5.17 - Arterial blood gases & acid base regulation Flashcards
What is PO2?
- partial pressure of oxygen
- indicates how much oxygen is dissolved in the arterial blood
- if it is particularly low it can suggest inadequate gas exchange in the lungs
What is PCO2?
- partial pressure of carbon dioxide
- indicates how much CO2 is dissolved in arterial blood
- if particularly high it can suggest inadequate gas exchange in the lungs
What is pH?
- the ‘power of hydrogen’
- describes the acidity, neutrality or alkalinity of the blood
- pH of arterial blood is finely tuned and small deviations can affect oxygen transport and delivery
What is HCO3-?
- plasma bicarbonate
- describes the concentration of bicarbonate dissolved in arterial blood
- if higher or lower than normal this could be evidence of gas exchange imbalance
What is base excess (BE)?
- describes the concentration of bases (predominantly bicarbonate) compared with the ‘expected concentration’
- an exact match is 0, an excess of base is positive and a base deficit is negative
What is PaO2, SaO2 and PaCO2 like in arterial blood?
- PaO2: >10 kPa
- SaO2: >95%
- PaCO2: 4.7-6.0 kPa
What is PaO2, SaO2 and PaCO2 like in venous blood?
- PaO2: 4.0-5.3kPa
- SaO2: ~75%
- PaCO2: 5.3-6.7 kPa
What is pulmonary transit time and gas exchange time, and what do these mean?
- pulmonary transit time: 0.75s - erythrocytes in contact with gas exchange surface for 0.75s
- gas exchange time: 0.25s (O2 moves slowest and takes 0.25s for exchange)
- CO2 is more soluble and is exchanged faster
What are the equations for pH and [H+]?
- pH = -log10[H+]
- [H+] = 10^(-pH)
What is an acid?
Any molecule that has a loosely bound H+ ion that it can donate
What are H+ ions also known as?
Protons (because a H atom with a +1 valency has no electrons or neutrons)
What is the relationship between [H+] and pH?
A greater concentration of H+ ions refers to a lower pH
What is a base?
- an anionic (negatively charged ion) molecule capable of reversibly binding protons (to reduce the amount that are ‘free’)
- H+A- <–> H+ and A-
What is the carbonic acid equilibrium?
- H2O + CO2 <-(carbonic anhydrase)-> H2CO3 <–> H+ + HCO3-
- this relationship is in an equilibrium - increasing something on one side will push the equation in the opposite direction
What is the balance of respiratory acids to metabolic acids in the body?
- 99% respiratory acids (carbonic acid - CO2 cleared by lungs)
- 1% metabolic acids (lactic acid, fatty acids etc from rest of body)
What is the difference in arterial and venous pH?
- arterial pH = 7.4
- venous pH = 7.36
How does the blood react to imbalances?
The blood has enormous buffering capacity that can react almost immediately to imbalances
What are the two methods of corrective compensation for acidosis/alkalosis?
- rapid - changes in ventilation can stimulate a rapid compensatory response to change CO2 elimination and therefore alter pH
- slow - changes in HCO3- and H+ retention/secretion in the kidneys can stimulate a slow compensatory response to increase/decrease pH
What is alkalaemia and acidaemia?
- alkalaemia - higher than normal blood pH
- acidaemia - lower than normal blood pH
What is acidosis and alkalosis?
- acidosis - circumstances that increase [H+] and decrease pH
- alkalosis - circumstances that decrease [H+] and increase pH
How do we get alkalaemia/acidaemia?
- an alkalaemia requires an alkalosis where either acid is lost or increased production/retention of a base
- an acidaemia requires an acidosis where either acid is overproduced/retained or base is lost
How is an acidosis and alkalosis corrected by the body?
- acidosis causes acidaemia which will need an alkalosis to correct
- alkalosis causes alkalaemia which will need an acidosis to correct
What four things do we look at in an ABG interpretation?
- type of imbalance?
- acidosis (or acidaemia) / alkalosis (or alkalaemia) / normal
- aetiology of imbalance?
- respiratory (acidosis or alkalosis) / metabolic (acidosis or alkalosis) / mixed (respiratory and metabolic) / normal
- any homeostatic compensation?
- uncompensated / partially compensated / fully compensated
- oxygenation?
- hypoxaemia / normoxaemia / hyperoxaemia
How do you report an ABG measurement?
CADO
- compensation?
- aetiology?
- disturbance?
- oxygenation?
e.g. uncompensated respiratory alkalosis with moderate hypoxia
What are the ranges for normal base excess (BE)?
- 0 = perfect (observed HCO3- = HCO3- needed for pO2)
- -2 to 2 is the normal range
What are the ranges for high, normal and low pH?
- high: >7.45
- normal: 7.35 to 7.45
- low: <7.35
What are the ranges for high, normal and low PaCO2?
- low: <4.7kPa
- normal: 4.7-6.4kPa
- high: >6.4kPa
What are the ranges for high, normal and low BE?
- low: <-2
- normal: -2 to 2
- high: >2
What are the ranges for high, normal and low PaO2?
- low: <10kPa (mild hypoxia 8-10, moderate hypoxia 6-8, severe hypoxia <6)
- normal: 10 to 13.5kPa
- high: >13.5kPa (rare)
What is the ABG like for uncompensated respiratory acidosis and alkalosis?
- uncompensated respiratory acidosis: pH low, PaCO2 high, BE normal
- uncompensated respiratory alkalosis: pH high, PaCO2 low, BE normal
What is the ABG like for uncompensated metabolic acidosis and alkalosis?
- uncompensated metabolic acidosis: pH low, PaCO2 normal, BE low
- uncompensated metabolic alkalosis: pH high, PaCO2 normal, BE high
What is the ABG like for uncompensated mixed acidosis and alkalosis?
- uncompensated mixed acidosis: pH low, PaCO2 high, BE low
- uncompensated mixed alkalosis: pH high, PaCO2 low, BE high
What is the ABG like for partially compensated respiratory acidosis and alkalosis?
- partially compensated respiratory acidosis: pH low, PaCO2 high, BE high
- partially compensated respiratory alkalosis: pH high, PaCO2 low, BE low
What is the ABG like for partially compensated metabolic acidosis and alkalosis?
- partially compensated metabolic acidosis: pH low, PaCO2 low, BE low
- partially compensated metabolic alkalosis: pH high, PaCO2 high, BE high
What is the ABG like for fully compensated respiratory acidosis / metabolic alkalosis?
pH normal, PaCO2 high, BE high
What is the ABG like for fully compensated respiratory alkalosis / metabolic acidosis?
pH normal, PaCO2 low, BE low
How does uncompensated respiratory acidosis occur?
- sub-optimal ventilation
- less minute ventilation = less fresh air in alveoli
- increase in CO2 in alveoli reduces diffusion gradient = less CO2 blood–>alveoli = more CO2 in blood
- increases CO2+H2O –> H2CO3 –> dissociates into protons which accumulate
- lower pH, increased PaCO2 and normal BE (since correct for the PaCO2)
How is respiratory acidosis compensated for?
- body tries to reduce [H+] by increasing HCO3- to bind H+
- acute phase - CO2 moving into RBC combines with H2O in presence of carbonic anhydrase to form HCO3-, which moves out of cell via AE1 transporter into plasma
- chronic phase - increase HCO3- reabsorption in kidneys
- pH still low but closer to normal, PaCO2 high as long as hypoventilating, BE high since plasma HCO3- higher than expected for the PaCO2
- partially compensated respiratory acidosis
- eventually pH will normalise, PCO2 and BE will remain high (fully compensated)
How does uncompensated respiratory alkalosis occur?
- hyperventilation - increased minute ventilation (e.g. through increase in tidal volume with same breathing frequency) → increases alveolar ventilation
- reduces alveolar PaCO2 and increases concentration gradient for CO2 diffusion out of blood so post-capillary blood has lower than normal CO2
- leftward shift in carbonic acid equilibrium meaning less H+
- higher pH, lower PaCO2, same BE
How is respiratory alkalosis corrected?
- body tries to increase [H+] in blood
- no acute phase, only chronic - reduces amount of HCO3- reabsorbed and more HCO3- secretion in collecting duct
- reduces plasma HCO3- meaning more dissociation of carbonic acid into H+ and HCO3-
- higher pH than normal, PaCO2 low and BE will be low (due to increased HCO3- excretion) - partially compensated
- eventually pH will normalise (fully compensated)
What happens to acid-base homeostasis in diarrhoea?
- lots of HCO3- lost in excretions
- increases H2CO3 dissociated to release more HCO3-
- also increases [H+] which decreases pH, PaCO2 same, BE decreased
What are some other causes of uncompensated metabolic acidosis (apart from diarrhoea)?
- other HCO3- losing conditions
- H+ gaining conditions e.g. increased lactic acid production
How do we compensate for metabolic acidosis?
- H+ conc needs to be reduced
- manipulation of ventilation helps with this- increases in ventilation reduces alveolar PCO2 and increases diffusion gradient of CO2 from blood so reduces systemic arterial PCO2
- this causes carbonic acid equation to shift left to correct the lower PCO2
- causes more H+ and HCO3- to combine to form carbonic acid which will be converted into H2O and CO2
- at this point pH will be low, PCO2 will be low and BE will be low
- this partially compensated metabolic acidosis
- eventually pH will normalise but PCO2 and BE will be lower than normal
- this is fully compensated metabolic acidosis
What happens to acid-base homeostasis in vomiting?
- HCl loss occurs which causes H+ loss
- HCO3- increases as there are less H+ to bind
- ABG shows high pH, normal PaCO2 and high BE (as HCO3- is disproportionately high for the PaCO2)
- uncompensated metabolic alkalosis
What else can cause uncompensated metabolic alkalosis (apart from vomiting)?
- other H+ losing conditions
- HCO3- gaining conditions
How is metabolic alkalosis corrected?
- need to increase H+ conc
- reducing ventilation increases PCO2 conc in alveoli, decreasing diffusion gradient from blood so increasing PCO2 in arterial blood
- this shifts carbonic acid equation to right to correct higher CO2 → this produces more H+ and further increasing HCO3-
- blood gas reads high pH, high PCO2 and high BE
- this is partially compensated metabolic alkalosis
- at one point, the pH normalises, PCO2 and BE are higher than normal
- this is fully compensated metabolic alkalosis
