Lecture 11: Acid-Base Balance #2 Flashcards

1
Q

What is base excess?

A

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-)

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2
Q

Normal base excess is?

A

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

BE - in metabolic acidosis

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3
Q

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

A

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)

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4
Q

Metabolic Acidosis: the anion gap (AG)

A

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-!)

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5
Q

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

A

Because some of the HCO3- is buffering the H+

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6
Q

Most common causes of acidosis with increased AG?

A
  1. Lactic Acidosis
  2. Ketoacidosis: betahydroxybutyrate is main anion
  3. Renal Failure: only slightly increased AG due to phosphate + sulfate retention
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7
Q

What type of Acid-base disturbance is this?

What else can we deduce

A

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

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

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8
Q

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

A

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

Ethanol and fomepizole competitively inhibit this

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9
Q

What type of acid-base disturbace is this?

What further tests should be performed?

A

Metabolic acidosis with respiratory compensation.

Normal AG therefore normal AG acidosis

Tests:

  • 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)

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10
Q

What’s normal Anion Gap Acidoses?

A

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

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11
Q

Why are those with a Normal AG acidosis hyperchloremic?

A

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

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12
Q

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

A
  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

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13
Q

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

A
  1. Diarrhoea (HCO3- and K+ loss)
  2. Renal Tubular acidoses: DT and PT both associated with hypokalemia
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14
Q

Causes of metabolic alkalosis

A

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- .

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15
Q

Chloride depletion alkalosis is?

A

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)

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16
Q

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

A

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!

17
Q

artefacts of arterial blood gases

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