RT Book, Section A1 Butterworth IV, John F. A1 Mackey, David C. A1 Wasnick, John D. SR Print(0) ID 1162427706 T1 Acid–Base Management T2 Morgan & Mikhail's Clinical Anesthesiology, 6e YR 2018 FD 2018 PB McGraw-Hill Education PP New York, NY SN 9781259834424 LK accessanesthesiology.mhmedical.com/content.aspx?aid=1162427706 RD 2024/04/19 AB KEY CONCEPTS The strong ion difference, PCO2, and total weak acid concentration best explain acid–base balance in physiological systems. The bicarbonate buffer is effective against metabolic but not respiratory acid–base disturbances. In contrast to the bicarbonate buffer, hemoglobin is capable of buffering both carbonic (CO2) and noncarbonic (nonvolatile) acids. As a general rule, PaCO2 can be expected to increase 0.25 to 1 mm Hg for each 1 mEq/L increase in [HCO3−]. The renal response to acidemia is three-fold: (1) increased reabsorption of the filtered [HCO3−], (2) increased excretion of titratable acids, and (3) increased production of ammonia. During chronic respiratory acidosis, plasma [HCO3−] increases approximately 4 mEq/L for each 10 mm Hg increase in PaCO2 above 40 mm Hg. Diarrhea is a common cause of hyperchloremic metabolic acidosis. The distinction between acute and chronic respiratory alkalosis is not always made, because the compensatory response to chronic respiratory alkalosis is quite variable: Plasma [HCO3−] decreases 2 to 5 mEq/L for each 10 mm Hg decrease in PaCO2 below 40 mm Hg. Vomiting or continuous loss of gastric fluid by gastric drainage (nasogastric suctioning) can result in marked metabolic alkalosis, extracellular volume depletion, and hypokalemia. The combination of alkalemia and hypokalemia can precipitate severe atrial and ventricular arrhythmias. Changes in temperature affect PCO2, PO2, and pH. Both PCO2 and PO2 decrease during hypothermia, but pH increases because temperature does not appreciably alter [HCO3−] and the dissociation of water decreases (decreasing H+ and increasing pH).