elimination of CO2 can cause a respiratory acid-base disorder. The PaCO2 is maintained within a range of 35–45 mm Hg in normal states. Alveolar ventilation is under the control of the respiratory center, which is located in the pons and the medulla. Ventilation is influenced and regulated by chemoreceptors for PaCO2, PaO2, and pH located in the brainstem, and in the aortic and carotid bodies as well as by neural impulses from lung stretch receptors and impulses from the cerebral cortex. Failure of ventilation quickly increases the PaCO2. In acute respiratory acidosis, compensation occurs in 2 steps. The initial response is cellular buffering (plasma protein buffers) that occurs over minutes to hours. Cellular buffering elevates plasma bicarbonate (HCO3−) only slightly, approximately 1 mEq/L for each 10-mm Hg increase in PaCO2. The second step is renal compensation that occurs over 3–5 days. With renal compensation, renal excretion of carbonic acid is increased and bicarbonate reabsorption is increased. For instance, PEPCK is upregulated in renal proximal tubule brush border cells, in order to secrete more NH3 and thus to produce more HCO3−. Estimated changes In renal compensation, plasma bicarbonate rises 3.5 mEq/L for each increase of 10 mm Hg in PaCO2. The expected change in serum bicarbonate concentration in respiratory acidosis can be estimated as follows: Acute respiratory acidosis: HCO3− increases 1 mEq/L for each 10 mm Hg rise in PaCO2. Chronic respiratory acidosis: HCO3− rises 3.5 mEq/L for each 10 mm Hg rise in PaCO2. The expected change in pH with respiratory acidosis can be estimated with the following equations: Acute respiratory acidosis: Change in pH = 0.08 X ((40 − PaCO2)/10) Chronic respiratory acidosis: Change in pH = 0.03 X ((40 − PaCO2)/10) Respiratory acidosis does not have a great effect on electrolyte levels. Some small effects occur on calcium and potassium levels. Acidosis decreases binding of calcium to albumin and tends to increase serum ionized calcium levels. In addition, acidemia causes an extracellular shift of potassium, but respiratory acidosis rarely causes clinically significant hyperkalemia. Diagnosis Diagnoses can be done by doing an ABG (Arterial Blood Gas) laboratory study, with a pH <7.35 and a PaCO2 >45 mmHg in an acute setting. Patients with COPD and other Chronic respiratory diseases will sometimes display higher numbers of PaCO2 with HCO3- >30 and normal pH. Terminology Acidosis refers to disorders that lower cell/tissue pH to < 7.35. Acidemia refers to an arterial