3s: Acid-Base Flashcards
Acid-base equation and bicarbonate in the proximal tubule
- As you buffer the H+, you use up the [HCO3-] ions
- The [HCO3-] buffer is only effective in the short term
- To maintain normal homeostasis, the kidney needs to excrete H+ ions and regenerate bicarbonate
- Bicarbonate is regenerated through the production of carbonic acid → [HCO3-] is reabsorbed back into the blood
- H+ ions CANNOT pass through the membrane by itself, so a transport system is necessary (Na+/H+ exchange)
Respiratory Control
- Respiration is controlled by chemoreceptors in the hypothalamic respiratory centre
- In health, any increase in CO2 stimulates respiration → maintain stable CO2 concentration
- Red blood cell buffer:
- The buffer in RBCs is hb
CO2 will be taken up by RBCs and it is buffered by hb, thereby controlling the concentration of H+ ions
ABG parameters
Metabolic acidosis
As soon as [H+] increases, your body will try to compensate by increasing RR and blowing off more CO2
In a compensated metabolic acidosis, you will see a low pCO2
Respiratory acidosis
- The primary abnormality is increased CO2 producing increased H+ (decreased pH) and a slight increase in HCO3
- This may be due to:
- Decreased ventilation (not necessarily RR)
- Poor lung perfusion
- Impaired gas exchange
- Compensation:
- Over a few days, this leads to increased renal excretion of H+ combined with generation of bicarbonate
- H+ may return to near normal but pCO2 and bicarbonate remain elevated
Metabolic alkalosis
- The primary abnormality is decreased H+ (increased pH) with increased HCO3
- This may be due to:
- H+ loss (i.e. pyloric stenosis)
- Hypokalaemia – cannot excrete H+
- Ingestion of bicarbonate
- Compensation:
- This tends to inhibit the respiratory centre (identified by a rise in pCO2)
- H+ may then return towards normal (as CO2 rises in the blood, and thus H+ levels)
Respiratory alkalosis
- This may be due to hyperventilation:
- Voluntary
- Artificial ventilation – be careful to identify this
- Stimulation of the respiratory centre
- If this mechanism is prolonged (chronic resp. alkalosis), this can lead to decreased renal excretion of H+ and less bicarbonate generation H+ may return to normal but pCO2 and bicarbonate will remain low
Summary
metabolic acidosis with partial respiratory compensation
metabolic alkalosis with partial respiratory compensation
- Other test results indicate renal failure, but the underlying problem is pyloric stenosis
- The loss of HCl leads to metabolic alkalosis
- Loss of fluid leads to dehydration (raised urea, creatinine and total protein)
- Dehydration stimulates the renin-angiotensin system
- The low potassium results from gastric and renal losses
respiratory alkalosis with partial metabolic compensation
- = respiratory acidosis with full metabolic compensation
- Low O2 shows a low respiratory effort tends to an acidosis
- Hx shows a 72yo man with long history of COPD on diuretics for cardiac failure with low potassium
- This hx lends you to think this is a respiratory-based acidosis
- mixed respiratory alkalosis and metabolic acidosis
- This classically happens with aspirin overdose:
- Stimulating RR resp. alkalosis
- Kidneys excretion of H+ ions met. acidosis
- This classically happens with aspirin overdose:
mixed respiratory and metabolic acidosis
Summary of causes
ABG steps
ABG steps
[H+] formula
Osmolar gap formula
2(Na+K) + G + U
in mmol/l
Normal osmolar gap = < 10
An elevated osmolar gap provides indirect evidence for the presence of an abnormal solute
The osmolar gap is increased by extra solutes in the plasma (e.g. alcohols, mannitol, ketones, lactate)
Can be raised in advanced CKD due to retained small solutes
Helpful in differentiating the cause of an elevated anion gap metabolic acidosis
mnemonic for elevated anion gap metabolic acidosis: KULT
Ketoacidosis (DKA, alcoholic, starvation)
Uraemia (renal failure)
Lactic Acidosis (shock, ischaemia, sepsis)
Toxins (ethylene glycol, methanol, paraldehyde, salicylate)
Drugs = metformin, aspirin
