--- module: 019-01 language: en chapter: 19 title: "Acid-Base Physiology and Clinical Interpretation" module_title: "Foundations" source_sha256: f40cd34c1174eeba883c639ec0de75d51d3c20361ab9d9fef621c6322f2dd1d2 --- # Acid-base physiology and clinical interpretation ## Why hydrogen ion concentration matters ### Proteins, enzymes, membrane excitability ### Vascular tone, potassium, oxygen binding ### Buffers, lungs and kidneys in sequence ### Disorders are processes, not numbers #### Coexisting disorders conceal one another ## Bicarbonate and carbon dioxide ### Carbon dioxide and water make carbonic acid ### Carbonic anhydrase in red cells and kidney ### pH follows bicarbonate over dissolved gas ### Lungs act in minutes, kidneys over days ### Bicarbonate is abundant and regulated ### Haemoglobin, plasma proteins, phosphate also buffer ### Bone buffers chronic load at mineral cost ## Renal acid handling ### Proximal tubule reclaims filtered bicarbonate #### Hydrogen secretion recovers existing buffer ### New bicarbonate needs urinary buffers ### Phosphate becomes titratable acid ### Glutamine yields ammonium and bicarbonate #### Ammonia trapped in the collecting system #### Acidosis increases ammoniagenesis ### Acidic urine may still mean low ammonium ## Systematic interpretation ### Assess the pH first ### Find the component explaining the direction ### Test whether compensation is appropriate ### Calculate the anion gap when acidotic ### Compare delta changes for mixtures ### Integrate electrolytes, history and treatment ### Compensation never overcorrects past normal ### Unexpected compensation means another disorder ## Metabolic acidosis ### Primary fall in bicarbonate ### Kussmaul breathing is respiratory compensation ### Gap: sodium minus chloride and bicarbonate #### Low albumin lowers the expected gap ### High gap: lactate, ketones, toxic alcohols ### Normal gap: loss or impaired excretion #### Diarrhoea, tubular acidosis, chloride-rich fluid ### Lactate when production exceeds clearance ### Ketoacidosis from insulin deficiency ## Metabolic alkalosis ### Primary rise in bicarbonate ### Generated by vomiting, diuretics, mineralocorticoid ### Persists when kidneys cannot excrete bicarbonate #### Volume, chloride and potassium depletion ### Urine chloride separates the two groups ### Severe alkalosis cuts cerebral and coronary flow ### Saline harms volume-overloaded alkalosis ## Respiratory disorders ### Acidosis from inadequate alveolar ventilation #### Sedation, weakness, obstruction, fatigue #### Acute retention, small bicarbonate rise #### Chronic retention brings renal compensation #### Acute-on-chronic hides behind normal pH ### Alkalosis when ventilation exceeds production #### Hypoxaemia, embolism, sepsis, salicylate #### Do not call hyperventilation anxiety first ## Mixed disorders and delta analysis ### Sepsis: lactic acidosis with hyperventilation ### Vomiting added to ketoacidosis ### Lung disease with diuretic alkalosis ### Compare gap rise with bicarbonate fall #### Larger fall adds a normal-gap acidosis #### Smaller fall suggests coexisting alkalosis ## Toxicological patterns ### Salicylate: alkalosis plus high-gap acidosis #### Tinnitus, fever, confusion, pulmonary oedema ### Toxic alcohols generate organic acids #### Osmolar gap falls as anion gap rises #### Visual toxicity points to methanol #### Oxalate and kidney injury with ethylene glycol ## Contexts, potassium and treatment ### Pregnancy lowers carbon dioxide physiologically #### Adult normal values may mean impairment ### Strong-ion difference complements bedside judgement ### Mineral acidosis shifts potassium outward ### Insulin drives potassium into cells ### Bicarbonate suits selected disorders only ### Definitive treatment corrects the cause