Metabolic alkalosis hypoventilation

Metabolic alkalosis is characterized by an increased arterial pH, a primary increase in the HCOf concentration, and a compensatory increase in the PaC02. Patients will always hypoventilate to compensate for metabolic alkalosis—even if it results in profound hypoxemia. For a metabolic alkalosis to persist there must concurrently be a process that elevates serum HC03 concentration (gastric or renal loss of acids) and another that impairs renal HC03 excretion (hypovolemia, hypokalemia, or mineralocorticoid excess). The etiologies of metabolic alkalosis are listed in Table 25-5. 

The respiratory response to metabolic alkalosis is to increase PaC02 by hypoventilation. 

AGC Line AG represents a metabolic alkalosis with a rise in HC03 to 35 mmol.l-1. Compensation occurs by hypoventilation along line GC. 

Hypoventilation causes retention of C02 by the lungs, which can lead to a respiratory acidosis. Hyperventilation can cause a respiratory alkalosis. Metabolic acidosis can result from accumulation of metabolic acids (lactic acid or the ketone bodies p-hydroxybutyric acid and acetoacetic acid), or ingestion of acids or compounds that are metabolized to acids (methanol, ethylene glycol). Metabolic alkalosis is due to increased HC03, which is accompanied by an increased pH. Acid-base disturbances lead to compensatory responses that attempt to restore normal pH. For example, a metabolic acidosis causes hyperventilation and the release of C02, which tends to lower the pH. During metabolic acidosis, the kidneys excrete NH4+, which contains H+ buffered by ammonia. 

The respiratory response to metabolic alkalosis is hypoventilation, which resnlts in an increased PaC02. Respiratory compensation is initiated within honrs when the central and peripheral chemoreceptors sense an increase in pH. The PaC02 increases 6 to 7 mm Hg for each 10-mEq/L increase in bicarbonate, np to a PaC02 of abont 50 to 60 mm Hg (see Table 51M) before hypoxia sensors react to prevent fnrther hypoventilation. If the PaC02 is normal or less than normal, one shonld consider the presence of a snperimposed respiratory alkalosis, which may be secondary to fever, gram-negative sepsis, or pain. 

Let us now consider what happens when the effect which was secondary in the primary respiratory disorder is instead the primary disorder. This would then be a primary metabolic alkalosis, as in the vomiting of gastric contents. In the uncompensated condition, there is a positive base excess with a normal partial pressure of carbon dioxide already noted (Table 4.4C). The respiratory compensation is hypoventilation, brought about by the partial withdrawal of the normal stimulus of hydrogen ions to the peripheral chemoreceptors. The partial pressure of carbon dioxide rises, adding a respiratory component to the acid-base disorder (Table 4.4D). 

Case 4, onset high pH, PCO2 normal, positive B.E., uncompensated metabolic alkalosis. Later PCO2 now high (hypoventilation), B.E. unaltered metabolic acidosis with respiratory compensation, no renal compensation. 

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