Pathology of Acidosis and Fistulae

Study Notes

Characterized by high [H+], low pH, low PCO2, and low [HCO3]
Compensation occurs through hyperventilation, which increases removal of carbon dioxide and lowers PCO2
Hyperventilation is a direct result of increased [H+] stimulating the respiratory center
Respiratory compensation cannot completely normalize [H+] since it is the high concentration itself that stimulates compensatory hyperventilation

Compensatory response is hyperventilation, leading to Kussmaul breathing
Increased [H+] leads to increased neuromuscular irritability, risking arrhythmias and cardiac arrest, especially with hyperkalaemia
Depression of consciousness can progress to coma and death

Characterized by primary increase in ECF bicarbonate concentration and reduction in [H+]
Normally, an increase in plasma bicarbonate concentration leads to incomplete renal tubular bicarbonate reabsorption and excretion of bicarbonate in the urine
However, in non-respiratory alkalosis, high renal bicarbonate reabsorption occurs due to factors such as:
- Decrease in ECF volume
- Mineralocorticoid excess
- Potassium depletion
Massive quantities of bicarbonate must be ingested to produce a sustained alkalosis

Hypoventilation, confusion, and eventually coma
Muscle cramps, tetany, and paraesthesia due to decrease in unbound plasma calcium concentration

Acidosis and alkalosis define primary acid-base disturbance, even when [H+] is within the normal range
Definitions:
- Non-respiratory (Metabolic) acidosis: Decrease in bicarbonate concentration
- Non-respiratory (Metabolic) alkalosis: Increase in bicarbonate concentration
- Respiratory acidosis: Increase in PCO2
- Respiratory alkalosis: Decrease in PCO2
Primary mixed acid-base disorders: Disorders of combined respiratory and non-respiratory origin
'Acidemia' and 'alkalaemia' refer to whether [H+] in blood is higher or lower than normal