Clinical Blood Gases Flashcards
why do we measure blood gases
to assess very sick patients
to diagnose resp failure
to diagnose metabolic problems
oxygen haemoglobin dissociation curve
Hb takes up o2 in lung
Hb liberates o2 in tissue
what initiates a right shift in the o2/Hb dissociation curve
increase co2
increase H+
increase temp
increase 2,3-DPG
how saturated does haemoglobin tend to be
97%
how is oxygen carriage quantified
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
how to measure Hb saturation
oxygenated blood red
deoxygenated blood blue
using absorption spectroscopy, is possible to estimate degree of saturation of haemoglobin
SpO2, pulse oximetry
how to measure ABG
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
what does blood gas measure
pao2
paco2
H+/pH
bicarbonate
some may measure electrolytes and Hb
other forms of Hb - carboxyhaemoglobin
normal blood gas values
H+ 36-44 nmol/L
PO2 12-15 kPa
PCO2 4.4-6.1
HCO3- 21-27.5
BE +2 to -2 mmol/L
oxygenation kPa
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
oxygenation
normal PaO2 = 12-15 kPa
breathing air
at normal atmospheric pressure
because amount of o2 available, alveolus (PAo2) around 14-15 kPa
carbon dioxide
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
carbon monoxide poisoning
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
resp failure
low o2 level in blood - hypoxaemia
resp failure = pao2 < 8 kPa
caused by vq mismatch or hypoventilation (or both)
asthma and resp failure
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
copd and resp failure
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
what is h+ increased by
increased pco2 - respiratory acidosis
increase in acid production or decrease in excretion - metabolic acidosis
acute vs chronic type 2 resp failure
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
what does increased bicarbonate retention by the kidney compensate for
acidosis
what does co2 normally stimulate
ventilation
what are some patients with chronic type 2 resp failure dependent on to stimulate breathing
hypoxia
what can a sudden increase in po2 with oxygen therapy worsen
hypoventilation
what is respiratory alkalosis not usually associated with
respiratory failure
what is resp alkalosis caused by
hyperventilation
what are there low levels of with resp alkalosis
low pco2 and low h+
metabolic problems involving blood gases
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
how is bicarbonate interpreted
bicarbonate calculated by blood gas machine
hco3- increased by increase in pco2
hco3- decreased by increase in acid production or decrease in excretion
actual bicarbonate
calculated with actual h+ and pco2 values
standard bicarbonate
calculated with actual h+ and pco2 of 5.3kPa
only influenced by metabolic effects
base excess
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
when is the patient in respiratory failure
if the po2 is low given the inspired o2
when is it type 1 resp failure
when co2 is low or normal
when is it type 2 resp failure
when co2 is high
what is high h+
acidosis
what is low h+
alkalosis
cause of acidosis - high pco2
respiratory
cause of acidosis - standard bicarbonate low or base excess has large negative value
metabolic
