Lecture 16

Question 1

Describe the 3 step approach to interpreting acid-base data?

Answer 1

1. Is it an acidosis or an alkalosis? Look at the pH.
2. Is the primary disturbance respiratory or metabolic? Look at the pCO2, bicarbonate and base excess.
3. Is it compensated or not? Look at the non-primary component.

Question 2

What is the primary change for metabolic acidosis?

Answer 2

Decrease in bicarbonate. 1.6kPa decrease in pCO2 for every 10mmol/L decrease in bicarbonate. If you re outside this, then it implies that a mixed process is going on.

Question 3

What is the primary change for metabolic alkalosis?

Answer 3

Increase in bicarbonate. 0.93kPa increase in pCO2 for every 10mmol/L increase in bicarbonate.

Question 4

What is respiratory acidosis divided into?

Answer 4

There is still an increase in pCO2 for both.
Acute = 1mmol/L increase in bicarbonate for every 1.3kPa increase in pCO2.
Chronic = 3.5mmol/L increase in bicarbonate for every 1.3kPa increase in pCO2.
Basically in acute you get a smaller increase in bicarbonate for the same amount of increase in pCO2.

Question 5

What is respiratory alkalosis divided into?

Answer 5

There is still a decrease in pCO2 for both.
Acute = 2mmol/L reduction in bicarbonate for every 1.3kPa decrease in pCO2.
Chronic = 4mmolL reduction in bicarbonate for every 1.3kPa decrease in pCO2.

Question 6

What is base excess?

Answer 6

The amount of acid or base needed to restore pH to 7.4 (at a pCO2 of 5.3kPa). It reflects all buffers in plasma (not only bicarbonate).

Question 7

What is normal base excess?

Answer 7

0 (-2 to +2).

Question 8

What is base excess in metabolic alkalosis?

Answer 8

It is positive.

Question 9

What is base excess in metabolic acidosis?

Answer 9

It is negative.

Question 10

Describe a patient with chronic lung disease on a ventilator in ICU?

Answer 10

pH has increased, pCO2 has stayed the same, bicarbonate has increased and base excess has increased. Metabolic alkalosis. This has occurred because when on a ventilator (ventilation has increased), the amount of CO2 in the blood has decreased. On admission the patient came in with respiratory acidosis with renal compensation (decrease pCO2 to try and decrease bicarbonate); however the metabolic alkalosis still remains (as it takes 3-5 days for change in renal compensation for metabolic alkalosis to occur).

Question 11

What is the anion gap?

Answer 11

It is the sum of the cations minus sum of anions.

AG = (Na + K) - (Cl - bicarb)
= (140 + 4) - (104 +24)
= 16.

The normal AG range is 14-18.

Question 12

What does the normal AG reflect?

Answer 12

Mainly the unmeasured protein anions. An increased AG indicates the presence of unmeasured anions e.g. if you add an acid to your blood.

Question 13

How does the AG work?

Answer 13

If you add acid i.e. lactic acid.
Na + K = Cl + HCO3 + Protein + lactate
140 + 4 = 104 + 16 + 14 + 10
AG = 24 (increased from 16).

Added H+ is buffered by bicarbonate and protein buffers.

Question 14

What are the common causes of acidosis with increased anion gap?

Answer 14

1. Lactic acidosis - poor perfusion, hypoxia.
2. Ketoacidosis - beta-hydroxybutyrate is the main anion.
3. Renal failure - slightly increased AG: retention of phosphate and sulphate.

Question 15

What are the rare causes of acidosis with increased anion gap?

Answer 15

1. methanol poisoning (formate anion).
2. Ethylene glycol poisoning (glycol ate, glyoxylate and oxalate anions).
3. Salicylate (aspirin) oversode.
4. Organic acidurias (children e.g. methylmalonic acuduria).
5. Pyroglutamic acuduria (adults).

Question 16

Describe the case with a 42yo man admitted with semi-comatose with seizures?

Answer 16

pH has decreased, bicarbonate has decreased, pCO2 has decreased as well and base excess has decreased. Metabolic acidosis with respiratory compensation. The AG is 34 (very elevated).

Question 17

Why do you give alcohol to a patient who is suspected to ethylene glycol poisoning?

Answer 17

Ethylene glycol is non-toxic itself by it is metabolised to glycol and oxalic acids (toxins) by alcohol dehydrogenase. Ethanol and the drug fomepizole competitively inhibit this enzyme and are used in this treatment.

However, you need to give ethanol before ethylene glycol has been fully metabolised.

Question 18

Describe the case with a 9yo girl who has presented with growth delay, there are features of rickets seen not he XRAYS?

Answer 18

Cl has increased, pH has decreased, pCO2 has decreased, bicarbonate has decreased and base excess has decreased as well. AG is normal. The girl has metabolic acidosis with respiratory compensation.

Question 19

What is a normal anion gap acidosis?

Answer 19

This is endogenous acid causing this (not an added) - hyperchloremic acidoses.

Question 20

What causes hyperchloremic acidoses?

Answer 20

1. GI bicarbonate loss.
2. Renal tubular acidoses (RTA).
3. Aldosterone deficiency or resistance (RTA type 4).
4. Glue or paint sniffing (toluene metabolised to hippuric acid).

Question 21

What can cause GI bicarbonate loss?

Answer 21

Diarrhoea, intestinal fistula, and ileostomy.

Question 22

What can cause renal tubular acidoses (RTA)?

Answer 22

Defects in acid excretion: urine pH >5.5 and urine ammonium has not increased (inappropriate for a metabolic acidosis) => proximal or distal types, may be associated with rickets or hypokalemia, may be associated with other renal tubular defects (falcon syndrome).

Question 23

What can cause aldosterone deficiency or restiance (RTA type 4)?

Answer 23

Addison’s disease, congenital adrenal hyperplasia syndromes (enzyme blocks in aldosterone synthesis), renin deficiency (e.g. in diabetic nephropathy), aldosterone resistance (pseuodhpyoaldosteronism).

Question 24

What further tests can you do for the 9yo girl?

Answer 24

1. Check the urine pH.
2. Check the urine ammonium.
3. Urine anion gap.
   In the presence of an acidosis, urine pH should be <5.5 and ammonium should be >100mmol/L. Therefore the girl has renal tubular acidosis.

Question 25

Why are normal anion gap acidoses hyperchloremic?

Answer 25

When bicarbonate is low, extra chloride needs to be reabsorbed to maintain sodium balance.

Question 26

What is the linkage between acidosis and hyperkalemia?

Answer 26

1. If you have primary acidosis (increase in H+ outside of the cells) it will drive potassium out of the cells and make you hyperkalemic (secondary). 2. If you have primary hyperkalemia (increase in potassium outside of the cell) it will drive H+ outside of the cell causing secondary acidosis.

Question 27

What is the linkage between alkalosis and hypokalemia?

Answer 27

1. If you have primary alkalosis (decrease in H+ outside of the cells) it will drive potassium into the cells as H+ is driven outside of the cells. This will cause secondary hypokalemia. 2. If you have primary hypokalemia (decrease of potassium outside of the cells) it will drive potassium out of the cells as H+ is drive into the cells. This will cause secondary alkalosis.

Question 28

What are the exceptions to the linkage between potassium and acid-base balance?

Answer 28

1. Diarrhoea (bicarbonate plus K+ loss). | 2. Renal tubular acidoses: distal and proximal types both associate with hypokalemia.

Question 29

Describe the case of a 21yo woman presented with muscle weakness?

Answer 29

The woman is a keen runner. She has a high pH, high bicarbonate, positive base excess, low chloride and low potassium. She has metabolic alkalosis with hypokalemia. The patient has said she is not vomiting - however, one fo the most common causes of alkalosis is GI contents loss. However, her chloride is <10mmol/L (at the lowest) this implies that her kidneys are trying their best to maintain what little chloride she has left. If you are using chloride through your kidney then it would appear high. Thus it turns out she was vomiting.

Question 30

Describe the pathogenesis of the 21yo case?

Answer 30

1. Loss of HCl due to vomiting causes alkalosis. 2. Hypokalemia is due to i) alkalosis and ii) potassium loss due to excessive laxative use (in chronic diarrhoea potassium loss predominates, due to Na/K exchange in the colon. In acute diarrhoea sodium loss predominates. 3. Hypokalemia causes muscle weakness (hyper polarises excitable cells).

Question 31

What are the causes of metabolic alkalosis?

Answer 31

1. Vomiting or gastric drainage. 2. Diuretic-induced alkalosis. 3. Secondary to hypokalemia. 4. Ingestion of alkali (antacids). 5. Mineralocorticoid excess. 6. Barterrs syndrome, riddles syndrome and variants (rare renal tubular disorders). Diarrhoea is more commonly associated with metabolic acidosis.

Question 32

Describe choroid-depletion alkalosis?

Answer 32

In metabolic alkalosis, the kidney attempts to increase bicarbonate loss. If chloride-depletion is present, bicarbonate reabsorption becomes obligatory to preserve sodium balance. The kidney cannot correct the alkalosis unless chloride is replaced. Gastric fluid loss and diuretics can cause chloride-depletion alkalosis.

Question 33

Describe an arterial blood gas?

Answer 33

Arterial punctures are very painful, occasional severe complications (thrombosis, haemorrhage); can result in nerve injuries.

Question 34

When is it ok to use venous blood for blood gases?

Answer 34

In patients with reasonable perfusion, pH, bicarbonate and BE are almost identical in venous and arterial blood. These gases are perfectly ok when pO2 is not needed and severe circulatory failure isn't present.

Question 35

What are the artefacts of using blood gases?

Answer 35

If you have air in the blood-gas syringe a falsely low pCO2 will show up and this will appear as respiratory alkalosis. There is also delayed separation of plasma from RBCs: RBCs produce lactic acid, leading to an apparent lactic acidosis (a metabolic acidosis with high AG).