Respiratory Acid-Base Imbalance

1. Respiratory Acidosis results from impaired lung function
   • Retention of carbon dioxide (pCO2 > 40)

     This animation has a minor glitch: the pH meter should stay still on the acid side rather than moving over with each loop--I'll fix it as soon as I can. JH

   • Renal compensation occurs in chronic respiratory acidosis

     Renal compensation of either respiratory acidosis or alkalosis develops slowly, requiring about a day to be fully expressed. It is a biochemical process involving gearing up of renal metabolism and changes in ion secretion by the kidney. Renal compensation is normally seen in chronic lung disease settings but may not be present after acute changes in lung function.

   • Causes
     • Severe (end stage) COPD: chronic bronchitis/emphysema (V/Q mismatch)

       Respiratory acidosis is seen only in the most severe cases of COPD (most COPD shows respiratory alkalosis--see below), but COPD is so common overall that this is a relatively frequent setting for acidosis.

     • Severe restrictive lung disease (pulmonary fibrosis)

       Movement of carbon dioxide from the blood to the alveolar air is limited by an increased tissue barrier as well as by restriction in lung motion.

     • CNS depression (trauma, anesthesia, drugs) -- hypoventilation

     • Neuromuscular disorders -- hypoventilation

       Both of the above are associated with limited chest wall motion and hypoventilation on that basis.

2. Respiratory alkalosis results from hyperventilation

   Under normal circumstances, expiration of carbon dioxide is dependent on respiratory rate. Increasing respiratory rate substantially increases the removal of carbon dioxide and thus effectively removes acid from the body.

   • Excess respiratory loss of carbon dioxide

   • Renal compensation in chronic settings

   • Causes
     • Hypoxia -- COPD

       Oxygen diffuses through tissue slower than carbon dioxide and is more affected by the V/Q mismatches typically present in COPD. COPD patients often breath faster than normal to maintain their oxygen tension and thus usually show low pCO2's and a chronic respiratory alkalosis. End stage COPD can become severe enough to limit carbon dioxide exchange and at that point the patients begin to show respiratory acidosis.

     • Excitement, anxiety

       Associated with increased respiratory rate and decreased pCO2 on that basis.

     • Moderate or early salicylate toxicity

       Salicylates (aspirin) directly stimulate the breathing center and induce hyperventilation and respiratory alkalosis. However, salicylates are themselves acids and in large overdoses a metabolic acidosis from acid ingestion will replace the initial respiratory alkalosis.