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*LSS Respiratory Y1* > Gas Transport > Flashcards

Gas Transport Flashcards

1
Q

What is the O2 cascade?

A

Describes increasing oxygen tension from inspired air to respiring cells; Fick’s law says flow rate proportional to pressure gradient - structural disease reduces the area, fluid in alveolar sacs increases thickness and hypoxic gas reduces gradient

Oxygen in air at highest partial pressure, decreasing from 21.3kPa (air) to 13.5 in alveoli, 13.3 in tissues to 5.3 in veins

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2
Q

What does a graph of PO2 against Location look like?

A
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3
Q

What are challenges to the oxygen cascade?

A

Alveolar ventilation:

  • V/Q matching: if blockage in respiratory tree and are not ventilating but are perfusing then will not gain oxygen and will drop
  • Diffusion capacity: thickness of exchange surface will reduce oxygen gain
    • Cardiac output: need high Q to move blood to tissues
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4
Q

What is the Altitude cascade, and what does it look like?

A

Reductions in ambient pressure reduces oxygen and gradient - harder to maintain homeostasis

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5
Q

What is the difference between Foetal and Maternal Haemoglobin?

A

Foetal gamma chains give greater affinity than HbA to extract oxygen from placental blood

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6
Q

How is myoglobin specialised?

A

Much greater affinity than HbA to extract oxygen from circulating blood for storage

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7
Q

What is Methaemoglobin?

A

Has Fe3+ not Fe2+; exists as <1% of total Hb in the body - does not bind oxygen, constantly in equilibrium with Hb, switching between Hb and MetHb

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8
Q

What does Methylene blue do?

A

Increases haemoglobin from MetHb

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9
Q

How much Oxygen is dissolved in the blood? (not Hb)

A

16mL min-1 at rest, so VO2 approx. 250 mL min-1(volume of oxygen consumed per minute) - so need Hb

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10
Q

What is the structure of Haemoglobin?

A

Monomers consist of Fe2+ ions at centre of tetrapyrrole porphyrin ring connected to globin protein chain, covalently bonded at proximal histamine residue

(Has two Hba subunits and two of Hb beta/sigma/gamma depending on type)

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11
Q

Describe the affinity of Hb:

A

Increases exponentially as oxygen binds (max 4) - cooperative binding

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12
Q

What is the change in shape of Hb as O2 binds?

A

Middle of Hb becomes binding site for 2,3-DPG (associated with metabolic activity) when 4 O2 bind; upon binding, pushed into tense shape (tightens) to eject oxygen - allosteric behaviour

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13
Q

What happens to CO2 that enters the blood?

A

Reacts slowly with water to form carbonic acid which can dissociate: CO2 + H2O -> H2CO3 -> H+ + HCO3- - CO2 IS ACID (non-enzymatic)

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14
Q

What is Carbonic anhydrase?

A

Enzyme that increases formation of H2CO3 by 5000x - CO2 can move into erythrocytes

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15
Q

What are the ways that CO2 can be transported in the blood?

A
  1. Dissolves in solution
  2. As bicarbonate
  3. Also binds to Hb (amine end of the globin chains, 1 Hb = 4 O2 and 4 CO2)
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16
Q

What is the chloride shift?

A

Negative chloride ions enter RBCs to maintain RMP with AE1 transporters

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17
Q

What are the 5 key gas laws you need to know?

A

Dalton’s

Fick’s

Henry’s

Boyle’s

Charles’

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18
Q

What is Daltons law?

A

Pressure of a gas mixture is equal to the sum of the partial pressures of all the gases in it

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19
Q

What is Ficks Law?

A

Molecules from regions of high concentration to lower concentration at a rate proportional to the concentration gradient, the exchange surface area, and the diffusion capacity of the gas; it is inversely proportional to the thickness of the exchange surface

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20
Q

What is Henry’s Law?

A

At a constant temperature, the amount of a given gas that dissolves in a given type and volume of liquid is directly proportional to the partial pressure of that gas in equilibrium with that liquid

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21
Q

What is Boyle’s Law?

A

At a constant temperature, the volume of a gas is inversely proportional to the pressure of that gas

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22
Q

What is Charles’ Law?

A

At a constant pressure, the volume of a gas is proportional to the temperature of that gas

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23
Q

What are Oxygen dissociation curves?

A

Not linear to ensure that high saturation occurs in lungs but that in systemic circuit a lot of oxygen can be unloaded when really needed, but at rest only remove ~25% of oxygen

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24
Q

What is P50?

A

Partial pressure of Oxygen when HbO2 = 50%

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25
Q

What causes a Left shift of the ODC?

A

(increased affinity): hypothermia, alkalosis, hypocapnia, decreased 2,3-DPG

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26
Q

WHat is 2,3-DPG?

A

The ease with which haemoglobin releases oxygen to the tissues is controlled by erythrocytic 2,3-diphosphoglycerate (2,3-DPG) such that an increase in the concentration of 2,3-DPG decreases oxygen affinity and vice versa.

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27
Q

What causes a right shift in the ODC?

A

(decreased affinity): hyperthermia, acidosis, hypercapnia, increased 2,3-DPG

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28
Q

What affects the P50?

A

Temp, pH, CO2, increased 2,3-DPG

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29
Q

What causes an Upward shift in the ODC?

A

Polycythaemia

(Increased oxygen carrying capacity)

30
Q

What causes a downward shift in the ODC?

A

Anaemia

31
Q

What causes a ODC to go Down and leftwards?

A

Decreased capacity and increased affinity results from increased HbCO (carboxyhaemoglobin)

32
Q

What allows Hb chains to accept protons?

A

Amino acids with negative chains that are proton acceptors

33
Q

What does the CO2 dissociation curve look like?

A

Practically linear, with slightly higher concentration in venous blood than arteries; the more oxygenated the Hb, the less CO2 accepted

34
Q

What is Alkalaemia?

A

Higher than normal blood pH

35
Q

What is Acidaemia?

A

Lower than normal blood pH

36
Q

What is Alkalosis?

A

Circumstances that will decrease [H+] and increase pH

37
Q

What is acidosis?

A

Circumstances that will increase [H+] and decrease pH

38
Q

What is the normal range of [Hb] in ABG?

A

130 to 170 g/L

39
Q

What is the normal pH of blood in an ABG?

A

7.35 to 7.45

40
Q

What is the normal PCO2 of blood in an ABG?

A

4.7 to 6.4 kPa

41
Q

What is the normal PO2 of blood in an ABG?

A

>10kPa

(>80mmHg)

42
Q

What is the normal range of HCO3 in the blood in an ABG?

A

22-26 mEq/L

43
Q

What is the normal range of Base excess in an ABG?

A

-2 to +2 mmol/L

44
Q

What are the compensatory mechanisms of Alka/acidosis?

A
  • Changes in ventilation can lead to rapid compensatory response to change CO2elimination
  • Changes in HCO3- and H+ retention/secretion in kidneys stimulate slow compensatory response to change pH
    • Acidosis needs an alkalosis to correct
    • Alkalosis needs an acidosis to correct
45
Q

What is respiratory acidosis?

A

May result from hypoventilation causing reduced diffusion gradient for CO2, leading to a greater PCO2 in post-alveolar blood, decreased pH and normal base excess (bicarbonate normal for pCO2)

46
Q

What are the two steps of partial compensation for respiratory acidosis?

A

Will have lower pH, high PCO2 and high base excess

  1. Acute phase: CO2 moves into erythrocytes, combines with H2O in presence of carbonic anhydrase to form bicarbonate, which moves out of cell by AE1 transporter; increased bicarbonate leads to raised base excess, shifting equilibrium backwards to carbonic acid and reducing [H+]
  2. Chronic phase: increases bicarbonate reabsorption in kidneys to stabilise pH
47
Q

What is full compensation of respiratory acidosis?

A

Will normalise pH with large PCO2 and base excess

48
Q

What is respiratory alkalosis?

A

May result from hyperventilation causing an increased gradient for CO2, leading to a lower PCO2 in post-alveolar blood, increased pH and normal base excess

49
Q

What is the acute compensation for resp alkalosis?

A

None

50
Q

What is the chronic partial compensation for respiratory alkalosis?

A

Reduces bicarbonate from nephrons and increases secretion in collecting duct, causing more carbonic acid dissociation, reducing base excess

51
Q

What is metabolic acidosis?

A

May result from diarrhoea (or H+ gaining/bicarb losing) as will lose bicarbonate in faeces, leading to increased dissociation of carbonic acid, causing pH reduction with normal PCO2 and low base excess

52
Q

What is partial compensation for metabolic acidosis?

A

Will have a lower pH, low PCO2 and low base excess; occurs by increasing ventilation rate to increase diffusion gradient and reduce PCO2, causing shift to left on equilibrium, forming carbonic acid, and then CO2

53
Q

What is Metabolic alkalosis?

A

May result from vomiting (or H+ losing/bicarb losing) as will lose protons in stomach acid, leading to increased bicarbonate, leading to high pH, normal PCO2 and high base excess

54
Q

What is partial compensation for Metabolic alkalosis?

A

Will have high pH, high PCO2 and high base excess; reducing ventilation rate to increase arterial PCO2 drives equation to right to increase protons and bicarbonate

55
Q

What is Base Excess?

A

The amount of acid required to restore a litre of blood to its normal pH at a PaCO2 of 40 mmHg. The base excess increases in metabolic alkalosis and decreases (or becomes more negative) in metabolic acidosis, but its utility in interpreting blood gas results is controversial.

56
Q

Recall the changes in pH, PCO2, BE and PO2 in the different types of alkalosis and acidosis.

A
57
Q

What is Respiratory failure?

A

Fundamentally a failure of pulmonary gas exchange

(V/Q Ventilation/Perfusion inequality)

58
Q

What is type 1 respiratory failure?

A

Hypoxic respiratory failure with normal CO2 and low O2; hypoventilation/diffusion issue - CO2 diffuses out easily, but oxygen moving in is impaired; can be due to pneumonia, pulmonary oedema or atelectasis (partial collapse)

59
Q

What is Type 2 respiratory failure?

A

Hypercapnic respiratory failure; failure to get gas to alveoli - oxygen has greater concentration gradient, so will still be exchanged, but CO2 has a lower concentration gradient so cannot leave alveoli (oxygen likely to be low as well); may be V/Q mismatch if pulmonary vessels not perfused well; hypercapnic failure usually due to pulmonary fibrosis, neuromuscular disease, obesity or increased dead space (increased CO2 production and/or decreased elimination)

60
Q

What is the equation for pH?

A

-log10[H+]

61
Q

What is the Henderson-Hasselbach equation?

A

pH = pK + log10([HCO3-]/[CO2])

62
Q

What does the Henderson-Hasselbach equation mean?

A

Links the pH of blood to the concentration of HCO3- and CO2 because of the equilibrium between H2O + CO2 <-> H2CO3 <-> H+ + HCO3-

63
Q

What is the difference between Hypoxia and Hypoxaemia?

A

Hypoxia - Describes specific enviroment - PO2 low

Hypoxaemia - Describes blood environment - PaO2 - BLOOD

64
Q

What is Hypoxic stress?

A

Can be brought on by altitude, exercise and disease e.g. COPD

65
Q

What is the bodies response to altitude?

(7 steps)

A
  1. Still 21% O2 but at lower partial pressure, decreasing PA/PaO2, which activates peripheral chemoreceptors (as opposed to central control using CO2)
  2. Increased SNS outflow increases ventilation to increase alveolar oxygen and oxygen loading
  3. Increased SNS will increase Q (HR/SV) to increase oxygen loading (and tissue delivery)
  4. Hyperventilation leads to hypocapnia, reducing central drive to breathe, reducing ventilation and hence oxygen loading
  5. CO2 loss increases pH, shifting ODC to left, increasing affinity decreasing oxygen unloading
  6. Alkalosis produced by increased pH detected by carotid bodies, increasing bicarbonate secretion (and causing kidneys recover/save/manufacture acid) to normalise ODC and increasing oxygen unloading
  7. Low blood oxygen increases erythropoietin production, increasing RBC production and oxygen loading
66
Q

What are the other changes in the body at altitude?

A

Oxidative enzyme/mitochondrial numbers increase to allow for greater oxygen utilisation to produce energy; small 2,3-DPG increase, causing shift to right and increased oxygen unloading

67
Q

What are prophylactics to altitude?

A

Acclimation: stimulated by artificial environments to lead to artificial acclimatisation (e.g. Hyperbaric chamber/breathing hypoxic gas)

Acetazolamide: carbonic anhydrase inhibitor, accelerates slow renal compensation to hypoxia induced hyperventilation

68
Q

What are the Causes, Pathophysiology, Symptoms, Consequences and Treatment of Acute mountain sickness?

A

Causes:

Maladaptation to HA - onset within 24h of ascent

Pathophysiology:

Mild cerebral oedema

Symptoms:

N&V, irritability, dizziness, insomnia, fatigue and dyspnoea

Consequences:

HAPE/HACE progression

Treatment:

Stop ascent, analgesia, fluids and hyperbaric O2therapy

69
Q

What are the Causes, Pathophysiology, Symptoms, Consequences and Treatment of Chronic Mountain sickness?

A

Causes:

Idiopathic

Pathophysiology:

Secondary polycythaemia increases blood viscosity (higher Hct), so blood sludges through systemic capillaries (impedes O2delivery)

Symptoms:

Cyanosis and Fatigue

Consequences:

Ischaemic tissue damage and HF/death

Treatment:

Must stay at low altitude

70
Q

What are the Causes, Pathophysiology, Symptoms, Consequences and Treatment of High-altitude Pulmonary Oedema?

A

Causes:

Rapid ascent/inability to acclimatise

Pathophysiology:

Pulmonary vessel vasoconstriction in response to hypoxia; increased pulmonary pressure, permeability and fluid leakage exceed lymph drainage

Symptoms:

Dyspnoea, dry cough, bloody sputum and crackling chest sounds

Consequences:

Impaired gas exchange

Treatment:

Descend, hyperbaric O2therapy, nifedipine, sildenafil

71
Q

What are the Causes, Pathophysiology, Symptoms, Consequences and Treatment of High Altitude Cerebral oedema?

A

Causes:

Rapid ascend/inability to acclimatise

Pathophysiology:

Cerebral vessel vasodilation in response to hypoxaemia; increased fluid leakage to cranium, compressing brain and raising ICP

Symptoms:

Confusion, ataxia, behavioural change, hallucinations, disorientation

Consequences:

Irrational behaviour, irreversible neuro damage, coma/death

Treatment:

Immediate descent,O2 therapy, hyperbaric O2 therapy and dexamethasone

*LSS Respiratory Y1* (11 decks)

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