a. Defect. Respiratory acidosis is caused by inadequate alveolar ventilation (eg, from medications that depress respiration, neuromuscular disorders, or increased CO2 production), or by ineffective gas exchange (eg, from airway obstruction, bronchoconstriction, or alveolar disease).
b. Laboratory manifestation. Increased Paco2; decreased pH.
c. Compensation. Normal respiratory response to hypercap-nia is to increase alveolar ventilation (through increased minute ventilation, respiratory rate, and depth of breaths). In addition to serum buffers (primarily proteins), renal compensatory mechanisms (increased HcO3 reabsorption) may be present after 24-36 hours.
d. Evaluate pH in conjunction with PaCO2. In general, pH will decrease by .008 for every 1 torr by which Paco2 is > 40 (eg, Paco2 of 60 is 20 torr > 40; pH would be expected to decrease by 20 x .008 = .16, as follows: serum pH = 7.40 - .16 = 7.24). If pH is above the calculated number, then there is some degree of metabolic compensation; if below it, then there is a metabolic acidosis in addition to respiratory acidosis.
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