acid-base balance Flashcards
normal pH of aterialised blood
7.4
sources of H+
respiratory acid
metabolic acid
respiratory acid
CO2 + H2O –> carbonic acid –> H+ and bicarbonate
metabolic acid sources
a) inorganic acid e.g. S containing amino acid, phosphoric acid from phospholipids
b) organic acids: fatty acids, lactic acids
major source of alkali
oxidation of organic anions such as citrate
buffer
minimise change in pH when H+ ions are added or removed
normal value and range ph
- 4
7. 37-7.43
normal value and range bicarbonate
24
22-26
what controls elimination of H+ from body
kidneys
this excretion is coupled to the regulation of plasma [HCO3-]
compensatory mechanisms
bicarb - renal
CO2 - resp
other buffers in ECF
plasma proteins
dibasic phsophate
primary intracellular buffers
proteins
organic and inorganic phosphates
haemoglobin (in RBCs)
how does increase in H+ lead to hyperkalaemia
buffering H+ by ICF buffers cn cause change in plasma electrolytes need to maintain electrochemical neutrality so must be exchanged for cation K+
how does kidney regulate [HCO3-]
- reabsorbing filtered bicarb
- generating new bicarb
both these processes depend on active H+ secretion from tubule into lumen
mechanism of HCO3- reabsorption
- active H+ secretion
- coupled to passive Na+ reabsorption
- filtered HCO3- reacts w H+ –> H2CO3 –> H2O + CO2
- CO2 is freely permeable and enters cell
- in cell CO2 –> H2CO3 –> H+ and HCO3-
- H+ ions are source of secreted H+
- HCO3- pass into peritubular capillaries with Na+
where does bulk of bicarb reabsorption take place
proximal tubule
is there excretion of H+ ions during HCO3- reabsorption?
no
minimum urine pH
4.5-5
maximum urine pH
8
titratable acidity
H+ buffered in urine
several weak acids an bases act as buffers - mostly dibasic phosphate, hydrogen phosphate and also uric acid and creatiine
why is urine buffering called titratable acifity
because its extent is measured by amount of NaOH needed to titrate urine pH back to 7.4 for a 24hr sample
why is tirtatable acifiy important
generates new bicarbonate and excretes H+
mechanism titratable acidity
- Na2HPO4 in lumen. One Na+ reabsorbed in exchange for H+. Monobasic phosphate removes H+ from body
- new HCO3- is indirectly from CO2 from blood. It enters tubule cell combines w water to form carbonic acid which dissociates to yeild H+ (secreted) and new bicarbonate which passes with Na+ into peritubular capillaries
where does titratable acidity predominanly occur
distal tubule
what is titrtable acidity dependent on
PCO2 of blood
why is distal tubule site for titratable acidity
because un-reabsorbed dibasic phosphate becomes highly concentrated by removal of volume of filtrate
ammonium excretion
major adaptive response to an acid load
generates new HCO3- and excretes H+
differential solubility basis of ammonium secretion
NH3 is lipid soluble
NH4+ is not
what is NH3 produced by
deamination of amino acids, primarily glutamine, by action of renal glutaminase within renal tubule cells
mechanism of ammonium excretion
- NH3 moves out into tubule lumen where it combines with secreted H+ ions to form NH4+ which combines with Cl- ions (from NaCl) to form NH4Cl which is excreted
- source of secreted H+ is CO2 from blood
- new HCO3- passes with Na+ ions into pertibular capillaries
what is activity of renal glutaminase depedent on
pH
when intracellular pH falls increase renal glutaminase acitivty and so more NH4+ produced and excreted
main adaptive response of kidney to acid loads
ability to augment NH4+ production
takes 4-5 days to reach maximal effect as required inc protein synthesis
also takes time to switch off when there is excess alkali
what do respiratory disorders effecr
PCO2
what do renal disorders effect
HCO3-
respiratory acidosis
pH has fallen due to respiratory change, so PCO2 must have increased
results from reduced ventilation and so retention of CO2
acute causes of respiratory acidosis
drugs which depress medullary resp centres e.g. opiates
obstruction of major airways
chronic causes of respiratory acidosis
lung disease e.g. bronchitis, emphysema, asthma
resp acidosis: response
need to protect pH so need to increase [bicarb]
renal compensation protects pH but doesn’t correct original disturbance, only restoration of normal ventilation can remove primary disturbance
respiratory alkalosis
alkalosis of respiratory origin so must be due to fall in PCO2 and this can only occur through increased ventilation and CO2 blow off
acute causes of resp alkalosis
voluntary hyperventilation
aspirin
first ascent to altitude
chronic causes of resp alkalosis
long term resifence at altitide
response to resp alkalosis
dealt with by HCO3- reabsorptive mechanism
if less PCO2 less H+ available for secretion and so less filtered load of bicarb reabsorbed and is lost in urine
venilation must be normalised to correct disturbace
metabolic acidosis
acidosis of metabolic origin must be due to decrease in bicarb
increase buffering of H+ or direct loss bicarb
to protect pH, PCO2 must be decreased
causes of metabolic acidoss
- inc H+ production: diabetic ketoacidosis, lactic acidosis
- failure excrete normal H+ dietary load (renal failure)
- loss bicarb in diarrhoea
metabolic acidosis response
stimulates ventilation so PCO2 falls
normally kidneys correct disturbance by restoring bicarb and getting rid H+
increase mtabolic H+ in body: what occurs
- immediate buffering in ECF and then ICF
- resp compensation within minute
- renal correction of disturbance takes longer to develop full response
resp compensation delays renal correction but protects pH
metabolic alkalosis
inccrease bicarbone
need to increase PCO2 to protect pH
causes of metabolic alkalosis
- inc H+ ion loss - vomiting
- inc renal loss H+ - aldosterone excess
- excess administration of bicarb if pt has renal impairment
response to metabolic alkalosis
increase PCO2 protects pH
increased bicarb exceeds level of H+ secretion to reabsorb it, so even in presence PCO2 increaed, excess is lost in urine
