8 - Acid Base 1 Flashcards
What is the definition of pH
pH = -log10 (H+) where H+ is mol/L (H+) = 10-pH
What is the normal ECF pH
7.4 (7.35-7.45)
Crucial for enzyme and organ function
ph below 7.35
acidaemia
ph above 7.45
alkalaemia
Difference between alkalaemia/acidaemia and alkalosis/acidosis
alkalaemia/acidaemia is that STATE of the blood pH while alkalosis/acidosis are PATHOLOGICAL processes that CHANGE pH
Acidosis
ph is usually an acidaemia i.e. less than 7.35 (but may not be if more than 1 acid-base disorder is present), 7.2 is severe acidosis and less than 6.9 is incompatible with life
What is a buffer
A buffer minimises pH changes due to either the addition or removal of H+ ions temporarily (the H+ is NOT eliminated)
When does the pK of a buffer = the pH
When the conc of A- and HA are equal as
pH = pK +log(A-/HA)
What are some buffers that are present in the blood?
- Bicarbonate: H+ + HCO3- > H20 + CO2
2. Proteins (albumin, HB): H+ + A- > HA
How do proteins act as buffers?
H+ is added onto the COO- and/or the NH3
With the bicarbonate buffer system how is pH determined>
Henderson Hasselbach equation
pH = 6.74 + log(HCO3-/pCO2)
What is the respiratory control of pCO2
metabolism creates a lot of co2, and the ventilation rate controls the pCO2. Low pH stimulates ventilation to increase excretion of CO2
Incr pco2 causes … decreased pco2 causes…
AcidOSIS and alkalosis
How are blood gas measurements made and what do they measure
- venous or arterial blood collection
- pH, pCO2, pO2 measured directly via blood gas analyser
- can then calculate HCO3- and base excess
What is normal HCO3- and pCO2?
HCO3- : 24
pCO2= 5.3
What are the 2 urinary buffers
- Phorphoric acid
- Ammonium ions
> allow H+ to be excreted
example of a resp acidosis
Severe asthma attack where can’t excrete co2
example of resp alkalosis
Panic attack/hyperventilation (also most asthma attacks)
Example of metabolic acidosis
Increase in acid load that exceeds the kidney’s ability to excrete acid and so HCO3- tries to buffer it and is depleted.
3 causes of metabolic acidosis
- Increased acid producion
- lactic acidosis (hypoxia, anaerobic metabolism, poor perfusion due to hypotension or ischaemia, CO/cyanide poisoning
- diabetic ketoacidosis due to beta-hydroxybutyric acids and acetoacetic acids - Decreased acid secretion due to renal failure or renal tubular acidosis
- Low HCO3-
- vomiting, severe diarrhoea, ileostomy
Why may you see a reduction in pCO2 despite ph being low and hco3- being low?
Degree of compensation for the metabolic acidosis
Describe resp compensation seen in metabolic acidosis
The low pH stimulates ventilation which lowers pCO2 (acidotic breathing)
Breathing symptoms can be a sign of what 2 things
Either the primary problem or compensation
Role of kidney in the acid-base balance?
- can generate new HCO3-
- reabsorbs HCO3-
- gets rid of acid by attaching it to ammonia or phosphoric acid
Why do kidneys excrete acid
To balance the non-volatile (non-CO2) acid that is generated through metabolism.
Net Acid Secretion by the kidneys
= urinary ammonium + urinary titratable acid - urinary HCO3- (NONE in normal state) x volume
What are the 3 main renal processes in acid-base balance
- HCO3- reabs
- generation of new HCO3-
- H+ secretion in the DT and CD primary by NH4+ and H3PO4
- Bicarbonate reabsorption?
- Most (80%) is reabsorbed in the PT
- na+ follows to maintain osmol
- New HCO3- generation?
CO2 from the ECF enters the cell and is converted by carbonic anhydrase in the cytoplasm and brush border of PT cells > H2CO3 > HCO3 + H+
The HCO3- is then released into the ECF and the H+ is secreted in to the lumen/urine
What is Acetazolamide
CA inhibitor and so causes metabolic acidoses
Via what 2 pumps is H+ actively excreted?
H+ ATPase and Na/H+ exchanger
How is new HCO3- generated?
CO2 from the blood is converted via CA into HCO3- + H+. HCO3- is reabsorbed while the H+ is either directly secreted or combined with titratable acids i.e. phosphate or ammonia
What drives H+ excretion in the DISTAL tubule and CD?
ALDOSTERONE drives expression of ENaC channels on the lumenal surface. This causes Na to be reabsorbed from the lumen into the blood and in exchange you get SECRETION of both K+ and H+
Renal handling of NH4+?
- ammonium is generated from glutamine metabolism in PT cells and secreted into the lumen and 2 HCO3- are also made and reabsorbed
- most is reabsorbed in the TAH
- in the CD diffusion trapping occurs where H+ combines with NH3 to secrete NH4+
What is the kidneys response to acidosis?
- Increased HCO3- and H+ transport along the nephron
- Increased ammoniagenesis
- Increased availability of urinary buffers
> increased acid secretion of which most is driven by NH4+
What renal compensation do you see in resp acidosis?
See a gradual increase in HCO3- reabsorption and generation over a couple of days.
Also excrete more acid primarily through ammonia
