4.1 Carbon dioxide in blood Flashcards
Carbon dioxide forms
- Dissolved co2 : 10%
- HCO3- : 60%
- Carbamino-Hb compound : 30%
Buffer
- Buffers are compounds which are able to release hydrogen ions such that they reduce slight alterations to the pH
- CO2 has a major role in controlling blood pH in a normal range of 7.35-7.45
Bicarbonate buffer system
CO₂ + H₂O H₂CO₃ H⁺ +HCO₃⁻
• [Dissolved CO₂] = 1.2mmol/L
• [HCO₃⁻] = 25 mmol/L
• [HCO₃⁻]:[CO₂] is maintained so that net reaction/equilibrium is towards CO₂
Dissolved CO₂
• [CO₂] dissolved = solubility factor x pCO₂
- Solubility factor for CO₂ = 0.23 mmol/L/kPa
- pCO₂ of arterial blood = 5.3 kPa
Henderson Hasselbalch Equation
pH = pKa + log ([conjugate base]/[weak acid])
• pKa at 37 degrees = 6.1
• Weak acid = [CO₂]
- Calculated by pCO2 x solubility constant (0.23)
• Conjugate base = [HCO₃⁻]
Ventilation affecting pCO2
- pCO2 of alveoli determines arterial pCO2
- Alveolar pCO2 controlled by altering rate of breathing
- Hyperventilation - causes [CO₂] to drop as increased expiration out of the body
- Hypoventilation - causes [CO₂] to increase as not expired enough
Bicarbonate production in RBC’s
- Carbon dioxide from tissues enters RBC’s
- Reacts with water to form bicarbonate and hydrogen ions
- Reaction sped up with carbonic anyhydrase - only present in RBC’s
- Reaction proceeds in forward direction to form bicarbonate to prevent build up of co2
- Bicarbonate is transported out of RBC via chloride:bicarbonate antiporter
- H+ ions formed are bound to the haemoglobin - to keep [H+] low and to keep equilibrium in forward direction
Bicarbonate concentration control
- Bicarbonate formed in RBC’s - reaction equilibrium controlled by H+ binding to Hb
- Kidney controls amount of bicarbonate by varying excretion - also can create more bicarbonate
Venous blood
- pCO2 is higher in venous blood - directly from metabolically active tissues
- More dissolved co2 will be found
- Most co2 is converted to bicarbonate on the way to the lungs to be eliminated
Haemoglobin buffering
- H+ ions can bind to Hb as to prevent build up H+ ions - acidosis
- Buffering of H+ depends on Hb level of oxygenation
- The more oxygenated Hb is (R state) - the less H+ ions will bind
- Therefore H+ binding is much lower at lungs - haemoglobin is saturated with oxygen
Why is CO2 transported to lungs as HCO3?
- At tissues to venous blood - oxygen saturation of Hb is low (T state)
- This allows more H+ ions to bind thus lowering [H+]
- pCO2 also increases in venous blood due to metabolically active tissues
- This drives reaction to the right (towards HCO3 + H+ )
- More bicarbonate is formed in RBC’s and transported into venous blood
When venous blood arrives at lungs
- Hb picks up oxygen at lungs and goes into R state
- Therefore gives up H+ ions/co2 (carbamino compounds)
- Increase in [H+] causes backward shift towards co2 + H20
- These products are exhaled
Carbamino compounds
- co2 can bind directly to amine group on globin of Hb
- This binding contributes to CO2 transport - not part of acid-base balance
- Carbamino compounds formed more readily at tissues - where [co2} is higher and less oxygen bound Hb
- T state Hb bind better to co2 - when oxygen saturation is lower
Haldane effect
- The co2 given up at lungs as Hb becomes oxygen rich - dissolution of carbamino compound
- Amount of co2 transported is affected by degree to which blood is oxygenated
Interpret acid-base status of following ABG.
pH: 7.48 (7.35-7.45) pO2: 13.5 kPa (10–14) pCO2: 6.2 kPa (4.5–6.0) HCO3: 34 mmol/L (22-26) Hb saturation: 99% (95-100)
- pH> 7.45 - alkalosis
- pCO2 elevated - therefore NOT respiratory
- Bicarbonate elevated - therefore metabolic alkalosis
- pCO2 elevated - compensation
- pH still abnormal - therefore partial compensation
We are very limited in respiratory compensation for
metabolic alkalosis because when we hypoventilate
oxygen falls - so pCO2 can only be elevated
limited amount.
