Electrolytes Part 1 PDF

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Summary

- Electrolytes are considered the most critical tests in the lab. This is because extremely high or low values for electrolytes can lead to very critical patient conditions. - Electrolytes are ionic compounds held together by electrostatic attraction between ions opposing charges. The compound itsel...

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MLSC-3111, Clinical Biochemistry II -

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Electrolytes are considered the most critical tests in the lab. This is because extremely high or low values for electrolytes can lead to very critical patient conditions. Electrolytes are ionic compounds held together by electrostatic attraction between ions opposing charges. The compound itself has no charge but when it dissociates in solution it creates charged elements that can react and conduct electricity. Cations are positively charged (sodium, potassium, calcium) and anions are negatively charged (chloride, bicarbonate, phosphate). The term electrolytes in the clinical lab only refers to sodium, potassium, chloride, and total CO2. Changes in any of these electrolytes can cause changes in other electrolytes and significant clinical conditions. Electroneutrality, the sum of all cations must equal the sum of all anions. It is essential for the body to remain in this state. Disturbances to electrolyte balance are extremely life threatening and require immediate intervention. Therefore, electrolytes are often ordered as stat. Electrolyte panels are prone to preanalytical error, so it is important to be careful when doing them.

Functions of Electrolytes -

Transmission of electrical impulses Act as cofactors in enzymatic reactions Aide in hormone release. Regulate blood volume and osmotic pressure. Regulate electrical balance between intra and extracellular fluid. Involved in blood coagulation. Because of these reasons, electrolytes are very helpful in identifying if clinical symptoms that are caused by a lack of electroneutrality. Electrolytes are also good markers for treatment response status and are used to monitor patient rehabilitation. Can also do the reverse to monitor problems that arise from treatment (side effects).

Types of Fluid/Electrolyte Imbalances -

Fluid Volume Imbalance, composition and concentration of electrolytes remains normal, but they change relatively due to a direct increase/decrease in water volume. Fluid Concentration Imbalance, Fluid volume and electrolyte composition are unchanged, but a disease is causing an overall excess or deficit of electrolytes. Fluid Composition Imbalance, fluid volume and overall electrolyte concentration is normal but the composition of electrolytes changes (High calcium, but low potassium makes the total electrolyte amount unchanged but individual levels different).

MLSC-3111, Clinical Biochemistry II Fluid and Electrolyte Regulation -

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The RAAS is an endocrine pathway that regulates blood pressure (activated in low blood pressure) and results in fluid retention and vasoconstriction. It also is a major regulator of electrolytes. The RAAS system is activated by decreased renal perfusion (low filtrate volume) or decreased Na+/Cl- levels. This affects the electrolyte and fluid balance. Angiotensinogen is made in the liver and is turned into angiotensin I by renin from the kidney. Both compounds are not biologically active, but once ACE from the capillaries turns angiotensin I into angiotensin II, it becomes biologically active and will act on the body (SNS stimulation, reabsorption of electrolytes, aldosterone release to retain electrolytes and water, arterial vasoconstriction, ADH secretion). All the products/symptoms from angiotensin II negatively influence the kidney to decrease the secretion of renin. This allows for a negative feedback loop to stop renin release when the body is at equilibrium. ADH, stops urine from being passed. Results in increased fluid retention. Released by the presence of angiotensin II. Stimulates thirst. Kidneys control body fluid volume by adjusting the amount of water secreted via urine in response to ADH. ADH will be inhibited when the body has too much water (results in transparent urine that is very diluted) Aldosterone, causes the retention of sodium and chloride in exchange for secreting potassium and hydrogen. If the body is low on sodium or chloride, aldosterone will cause tubular reabsorption of the sodium and chloride rich urine (causes dilute urine). If the body is high in sodium and chloride, aldosterone is inhibited to stop sodium and chloride reabsorption (causes concentrated urine). Aldosterone and ADH work together the regulate fluid and electrolyte balance, If ADH worked alone, it can increase the hydrostatic pressure in the body, causing potential brain edema and coma. In increased aldosterone release, urine becomes diluted and urine SG is lower than 1.005. In decreased aldosterone, urine is concentrated and urine SG is greater than 1.025 – 1.035.

Sodium -

The largest contributor to the extracellular fluid osmolality (2Na + GLU + UREA). It is 10 times more concentrated in extracellular fluid compared to intracellular fluid. The typical reference range for sodium is 135 – 147 mmol/L. Hyponatremia, low plasma Na. Most common abnormality in clinical biochemistry. Can lead to edema, seizures, respiratory arrest, coma (from brain edema) and death. o Dilutional Hyponatremia, sodium is diluted due to an increase of water volume in the body. Causes edema from dilute fluid being pushed out of blood vessels from high hydrostatic pressure. o Depletional Hyponatremia, sodium content is lost from the body from other clinical situations. Usually does not cause edema or serious symptoms.

MLSC-3111, Clinical Biochemistry II -

Hypernatremia, high plasma Na. Less common but also extremely fatal, especially if it is acute. Can be due to water loss from dehydration (increases Na from water loss) or increased sodium retention (not usually from diet alone but can be caused by drowning in/drinking sea water).

Chloride -

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The major anion in the extracellular fluid. Secreted by the stomach’s parietal cells as HCl. Acts as a buffer with CO2. Has a direct relationship with sodium. It maintains electroneutrality by being reabsorbed by the kidneys along with Na+ proportionally (balance the charges). It also has a reciprocal relationship with TCO2 via the Cl- shift. As bicarbonate moves out of the cell, Cl- moves in (and vice versa) to maintain electroneutrality. It also has a reciprocal relationship with H+ via isohydric shift. Enables the exchange with H+ (HCO3 buffers H+) to maintain blood pH. The typical reference interval for Chloride is 96 – 108 mmol/L. Hypochloremia, low plasma Cl-. Seen in metabolic alkalosis where high concentrations of negative bicarbonates causing a negative shift away from electroneutrality. The body responds by excreting chloride to compensate. Hyperchloremia, high plasma Cl-. Causes similar symptoms to Na+ since Cl- regulation is like Na+. Seen in metabolic acidosis where bicarbonate levels are too low. Low bicarbonate doesn’t allow for H+ buffering (increased pH), leading to a positive shift away from electroneutrality. The body responds to this by reabsorbing negatively charged chloride to compensate. Cl- testing is of little value in non-acid/base disturbances. It is useful in acid base disorders that involve altered levels of bicarbonates. Exchange with bicarbonate in acid-base metabolism and disturbances can cause Cllevels to not correlate with Na+ levels anymore (Na+ is not significant in acid base imbalances). Chloride levels are collected in sweat to assess for cystic fibrosis. Also, bacterial meningitis raises the negatively charged protein level in CSF. The body lowers the concentration of chloride anions in the fluid to compensate for the charge imbalance in the CSF, which can be seen in analysis.

Preanalytical Considerations for Na+ and Cl-

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The sample can be collected as serum or heparinized plasma for testing. Stored at RT or 4 degrees Celsius. All green tubes are not created equal, since some use sodium heparin tubes which will throw off electrolyte values. Purple top EDTA tubes cannot be used either since EDTA is a weak acid. This will damage the electrodes used in analysis. Grey top NaF tubes cause positive interferences when the Fluoride (or any other halides like Bromide and Iodide) in the tube is mistaken for chloride in the analyzer.

MLSC-3111, Clinical Biochemistry II -

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Cells must be separated from plasma ASAP and are to be remained capped. The longer the plasma is exposed to RBCs, the more the RBCs will metabolize. Prolonged RBC metabolism in the tube will increase bicarbonate levels and decrease Cl-. Exposure to air will increase Cl- as CO2 escapes into the atmosphere. Hemolysis in the tube will falsely increase potassium levels since RBCs are very high in intracellular potassium. Lipemic samples can cause some analyzers to produce falsely low Na+ readings. These samples are either ejected, analyzed differently, or separated from the lipids in the sample.

Collection Considerations for Na+ and Cl-

Urine Collection, usually done through timed or 24-hour urine collections without preservatives. This is because of the large diurnal variation for urine Na+ (lower at night). Spinal Fluid, it is similar to plasma. Stool and Gastric Fluid, usually requires sample prep to remove particulate matter. Catheters, often flushed with saline and can affect results. You must remove 5.5 times the dead space (tube volume between the catheter and the sampling port) and discard the blood prior to sample collection.

Potassium -

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Functions to regulate heart rhythm but does not have a strong effect on osmolality. The reference ranges for potassium are 3.5 – 5.0 mmol/L. Hypokalemia, low plasma K+. More common than hyperkalemia and can cause death. o Fanconi Syndrome, tubular acidosis that affects K+ reabsorption. Results in a lose of K+ by the kidneys. o Increased loss via GI Tract, diarrhea and vomiting or misuse of laxatives (water loss increased). Increased Cellular Uptake of K+, Insulin also lowers K+ since insulin causes cellular uptake of glucose. When glucose moves into the cells, potassium follows it causing decreased sodium concentration in the ECF. o Reduced Dietary Intake, starvation. o Excessive use of Diuretics, promotes K+ excretion. Aldosterone lowers potassium via secretion into the urine when it saves sodium. pH causes a change in potassium levels since there is a reciprocal movement of K+ and H+. Acidosis increases H+ plasma concentration which causes H+ to go into the cells and potassium to come out of the cells (increases plasma K+). Alkalosis decreases H+ plasma concentration which causes H+ to exit the cells and potassium to enter the cells (decreases plasma K+).

Hyperkalemia, high plasma K+. Less common but one of the most serious electrolyte emergencies. Causes include…

MLSC-3111, Clinical Biochemistry II

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o Increased Dietary/Oral Intake o Renal Failure, decreased GFR will disrupt the kidneys ability to excrete potassium, causing it to back up into the plasma. o Metabolic Acidosis, H+ goes into the cells as K+ goes out to balance the ECF pH. o Hypoaldosteronism, K+ reabsorption to balance the loss of Na+. o Uncontrolled Type I Diabetes, glucose and K+ are not entering the cells since insulin isn’t working to bring glucose into the cell. Considered the most important electrolyte affected by diabetes. o Cellular Destruction, cells are filled with K+ so when they are destroyed (hemolysis) all their intracellular K+ is released in the plasma. o Excessive K+ Replacement Therapy o Following Exercise, excessive exercise can cause damaged cells which increases ECF K+. Critical values for hyperkalemia are < 2.5 mmol/L or > 6.0 mmol/L. Death will occur at > 10.0 mmol/L. Both severe hypokalemia and severe hyperkalemia are medical emergencies requiring prompt intervention. K+ is a critical assay and ordered STAT. Critical values are to be reported immediately to the physician because treatment occurs immediately but slowly to avoid shocking the body with a change in concentration.

Preanalytical Considerations for K+ -

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Potassium is 37 times higher within RBCs than in plasma. This means that hemolyzed samples gives us extremely falsely elevated K+ levels. Do not ever report a potassium level on a hemolyzed sample without consulting your lab’s policies. Hemolysis, as hemolysis increases sodium decreases relatively because of the dilution effect. The lysis of the RBCs also releases ICF water into the plasma, diluting the Na+ levels. If a whole blood sample has a high potassium result, you can check if it is due to hemolysis by centrifuging the sample or allowing the RBCs to settle to look for hemolysis. Storage at Cold Temperatures, the cold will slow down the Na/K pumps on RBCs as it slows down their metabolism. Results in less potassium going into the cells and more leaking into the plasma. K+ will increase in the tube 0.1 mmol/L/hour in the first hour of storage and 0.4 mmol/L/hour afterwards at 4 degrees Celsius. Because of this, samples for potassium should not be collected on ice or stored in the cold. If multiple samples are ordered alongside K+ that require refrigeration, then run the LYTES asap and then refrigerate. You could also collect 2 tubes for LYTES and the others. Delayed Centrifugation, sample should be spun within 3 hours to avoid false increases. Inappropriate Transportation, Hot trucks can falsely decrease K+ since heat accelerates the Na/K pump resulting in more K+ being pumped into the RBCs.

MLSC-3111, Clinical Biochemistry II -

Evaporation, leaving tubes uncapped will falsely increase K+ due to evaporation of plasma water. Serum vs. Plasma levels, K+ is higher in serum than plasma since clotting releases K+ from platelets. Inappropriate Blood Collection, excessive tourniquet and fist pumping causes K+ to falsely increase by up to 10-20%. Uncapped Centrifuging, falsely increases electrolyte concentration by up to 132% through losing water components as they spill out during centrifugation....