Metabolic acidosis

[Ref: KB's online acid-base text]

Major effects of a metabolic acidosis

Respiratory effects

• Hyperventilation (Kussmaul respiration)
  * Compensatory response
• Shift of oxyhaemoglobin dissociation curve to the right
• Decreased 2,3 DPG levels in red cells
  --> Tends to move ODC towards left

Cardiovascular effects

• Depression of myocardial contractility
• Sympathetic overactivity, including
  * Tachycardia
  * Vasoconstriction
  * Decreased arrhythmia threshold
• Resistance to the effects of catecholamines
• Peripheral arteriolar vasodilation
• Venoconstriction of peripheral veins
• Vasoconstriction of pulmonary arteries

Other effects

• Increased bone resportion
  * Chronic acidosis only
• Hyperkalaemia
  * Shift K+ out of cells
  * Can have effects on the heart

 

NB:

• Acidosis shifts ODC to the right rapidly
• After 6 hours of acidosis
  --> RBC 2,3 DPG level declines
  --> ODC is shifted back to normal

Respiratory compensation in metabolic acidosis

Hyperventilation

Increase in ventilation
--> Decrease pCO2
--> Central chemoreceptor inhibits the extent of hyperventilation
--> As HCO3 stabilized across BBB
--> Inhibition is removed

Thus,

• Increase in ventilation starts within minutes
• Well-advanced at 2 hours of onset
• Maximal compensation may take 12-24 hours to develop

 

 

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The arterial pCO2 at maximal compensation has been measured in many patients with a metabolic acidosis. A consistent relationship between bicarbonate level and pCO2 has been found. It can be estimated from the following equation:

Expected pCO2 = 1.5 (Actual [HCO3] ) + 8 mmHg
* Units: mmols/l for [HCO3], and mmHg for pCO2

The limiting value of compensation is the lowest level to which the pCO2 can fall - this is typically 8 to 10mmHg, though lower values are occasionally seen.

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If the measured HCO3 is 12 mmols/l, then the expected pCO2 (at maximal compensation) would be: (1.5 x 12) + 8 = 18 + 8 = 26 mmHg. If the actual pCO2 was within +/- 2 mmHg of this (and 12 to 24 hours have passed from onset) then the respiratory compensation has reached it maximal value (and there would be no evidence of a primary respiratory acid-base disorder).

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1. Kidney: Renal generation of new bicarbonate
This usually occurs as a consequence of an increase in ammonium excretion.

2. Liver: Hepatic metabolism of acid anions to produce bicarbonate
The normal liver has a large capacity to metabolise many organic acid anions (eg lactate, ketoanions) with the result that bicarbonate is regenerated in the liver. In severe ketoacidosis there is often a large loss of ketoanions due to the hyperglycaemia induced osmotic diuresis. This leaves a shortfall of ketoanions to be used to regenerate bicarbonate as a consequence of their metabolism in the kidney.

3. Exogenous Administration of sodium bicarbonate
This is the time honoured method to 'speed up' the return of bicarbonate levels to normal. Indeed, this may be useful in mineral acidosis (hyperchloraemic metabolic acidosis) where there are no endogenous acid anions which can be metabolised by the liver. However, in most other cases of metabolic acidosis this administration is either not helpful or may be disadvantageous.

Sodium bicarbonate solutions should NOT be given on a routine basis no matter what the arterial pH is.

 

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