will not affect dissolved oxygen and therefore PO2 will remain normal.

21
Q

CO affect on O2-Hb dissociation cruve

A

Carbon monoxide also changes the affinity between O2 and Hb, shifting the dissociation curve to the left and decreasing offloading at the tissues.

22
Q

CO treatment

A

Treated by administering 100% oxygen to displace CO (shortens half-life).

23
Q

Factors which shift the O2-Hb curve

A
  1. CO2
  2. pH
    3, Temperature
  3. 2, 3 -DPG (BPG)
24
Q

Bohr effect

A

At the tissues, the increase in blood CO2 and H+ enhances the release of O2 from the blood into the tissues.

Decreased affinity –> right shift, increase P50 (increase oxygen off-loading)

At the lungs, decrease in CO2 and H+ enhances oxygenation

Increased affinity –> left shift, decrease P50 (increase oxygen offloading)

25
Q

Temperature affect on O2-Hb curve

A

Increase in temperature causes a shift to the right.

26
Q

Affect of exercise on O2-Hb curve

A

During exercise:

  1. Increase metabolism
  2. Release CO2
  3. Release metabolic acids
  4. Increase temperature

All act to shift the curve to the right, and enhance O2 release at the tissues.

27
Q

2,3-diphosphoglycerate

A

2,3-DPG is an end product of RBC metabolism (glycolysis). Interacts with the beta chain of Hb .

DPG is normally present in RBC at a concentration of 15mmol/g Hb.

Without 2,3-DPG, Hbs high affinity for O2 would impair the oxygen supply at the tissues.

Increased in hypoxia (at altitude, COPD). Decreased in ‘stored blood’ (blood bank).

28
Q

2,3-diphosphoglycerate affect of O2-Hb dissociation curve.

A

Increased binding of DPG shifts dissociation curve to the right.

29
Q

Foetal Hb

A

HbF has a greater affinity for O2 than adult haemoglobin (HbA).

P50 = 19 vs 27 mmHg in adult.

Instead of beta-chain –> gamma-chain. .

Doesn’t bind 2,3-DPG as readily as beta chain, therefore, less DPG causes a shift to the left (and therefore greater affinity for O2).

Newborn has both HbA and HbF

30
Q

Significance of the curve shift.

A

A shift in the O2-Hb dissociation curve has little effect on saturation at higher PP where the curve is flat. The shift has most influence over the steep part of the curve and oxygen offloading.

31
Q

Affect of lung disease on the O2-Hb dissociation curve.

A

Many are characterised by decrease PaO2, but due to the flat part of the curve saturation is still adequate at approximately 90%.

However, any decrease in pH/increase in PCO2 will dhift the curve to the right and may result in a decreased in saturation to <80%, impairing oxygen delivery to the tissues (hypoxia).

Conditions resulting in retention of CO2.
Problematic during during exercise.

32
Q

Hypoxia

A

Low PO2 at tissues.

Occurs when there is insufficient oxygen available to the cells to maintain adequate aerobic metabolism.

Results in anaerobic metabolism, decrease in pH.

Severe hypoxia may result in cyanosis (blue colour –> deoxyhaemoglobin).

33
Q

Hypoxic hypoxia

A

Low arterial PO2.

Caused by high altitude, alveolar hypoventilation, decrease lung diffusion capacity, abnormal ventilation-perfusion ratio.

34
Q

Anaemic hypoxia

A

Decreased total amount of O2 bound to haemoglobin.

Caused by blood loss, anaemia (low [Hb] or altered HbO2 binding), carbon monoxide poisoning.

35
Q

Ischaemic hypoxia

A

Reduced blood flow.

Heart failure (whole-body hypoxia), shock (peripheral hypoxia), thrombosis (hypoxia in a single organ).

36
Q

Histotoxic hypoxia

A

Failure of cells to use O2 because cells have been poisoned.

Caused by cyanide and other metabolic poisons.

37
Q

Oxygen transport reserve mechanisms

A
  1. Pulmonary reserve
  2. Circulatory reserve
  3. Erythropoietic reserve
  4. P50 (chemical reserve)
38
Q

Pulmonary reserve

A

Increased ventilation

39
Q

Circulatory reserve

A

Increased cardiac output (global)

Increased tissue perfusion (local)

40
Q

Erythropoietic reserve

A

Increased production of RBCs (and therefore Hb)

41
Q

P50 (chemical reserve)

A

Factors which change the affinity between Hb and O2:

  • increased affinity at the lung to facilitate oxygen loading
  • decreased affinity at the tissues which facilitates oxygen offloading.
42
Q

How do we carry CO2 in the blood?

A

7% Dissolved (PCO2)
10% Bound to protein (carbaminohaemoglobin)
80-90% Bicarbonate ions

43
Q

CO2 binding to haemoglobin (protein)

A

Reacts with terminal amine group to form carbaminohaemoglobin.
Hb-NH2 + CO2 –> Hb-NH-COO- + H+
Rapid, reversible reaction, no enzyme required.

Reduced Hb can bind more CO2 than oxygenated Hb

  • more CO2 offloading at lungs when Hb saturation is increased.
  • more CO2 loading at tissues when Hb is less saturated
44
Q

Bicarbonate ion equation

A

CO2 +H2O↔H2CO3 ↔H+ +HCO3-

Firs reaction occurs slowly in plasma, but very quickly in RBC due to presence of carbonic anhydrase (CA).

H+ is then buffered by Hb or plasma proteins.

HCO3- diffuses out of the RBC via a HCO3-/Cl- carrier protein = chloride shift

Reverse reaction occurs at lungs.

Hb is a better bugger of H+ ions in reduced state. Facilitates CO2 loading at tissues, offloading at lungs.

45
Q

Haldane effect

A

How oxygen affects Hb affinity for CO2 and H+ The protons produced from the dissociation of carbonic acid are buffered by Hb.

Deoxygenation of Hb enhances its ability to carry H+ ions.

As Hb becomes more deoxygenated it becomes a more effective buffer - Haldane effect.

At the lung binding of oxygen with Hb releases excess H+ ions and displaces carbon dioxide.

46
Q

CO2 concentration and ventilation

A

Excretion of CO2 by the lungs is an important mechanism in the regulation of acid-base balance.

Changes in PCO2 are a very strong stimulus to the control of breathing.

There is a strong relationship between alveolar ventilation and the concentration of CO2 in the blood.

In healthy people, alveolar PCO2 is in equilibrium with arterial PCO2

PICTURE OF EQUATION

47
Q

Hypercapnia

A

Elevated PaCO2.

May be caused by:
1. Reduced alveolar ventilation (VA) with normal/constant CO2 production (VCO2).

Decreased total/minute ventilation.

Increase in dead space due to ventilation pattern e.g. rapid shallow breathing; ventilation/perfusion mismatch.

  1. Increased CO2 production without compensatory change in ventilation.

Control problem (suppression of respiratory centre)

Abnormality of ventilatory pump (severe/advanced emphysema)

48
Q

Alveolar gas equation

A

PAO2 = PIO2 (PB – PH2O) – ( PACO2/RQ)

Alveolar PO2 will increase with increasing ventilation - however… doubling ventilation will not necessarily double alveolar PO2 as the highest PO2 achieved is = inspired PO2 (149mmHg at sea level). As alveolar ventilation increases, alveolar air becomes closer to atmospheric concentrations (decreased PCO2 and increased PO2).

49
Q

Respiratory quotient

A

RQ = rate of CO2 output/ rate of O2 uptake. The ‘normal’ RQ = 0.825

The amount of CO2 produced will vary with fuel source.

  • exclusive carbohydrate metabolism: R = 1
  • exclusive fat metabolism: R = 0.7

CAM201 Physiology (18 decks)

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