1.
Respiratory Acidosis:
a. Primary defect: Increase pCO2
b. Cause:
·
Ventilatory failure
·
Chronic bronchitis and bronchial asthma
·
Emphysema
·
Depression of nervous system
·
Morphine poisoning
c. Compensation: Compensated by renal mechanism. Excess CO2
is counteracting by renal HCO3 retention and increased H+
secretion and excretion.
2.
Respiratory alkalosis:
a. Primary defect: Decrease in pCO2 as result of
hyperventilation.
b. Causes:
·
Hyperventilation (voluntary, forced, hysterical)
·
CNS disease affecting the respiratory centers
·
Salicylate poisoning
·
Hepatic coma.
c. Compensation: Compensated by kidneys. Low pCO2
in the arterial blood is compensated by increased HCO3 excretion in
urine.
3.
Metabolic acidosis:
a. Primary defect: Decrease HCO3
b. Causes
1) Metabolic
acidosis with normal anion gap
a) Increased
gastrointestinal bicarbonate loss
i)
Diarrhea
ii) Fistulae
iii) Uretero-sigmoidostomy
b) Increased
renal bicarbonate loss
i)
Renal tubular acidosis
ii) Carbonic
anhydrase inhibitors
iii) Tubular damage
c) Increased
HCl production
i)
Ammonium chloride production
2) Metabolic
acidosis with an increased anion gap
i)
Diabetic ketoacidosis
ii) Lactic
acidosis
iii) Exogenous
acid
iv) Renal
failure
c. Compensatory mechanism: Primarily compensated by
respiratory system. A low PH stimulates respiratory centers, the
patient hyperventilates and blow out CO2.
4.
Metabolic Alkalosis:
a. Primary defect: Increase in plasma HCO3
Concentration.
b. Causes:
·
Loss of acid (Vomiting)
·
Diuretic therapy
·
Potassium deficiency
·
Extracellular volume depletion
·
Excess mineralocorticoids (Primary and secondary
aldosteronism, Cushing’s syndrome)
·
Excess alkali administration
·
Post hypercapnic alkalosis
c. Compensation:
Compensated by respiratory system by hypoventilation resulting in an increase
in plasma pCO2.
No comments:
Post a Comment