Clinical Blood Gases Flashcards

1
Q

why do we measure blood gases

A

to assess very sick patients
to diagnose resp failure
to diagnose metabolic problems

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2
Q

oxygen haemoglobin dissociation curve

A

Hb takes up o2 in lung
Hb liberates o2 in tissue

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3
Q

what initiates a right shift in the o2/Hb dissociation curve

A

increase co2
increase H+
increase temp
increase 2,3-DPG

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4
Q

how saturated does haemoglobin tend to be

A

97%

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5
Q

how is oxygen carriage quantified

A

Hb saturation
- very easy to do
- assuming Hb is normal, is an accurate reflection of oxygen content
arterial blood gases
- more complicated and invasive
- PaO2 reflects haemoglobin saturation but is a measure of partial pressure of O2 in blood

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6
Q

how to measure Hb saturation

A

oxygenated blood red
deoxygenated blood blue
using absorption spectroscopy, is possible to estimate degree of saturation of haemoglobin
SpO2, pulse oximetry

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7
Q

how to measure ABG

A

single arterial puncture technique
- radial a.
- femoral a.
- brachial a.
measurement from in-dwelling arterial catheter or a-line
- only really an option in HDU/ITU

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8
Q

what does blood gas measure

A

pao2
paco2
H+/pH
bicarbonate
some may measure electrolytes and Hb
other forms of Hb - carboxyhaemoglobin

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9
Q

normal blood gas values

A

H+ 36-44 nmol/L
PO2 12-15 kPa
PCO2 4.4-6.1
HCO3- 21-27.5
BE +2 to -2 mmol/L

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10
Q

oxygenation kPa

A

partial pressure of o2 in air is 21 kPa
total pressure in atmosphere is 100 kPa
21% of air is oxygens, therefore 21% of total pressure is partial pressure of oxygen
depends on environment

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11
Q

oxygenation

A

normal PaO2 = 12-15 kPa
breathing air
at normal atmospheric pressure
because amount of o2 available, alveolus (PAo2) around 14-15 kPa

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12
Q

carbon dioxide

A

normal PaCO2 = 4.4-6.1 kPa
pco2 and co2 content vary with ventilation
more v = low pco2 and content
less v = high pco2 and content
hypoventilation causes build up of alveolar co2 and therefore less likely to be removed from blood
increase in blood co2 leads to acidosis

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13
Q

carbon monoxide poisoning

A

CO produced from incomplete combustion of hydrocarbons
CO bind to Hb in place of O2 to form carboxyhaemoglobin
also interferes with mitochondrial respiration
death by asphyxia
treatment is high concentration o2 - displaces CO from Hb

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14
Q

resp failure

A

low o2 level in blood - hypoxaemia
resp failure = pao2 < 8 kPa
caused by vq mismatch or hypoventilation (or both)

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15
Q

asthma and resp failure

A

hypoxaemia suggest significant asthma attack
bronchospasm and mucous plugging causes ventilation defects and vq mismatch
T2 resp failure develops when severe bronchospasm causes hypoventilation of alveoli or exhaustion
patient need o2 to survive
invasive ventilation may be required

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16
Q

copd and resp failure

A

copd - mixture of chronic airway inflammation and narrowing and emphysema
problems with vq mismatch and hypoventilation
may present acutely with resp failure T1 or T2
may have chronic T2 resp failure in advanced disease
treat resp failure with o2 but with caution in chronic T2

17
Q

what is h+ increased by

A

increased pco2 - respiratory acidosis
increase in acid production or decrease in excretion - metabolic acidosis

18
Q

acute vs chronic type 2 resp failure

A

acute hypoventilation - e.g. due to opiate toxicity leads to hypoxia, hypercapnia and acidocis
chronic hypoventilation e.g. neuromuscular disease or severe copd leads to hypoxia and hypercapnia but may not have acidosis due to compensation

19
Q

what does increased bicarbonate retention by the kidney compensate for

A

acidosis

20
Q

what does co2 normally stimulate

A

ventilation

21
Q

what are some patients with chronic type 2 resp failure dependent on to stimulate breathing

A

hypoxia

22
Q

what can a sudden increase in po2 with oxygen therapy worsen

A

hypoventilation

23
Q

what is respiratory alkalosis not usually associated with

A

respiratory failure

24
Q

what is resp alkalosis caused by

A

hyperventilation

25
Q

what are there low levels of with resp alkalosis

A

low pco2 and low h+

26
Q

metabolic problems involving blood gases

A

excess acid production by body - e.g. lactic acidosis or diabetic ketoacidosis
kussmal breathing - clinical sign of acidosis as a compensatory mechanism to increase co2 removal from blood
full compensation difficult - need to treat underlying cause of increased acid load

27
Q

how is bicarbonate interpreted

A

bicarbonate calculated by blood gas machine
hco3- increased by increase in pco2
hco3- decreased by increase in acid production or decrease in excretion

28
Q

actual bicarbonate

A

calculated with actual h+ and pco2 values

29
Q

standard bicarbonate

A

calculated with actual h+ and pco2 of 5.3kPa
only influenced by metabolic effects

30
Q

base excess

A

amount of base needed to be removed from a litre of blood at normal pco2 in order to bring h+ back to normal
- calculated with normal co2, so only looks at metabolic component
- normal value is zero (-2 to 2 mmol/L)
- big negative value indicated metabolic acidosis
- positive value seen in compensated resp acidosis

31
Q

when is the patient in respiratory failure

A

if the po2 is low given the inspired o2

32
Q

when is it type 1 resp failure

A

when co2 is low or normal

33
Q

when is it type 2 resp failure

A

when co2 is high

34
Q

what is high h+

A

acidosis

35
Q

what is low h+

A

alkalosis

36
Q

cause of acidosis - high pco2

A

respiratory

37
Q

cause of acidosis - standard bicarbonate low or base excess has large negative value

A

metabolic