9 - Acid Base Balance Flashcards
What is the normal pH of blood?
- 35 - 7.45
- 5 - 35.5 nmol per litre H+
What is more dangerous, alkalemia or acidaemia?
Alkalaemia
What pH range causes high mortality in alkalosis and why?
Reduces solubility of Ca salts so more free Ca leaves the ECF to bind to bones and proteins. Hypocalcaemia leads to excitable nerves, paraesthesia and tetany
- Paraesthesia and tetany above 7.45
- 45% mortality at 7.5
- 80% mortality at 7.65
What pH range causes high mortality in acidosis and why?
High H+ affects enzyme function and leads to K+ movement out of cells so hyperkalaemia leading to arrythmias.
- Effects seen at 7.1
- Life threatening below 7
What is the main buffer system for pH in the ECF?
- Carbon Dioxide/Hydrogen carbonate system
- pCO2 determined by ventilation* so disturbed by respiratory disease
- HCO3- determined by kidneys* so disturbed by metabolic or kidney disease
How do the kidneys maintain plasma pH in general terms?
- Variable recovery of HCO3- produced by RBC
- Secretion of H+
What parameters change to get the following outcomes in the blood:
- Respiratory acidosis
- Respiratory alkalosis
- Metabolic acidosis
- Metabolic alkalosis
- Resp acid: increased pCO2
- Resp alk: decrease pCO2
- Met acid: decreased HCO3- due to reaction with metabolic acids, e.g lactate and ketoacids
- Met alk: increased HCO3-
How does the body compensate for the following:
- Respiratory acidosis
- Respiratory alkalosis
- Metabolic acidosis
- Metabolic alkalosis
- Respiratory acidosis: kidneys retain more HCO3-
- Respiratory alkalosis: kidneys lose more HCO3-
- Metabolic acidosis: hyperventilation
- Metabolic alkalosis: limited by the hypoxia that comes with hypoventilation
How do we stop HCO3- depleting in the body when the body produces metabolic acids like lactate that react with HCO3- ?
- Kidneys recover all filtered HCO3- (80% PCT and 15% DCT in intercalated cells)
- PCT makes HCO3- from AA putting NH4+ onto urine
- DCT makes HCO3- from CO2 and H2O and the H+ is buffered by ammonia and phosphate
How is HCO3- in the kidney produced?
- H+ ions actively secreted in the DCT
- H+ buffered by phosphate (titratable) and ammonia
What is the major adaptive response of the kidney to an increased acid load?
- Production of NH3 from glutamate that moves throughout interstitiums
- H+ actively pumped into lumen of DCT and CT
- H+ reacts with NH3 to make NH4+ which is excreted in urine
- Allows HCO3- to be reabsorbed to buffer and loses H+
What is the minimum pH of urine?
- 4.5
- All HCO3- has been recovered
- Some H+ in the urine buffered by ammonia to ammonium and phosphate to stop urinary tract being damaged
What can happen to potassium levels in alkalosis and acidosis?
Hyperkalaemia can cause metabolic acidosis or the acidosis can cause hyperkalaemia etc.
Why does hyper/hypokalaemia lead to acidosis/alkalosis?
What will the following blood parameters look like:
- Compensated respiratory acidosis
- Compensated respiratory alkalosis
- Compensated metabolic acidosis
- Comp Resp Acidosis: high pCO2, high HCO3-, normal pH
- Comp Resp Alkalosis: low pCO2, low HCO3-, normal pH
- Comp Met Acidosis: low HCO3-, low pCO2, normal pH
What is the anion gap and what can it tell us?
- Difference between measure cations and ions
- Normal 10-18 mmol/L
- Gap increased if HCO3- is replaced by ions other than Cl-, e.g metabolic acids
- If metabolic acidosis but no change in ion gap then this is a renal cause as not making enough HCO3- but replaced by Cl-
If the pH drops due to a metabolic acidosis what processes occur to correct this?
- Peripheral chemoreceptors detect
- Increase ventilation
- Decreased pCO2
What conditions can lead to metabolic and respiratory acidosis?
Respiratory:
- Type 2 resp failure with low pO2 and high pCO2
- Severe COPD
- Severe asthma
- Drug OD
- Neuromuscular diseases
(chronic are compensated to near normal pH by HCO3-)
Metabolic:
Increased anion gap:
- Ketoacidosis in diabetes
- Lactic acidosis, poor tissue perfusion
- Uraemic acidosis in advanced renal failure so reduced acid seccretion
Normal anion gap:
- Renal tubular acidosis
- Persistant diarrhoea (replaced by Cl-)
What conditions can lead to metabolic and respiratory alkalosis?
Respiratory:
- Hyperventilation in panic attack/anziey
- Type 1 Resp failure leading to chronic hyperventilation but compensated
Metabolic:
- Severe vomiting or mechanical drainage of stomach as HCO3- produced in response to H+ in stomach but no H+
- Potassium depletion/excess mineralcorticoid excess
- Certain diuretics, e.g loops
What is renal tubular acidosis?
- Type 1 (distal) = inability to pump out H+
- Type 2 (proximal) = issues with HCO3- reabsorption
RARE
What can be an issue with correcting metabolic alkalosis e.g in persistent vomiting?
- Increased HCO3- so just excrete more
- HOWEVER: if patient is volume depleted then their capacity to lose HCO3- is reduced due to high rate of Na+ recovery to raise volume. In PCT
What does metabolic alkalosis do to potassium levels in the blood?
If pCO2 is high, HCO3- is high and pH relatively normal, what is this called?
Compensated respiratory acidosis as can’t have compensated metabolic alkalosis
If pCO2 is low, HCO3- is low and pH relatively normal, what is this called?
- Compensated resp alkalosis or compensated metabolic acidosis
- If no respiratory disease or altitude exposure unlikely to be respiratory
- Check anion gap as this will be increased in metabolic acidosis
For each set of ABG results, state the acid base status:
How should you treat someone with hypoxia and chronic hypercapnia?
- Hypercapnia would occur as the central chemoreceptors set to a new high pCO2 (by choroid plexus)
- If given oxygen their peripheral chemoreceptors detect increase in pO2 and lower respiratory rate but this raises the pCO2
