Acid

The clinician integrates acid-base and electrolyte physiology to manage complex, multi-disturbance clinical scenarios. Hydrogen ion homeostasis maintains arterial pH within the narrow range of 7.35-7.45 through three mechanisms: chemical buffering (bicarbonate system is the primary extracellular buffer: H2CO3 equilibrium with CO2 + H2O via carbonic anhydrase; the Henderson-Hasselbalch equation pH = 6.1 + log[HCO3-/0.03 x PaCO2] defines this relationship), respiratory compensation (chemoreceptors in the medulla and carotid bodies adjust minute ventilation within minutes to modulate PaCO2), and renal regulation (proximal tubule reclaims filtered bicarbonate, intercalated cells of the collecting duct secrete hydrogen ions or bicarbonate, and ammoniagenesis produces new bicarbonate -- full renal compensation requires 3-5 days). Electrolyte disturbances frequently accompany acid-base disorders: metabolic acidosis causes transcellular potassium shift (hydrogen ions enter cells, potassium exits to maintain electroneutrality -- for every 0.1 decrease in pH, serum potassium increases approximately 0.6 mEq/L), while metabolic alkalosis causes hypokalemia through the reverse mechanism. Chloride-responsive metabolic alkalosis (urine chloride less than 20 mEq/L -- vomiting, nasogastric suction, diuretics) responds to saline and chloride repletion, while chloride-resistant metabolic alkalosis (urine chloride greater than 20 mEq/L...