Acid Base Balance II

Question 1

If renal or respiratory function is abnormal, or any acid or base load overwhelms the body, a change in pH occurs.

What are these individually called?

Answer 1

Decreased pH = Acidosis

Increased pH = alkalosis

Question 2

Respiratory disorders effect what in the acid base balance?

Answer 2

Pco2

Question 3

Renal disorders effect what in the acid base balance?

Answer 3

[HCO3-]

Question 4

What is respiratory acidosis?

Answer 4

pH has fallen and it is due to a respiratory change, so Pco2 must have increased.

Respiratory acidosis results from reduced ventilation and therefore retention of CO2.

Question 5

What are the acute causes of respiratory acidosis?

Answer 5

Drugs which depress the medullay respiratory centres, such as barbiturates and opiates.

Obstructions of major airways

Question 6

what are the chronic causes of respiratory acidosis?

Answer 6

Lung disease:

• Bronchitis
• Emphysema
• Asthma

Question 7

What is the bodies response to respiratory acidosis?

Answer 7

Need to protect pH so need to increase bicarbonate to keep Pco2/[HCO3-] ratio.

The increase in Pco2 will increase secretion of H+ and increase HCO3-

Acid conditions stimulate renal glutaminase so get more NH3 produced, BUT it takes time

So there is incraesed generation of new HCO3- as well as increased reabsorption, because having generated more HCO3- the increased Pco2 will also increase the ability to reabsorb it

Question 8

What is the downside to renal compensation of respiratory acidosis?

Answer 8

Increased HCO3- protects the pH, it does not correct the original disturbance.

ONLY restoration of normal ventilation can remove the primary disturbance.

This means that in chronic respiratory acidosis blood gas values are never normalised. The underlysing disease process prevents the correction of ventilation, but because the kidney maintains high [HCO3-] the pH is protected.

Question 9

What is respiratory alkalosis?

Answer 9

Alkalosis of respiratory origin so must be due to a fall in Pco2 and this can only occur through increased ventilation and CO2 blow off.

Question 10

What are the causes of acute respiratory alkalosis?

Answer 10

Voluntary hyperventilation
Aspirin
First ascent to altitude

Question 11

What are the chronic causes of respiratory alkalosis?

Answer 11

Long term residense at altitude.

Decreased Po2 to

Question 12

How is pH protected in respiratory alkalosis?

Answer 12

[HCO3-] should decrease.

Alkaline conditions are dealt with by the HCO3- reabsorptive mechanism.

If decreased Pco2, less H+ is available for secretion, therefore less of the filtered load of HCO3- is reabsorbed so HCO3- is lost in the urine.

(Ventilation must be normalised to correct the disturbance)

Question 13

What is metabolic acidosis?

Answer 13

An acidosis of metabolic origin must be due to a decreased bicarbonate.

So decreased [HCO3-], either due to increased buffering of H+ or direct loss of HCO3-.

To protect the pH, Pco2 must be decreased

Question 14

What are the causes of metabolic acidosis?

Answer 14

1. Increased H+ production, as in ketoacidosis of a diabetic or in lactic acidosis
2. Failure to excrete the normal dietary load of H+ as in renal failure
3. Loss of HCO3- as in diarrhoea
   i. e. failure to reabsorb intestinal HCO3-

Question 15

What effect does metabolic acidosis cause?

Answer 15

Stimulates ventilation so that Pco2 falls.

The increase in ventilation is in depth rather than rate, may be very striking, reaching a max 30l/min compared to normal 5-6l/min when the arterial pH falls to 7.

This degree of hyperventilation = Kussmaul breathing = an established clinical sign of renal failure or diabetic ketoacidosis. Very serious.

Question 16

What problem does respiratory compensation of metabolic acidosis cause?

Answer 16

Normally the kdineys correct the disturbance by restoring [HCO3-] and getting rid of H+ ions

The source of H+ ions is the CO2 in the peritubular capillaries but respiratory compensation lowers the Pco2 to protect the pH.

This lowers the driving force for renal compensation through renal glutaminase.

Respiratory compensation DELAYS the renal correction, BUT PROTECTS THE pH, much more important

Question 17

Why do compensatory mechanisms not restore pH exactly back to original?

Answer 17

Complete compensation would remove the drive to correct the original disturbance. Survival value of this is that if there were no pressure to correct initial disturbance, a further perturbation may push the system so far that compensation can no longer be effective

Question 18

How does renal compensation in metabolic acidosis take place when respiratory compensation has taken place?

Answer 18

Decreased Pco2 due to respiratory compensation.

Lowers H+ but also lowers bicarbonate even more (lowered bicarbonate original problem).

Less H+ needed for bicarbonate reabsorption as less bicarbonate will be filtered.

More H+ available for excretion through NH4+

Question 19

What is metabolic alkalosis?

Answer 19

[HCO3-] must have increased and Pco2 will have to increase to protect the pH

Question 20

What causes metabolic alkalosis?

Answer 20

1. Increased H+ ion loss -> vomiting loss of gastric secretions
2. Increased renal H+ loss
   - > Aldosterone excess, excess liquorice ingestion
3. Excess administration of HCO3- is unlikely to produce a metabolic alkalsis in subjects with normal renal function, but may do so if renal function impaired.
4. Massive blood transfusions

Question 21

How can massive blood transfusions cause metabolic alkalosis?

Answer 21

Can lead to metabolic alkalosis because bank blood contains citrate to prevent coagulation, which is converted to HCO3- but need at least 8 units to have this effect.

The greatly increased filtered load of HCO3- exceeds the level of H+ secretion to reabsorb it, even in the presence of increased Pco2, so the excess is lost in the urine

Question 22

How does respiratory compensation effect renal compensation in metabolic ketoacidosis?

Answer 22

Once again respiratory compensation delays renal correction, but protects the pH.

Question 23

What is the H+, pH, Primary disturbance and compensation in Respiratory acidosis?

Answer 23

H+ = Increased

pH = Decreased

Primary Disturbance = Increased Pco2

Compensation = Increased [HCO3-]

Question 24

What is the H+, pH, primary disturbance and compensation in Respiratory alkalosis?

Answer 24

H+ = decreased

pH = Increased

Primary disturbance = Decreased Pco2

Compensation = Decreased [HCO3-]

Question 25

What is the H+, pH, primary disturbance and compensation in metabolic acidosis?

Answer 25

H+ = Increased

pH = decreased

Primary disturbance = Decreased [HCO3-]

Compensation = Decreased Pco2

Question 26

What is the H+, pH, primary disturbance and compensation in metabolic alkalosis?

Answer 26

H+ = decreased

pH = increased

Primary disturbance = increased [HCO3-]

Compensation = increased Pco2

Question 27

When looking at ABGs why do you need to take all the values into account?

Answer 27

Need to distinguish between cause and effect.

e.g. a decrease in pH (acidosis) is caused by either decreased HCO3- or increased Pco2

Question 28

For a given Pco2, there is a smaller decrease in pH in chronic respiratory acidosis than in acute respiratory acidosis.

Why is this?

Answer 28

NH3 production takes 4-5 days to be fully turned on. So initially can only raise [HCO3-] by titratable acid, so limited.

With time, can use NH3 production which has a considerable capacity to raise [HCO3-].

Question 29

How long do renal compensations take to kick in compared to respiratory compensations?

Answer 29

Respiratory compensations can take minutes

Renal compensations can take 4-5 days

(Turning on or off NH3 production takes time)

Question 30

What electrolyte should you always be aware of in acidosis?

Answer 30

K+
Hyperkalaemia

H+ taken into cells to buffer in exchange for K+

Question 31

In hyperkalaemia due to acidosis what treatments can you consider?

Answer 31

Insulin (+ glucose if non-diabetic), stimulates cellular uptake of K+

Calcium resonium, either oral or per rectum, exchanges Ca2+ for K+ ions.

Ca gluconate (IV) -> decreased excitablility of the heart, stabilizes cardiac muscle cell membranes

Question 32

Consider a bad case of vomiting:

Loss of NaCl and H2O -> hypovolaemia

Loss of HCl -> metabolic alkalosis

Why might the kidneys response cause further alkalosis?

Answer 32

Hypovolaemia will stimulate aldosterone to increase distal tubule Na+ reabsorption.

Under conditions of avid Na+ reabsorption (and due to loss of Cl-), the main ion exchanged for Na+ is H+

The respiratory compensation for the metabolic alkalosis i.e. increased Pco2 helps drive the H+ secretion and exacerbates the metabolic alkalosis by adding yet more HCO3- to the plasma

Question 33

Why in vomiting and diarrhoea, although you lose acid and alkali, you become alkalotic?

Answer 33

Decrease in ECF volume takes precedence over correction of metabolic alkalosis

Increased aldosterone -> increased reabsorption of Na+ and therefore increased loss of H+ and reabsorption of HCO3-

“Contraction alkalosis’

Question 34

What is the anion gap?

Answer 34

The difference between the sum of the principle cations (Na+ and K+) and the principal anions in the plasma (Cl- and HCO3-)

Normally 14-18mmoles/l

Question 35

Why is the anion gap useful?

Answer 35

Useful to measure in metabolic acidosis.

There are 2 patterns of metabolic acidosis in terms of anion gap, in one there if no change from normal and in the other the anion gap increases.

If the acidosis is due to a loss of bicarbonate from the gut for example, then the reduction of bicarbonate is compensated by an increase in chloride and so there is no change in ion gap.

However in e.g. lactic or diabetic acidosis, the reduction in bicarbonate is made up by other anions such as lactate, acetoacetate, B-OH butyrate and so the anion gap is increased