• Respiratory acidosis is a process in which the low pH is primarly due to a rise in PCO2.
• In critically ill patients the CO2 load may be greatly increased due to hypermetabolism, excess parenteral nutrition, or titration of HCO 3- by fixed acids.
• The arterial PCO2 for a given acid load is a function of alveolar ventilation and cardiac output.
• CO2 is buffered by fixed buffers, i.e. hemoglobin, phosphates, and proteins.
• CO2 buffering in vivo leads to an increase in HCO3- of 1 mmol/l for every increase of 10 mmHg (1.33 kPa) in PCO2 above 40 mmHg (5.33 kPa).
• The decrease in pH stimulates the generation of more HCO3- in the tubular kidney cells by increased ammonium ion production. This mechanism leads to an increase in plasma HCO3- of approximately 3.5 mmol/l for every increase of 10 mmHg (1.33 kPa) in PCO2 above 40 mmHg (5.33 kPa).
• Every step of acid-base regulation may be affected in critically ill patients: abnormal increase in acid load, decreased concentration of fixed buffers, altered cardiac output, inadequate alveolar ventilation, and impaired production of HCO 3- in the presence of renal failure.
• Respiratory failure may orginate from changes in the central nervous system, the conductive system (airways), the lung parenchyma, the inspiratory muscles, or the chest wall.
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