CHAPTER 15: ELECTROLYTES

Electrolytes- ions capable of carrying an electric charge Classification: 1. Anions- negative charge and move toward the anode 2. Cations- positive charge, migrate toward the cathode Functions:  volume and osmotic regulation (sodium, chloride, potassium)  myocardial rhythm and contractility (potassium, magnesium,calcium)  cofactors in enzyme activation (magnesium, calcium, zinc)  regulation of ATPase ion pumps (magnesium)  acid-base balance (bicarbonate, potassium, chloride)  blood coagulation (calcium, magnesium)  neuromuscular excitability (potassium, calcium, magnesium)  production and use of ATP from glucose (magnesium, phosphate) WATER  40% to 75% of total body weight  values declining with age and obesity  women have lower water content than men as a result of higher fat content  solvent for all processes in the human body  transports nutrients to cells  determines cell volume by its transport into and out of cells  removes waste products by way of urine  body’s coolant by sweating Intracellular Fluid- fluid inside the cells, 2/3 of body water Extracellular Fluid- 1/3 of total body water, subdivided into the intravascular extracellular fluid (plasma) and the interstitial cell fluid that surrounds the cells in the tissue Normal plasma- 93% water, the rest is composed of lipids and proteins Active transport- requires energy to move ions across cellular membranes Diffusion- passive movement of ions across membrane, depends on size, charge of ion and nature of membrane

OSMOLALITY  physical property of a solution based on the concentration of solutes (mmoles per kg of solvent, w/w) Freezing point depression & Vapor pressure decrease- basis for routine measurement of Osmolality Osmolarity- reported as milliosmoles per liter  parameter to which hypothalamus responds  thirst and arginine vasopressin hormone (AVP) secretion- stimulated by the hypothalamus in response to an increased osmolality of blood Thirst- important in mediating fluid intake AVP- secreted by posterior pituitary gland  water conserved, osmolality , turns off AVP secretion Clinical Signifance of Osmolality  Na+, and its associated anions account for approx. 90% of osmotic activity in plasma  osmolality (Na+) –regulated by changes in water balance  volume- regulated by changes in Na+ balance Normal plasma osmolality: (275–295 mOsm/kg of plasma H2O)  1%–2% osmolality, fourfold in circulating concentration of AVP  1%–2% osmolality, shuts off AVP production AVP- increases reabsorption of water in the Cortical and medullary collecting tubules; has half life of 15-20 mins.  Renal water excretion- controls water excess  Thirst- controls water deficit/ dehydration Water Load  plasma osmolality, AVP and thirst are suppressed, vol. of dilute urine excreted (10-20 L daily) Water Deficit  plasma osmolality, AVP & thirst are activated Thirst- major defense against hyperosmolality and hypernatremia

Inside the cells ATPase ion pumps. headache.nephritic syndrome. Retention of Na+ & water that accompanies Na+ Factors affecting blood vol.neuropsychiatric symptoms including nausea and vomiting.serum/plasma level <135mmol/L. result of plasma/serum water displacement Symptoms of Hyponatremia:  125 and 7130 mmol/L.assoc. methanol. Atrial natriuretic peptide (ANP) 2. Excretion of H2O 3. water imbalance  Urine Na+ > 20mmol/day – acute/ chronic renal failure  Urine Na+ <20mmol/day. muscular weakness. Volume receptors independent of osmolality 3. one of the most common electrolyte disorders  May be caused by Na+ loss.assoc. urea.difference bet. moves 3 Na+ ions out and 2 K+ ions into the cell K+ . Blood vol.Hypernatremia. Renin is secreted due to renal blood flow 2. status  60% to 75% of filtered Na+ is reabsorbed in the proximal tubule. Renin converts angiotensin I to angiotensin II 3.common in infants. w/ pulmonary disease. Glomerular filtration rate 4.gastrointestinal  Below 125 mmol/L. freezing pt temp and vapor pressure  Turbid serum and urine samples should be centrifuged before analysis Osmometers.medical emergency Treatment of Hyponatremia:  fluid restriction and providing hypertonic saline and/or other pharmacologic agents  correcting it too rapidly. w/ liver cirrhosis w/ ascites. hepatic cirrhosis  Defect in AVP – assoc. hypothyroidism. some in the loop and distal tubule Clinical Applications Hyponatremia.: 1.Na+ is measured using indirect ion-selective electrodes (ISEs) in a patient who is hyperproteinemic or hyperlipidemic. Intake of H2O in response to thirst 2. solns.cerebral edema Conivaptan. w/ 270mmol/L being the result of Na+ and anions  Much larger conc. CNS disorders. ethylene glycol. Angiotensin II causes vasoconstriction 4. and ataxia  Below 120 mmol/L for 48 hours or less (acute hyponatremia).prevent equilibrium from occurring.excessive H2O intake Determination of Osmolality Specimen  Serum or urine Discussion  Osmolality.cerbral myelinolysis  correcting it too slowly. water retention. Osmolal gap. infections or trauma Pseudohyponatremia.dilutes the sample prior to analysis. lactate. ethanol.major intracellular cation Regulation 3 processes: 1. Increased plasma Na+ Polydipsia.that operate by freezing point depression are standardized using NaCl ref.blocks the action of AVP in the collecting ducts of nephron. seen w/ in vitro analysis Indirect ISE. unconscious patients or anyone who is unable to either drink or ask for water Regulation of Blood Volume  Essential to maintain blood pressure & ensure good perfusion to all tissue and organs 1. w/ SIADH. or Bhydroxybutyrate THE ELECTROLYTES SODIUM  Most abundant cation in ECF (90%)  Normal plasma osmolality is 295mmol/L. overhydrated postoperative patients . the measured and calculated osmolality  Indirectly indicates presence of osmotically active substances other than Na+. glucose. Blood pressure and aldosterone 5. CHF. adrenal insufficiency Hypervolemic hyponatremia. lethargy. not effective for hypovolemic hyponatremia Euvolemic hypernatremia. malignancies.

plasma K conc.promote cellular entry Propranolol. nausea/vomiting. muscle twitching. Indirect. digoxin overdoes 2. less commonly seen in hospitalize patients  Loss of hypotonic fluid may occur either by the kidney or through profuse sweating. impairment of urinary K excretion  Therapeutic K admin. 20x greater inside than outside of cell  Only 2% of total K circulates in plasma  Major effect on contraction of skeleteal and cardiac muscles  Plasma K resting membrane potential.most common cause Symptoms of Hypokalemia:  Weakness. decreased water intake.Hypernatremia. Catecholamines: Epinephrine. seizures. Contraction of heart 3. whole blood w/ analyzers.decreases cell excitability.most common cause Symptoms of hyperkalemia: .not significant  24 hr collection. net difference  Lower than normal difference – increases cell excitability.usually have an underlying disorder.specimen of choice for urine Na analyses Method  flame emission spectrophotometry (FES).hypoxia. difficult respiration. Insulin promotes acute entry of K into skeletal muscle & liver 3. restlessness. constipation. w/ defect in the osmoreceptors Symptoms of Hypernatremia:  altered mental status.releases K into the Clinical Applications Hypokalemia.principal determinant of urinary K excretion Factors affecting K Distribution: 1. maximal rate should be 0.protein buildup POTASSIUM  Major intracellular cation. paralysis. K loss.lack of muscle excitability. Hypokalemia. hyperreflexes. H+ concentration Hyperkalemia. fatigue.undiluted sample react w/ ISE.. ammonium heparin.most routinely done. atomic absorption spectrophotometry (AAS)  Chemical methods. lethargy. hypomagnesemia. measures plasma water only. w/ 60-75% mortality rate Treatment of Hypernatremia:  should be corrected gradually  rapid correction.impairs cellular entry   ECF Exercise – K is released from cells Cellular breakdown. or severe burns  Chronic hypernatremia in alert patientsindicative of hypothalamic disease. paralysis. ICF volume 4.excess loss of H2O relative to Na+ loss.5 mmol/L per hr Determination of Sodium Specimen Serum. Regulation of neuromuscular excitability 2.. bananas) Hyperkalemia. sweat  hemolysis. diarrhea. plasma (w/ lithium heparin.  Thiazide diuretics. or increased Na intake or retention. lack of precision  ISE. fever. arrhythmia. urine. increased risk of arrhythmia Treatment of hypokalemia:  Oral KCl replacement of K  Intravenous replacement  Food high in K content (nuts. Direct.outdated due to large sample vol. and increased thirst  Serum Na >160mmol/L – assoc. uses 2 electrodes: reference electrode (constant potential). muscle weakness  Excess K is secreted in urine Funtions: 1. irritability. fatal cardiac. more accurate 2. lithium oxalate). cereals.induce cerebral edema and death. measuring electrode Types of ISE: 1.arrhythmia. paralysis Regulation  Kidneys are important in K balance  Distal nephron.diluted sample  Source of error in ISE.

and >1% in serum and red blood cells  Essential cofactor of more than 300 enzymes Regulation  Sources. and metabolic abnormalities Treatment of Hypomagnesemia: . sweat  excessive sweating.uses acid reagent  enzymatic method MAGNESIUM  4th most abundant cation  2nd most abundant intracellular ion  Average human body contains 1 mole of Mg  53% of Mg2 is found in bone. 46% in muscle and other organs and soft tissue.excess loss of HCO3 as a result of GI losses.most common Specimen Serum.excessive loss of Cl from prolonged vomiting. numbness. uses ion-exchange membrane  amperometric-coulometric titration.etc. diabetic ketoacidosis. Muscle weakness. and colorimetry BICARBONATE  2nd most abundant anion in ECF  Composes the largest fraction of total CO2  Major component of the buffering system in the blood Regulation  85% is reabsorbed in proximal tubules  15% in distal tubules Clinical Application  Acid-base imbalances cause changes in HCO3 and CO2 levels  HCO3 – metabolic acidosis  Metabolic alkalosis. plasma (sample is capped until examination to prevent CO2 escapes) Method  ISE.maintains electroneutrality Hyperchloremia.uses valinomycin membrane CHLORIDE  major extracellular anion  maintains osmolality. thyroxine. tingling. mental confusion.. or insulin. cardiac arrhythmia Treatment of hyperkalemia:  Ca 2+ provides immediate but short-lived protection to the myocardium  sodium bicarbonate.uses silver ions  mercurimetric titration. or salt losing renal diseases such as pyelonephritis Specimen Serum. may also be administered  hemodialysis Collection of Samples Causes of Artifactual Hyperkalemia: 1. RTA. coagulation 2. glucose. hypokalemia. blood vol. neuromuscular.anticoagulant of choice Method ISE. excessive alkali intake Determination of Carbon Dioxide Specimen Venous serum. 24hr urine. hemolysis.severe vomiting. urine  heparin.increases renal reabsorption of Mg  Aldosterone. Plasma (lithium heparinanticoagulant of choice). or metabolic acidosis Hypochloremia. aldosterone deficiency. psychiatric. sweat Methods  ISE – most common.increases renal excretion of Mg Hypomagnesemia. and “hard” drinking water.mostly observed in ICU or those receiving diuretic therapy/ digitalis therapy Symptoms of Hypomagnesemia:  cardiovascular. long tourniquet application 3.raw nuts. whole blood w/ analyzers. storage in ice 4.  Henle’s loop is the major renal regulatory site  Parathyroid hormone. electric neutrality  completely absorbed in the GI tract  excess is secreted in urine. dry cereal. plasma.stimulates aldosterone secretion Chloride shift.

nephrolithiasis and nephrocalcinosis Treatment of hypercalcemia:  estrogen replacement therapy  Parathyroidectomy may be necessary in some hyperparathyroidic patients  Salt and water intake  Biphosphanates.main drug Specimen Serum.active form of Vit.cardiovascular. EDTA-not acceptable Methods Colorimetric:  Calmagite method.electrocardiogram changes. urine acidified w/ 6mol/L of HCl  No liquid heparin should be used Methods  ortho-cresolphthalein complexone (CPC)uses 8-hydroxyquinoline to prevent Mg interference .colored complex AAS.mild drowsiness/weakness. and lethargy  life-threatening.most common cause  dehydration.constipation. tetany.inactive form of vitamin D  1.D resistance  Pseudohypoparathyroidism.for it inhibits glandular secretion of PTH. 24 hr urine acidified w/ HCl  oxalate. anorexia. coma. respiratory depression or arrest. and paralysis treatment of hypermagnesemia:  discontinue the source of Mg2  hemodialysis  diuretic. sedation. nausea. depression. lethargy. calcitonin.frequent cause is hypomagnesemia. increased skin temperature. neurologic. and hemostatic abnormalities  moderate. seizures  cardiac irregularities.arrhythmia. muscle cramps.from the medullary cells of thyroid gland.colored complex  Methylthymol blue.main cause is primary hyperparathyroidism (excess secretion of PTH)  2nd cause. or magnesium chloride or an antacid w/ Mg2  severely ill patients. neuromuscular. bradycardia.reddish-violet complex  Formazen dye. heart block. oral intake using magnesium lactate.rare hereditary disorder in w/c PTH target tissue response is decreased  blood-ionized Ca concentrations in neonates are high at birth and then decline Symptoms of hypocalcemia:  Neuromuscular irritability.regulates serum Ca  PTH secretion stimulated. Of vitamin D  25-hydroxycholecalciferol. asystole.causes pseudohypermagnesemia Symptoms of hypermagnesemia:  most frequent. vomiting.parasethesia.activates bone resorption. dermatologic. causes vit. may cause neuromuscular irritability (tetany-irregular muscle spasm) Regulation  PTH. citrate.malignancy  Thiazide diuretics Symptoms of hypercalcemia:  Neurologic. D. vomiting. stimulates renal prod. coma  GI.25-dihydroxycholecalciferol.ionized Ca  PTH. D  Calcitonin. 1% in blood & ECF Hypocalcemia. peptic ulcer  renal symptoms. heart block Treatment of hypocalcemia:  Oral or parenteral Ca  Vitamin D Hypercalcemia. skin flushing. IV fluid Specimen Nonhemolyzed serum. an MgSO4 solution is given parenterally Hypermagnesemia. lithium heparin plasma w/o venous stasis. magnesium oxide. GI.reference method for measuring Mg CALCIUM  Essential for myocardial contraction  Decreased ionized Ca impairs mycordial function. lithium heparin plasma. metabolic. Distribution  99% is part of bone. secreted when Ca conc. vit. impairs PTH action.hypotension. increases tubular reabsorption of Ca.less frequently than hypomagnesemia  renal failure. nausea.

base-excess determinations. arsenzo III dye  can be reduced to molybdenym blue-stable blue chromophore LACTATE  by-product of an emergency mechanism that produces a small amount of ATP when oxygen delivery is severely diminished  pyruvate-normal end product of glucose metabolism  conversion of pyruvate to lactate is activated when a deficiency of oxygen leads to an accumulation of excess NADH  citric acid cycle.major cause of hypophosphatemia. creatine phostphate.hyperparathyroidism. pulmonary edema.should be avoided  phosphate levels. severe infection. longterm treatment with total parenteral nutrition. increases lactate levels  Heparinized blood on ice. salicylate poisoning) Specimen  Tourniquet. lowers blood conc by increasing renal excretion  Vitamin D. or severe blood loss) 2.high in morning. fluoride. Type 2. 1% serum/plasma Hypophosphatemia. chronic obstructive pulmonary disease (COPD). peroxidase *Kindly check the tables found in the book (very useful). pulse oximeters. Also. inflammatory bowel disease. 20% in soft tissue. and measurements of oxygen consumption  enzymatic method. Anion Gap is not included here (sorry).major organ in lactate removal  Gluconeogenesis. lost from bone  PTH. toxins (ethanol.produces 38 moles of ATP  accumulation of excess lactate. Reservoirs of biochemical energy Transcellular shift.high risk w/ acute or chronic renal failure  Neonates are susceptible. laxative  severe infections. leukemia. malignancy.satisfactory additives Methods  Lactate-sensitive indicator of inadequate tissue oxygenation  indwelling catheters that measure blood flow. reabsorption in kidney  Growth hormone.increases phosphate absorption in intestine. Feel free to read the book for more elaborate explanations. lithium heparin plasma.causes venous stasis.increased incidence in patients w/: diabetic ketoacidosis. vitamin D deficiency or antacid use Hyperphosphatemia.most impt. low in evening Methods  mostly involves formation of ammonium phosphomolybdate complex  read at 340nm . increased shift of phosphate into the cell Regulation  Absorbed in the intestine from dietary sources.assoc.  Goodluck! MERRY CHRISTMAS! PHOSPHATE  predominant intracellular anion  Important in biochemical processes  ATP. This is just a summary. asthma.indicator of oxygen deprivation Regulation  oxygen delivery lactate conc.uses lactate oxidase.  intensive exercise.from cow’s milk. lymphoblastic leukemia Specimen Serum. anorexia nervosa. sepsis  Other causes.increases phosphate Distribution  Mostly organic phosphate  80% in bone. plasma must be quickly separated  Iodoacetate. neoplastic disorders. or intravascular hemolysis.metabolic origin (DM.most important factor. Type A. myocardial infarction. severe congestive heart failure. liver or renal disease. methanol.  Liver. released from cells into blood. w/ hypoxic conditions (shock. phosphoenolpyruvate.urine 24 hr  hemolysis. and alcoholism.lactate to glucose Clinical applications Lactic acidosis: 1.