Acid-Base Physiology

5.4 Metabolic Acidosis - Metabolic Effects

5.4.1 Cardiorespiratory Effects

A metabolic acidosis can cause significant physiological effects, particularly affecting the respiratory and cardiovascular systems.

Major Effects of a Metabolic Acidosis

Respiratory Effects

  • Hyperventilation ( Kussmaul respirations) - this is the compensatory response
  • Shift of oxyhaemoglobin dissociation curve (ODC) to the right
  • Decreased 2,3 DPG levels in red cells (shifting the ODC back to the left)

Cardiovascular Effects

  • Depression of myocardial contractility
  • Sympathetic overactivity (incl tachycardia, vasoconstriction,decreased arrhythmia threshold)
  • Resistance to the effects of catecholamines
  • Peripheral arteriolar vasodilatation
  • Venoconstriction of peripheral veins
  • Vasoconstriction of pulmonary arteries
  • Effects of hyperkalaemia on heart

Other Effects

  • Increased bone resorption (chronic acidosis only)
  • Shift of K+ out of cells causing hyperkalaemia

5.4.2 Some Effects have Opposing Actions.

The cardiac stimulatory effects of sympathetic activity and release of catecholamines usually counteract the direct myocardial depression while plasma pH remains above 7.2. At systemic pH values less than this, the direct depression of contractility usually predominates.

The direct vasodilatation is offset by the indirect sympathetically mediated vasoconstriction and cardiac stimulation during a mild acidosis. The venoconstriction shifts blood centrally and this causes pulmonary congestion. Pulmonary artery pressure usually rises during acidosis.

The shift of the oxygen dissociation curve to the right due to the acidosis occurs rapidly. After 6 hours of acidosis, the red cell levels of 2,3 DPG have declined enough to shift the oxygen dissociation curve (ODC) back to normal.

Acidosis is commonly said to cause hyperkalaemia by a shift of potassium out of cells. The effect on potassium levels is extremely variable and indirect effects due to the type of acidosis present are much more important. For example hyperkalaemia is due to renal failure in uraemic acidosis rather than the acidosis. Significant potassium loss due to osmotic diuresis occurs during diabetic ketoacidosis and the potassium level at presentation is variable (though total body potassium stores are invariably depleted). Treatment with fluid and insulin can cause a prompt and marked fall in plasma potassium. Hypokalaemia may then be a problem.