TY - CHAP M1 - Book, Section TI - Acid–Base Management A1 - Butterworth IV, John F. A1 - Mackey, David C. A1 - Wasnick, John D. PY - 2022 T2 - Morgan & Mikhail’s Clinical Anesthesiology, 7e AB - KEY CONCEPTS The strong ion difference, PaCO2, 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 filtered [HCO3–], (2) increased excretion of titratable acids, and (3) increased production of ammonia. With 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 PaCO2, PaO2 and pH. Both PaCO2 and PaO2 decrease during hypothermia, but pH increases because temperature does not appreciably alter [HCO3–] and the dissociation of water decreases (decreasing H+ and increasing pH). SN - PB - McGraw-Hill Education CY - New York, NY Y2 - 2024/04/16 UR - accessanesthesiology.mhmedical.com/content.aspx?aid=1190611009 ER -