Key messages

• 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.

Healthy Fat Loss For A Longer Life

Healthy Fat Loss For A Longer Life

What will this book do for me? A growing number of books for laymen on the subject of health have appeared in the past decade. Never before has there been such widespread popular interest in medical science. Learn more within this guide today and download your copy now.

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