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Respiratory Block > 1- oxygen & respiratory failure > Flashcards

1- oxygen & respiratory failure Flashcards

1
Q

what happens in type 1 respiratory failure?

A

short of oxygen (low pO2)

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2
Q

what happens in type 2 respiratory failure?

A

short of oxygen AND too much CO2 (low pO2 and high pCO2)

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3
Q

what is primary hypoxaemia?

A

not enough oxygen in blood

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4
Q

what is hypoxic?

A

not enough oxygen in tissues

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5
Q

what is the response to primary hypoxaemia if good lungs?

A

2 responses: increased tidal volume & increased frequency of breaths
= this makes normal pO2 and low pCO2 (since compensating for low pO2 by breathing more)

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6
Q

what happens with primary hypoxaemia with bad lungs?

A

low pO2 and normal pCO2 as your body can’t take big or frequent breaths = type 1 failure

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7
Q

what happens with primary hypoxaemia in good lungs after you start to get tired?

A

you can’t maintain high tidal volume & frequency to compensate so pO2 drops = type 1 failure

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8
Q

what happens when people with bad lungs come into contact with bacteria, virus or something like that?

A

the bacteria etc causes inflammation and mucous protection of airways worsening airflow that reduces ventilation and gas exchange which means get low pO2 & very high pCO2. the compensatory mechanisms of making HCO3 not enough→acidosis

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9
Q

why is the pH of the blood in people with bad lungs slightly lower than normal?

A

people with bad lungs often run with high pCO2 and normal HCO3 →the build up CO2 leads to compensatory mechanisms = the kidneys (body) compensates by increasing bicarbonate→this helps slightly buffer the acidity but often the pH of the blood still lower than normal

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10
Q

what is FiO2?

A

the concentration of oxygen in the gas mixture

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11
Q

why is it bad to give 100% (high) FiO2 as treatment?

A

very high oxygen and due to shape of oxygen haemoglobin/pO2 graph curve it means that the stats will say fine even if not as straight line

  • difference in 10 pKa of pO2 of lungs will both show same stats
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12
Q

why do we now give controlled FiO2?

A

controlled FiO2 dose is at point on graph at edge of flat section so if lung pO2 dropped by 10 pKa then would be over edge of steep curve so would show different stats

*hard to explain - look at notes if don’t get cause not too complicated

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13
Q

why can too much oxygen be bad in some people who are sensitive to it?

A

in these people as pO2 rises, pCO2 rises = acidosis which can be severe & life threatening

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14
Q

what are symptoms of severe hypoxaemia bad?

A

drowsy, altered mental state, cyanosis, dyspnoea, tachypnoea, arrhythmias

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15
Q

what pO2 level do you
a) start hyperventilating?
b) lose consciousness?
c) death?

A

a) pO2 < 5.3 kPa
b) 4.3 kPa
c) 2.7 kPa

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16
Q

what determines amount of oxygen that gets to tissues?

A
  • requires cardiac output (needs heart beating)
  • also need haemoglobin (that is saturated)
  • also slightly depends on how much oxygen in blood
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17
Q

what are causes of circulatory hypoxia?

A
  • anaemia (less haemoglobin to carry O2)
  • carbon monoxide (higher affinity that O2)
  • cyanide poisoning (stops cells from using O2 well)
  • ferrous iron oxidised to ferric iron (different state binds O2 worse)
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18
Q

how does anaemia cause circulatory hypoxia? and what is anaemia caused by?

A

anaemia = decreased number of haemoglobin = less oxygenated blood to tissues

anaemia caused by B12 deficiency, folic acid deficiency, iron deficiency, loss of blood

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19
Q

how does carbon monoxide cause circulatory hypoxia?

A

carbon monoxide irreversibly binds to haemoglobin = toxic hypoxia

sign = bright red venous blood

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20
Q

what is treatment of carbon monoxide?

A

give people 100% oxygen (binds competitively with haemoglobin) = hyperbaric oxygen is treatment if life threatening problem (not common)

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21
Q

how does cyanide poisoning cause circulatory hypoxia?

A
  • Cyanide inhibits ATP at a cellular level, shifting cells from aerobic to anaerobic respiration
  • Cells no longer take up oxygen, so blood remains oxygenated and bright red
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22
Q

what is treatment for cyanide poisoning?

A
  • give Nitrites (Amyl Nitrite), but this can cause dangerously high levels of methaemoglobin
  • Alternative is hydroxy-cobalamin (Vitamin B12 derivative)
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23
Q

what can give you cyanide poisoning?

A

burning polystyrene

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24
Q

how can you tell difference between cyanide poisoning and carbon monoxide poisoning clinically?

A

you can’t clinically

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25
Q

how does ferrous ions cause circulatory hypoxia?

A

functioning haemoglobin contains ferrous iron (Fe2+)
oxidation to ferric iron (Fe3+) creates met-haemoglobin which can’t bind oxygen and therefore causes reduced deliver of oxygen to tissues

26
Q

what are causes of oxidation of ferrous iron?

A
  • Fava-ism (G6PD deficiency) = when they fava beans
  • Amyl nitrate (poppers) = drug poppers
  • Chloroquine, dapsone, primaquine, quinones, sulphonamides
  • Aromatic amines
  • Nitrates/Nitrites
27
Q

what is hypoxaemic hypoxia and causes?

A

decreased partial pressure of oxygen (decreased inspired) leading to decreased oxygen concentration

causes:
- drug use
- upper airway obstruction
- obesity
- chest wall deformities
- anaesthesia
- bronchial obstruction

28
Q

how do drugs cause hypoxaemic hypoxia?

A

Opiates cause respiratory depression by suppressing the central nervous system

29
Q

what can cause laryngeal obstruction and why does that matter?

A

Laryngeal obstruction can be caused by anaphylaxis, or physical obstruction = hypoxaemic hypoxia

30
Q

how can obesity cause hypoxaemic hypoxia?

A

causes hypoventilation by stenting the diaphragm, preventing diaphragmatic excursion inferiorly, reducing tidal volume, and lung volumes

31
Q

how can anaesthesia cause hypoxaemic hypoxia?

A

the drugs reduce respiratory effort, having a tube in the airway restricts airflow, paralysis prevents normal respiratory effort, artificial ventilation is not as good as natural respiratory effort. The longer the anaesthetic the worse it is for the patient, in many ways

32
Q

what are ways that impaired diffusion causes hypoxaemia?

A
  • interstitial thickening e.g. pulmonary fibrosis, lymphangitis, sarcoidosis
  • vascular dysfunction e.g. pulmonary vasculitis
33
Q

how does interstitial thickening cause hypoxaemia?

A

If the interstitium (the gap between the pneumocytes and the endothelial cells) is thickened, or swollen with additional cells, or fluid, the diffusion is less efficient.

34
Q

what effect does abnormal or thickened blood vessels have?

A

it means less diffusion
= Some rarer diseases cause inflammatory infiltrates in the lungs – extrinsic allergic alveolitis (Type 3 and type 4 hypersensitivity reaction in the lungs) and Goodpasture’s syndrome (Type 2 hypersensitivity to Glomerular Basement Membrane cell proteins). Both inhibit oxygen transfer to the pulmonary bed.

35
Q

how do lungs themselves cause hyperaemia?

A

an unbalance between ventilation & perfusion = v/q mismatch

36
Q

what is ventilation & perfusion like at lung apex & lung base?

A
  • Lung Apex - Good V, Poor Q
  • Lung Base - Poor V, Good Q

= areas of lung have varying degrees of perfusion & ventilation, perfusion should be directed to areas of best ventilation

37
Q

when someone has tissue hypoxia what questions should you think to find out which bit is failing?

A

cardiac output?

haemoglobin?

poisoning?

then the lungs?

38
Q

what can result in decompensatory acidosis?

A

(when not enough compensation so leads to acidosis)

  • too much oxygen
  • viruses
39
Q

who is more likely to develop type 2 respiratory disease?

A
  • cystic fibrosis & bronchitis 9end stage)
  • neuromuscular diseases
  • COPD
  • morbidly obese (associated with obesity hypoventilation syndrome in which hypercarbia is a component)
40
Q

why does giving excessive oxygen cause acute respiratory failure?

A

= v/q mismatch

  • when excess oxygen administered it can reverse reactive vasoconstriction as with higher oxygen levels the body perceives less of a need for vasoconstriction in poorly ventilated areas so perfusion becomes good, but ventilation is still poor
  • Inadequate ventilation means CO2 is trapped in the lung as not effectively removed, and diffuses back into the arterial system
41
Q

what is reverse vasoconstriction - why does it occur in areas of poor ventilation?

A

In areas of poor ventilation (inadequate air to oxygenate blood) the bodies response is reactive vasoconstriction = purpose is to redirect blood flow away from poorly ventilated towards well ventilated to optimize oxygenation

42
Q

what is haldane effect?

A

= when hemoglobin binds with oxygen, it has a reduced affinity for CO2 and vice versa

oxygen can displace CO2 from HCO3 when deoxygenated haemoglobin (HHb) becomes HbO2 (oxygenated haemoglobin)

= when hemoglobin releases oxygen to tissues (becoming deoxygenated), it becomes more effective at picking up CO2. When it picks up oxygen (becoming oxygenated), it becomes less effective at holding onto CO2 (think like attractive party analogy)

43
Q

what is bohr effect?

A

high concentrations of CO2 prevent O2 binding to haemoglobin = pCO2 shifts the dissociation curve

as the concentration of CO2 increases or as the pH decreases (resulting in higher acidity), the affinity of hemoglobin for oxygen decreases so to tissues

44
Q

what does pCO2 affecting haemoglobin dissociation curve mean?

A

means that patients with chronically elevated pCO2 have right shift of their Hb-O2 curve
- so at any given pO2 their SaO2 is lower.
- This figure can be very low
- Many people are wandering around Dundee with SaO2 of less than 80 %

45
Q

who is oxygen sensitive?

A

people with chronically poor localised ventilation due to v/q mismatch

46
Q

what is a good test for who has oxygen sensitivity (v/q mismatch)?

A

Chronic CO2 retention is a good marker, so look for a high pCO2 and high HCO3 (renal compensation)

*takes a while to flush oxygen in & out

47
Q

what effect means some patients have very low SaO2 despite relatively normal pO2?

A

bohr effect

48
Q

what effect means Chronically hypoxaemic patients without CO2 retention can still become acidotic with too much O2?

A

haldane effect

49
Q

what people are allowed unlimited oxygen? (100%)

A
  • cluster headaches (don’t know why but evidence based)
  • carbon monoxide or cyanide poisoning
  • sickle cells crisis
  • pneumothorax (only for people who have who don’t have chest drain)
50
Q

what people require cautious oxygen prescription?

A
  • large stroke
  • MI
  • aim for 94-98% for this group
  • don’t start giving stats at or above 93% for this group
51
Q

when should you stop oxygen? at what stat?

A

at 96%

52
Q

what stats should be given for people at risk of respiratory failure e.g obesity, COPD etc?

A

88-92%

53
Q

what should stats be aimed for for pulmonary embolism, sepsis etc (anything else that isn’t high risk or unlimited etc)?

A

94-98%

54
Q

why is nasal cannulae not good?

A

only has low flow and needs dependant on nasal breathing

55
Q

why is variable performance mask good/bad?

A

cheap & simple, can have 5-15 Lmin but also unable to cope with high flow

56
Q

why is venturi mask good?

A

fixed performance and flows of up to 250 L/min

*colour coded by flow

57
Q

why is non-rebreathing mask good/bad? (bag mask)

A

Up to 85 % FiO2
Uncontrolled FiO2
Flow limited to outflow of wall
Beware large VT

58
Q

what are the few indications for using re-breathing mask?

A
  • CO poisoning
  • PTX
  • Cluster headaches
  • Sickling crisis
59
Q

what is aim for saturated oxygen if risk of chronic type 2 respiratory failure?

A

88-92%

60
Q

does type 1 respiratory failure require oxygen?

A

yes

61
Q

can type 2 respiratory failure occur in anyone?

A

yes

62
Q

what is treatment for hypercarbia?

A

non invasive ventilation

Respiratory Block (46 decks)

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