Anaes · Applied cardiovascular & respiratory physiology

Acid-base: buffers & compensation

Also known as Acid-base balance · Henderson-Hasselbalch equation · Bicarbonate buffer system · Open buffer system · Haemoglobin buffer · Haldane effect · Winter formula · Compensation rules · Base excess · Anion gap · Davenport diagram · Renal acidification

Arterial pH is held between 7.35 and 7.45 by a system of buffers and two excretory organs, and the anaesthetist reads its output every time a blood gas is drawn. Six exam-critical ideas frame the topic. First, pH is governed by the Henderson-Hasselbalch relationship, in which pH equals pKa plus the log of the ratio of bicarbonate to dissolved carbon dioxide (0.03 times PaCO2), so the bicarbonate to PaCO2 ratio sets the pH. Second, the bicarbonate buffer dominates the extracellular fluid not because its pKa (6.1) is well matched to pH 7.4 but because it is an OPEN system, the lungs exhaling the acid (CO2) and the kidneys regenerating the base (bicarbonate). Third, the non-bicarbonate buffers, chiefly haemoglobin (imidazole of histidine, pKa about 7.0, with deoxyhaemoglobin the better buffer, the Haldane effect), plasma proteins and phosphate, supply the buffer base. Fourth, there are four primary disorders, respiratory acidosis and alkalosis (a PaCO2 problem) and metabolic acidosis and alkalosis (a bicarbonate problem), each compensated by the opposite system, respiratory compensation fast (minutes to hours) and renal compensation slow (two to five days). Fifth, the expected compensations are rule-based and must be checked, the chief being Winter's formula (expected PaCO2 equals 1.5 times bicarbonate plus 8, plus or minus 2 for metabolic acidosis) and the acute versus chronic respiratory rules (acute respiratory acidosis adds about 1 mmol per litre of bicarbonate per 10 mmHg rise in PaCO2, chronic adds about 4; acute respiratory alkalosis drops about 2 per 10, chronic about 4 to 5). Sixth, base excess (the metabolic component at a standardised PaCO2 of 40 mmHg) and the anion gap (sodium minus chloride minus bicarbonate) are the two derived variables that refine the diagnosis. Built on the Adrogue and Madias acid-base reviews (NEJM 1998), the Berend base-excess review (NEJM 2018), the Story acid-base history (Critical Care 2004), the Kellum determinants review (Critical Care Clinics 2005), the Figge serum-protein buffer study (1991), the Madias renal acidification reviews (Nephron Physiology 2003, Journal of Nephrology 2010), the Fulop PaCO2-prediction study (1997), the Kraut and Madias lactic-acidosis review (2016), the Lang and Zander base-excess calculation study (2002), the Figge anion-gap correction study (1998), the SMART and SALT-ED balanced-crystalloid trials (2018), and the Berend acid-base pathophysiology review (2013).