Electrolytes

Chloride Major Extracellular anion (~103 mEq/L) Maintains hydration, osmotic pressure, ionic balance Changes parallel changes in Na ISE Silver Chloride/silver sulfide sensing element Also colorimetric and coulometric- amperometric (Ag + + Cl -  AgCl) Sweat Chloride Cystic Fibrosis

Chloride Metabolism Obtained from the diet and completely absorbed in the gut Excreted through the GI tract, skin, urine Reabsorbed by the proximal tubule and the Loop of Henle

Chloride Clinical Significance Normal Range ( mmol/L) Increased Hyperparathyroidism, renal tubular disease, diarrhea, dehydration, Chronic Heart Failure CHF Decreased Salt losing renal disease, overhydration, prolonged vomiting, burns

Sweat Chloride 17 th Century Saying “Woe to that child who when kissed on the forehead taste salty. He/She is bewitched and soon must die” Pilocarpine nitrate A stimulant which causes localized sweating so that sweat may be collected and analyzed

Sweat Chloride for Cystic Fibrosis / Gauze soaked in pilocarpine nitrate and potassium sulfate reagents Gauze is placed on the arm and connected to the electrodes Sweat is then analyzed for chloride Ranges –Normal = 0 – 35 mmol/L –Ambiguous = mmol/L –Cystic Fibrosis = >60 mmol/L

CO 2 Primarily bicarbonate Keep sample capped to prevent loss of CO 2 –Dissolved CO 2 escapes rapidly once the sample is opened

CO 2 Specimen Serum or heparinized plasma (venous blood)

CO 2 Measurement Sample must be acidified or alkalinized Acidification converts various forms of CO 2 to gaseous CO 2 Alkalinizing converts all CO 2 to HCO 3 - Measurements involve electrode-based or enzymatic methods –Electrodes – use PCO2 electrode –Enzymatic – convert to bicarbonate HCO 3 - react with phosphoenolpyruvate, measure a decrease in absorbance at 340nm (NADH + H +  NAD + )

CO 2 Clinical Significance Normal Range (23-30 mmol/L) Increased Metabolic Alkalosis, Compensated respiratory acidosis, Emphysema Decreased Metabolic Acidosis, Compensated respiratory alkalosis, Hyperventilation

Sodium Major extracellular cation (serum/plasma concentration mEq/L, urine concentration mEq/24hr) Functions in maintaining osmotic pressure in the ECF Highly regulated by the kidneys –70%-80% reabsorbed in the proximal tubules –20%-25% reabsorbed in the loop of Henle

Sodium Specimen Serum or heparinized plasma (no sodium- containing anticoagulants) –Must be centrifuged in <30 min from collection Serum/plasma may be stored at 2-4°C Urine collected unpreserved Hemolysis DOES NOT cause significant errors Lipemic samples should be measured by direct ion-selective electrode Avoid IV line draws (draw below IV)

Sodium Measurement Atomic Absorption Spectra (AAS) Flame Emission Spectra (FES) Ion-selective Electrode (IES) –Sodium electrode with a glass membrane –Potentiometric method –Indirect = sample is diluted with a high ionic strength buffer –Direct = no dilution –Subject to error by lack of selectivity, protein coating, and salt-bridge competition with the selected ion

Clinical Significance: Sodium Hypernatremia –Water deficiency –Excessive sweating –Fever –Burns –Hyperventilation –Diabetes insipidus –Diarrhea and vomiting

Clinical Significance: Sodium Hyponatremia –Water excess (dilutional hyponatermia) –Heart failure, liver disease, nephrotic syndrome, renal failure –Inappropriate ADH –Sodium deficit > water deficit – vomiting diarrhea, GI obstruction, burns, diuretics, hypoaldosterone –ECF to ICF –Psuedohyponatremia – hyperglycemia, hyperlipidemia, hyperglobulinemia

Potassium Major intracellular cation (serum/plasma concentration of mEq/L, urine concentration mEq/24hr) Highly reabsorbed in the proximal tubules Secreted by the distal tubules for Na + exchange when influenced by aldosterone Potassium is required for muscle irritability, respiration, and myocardial function

Potassium Specimen MUST avoid hemolysis Levels in plasma and whole blood are mEq/L lower than serum (due to platelet release of K + in serum) CANNOT refrigerate whole blood sample –Falsely increased due to poor K-ATPase pump regulation = leaking CANNOT store unseparated at room temp –Glycolysis occurs and shifts K + to ICF Therefore, collect the sample between C, and centrifuge within 30 min.

Potassium Measurement Atomic Absorption Spectra (AAS) Flame Emission Spectra (FES) Ion-selective Electrode (IES) –Potassium electrode with liquid ion-exchange membranes which incorporate valinomycin –Potentiometric method –Indirect = sample is diluted with a high ionic strength buffer –Direct = no dilution –Subject to error by lack of selectivity, protein coating, and salt-bridge competition with the selected ion

Clinical Significance: Potassium Hyperkalemia (Addison’s, Acidosis, Cardiac Arrest) –Pseudohyperkalemia – hemolysis, leukocytosis –High intake/Decreased excretion – renal failure, hyperalsodteronism, diuretics –SYMPTOMS: changes in EKG, arrhythmia, muscle weakness, paresthesias, cardiac arrest

Clinical Significance: Potassium Hypokalemia (Cushings, Alkalosis, Arrhythmias) –ECF to ICF due to alkalosis, increased insulin –Decreased intake –Increased GI loss – vomiting, diarrhea, malabsorption, laxatives –Increased urinary loss – increased aldosterone, renal disease, tubular acidosis, Fanconi syndrome –SYMPTOMS: nausea, vomiting, abdominal distension, muscle cramps, EKG changes, lethargy, confusion No renal threshold for potassium!

Electrolyte Exclusion Principle The exclusion of electrolytes from the fraction of plasma which is occupied by solids Solids occupy 7% of plasma (93% is water) Therefore, 145 x (100/93) = 156 mEq/L Becomes a problem during hyperlipidemia or hyperproteinemia

Anion GAP (Na + K) – (Cl+ CO 2) (10 -20) Or Na – (Cl +CO 2) (8-16) Difference between unmeasured anions and unmeasured cations Increased Renal failure, diabetic acidosis, lactic acidosis, drugs or toxins or lab error Decreased QC Check Can’t be a negative number Analytical error, such as false elevated Cl or low Na Lipemia

Correlations