Acid-Base Balance #2 Flashcards Preview

Genitourinary System > Acid-Base Balance #2 > Flashcards

Flashcards in Acid-Base Balance #2 Deck (17)

What is base excess?

The amount of acid or base needed to restore the pH to 7.4 (at a pCO2 of 5.3kPa) Calculated from pH, pCO2 and haemaglobin and it reflects ALL buffers in plasma (not just HCO3-)


Normal base excess is?

Normal base excess = 0 (-2 to +2)
BE + in metabolic alkalosis

BE - in metabolic acidosis


This is a patient with chronic lung disease. What kind of acid-base disturbance is this?

On admission: Respiratory acidosis with renal compensation

On Ventilator: Metabolic alkalosis (as the respiratory component is corrected, but the 'compensating' metabolic alkalosis remains, and takes ~3-5 days to return to normal)


Metabolic Acidosis: the anion gap (AG)

AG = (sum of cations) - (sum of main anions)
       = (Na+ + K+)          -  (Cl- + bicarb)
       = (140 + 4)             - (104 + 24)
       = 16 (the left over protein anions!)

Normal range AG = 14-18

Therefore increased AG reflects the presence of unmeasured anions (eg lactate-!)


This shows an anion gap due to metabolic acidosis. Why is it that although 10 lactate was added, it is ony increased by 8??

Because some of the HCO3- is buffering the H+


Most common causes of acidosis with increased AG?

  1. Lactic Acidosis
  2. Ketoacidosis: betahydroxybutyrate is main anion
  3. Renal Failure: only slightly increased AG due to phosphate + sulfate retention


What type of Acid-base disturbance is this? 

What else can we deduce

Metabolic acidosis (low pH, low HCO3-. -BE) with respiratory compensation (low pCO2)


Check lactate, betahydroxybutyrate (ketoacidosis), Ethylene glycol poisoning?




Why are patients with ethylene glycol poisoning given alcohol as treatment??

Ethylene glycol is non-toxic but metabolised → toxic acids via alcohol dehydrogenase.

Ethanol and fomepizole competitively inhibit this 


What type of acid-base disturbace is this?

What further tests should be performed?

Metabolic acidosis with respiratory compensation.

Normal AG therefore normal AG acidosis


  • Check urine pH and NH4+ (if pH high and NH4+ low → RTA)
  • Urine Anion Gap

as urine pH should be <5.5 and NH4+ >100mmol/L this indicates Renal Tubular Acidosis, defects in H+ secretion)



What's normal Anion Gap Acidoses?

Where the acidosis is occuring due to an endogenous acid (not added). 

GI HCO3- loss: poops, fistula

Renal Tubular acidosis (RTA): can't secrete H+, urine pH >5.5 and urine NH4+ not increased

Aldosterone deficiency: addisons disease


Why are those with a Normal AG acidosis hyperchloremic?

When bicarb. is low, extra Cl- needs to be reabsorbed to maintain Na+ balance


What is the linkage between K+ and acid-base?

  1. the general rule is

Acidosis ⇔ hyperkalemia

Alkalosis ⇔ hypokalemia

These cause shifts of H+ or K+ in/out of the cells

** H+ and K+ compete with each other for secretion


What are the 2 exceptions to the potassium and acid-base balance rule?

  1. Diarrhoea (HCO3- and K+ loss)
  2. Renal Tubular acidoses: DT and PT both associated with hypokalemia


Causes of metabolic alkalosis

If you decrease acid and nothing else you still can't get alkalosis without a secondary issue as the kidneys can compensate. If you also lose Cl- then the kidneys cannot remove HCO3


Chloride depletion alkalosis is?

In metabolic alkalosis, the kidney attempts to increase HCO3- loss. If Cl- depletion is present, HCO3- reabsorbtion becomes obligatory to preserve Na+ balance. 

The kidney can't correct the alkalosis until Cl- is replaced


Causes of Cl- depletion: gastric Fluid loss, diuretics (laxitaves and vomiting)


When's it ok to use venous blood for blood gases? (s arterial punctures are painful and more dangerous)

Venous blood useful most of the tim in patient with good perfusion (the pH, HCO3- and BE are identical. NOT good for hypoxia, if pO2 is needed and the patient has circulatory failure.


Venous good bc its rapid! 


artefacts of arterial blood gases

  • Air in blood-gas syringe → falsely low pCO2
  • Delayed seperation of plasma from RBCs