L23 Acid and Base 1 Flashcards
What are the sources of acid produced in the body and examples of acid.
- Volatile acid: produced by oxidative metabolism
- CO2 and carbonic acid in equilibrium. H2O + CO2 H2CO3 (carbonic acid) H+ + HCO3- - Non-volatile: produced by protein catabolism: not in equilibrium with volatile component so can’t be excreted by lungs
- eg. oxidation of sulphur containing amino acid residues to make H2SO4
- minority
What are the 3 ways and speed we deal with increased acid to maintain physiological pH at 7.37-7.42 - what is the difference for non-volatile and volatile
- Immediate for non volatile: (s-min) bicarbonate buffer system (adding H+ to HCO3-) + other buffers
- Immediate for volatile: Lungs excrete CO2 via gas exchange
- Hr-days for non volatile: excretion via kidneys
What are situations for volatile/non volatile acid production to increase
Vol
-bigger size, more exercise
Non-Vol
- ischaemia
- extreme exercise: lactic acid formation
- DKA: acetoacetic acid, b hydroxybutyric acid
What are the 4 systems for buffering on a non-volatile acid.
- Bicarbonate buffering system: mainly plasma, interstitial fluid
- Red cells: effective short term (s-min)
- H+ combine intracellular proteins,Organic phosphates in tissue and bone.
- H+ transported across cell membrane in exchange for Na+ or K+
What is the Isohydric principle and what type of fluid is it accurate for
For a homogenous solution of multiple buffer systems at equilibrium: the pH can be evaluated from the status of any buffer system.
This is only accurate for blood/interstitial phases not rlly for intracellular phase which isn’t same composition as ECF.
How does pH change when bicarbonate is buffering non volatile acid (give hasselbach equation) vs when buffering CO2
- Non volatile acid = adding extra H+ means that bicarb falls down, reducing pH. This is based on a curve depending on PCO2.
pH= 6.1 + log (HCO2-/ (solubility of CO2:0.03 x PCO2)
- Volatile acid: CO2–> increases the plasma HCO3 (and H+) which decreases the pH
Describe the steps of CO2 from tissue being buffered at the capillary bed by the RBC (and plasma)
- CO2 diffuses into plasma
a) some dissolves
b) some buffered by non-bicarbonate buffers (pi and protein) - (c) most follows conc gradient into the RBC where a) some dissolve
b) some join with Hb-NH2 to make carbamino Hb and H+
3.(c) Some combines with H2O to make H2CO3 (via Carbonic anhydrase)
- This dissociates into HCO3- and H+.
The HCO3- shifts down conc gradient to the plasma, and Cl- is exchanged
5.The H+ from the dissociation + the H+ from carbaminoHb
is buffered by Histidine (on deoxy Hb).
What happens when Hb goes to the capillaries and how does this relate to the haldane effect
In capillaries Hb becomes reduced to deoxyHb- a better base-because of the falling O2.
Deoxy Hb is
- 3.5 x more effective at forming carbamino compounds
- better buffer than oxyHb thus improving CO2 carriage
Haldane e: Increased ability of blood to carry CO2 when oxyHb is low.
How does reduced haematocrit effect the blood buffer line (linear relationship between CO2 HCO3- conc and resultant pH)
If you reduce Hb you reduce buffering capacity so for a given CO2, the HCO3- is a little higher –> greater acidosis
What does base excess and base deficit mean, what are potential causes, and how is this measured in real life
Base excess means there is higher than normal HCO3- in the blood mopping up the H+ ions.
Indicates
-1’ metabo alk, compensated resp acidosis
Base deficit: (- base excess) If lower than normal HCO3- so
- 1’ metab acidosis, compensated resp alkalosis
This is calculated from henderson-hasselbalch equation from Arterial blood gas CO2 values so if thats wack can’t trust it
Give examples of acute conditions that could lead to metabolic and respiratory acidosis and alkalosis and the mechanics
Resp. acid: asthma, copd (obstructive conditions): prevent release of CO2
Resp: alk: hyperventilation: increased excretion of CO2
Metab acid: diarrhoea: failure to reabsorb + active loss of HCO3-
Metab alk: vomiting: loss of gastric acid
How do you differentiate a metabolic from respiratory acidosis, alkalosis
- Firstly look at pH to determine if acid or alk
- Then look at CO2. If normal then likely 1’ metabolic.
- Look at HCO3- changes. Likely normal in 1’ resp.
- Base excess changes indicate metab
Where are normal blood samples taken from and which is more acidic : arterial or venous blood.
What do central chemoreceptors respond to vs peripheral more to increase ventilatory drive
Normal samples taken from venous or capillary blood.
Venous blood more acidic: every transport around the body is a shift towards acidosis
Central chem: hypercapnia (strong)
Peripheral: hypoxia.
What 3 jobs need to be done to control bicarbonate
- Reabsorption of HCO3- filtered by the kidney. and secretion of H+ by nephron - amount alterable depending on acidosis/alkalosis state
- Regeneration of all HCO3- lost in buffering non-volatile acids
- Removal of fixed acids incorporated into non-bicarb buffer systems
How is HCO3- reabsorbed by the kidney, where and steps
Proximal tubule lumen
1. HCO3- free and some dissociated from NaHCO3 join with H+ excreted by Na/H+ antiporter (Na+ has gone into the cell and been exchanged - gradient driven by NaKATPase)
- H2CO3 is then converted to H2O and CO2 by Carbonic anhydrase on cell surface.
- Water is excreted, CO2 follows conc gradient into cell where it joins with water to make H2CO3 inside cell
- This equilibrates into H+ which is excreted via exchanger and HCO30 which is transported out into interstial fluid–> plasma via the Na- HCO3 symporter
