acid base handling Flashcards
normal pH and H+ conc
7.35-7.45
H+ = 35-45
pH = log1/[H+]
how is H+ produced and excreted
Metabolism of proteins, carbohydrates and fats
-> produce carbon dioxide, water and hydrogen ions
Production of H+
(50-100 mmol/day)
excreted through kidney
what is the acid-base balance
what is a buffer and examples
Buffer – weak acid and its base – used to mop up H ions
why does H+ need to be excreted
because bicarb needed to buffer - and this needs to be regenerated otherwise the capacity is reached
role of the kidney in H+ control
As buffer H – use up bicarb
Bicarb regenerated through carbonic acid (CO2 and water)
Square is renal tubule cell
Bicarb ion is reabsorbed
H+ is produced when regen bicarb – get H into the renal tubles – cant excrete H from luminal surface – because impermeable
Need transport system – this is Na
Bicarb is reabsorbed and H are excreted in return for Na
resp control of acidosis
In health CO2 produced in the tissues is transported via the circulation to the lungs where it is excreted
respiration is controlled by chemoreceptors in hypothalamic resp centre
any rise in CO2 -> resp -> maintain stable CO2
if COPD = chronically raised CO2
how is acid base buffered in the blood
In RBC – main buffer is Hb
CO2 taken by RBC – buffered by Hb
About control conc of hydrogen ions
summary of buffer equation
what is metabolic acidosis and what is it caused by
increased H+ (decreased pH) with decreased bicarbonate
Due to:
1. Increased H+ production e.g. diabetic ketoacidosis
2. Decreased H+ excretion e.g. Renal tubular acidosis
3. Bicarbonate loss ie not mopping it up e.g. intestinal fistula
how do we compensate for metabolic acidosis
reducing amount of CO2 – shift equation to R
Compensated met acidosis – see high H and low CO2 – will try and limit the rise in H ions
Might see very small pH change
If situation where cant excrete CO2 – then hydrogen ion will increase further
what is resp acidosis
high CO2 -> high H+ = low pH and slight increase in bicarb
due to:
* Decreased Ventilation- PE
* Poor Lung Perfusion
* Impaired Gas Exchange
compensation of resp acidosis
increased renal H+ excretion
increased bicarb generation
H+ may return to near normal but pCO2 and bicarbonate remain elevated
slow - only happens in chronic
what is met alkalosis
low H+ = increased pH
high bicarb
due to:
* H+ loss (e.g. pyloric stenosis in children)
* Hypokalaemia – K one of transport agents with Na-K ATPase pump to exclude H – so if that cant work – cant exclude H
* Ingestion of Bicarbonate - antiacids
compensated metabolic alkalosis
This tends to inhibit the respiratory centre
Identified by a rise in pCO2
H+ returns towards normal
This is a limited response – because increase in CO2 trigger resp response to breath off CO2
what is resp alkalosis
low CO2
Due to excessive CO2 hyperventilation
Very rare in clinical practice unless –
* anxiety,
* artificial ventilation/CPAP,
* some rare drugs that stim resp centre.
More co2 expired by lungs -> fall in CO2 -> drive to R – so H used up
compensation of resp alkalosis
If prolonged this leads to decreased renal excretion of H+ and less bicarbonate generation
H+ may return to near normal but pCO2 and bicarbonate remain low
what is the relationship between bicarb, CO2 and pH
causes of breathlessness and where they lie on acidosis-alkalosis scale
bicarb, CO2 and pH in met acidosis
bicarb, CO2 and pH in met alkalosis
blood gas with aspirin OD
Mixed condition associated with aspirin – resp alkalosis and met acidosis
Aspirin stim resp centre -> low co2
And aspirin stim excretion of H ions from kidney
