Oxygen and Respiratory Failure

Question 1

describe type 1 respiratory failure

Answer 1

short of oxygen

requires oxygen treatment

Question 2

describe type 2 respiratory failure

Answer 2

short of oxygen
too much carbon dioxide

(anyone can develop type 2)

Question 3

describe progression to type 1 respiratory failure - good lungs

Answer 3

response to hypoxaemia - increase in tidal volume
increase in respiratory rate (hyperventilation)

normal pO2
low pCO2

low pO2
normal pCO2

Question 4

describe progression to type 1 respiratory failure - bad lungs

Answer 4

response to hypoxaemia - low pO2

normal pCO2

Question 5

describe progression to type 2 respiratory failure

Answer 5

patinet tires, less able to ventilate -
low pO2
high CO2

life threatening

Question 6

describe progression to acidosis - type 2 failure

Answer 6

low pO2
high pCO2
normal HCO3

chronic acidosis - clears via kidneys

low pO2
high pCO2
high HCO3

invasion (e.g. oxygen, virus)

low pO2 (high if prescribed oxygen)
very high pCO2
high HCO3

decompensated acidosis

Question 7

explain the precautions when prescribing oxygen

Answer 7

only give oxygen if the risk/benefit ratio is in favour of oxygen (no patient prescribed oxygen should have sats >98%)
oxygen is the treatment for hyoxaemia but can do harm
some people may be sensitive to oxygen

too much oxygen can kill;
as pO2 rises, pCO2 rises (leading to acidosis, severe and life threatening)
acute on chronic type 2 respiratory failure is triggered by over oxygenation

normal pO2 = 12-15kPa
lung damage causes a 10kPa fall in pO2 but shows minimal drop in sats (presume patient is well when they are not)
gross deterioration in oxygenation

controlled oxygen prescription only causes a 5kPa fall in pO2

Question 8

describe oxygen prescribing to COPD patients

Answer 8

not all patients retain CO2 and are sensitive to oxygen but we are unable to tell them apart
most COPD patients are at risk of developing type 2 but not all of them

chronic CO2 retention is a good mark so look for pCO2 and high HCO3 (renal compensation)
takes a while to flush oxygen in and out
chronically hypoxaemic patients without CO2 retention can still become acidotic with too much oxygen (Haldane effect)
Bohr effect means some patients have very low sats despite relatively normal pO2

Question 9

describe different causes of type 2 respiratory failure

Answer 9

kyphoscoliosis
end stage cystic fibrosis
morbid obesity

Question 10

describe hypoxic drive theory

Answer 10

normal respiration driven by CO2 receptors
chronic hypercarin leads to desensitisation of receptors
oxygen chemoreceptors then become primary drive for respiration

Question 11

state the aim for sats for patients with any risk of chronic type 2 respiratory failure

Answer 11

88-92%

Question 12

state the aim for sats for patients with any risk of ischaemia/infarction

Answer 12

no oxygen is sats >_90%

Question 13

state the normal range for sats

Answer 13

94-98%

Question 14

describe cases when there should be an unrestricted use of oxygen

Answer 14

patients with cluster headaches, carbon monoxide poisoning, pneumothorax not treated with a chest drain and sickle cell crisis
these patients should receive high flow, high concentration oxygen therapy

Question 15

describe non invasive ventilation

Answer 15

provides positive pressures in inspiration and expiration - the high the pressure in inspiration increases Vt thereby increasing minute ventilation and exhalation of carbon dioxide
recruits alveoli by opening uo closed alveoli - improving V/p mismatch and helping to recuse arteriolar pCO2

Question 16

describe severe hypoxaemia

Answer 16

abnormally low concentration of oxygen in blood
causes an alteration in mental sate, cyanosis, dyspnoea, tachypnoea, arrhythmias - tissue hypoxia (cells switch to anaerobic respiration leading acidosis)

hyperventilation increases dramatically when pO2<5.3 kPa
loos of consciousness ` 4.3 kPa
death ` 2.7 kPa

Question 17

describe circulatory hypoxia

Answer 17

oxygenated blood needs to get to tissues
‘heart failure’
local reception - obstruction of vessels, oedema, compression, compartment syndrome

cause of mortality post MI (MI reduces cardiac output, oxygenated blood cannot go anywhere)

Question 18

state the aim for sats with patients with ‘everything else’

Answer 18

90-94%