Body Fluid Composition

Body Fluid Composition Main Electrolyte Composition (Pattern) Fluid Acid–Base Effect if Lost Common Clinical Scenario Replacement Regimen High Na ? Serum (ECF) High Cl ? Haemorrhage, Neutral (baseline) dehydration 0.9% NaCl or Hartmann’s (balanced crystalloid) ± blood if needed low K ? High H ? High Cl ? Gastric aspirate moderate Na Metabolic alkalosis Prolonged vomiting, 0.9% NaCl + KCl (corrects Cl? NG suction depletion + K? loss) Mild metabolic acidosis Biliary fistula, Ttube loss ? L ow K ? High Na ? Moderate Bile HCO? ? Cl ? Hartmann’s or 0.9% NaCl ± K ? High HCO? Pancreatic fluid ? Na Metabolic acidosis (loss of base) Pancreatic fistula Hartmann’s (contains lactate ? converted to HCO??) Metabolic acidosis High-output ileostomy 0.9% NaCl + K? (often large volumes required) Usually minimal acid–base effect Excess sweating, burns Oral fluids if mild; 0.9% NaCl if significant loss ? High Na ? Ileostomy fluid High HCO? ? some K ? Hypotonic; low Na ? Perspiration & Cl ? relative to plasma Calculation of Body Compartment Composition 60 – 40 – 20 Rule Compartment % of Body Weight % of TBW Volume in 70 kg Adult Total Body Water (TBW) 60% 100% 42 L Intracellular Fluid (ICF) 40% ? of TBW 28 L Extracellular Fluid (ECF) 20% ? of TBW 14 L Interstitial 15% ¾ of ECF 10.5 L Intravascular (plasma) 5% ¼ of ECF 3.5 L Acid/Base and Electrolyte Disturbances in Surgical Conditions Condition Acid–Base Disturbance Key Electrolyte Changes Why (Mechanism) Excessive gastric losses (vomiting/NG suction) Metabolic alkalosis ? Cl?, ? K?, ? Na? Loss of HCl ? alkalosis; volume depletion ? RAAS ? K? wasting Pancreatic fistula Metabolic acidosis ? HCO??, ? Na?, Loss of bicarbonate-rich ? K? pancreatic fluid Small intestinal fistula Metabolic acidosis ? Na?, ? K?, ? HCO?? Loss of alkaline small bowel contents Biliary fistula Mild metabolic acidosis ? Na?, ? HCO?? Loss of sodium + bicarbonatecontaining bile Diarrhoea Metabolic acidosis (normal ? HCO??, ? K? anion gap) Bicarbonate loss from colon Intestinal obstruction Early: Metabolic alkalosis; ? K?, ? Cl? Late: Metabolic acidosis Vomiting early; later ischemia ? lactic acidosis Pyloric obstruction Severe metabolic alkalosis ? Cl? (very low), Persistent vomiting of gastric ? K?, ? Na? acid Peritonitis Metabolic acidosis ? Na?, ? K? (may Sepsis ? lactic acidosis; third occur) spacing Burns Early: Metabolic acidosis ? K? (early), ? Na Cell lysis ? K? release; capillary ? leak ? fluid shifts Urine Electrolyte and Osmolarity Changes Condition Urine Na? Urine Osmolality Why? (Mechanism) ATN (Acute Tubular ? (>40 Necrosis) mmol/L) Low–normal (<350 mOsm/kg) Tubules damaged ? cannot reabsorb Na? or concentrate urine Dehydration (prerenal) ? (<20 mmol/L) High (>500 mOsm/kg) Kidneys conserve Na? + water SIADH ? (>40 mmol/L) High (>100–300 mOsm/kg) ADH causes water retention ? concentrated urine despite low serum Na? DI (Diabetes Insipidus) Normal–low Very low (<300, often <100 mOsm/kg) No ADH effect ? cannot concentrate urine CHF ? (<20 mmol/L) High (>300–500 mOsm/kg) Low effective circulating volume ? RAAS + ADH activation Renal Control of Electrolytes and Fluids Sodium Factor Effect Aldosterone increased Na+ reabsorption at the PCT increased Na+ levels RAAS SNS SNS renal vasoconstriction and indirect activation of Na+ channels increased Na+ levels Natriuretic Peptides (ANP and High arterial pressure inhibit Na+ reabsorption at the DCT decrease Na+ BNP) levels decrease Na+ levels Arterial Pressure/Blood Volume Increased renal perfusion indirect decrease in Na+ and H2O reabsorption decrease Na+ levels High GFR low Na+ GFR Low GFR high Na+ Peritubular Capillary High hydrostatic pressure or low oncotic pressure in peritubular capillaries inhibit Na+ reabsorption Acidosis Decrease Na+ Potassium Factor Effect Aldosterone (main regulator) Increased Na+/K+ activity increase K+ excretion decrease serum K+ High K+ levels Stimulates aldosterone production increased K+ excretion decrease serum K+ Alkalosis Alkalosis intracellular K+ shift increases K+ excretion decrease serum K+ Acidosis Acidosis inhibits K+ excretion increases serum K+ Diuretics Inhibit K+ absorption K+ excretion increased serum K+ Water Factor Effect ADH (main regulator) Increases water reabsorption increases water retention Plasma osmolality High plasma osmolality stimulates osmoreceptors in the hypothalamus ADH release increased water retention Effective arterial blood volume Hypovolemia or hypotension baroreceptors ADH increased water retention overrides osmotic regulation Medullary osmotic gradient Concentration gradient at loop of henle SNS SNS reduce GFR decrease water excretion increased water retention