--- module: 019-02 language: en chapter: 19 title: "Acid-Base Physiology and Clinical Interpretation" module_title: "Quantitative compensation, hidden mixtures, and acid-base treatment traps" source_sha256: f84635f2d747d94bd6530a6e1cfffc0058ac459ca86b2388bcaf7e3267f40b48 --- # Quantitative compensation and hidden mixtures ## Process before equations ### Carbon dioxide changes within minutes ### Renal handling shifts over hours to days ### Timing is part of the diagnosis ### Low bicarbonate: acidosis or compensation ### High bicarbonate: alkalosis or compensation ### Rules give ranges, not exact targets ### A value outside the range means another process ## Respiratory compensation in metabolic disease ### Expected value: one and a half times bicarbonate #### Then add eight, with a small range #### A higher measured value means ventilatory failure #### A lower measured value means respiratory alkalosis ### High minute ventilation must be sustained #### Sedation, fatigue and weakness remove it #### Intubation must match compensatory demand ### Alkalosis compensation limited by oxygenation ## Acute and chronic respiratory change ### Acute retention raises bicarbonate a little ### Chronic retention raises it through the kidney ### Less bicarbonate than expected: added acidosis ### More bicarbonate: alkalosis or higher baseline ### Pregnancy is chronic mild respiratory alkalosis ### Post-hypercapnic alkalosis after rapid correction #### Volume, chloride, potassium and diuretics maintain it ## Correcting and dissecting the gap ### Low albumin lowers the expected gap #### Correction reveals hidden organic acids ### Delta: gap rise against bicarbonate fall #### Much larger fall adds normal-gap acidosis #### Smaller fall suggests coexisting alkalosis ### Chloride-rich fluid replaces the organic gap #### Hyperchloraemic acidosis as lactate clears #### Serial values prevent a false failure ## Normal-gap acidosis and urine ### Bicarbonate loss or impaired acid excretion ### Diarrhoea loses gastrointestinal bicarbonate ### Proximal disease loses filtered bicarbonate ### Distal disease cannot acidify the urine ### Urine gap: sodium plus potassium minus chloride #### Negative value: appropriate ammonium excretion #### Positive value: reduced ammonium production ### Urine pH alone is insufficient ## Alkalosis: generation and maintenance ### Vomiting removes hydrogen and chloride ### Volume depletion drives sodium reclamation ### Chloride unavailable for bicarbonate exchange ### Mineralocorticoid signalling secretes hydrogen distally ### Low urine chloride after remote losses ### High urine chloride with ongoing diuretics ### Potassium depletion sustains the alkalosis #### Magnesium depletion blocks potassium replacement ## Lactate, ketones and toxins ### Lactate is a shared endpoint #### Hypoxia, ischaemia, seizures, thiamine deficiency #### Normalisation need not precede improvement ### Ketoacidosis carries several changes at once #### Osmotic diuresis loses volume and electrolytes #### Potassium high while stores are depleted ### Toxic alcohols move osmolar gap to anion gap #### A late normal osmolar gap excludes nothing ### Salicylate: ventilation plus organic acids ## Physicochemical interpretation ### pH from gas, strong ions and weak acids ### Albumin and phosphate are the weak acids ### Chloride narrows the strong-ion difference #### Narrowing promotes acidosis ### Chloride loss or added sodium widens it #### Widening promotes alkalosis ### Low albumin has an alkalinising effect ### Complements bicarbonate-centred analysis ## Treatment follows the cause ### Bicarbonate for selected severe states #### It adds sodium and carbon dioxide #### It lowers ionised calcium and shifts potassium #### Central acidity worsens if ventilation fails ### Restore ventilation without erasing adaptation ### Chloride-responsive alkalosis needs volume and chloride ### Dialysis removes selected acids and toxins ### State every process and its danger ### A normal pH must not end the analysis ### Serial measurements confirm recovery