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Respiratory Acidosis

  • Respiratory Acidosis is a pathophysiological category of acidosis and refers to those acidoses caused by primary disturbances in ventilation. Although ventilatory defects can cause significant decreases in the blood pH, renal compensatory mechanisms can largely correct the pH over several days.
Primary Disturbance
  • The fundamental cause of all respiratory acidoses is insufficient alveolar ventilation, resulting in an increase in the partial pressure of arterial carbon dioxide (PaCO2). Increased PaCO2 results in an misalignment of the Henderson-Hasselbalch Equation for the bicarbonate buffer which largely determines the pH of the extracellular fluid. Mathematically, the reduced ECF pH results from an increase in the ratio between PaCO2 relative to the ECF concentration of bicarbonate ([HCO3-]). More colloquially, deficiencies in alveolar ventilation result in an inability of the lungs to "Breathe Off" gaseous CO2 which is immediately converted to carbonic acid H2CO3 in the extracellular fluid. H2CO3 immediately releases a free hydrogen ion (H+) which serves to reduce the ECF pH, thus causing acidosis.
  • Respiratory Acidoses can be compensated by the actions of the kidneys which serve to realign the bicarbonate buffer Henderson-Hasselbalch Equation over a period of several days. As described in Renal Response to Acid-Base Imbalance, the kidneys respond to acidosis by secreting free hydrogen ions in the urine, synthesizing novel bicarbonate which is added to the ECF, and reducing any urinary excretion of bicarbonate. By secreting acid in the urine, the kidneys may slightly reduce the PaCO2 over several days. However, the most important renal contribution is the synthesis of novel bicarbonate and reduction in urinary bicarbonate excretion which serve to slowly increase the ECF bicarbonate concentration over several days. The increased bicarbonate concentration realigns the Henderson-Hasselbalch Equation for the bicarbonate buffer and thus largely corrects the ECF pH. Consequently, a renally-compensated respiratory acidosis is characterized by increased levels of PaCO2 (caused by the primary ventilatory disturbance) as well as increased levels of ECF bicarbonate (caused by the renal compensation). However, it is important to point out that renal compensation cannot completely correct the ECF pH and thus the ECF will still remain slightly acidotic even after compensation.
  • A large number of etiologies can result in pathologic hypoventilation and thus respiratory acidosis. Defects of the brainstem respiratory centers may occur due to ingestion of certain drugs such as opiates or a stroke. Obstruction of airways may result from causes of airway obstruction or in contexts of asthma exacerbation. A variety of parenchymal diseases may reduce alveolar ventilation such as Acute Respiratory Distress Syndrome, emphysema, bronchitis, or pneumoconioses. Neuromuscular defects may affect breathing such as following Polio Virus infection or Muscular Dystrophy. Finally structural defects may prevent proper breathing such as obesity.
  • An uncompensated respiratory acidosis is characterized by a blood pH far below 7.35, increased PaCO2, and a largely normal blood bicarbonate. A renally-compensated respiratory acidosis is characterized by a blood pH only slightly below 7.35, increased PaCO2, and an increased blood bicarbonate.