Electrolytes 2024 PDF

 are ions capable of carrying an electric charge.  Anions (-) move toward the anode, whereas cations (+) migrates in the direction of the cathode.  Examples: ▪ volume and osmotic regulation (Na, Cl, K) ▪ myocardial rhythm and contractility (K, Mg, Ca) ▪ cofa...

 are ions capable of carrying an electric charge.  Anions (-) move toward the anode, whereas cations (+) migrates in the direction of the cathode.  Examples: ▪ volume and osmotic regulation (Na, Cl, K) ▪ myocardial rhythm and contractility (K, Mg, Ca) ▪ cofactor in enzyme activation (Mg, Ca, Zn) ▪ regulation of ATPase ion pumps (Mg) ▪ acid base balance (HCO₃, K, Cl) ▪ blood coagulation (Ca, Mg) ▪ neuromuscular excitability , glucose metabolism (K, Ca, Mg)  40-75% of total body weight, with the values declining with age and especially with obesity.  Water is the solvent for all processes In the human body. it transports nutrients to cells, removes waste products by way of urine and acts as the body’s coolant by way of sweating.  located in intracellular and extracellular compartments, intracellular fluid (ICF) is the fluid inside the cells and accounts for about two thirds of total body water  extracellular fluid (ECF) accounts for the other one third of total body water and can be subdivided in the intravascular and extracellular fluid.  normal plasma is about 93% water, with the remaining volume occupied by lipids and proteins. the concentrations of ions within cells and in plasma are maintained both by energy –consuming active transport processes and by diffusion or passive transport processes.  Active transport is a mechanism that requires energy to move ions. because most biologic membranes are freely permeable to water but not to ions or proteins, the concentration of ions and proteins and blood pressure influence the flow of water across a membrane.  the concentration of solutes/kilogram of solvent  the parameter to test hypothalamus responds.  the regulation of osmolality also affects the sodium concentration in plasma, sodium and its associated anions account for approximately 90% of the osmotic activity in plasma. affecting the sodium concentration in blood volume.  normal plasma osmolality (275-295 mOsm/kg of plasma)  Respond to: sensation of thirst and ADH ▪ as excess intake of water lowers plasma osmolality, both ADH and thirst are suppressed. ▪ deficits of water will increase plasma osmolality, both ADH secretion and thirst are activated.  Compensation: ▪ renal water excretion prevents water overload ▪ thirst prevents water deficit or dehydration.  as excess intake of water (e.g in polydipsia) begins to lower plasma osmolality, both ADH and thirst are suppressed.  in the absence of ADH, water is not reabsorbed causing a large volume of dilute urine to be excreted as much as 10-20 L daily.  Hypoosmolality and Hyponatremia usually occur in patients with impaired renal excretion of water.  as a deficits of water begins to increase plasma osmolality, both ADH secretion and thirst are activated.  although ADH contributes by minimizing renal water loss, thirst is the major defense against hyperosmolality and hypernatremia.  At risk are infants and unconscious patients or anyone who is unable to either drink or ask for water.  Osmotic stimulation of thirst progressively diminishes in people who are older than age 60.  In older patient w/ illness and diminished mental status, dehydration becomes increasingly likely.  Blood volume is essential to maintain blood pressure and ensure good perfusion to all tissue and organs. sodium and water Renin-angiotensin- aldosterone system responds to decreased blood volume. ▪ renin is secreted near the renal glomeruli to decreased renal blood flow ▪ Renin converts angiotensinogen to angiotensin I which then becomes angiostensin II. ▪ angiostenin II causes vasoconstriction which quickly increases retention of sodium and the water accompanies in sodium.  Atrial natriuretic peptide (ANP) released from the myocardial atria in response to volume expansion, promotes sodium excretion in the kidney (B-type natruiretic peptide (BNP) and ANP act together in regulating blood pleasure and fluid balance.  volume receptors independent of osmolality stimulate the release of ADH which conserves water by renal absorption  Glomerular filtration rate (GFR) increase with volume expansion and decreases with volume depletion and  all other things equal, an increased plasma sodium will increase urinary sodium excretion and vice versa.  serum or urine sample.  Plasma use in not recommended because osmotically active substances may be introduced into specimen from the anticoagulant.  measurement of: ▪ freezing point depression ▪ vapor pressure. ▪ Osmolal Gap ▪ difference between the measured and calculated osmolality. ▪ indirectly indicates the presence of osmotically active substances other than Na, urea, or glucose, such as ethanol, methanol, ethylene glycol, lactate, or hydroxybutyrate.  Reference values ▪ Serum 275–295 mOsm/kg ▪ Urine(24-h) 300–900 mOsm/kg ▪ Urine/serum ratio 1.0–3.0 ▪ Random urine 50–1200 mOsm/kg ▪ Osmolal gap 5–10 mOsm/kg  Serum 275–295 mOsm/kg  Urine(24-h) 300–900 mOsm/kg  Urine/serum ratio 1.0–3.0  Random urine 50–1200 mOsm/kg  Osmolal gap 5–10 mOsm/kg THE ELECTROLYTES  most abundant cation in the ECF (90% of extracellular cations)  determines the osmolality of the plasma.  Na-K-ATPase ion pump moves three (3) Na+ ions out of the cell in exchange for two (2) K ions moving into the cell as ATP is converted to ADP  Three processes are of primary importance: (1) The intake of water in response to thirst, as stimulated or suppressed by plasma osmolality; (2) The excretion of water, largely affected by AVP release in response to changes in either blood volume or osmolality; (3) the blood volume status, which affects Na_ excretion through aldosterone, angiotensin II, and ANP (atrial natriuretic peptide)  60% to 75% of filtered Na is reabsorbed in the proximal tubule  Electroneutrality is maintained by either Cl- reabsorption or hydrogen ion secretion.  Hyponatremia, the most common electrolyte disorder, is defined as reduced plasma sodium concentration to a value less than 135 mmol/L  Generally, clinical concern arises when the concentration is less than 130 mmol/L.  If renal failure occurs, the kidneys ultimately fail to concentrate the urine, resulting to hyponatremia.  For every 100mg/dl increase in blood glucose, serum sodium decreases by 1.6 mmol/L-glucose is osmotically active and induces flow of water from the cells to the ECF, diluting its electrolytes. Accumulation of glucose or mannitol in the ECF is a well-known cause of hyponatremia because, glucose is osmotically active and induces diffusion of water from the cells to the ECF, thus diluting its electrolytes. In diabetes mellitus, sodium loss occurs with ketonuria.  Decreased serum sodium in SIADH is due to excess retention of water in the collecting ducts.  Potassium deficiency also causes loss of sodium because of the inverse relationship of the two  Symptoms of hyponatremia occurs if the serum level is 125-130 mmol/L  Serum sodium level of < 125 mmol/L may result to severe neuropsychiatric symptoms.  By examining the urinary sodium, potassium, and osmolarity, the causes of hyponatremia and hypernatremia can be readily determined.  Hyponatremia: Na Serum levels less than 133 mmol/L.  INCREASED WATER RETENTION  Levels below 130 mmol/L are ▪ Renal failure clinically significant ▪ Nephrotic syndrome ▪ Hepatic cirrhosis  INCREASED SODIUM LOSS ▪ Congestive heart failure ▪ Hypoadrenalism ▪ Potassium deficiency  WATER IMBALANCE ▪ Diuretic use ▪ Excess water intake ▪ Ketonuria ▪ SIADH ▪ Salt-losing nephropathy ▪ Pseudohyponatremia ▪ Prolonged vomiting or diarrhea ▪ Severe burns  WITH LOW OSMOLALITY  WITH HIGH OSMOLALITY ▪ Increased sodium loss ▪ Hyperglycemia ▪ Increased water retention ▪ Mannitol infusion  WITH NORMAL OSMOLALITY ▪ Increased nonsodium cations ▪ Lithium excess ▪ Increased _-globulins—cationic (multiple myeloma) ▪ Severe hyperkalemia ▪ Severe hypermagnesemia ▪ Severe hypercalcemia ▪ Pseudohyponatremia ▪ Hyperlipidemia ▪ Hyperproteinemia ▪ Pseudohyperkalemia as a result of in vitro hemolysis Symptoms  Between 125 & >130 mmol/L: gastrointestinal  < 125 mmol/L: Neuropyschiatric  < 120 mmol/L : medical emergency. Treatment  Treatment is directed at correction of the condition that caused hyponatremia  Treatment: ▪ fluid restrictions ▪ hypertonic saline ▪ pharmacologic agents. ▪ AVP antagonist (Conivaptan)  correcting severe hyponatremia too rapidly can cause cerebral myelinolysis and too slowly can cause cerebral edema.  Hypernatremia is  DECREASED WATER increased serum Na INTAKE concentration ▪ Older persons ▪ Infants  EXCESS WATER LOSS ▪ Mental impairment ▪ Diabetes insipidus ▪ Prolonged diarrhea  INCREASED INTAKE OR ▪ Profuse sweating RETENTION ▪ Severe burns ▪ Hyperaldosteronism ▪ Sodium bicarbonate excess ▪ Dialysis fluid excess  URINE OSMOLALITY 700 mOsm/kg ▪ Loss of thirst ▪ Insensible loss of water (breathing, skin) ▪ GI loss of hypotonic fluid ▪ Excess intake of sodium Symptoms  altered mental status, lethargy, irritability, restlessness, seizures, muscle twitching, hyperreflexes, fever, nausea or vomiting, difficult respiration, and increased thirst Treatment  Directed at correction of underlying conditions that caused hypernatremia  Hypernatremia must be corrected gradually because too rapid a correction of serious hypernatremia (> 160 mmol/L) can induce cerebral edema and death.  Specimen ▪ Plasma w/ lithium heparin, ammonium heparin, and lithium oxalate ▪ Hemolysis does not cause a significant change ▪ Marked hemolysis Na levels may be decreased as a result of a dilutional effect. ▪ Whole blood samples may be used with some ▪ 24-hr urine specimen for urine Na analyses ▪ Sweat is also suitable for analysis  Methods ▪ Flame emission spectrophotometry (FES) ▪ Atomic absorption spectrophotometry (AAS) ▪ ISEs.  Reference values ▪ Serum, plasma 36–145 mmol/L ▪ Urine (24-h) 40–220 mmol/day, varies with diet ▪ CSF 136–150 mmol/L  major intracellular cation in the body  Only 2% of the body’s total K circulates in the plasma.  It is the single most important analyte in terms of an abnormality being life threatening. Functions of K: ▪ regulation of neuromuscular excitability ▪ contraction of the heart ▪ ICF volume and ion concentration Regulation  Kidneys :proximal tubules reabsorb K+, Distal nephron is for excretion.  Exercise: Potassium is released from cells during exercise  Hyperosmolality: as with uncontrolled diabetes mellitus  Cellular Breakdown: Cellular breakdown releases K into the ECF. ▪ Eg: severe trauma, tumor lysis syndrome, and massive blood transfusions. (1) Na, K-ATPase pump - inhibited by hypoxia, hypomagnesemia, or digoxin overdose = K loss (1) Insulin promotes entry of K into skeletal muscle and liver by increasing Na, K-ATPase activity (1) Cathecholamines: epinephrine promotes cellular entry of K, propranolol impairs cellular entry of K+  Hypokalemia is a plasma K  RENAL LOSS concentration below the ▪ Diuretics—thiazides, lower limit of the reference mineralocorticoids range. ▪ Nephritis ▪ Renal tubular acidosis (RTA)  GI LOSS ▪ Hyperaldosteronism ▪ Vomiting ▪ Cushing’s syndrome ▪ Diarrhea ▪ Hypomagnesemia ▪ Gastric suction ▪ Acute leukemia ▪ Intestinal tumor  CELLULAR SHIFT ▪ Malabsorption ▪ Alkalosis ▪ Cancer therapy ▪ Insulin overdose ▪ Large doses of laxatives  DECREASED INTAKE Symptoms  weakness, fatigue, paralysis and constipation.  At risk are patients w/ cardiovascular disorders because of an increased risk of arrhythmia w/c can cause death Treatment  Oral or intravenous (IV) replacement  In some cases, chronic mild hypokalemia may be corrected simply by including food in the diet with high K content, such as dried fruits, nuts, bran cereals, bananas, and orange juice.  Plasma electrolytes are monitored as treatment to return K levels to normal occurs.  Patients with ▪ Chemotherapy hyperkalemia often have ▪ Leukemia an underlying disorder, ▪ Hemolysis such as renal insufficiency,  Increased intake diabetes mellitus, or ▪ Oral or IV potassium metabolic acidosis replacement therapy  Artifactual  Decreased renal excretion ▪ Sample hemolysis ▪ Acute or chronic renal ▪ Thrombocytosis failure ▪ Prolonged tourniquet or ▪ Hypoaldosteronism excessive fist clenching ▪ Addison’s disease ▪ Drugs (captropil, ▪ diuretics nonsteroidal anti-  Cellular shift inflammatory agents, ▪ Acidosis digoxin, cyclosporine and heparin treatment) ▪ Muscle/cellular injury Symptoms  muscle weakness (plasma K+ > 8mmol/L) , tingling, numbness, or mental confusion, cardiac arrhythmias and possible cardiac arrest. Treatment ▪ Calcium lowers the resting potential of myocardial cells ▪ sodium bicarbonate, glucose, or insulin - acutely shift K back into cells ▪ Diuretics ▪ sodium polystyrene sulfonate (Kayexalate) enemas ▪ Hemodialysis Specimen  Proper collection & handling of samples for K analysis is important.  artifactual hyperkalemia:. ▪ serum K higher than plasma K, ▪ Thrombocytosis can elevate K ▪ Prolonged application of tourniquet ▪ excessively clenching of fists  Serum, plasma, and 24-urine may be acceptable for analysis.  Heparin is anticoagulant of choice  whole blood samples for K determinations should be stored at room temperature, never iced (ice promotes the release of K from cells  analyzed promptly or centrifuged to remove the cells.  if hemolysis occurs after the blood is drawn, K may be falsely elevated—the most common cause of artifactual hyperkalemia. Method ▪ ISE w/ valinomycin membrane Reference Values ▪ Serum 3.5–5.1 mmol/L ▪ Plasma (Heparin) ▪ Males: 3.5–4.5 mmol/L ▪ Females: 3.4–4.4 mmol/L ▪ Urine (24-h) 25–125 mmol/day  Chloride (Cl) is the major extracellular anion.  maintains osmolality, blood volume, and electric neutrality (HCO3)  In most processes, Cl shifts secondarily to a movement of Na or HCO3 ions  absorbed by the intestinal tract and reabsorbed in proximal tubules  Excess Cl is excreted in the urine and sweat.  Excessive sweating stimulates aldosterone secretion w/c will conserve Na+ and Cl-  Chloride maintains electrical neutrality in two ways. ▪ Chloride acts as the rate-limiting component, in that Na reabsorption is limited by the amount of Cl available. ▪ Electroneutrality is also maintained by Cl through the chloride shift. ▪ bicarbonate diffuses out into the plasma and Cl- diffuses into the RBC to maintain electric balance of the cell  CO2 generated by cellular metabolism w/in tissue diffuses out into both plasma and rbc  In the RBC, CO2 forms carbonic acid, which splits into H+ and bicarbonate.  Deoxyhemoglobin buffers H+ whereas the bicarbonate diffuses out into the plasma and Cl- diffuses into the rbc to maintain electric balance of the cell  Chloride disorders are often a result of the same causes that disturb Na levels because Cl passively follows Na.  Hyperchloremia occurs due to excess loss of HCO3: ▪ GI losses ▪ RTA ▪ metabolic acidosis.  Hypochloremia occurs with excessive loss of Cl from: ▪ prolonged vomiting ▪ diabetic ketoacidosis ▪ aldosterone deficiency ▪ salt losing renal diseases (pyelonephritis)  Specimen ▪ Serum, plasma, 24-urine and sweat ▪ lithium heparin being the anticoagulant of choice. ▪ Hemolysis does not cause a significant change in serum or plasma values as a result of decreased levels of intracellular Cl-. However, with marked hemolysis, levels may be decreased as a result of a dilutional effect. ▪ Whole blood samples may be used with some analyzers. ▪ Sweat is also suitable for analysis.  Methods ▪ ISEs, amperometric-coulometric titration, mercuric titration, and colorimetry  Reference values ▪ Plasma, serum 98–107 mmol/L ▪ Urine (24-h) 110–250 mmol/day, varies with diet  Bicarbonate is the second most abundant anion in the ECF.  Total CO2: ▪ bicarbonate ion = 90%: ▪ carbonic acid ▪ dissolved CO2  HCO3 is the major component of the buffering system CO2 + H2O H2CO3 < -----→H+ + HCO3 CA CA  bicarbonate in the kidney is reabsorbed in the proximal tubules.  Acid-base imbalances cause changes in HCO3 and CO2 levels.  A decreased HCO3 may occur from metabolic acidosis  An increased HCO3 may occur from metabolic alkalosis  s/s of metabolic alkalosis include severe vomiting, hypokalemia and excessive alkali intake  Acid-base imbalances cause changes in HCO3 and CO2 levels.  A decreased HCO3+ may occur from metabolic acidosis as HCO3+ combines with H ion to produce CO2, which is exhaled by the lungs.  The typical response to metabolic acidosis is compensation by hyperventilation, which lowers pCO2.  Elevated total CO2 concentration occurs in metabolic alkalosis as HCO3 is retained.  s/s of metabolic alkalosis include severe vomiting, hypokalemia and excessive alkali intake  Specimen ▪ Serum or lithium heparin plasma is suitable for analysis under anerobic conditions. ▪ sample is capped until the serum or plasma is separated and the sample is analyzed immediately. ▪ If the sample is left uncapped before analysis, CO2 escapes. Levels can decrease by 6 mmol/L per hour.  Method ▪ ISE ▪ Enzymatic method  Reference Range: ▪ CO2 23 – 29 mmol/L  4th most abundant cation in the body  2nd most abundant intracellular ion  Approximately 53% of Mg2 in the body is found in bone, 46% in muscle and other organs and soft tissue, and less than 1% is present in serum and red blood cells.  Of the Mg2_ present in serum, about one third is bound to protein, primarily albumin. Of the remaining two thirds, 61% exists in the free or ionized state and about 5% is complexed with other ions, such as PO4+ and citrate. Similar to Ca2+, it is the free ion that is physiologically active in the body  cofactor of more than 300 enzymes  abnormal serum Mg levels is indicated in: ▪ Cardiovascular ▪ Metabolic disorders ▪ neuromuscular disorders.  The small intestine may absorb 20%–65% of the dietary Mg2+, depending on the need and intake of body Mg2+ is controlled largely by the kidney, which can reabsorb Mg2+ in deficiency states or readily excrete excess Mg2+ in overload states.  Of the nonprotein-bound Mg2+ that gets filtered by the glomerulus, 25%–30% is reabsorbed by the proximal convoluted tubule (PCT), unlike Na, in which 60%–75% is absorbed in the PCT. Henle’s loop is the major renal regulatory site, where 50%–60% of filtered Mg2+ is reabsorbed in the ascending limb.  The renal threshold for Mg2_ is approximately 0.60–0.85 mmol/L (1.46– 2.07 mg/dL) only about 6% of filtered Mg2+ is excreted in the urine per day  Mg2+ regulation appears to be related to that of Ca2_ and Na.  Parathyroid hormone (PTH) increases the renal reabsorption of Mg2_ and enhances the absorption of Mg2+ in the intestine. However, changes in ionized Ca2+have a far greater effect on PTH secretion.  Aldosterone and thyroxine apparently have the opposite effect of PTH in the kidney, increasing the renal excretion of Mg2+  most frequently observed in hospitalized individuals in ICUs or those receiving diuretic therapy or digitalis therapy.  Causes and Symptoms  oral intake: ▪ magnesium lactate ▪ magnesium oxide ▪ magnesium chloride ▪ antacid that contains Mg.  Parenteral MgSO4 solution  Before initiation of therapy, renal function must be evaluated to avoid inducing hypermagnesemia during treatment. Causes Symptoms of hypermagnesemia  Decreased excretion typically do not occur until the ▪ Acute or chronic renal failure serum level exceeds 1.5 mmol/L ▪ Hypothyroidism ▪ Hypoaldosteronism  CARDIOVASCULAR NEUROMUSCULAR ▪ Hypopituitarism (↓GH) ▪ Hypotension Decreased reflexes  Increased intake ▪ Bradycardia Dysarthria ▪ Heart block Respiratory depression ▪ Antacids ▪ Paralysi ▪ Enemas  Dermatologic Metabolic ▪ Cathartics ▪ Flushing Hypocalcemia ▪ Warm skin ▪ Therapeutic—eclampsia,  GI Hemostatic cardiac arrhythmia ▪ Nausea Decreased thrombin  Miscellaneous generation  Dehydration ▪ Vomiting Decreased platelet adhesion  Bone carcinoma  Neurologic  Bone metastases ▪ Lethargy ▪ Coma  Supportive therapy for cardiac, neuromuscular, respiratory, or neurologic abnormalities.  Hemodialysis - Patients with renal failure  Diuretic and IV fluid -Patients with normal renal function  Specimen ▪ Nonhemolyzed serum or lithium heparin plasma may be analyzed. Because the Mg2_ concentration inside erythrocytes is 10 times greater than that in the ECF, hemolysis should be avoided and the serum should be separated from the cells as soon as possible Oxalate, citrate, and (EDTA) anticoagulants are unacceptable because they will bind with Mg. ▪ A 24-hour urine sample is preferred for analysis because of a diurnal variation in excretion. ▪ The urine must be acidified with HCl to avoid precipitation.  Methods ▪ Colorimetric method ▪ calmagite, ▪ formazen dye ▪ methylthymol blue. ▪ AAS is the reference method  Reference Range ▪ Serum, colorimetric:.63–1.0 mmol/L (1.26–2.10 mEq/L)  essential for myocardial Contraction.  decreased concentrations can cause: ▪ neuromuscular irritability ▪ spasms (tetany) Regulation ▪ PTH, ▪ vitamin D ▪ Calcitonin  99% of Ca2_ in the body is part of bone.  The remaining 1% is mostly in the blood and other ECF.  Ionized calcium is a sensitive and specific marker for calcium disorders  Three hormones, PTH, vitamin D, and calcitonin, are known to regulate serum Ca2_ by altering their secretion rate in response to changes in ionized Ca2_.  PTH secretion in blood is stimulated by a decrease in ionized Ca2 and, conversely, PTH secretion is stopped by an increase in ionized Ca2_  PTH exerts three major effects on both bone and kidney. In the bone, PTH activates a process known as bone resorption, in which activated osteoclasts break down bone and subsequently release Ca2_ into the ECF. In the kidneys, PTH conserves Ca2_ by increasing tubular reabsorption of Ca2_ ions. PTH also stimulates renal production of active vitamin D.  Vitamin D3, a cholecalciferol, is obtained from the diet or exposure of skin to sunlight. Vitamin D3 is then converted in the liver to 25- hydroxycholecalciferol (25-OH-D3), still an inactive form of vitamin D. In the kidney, 25-OH-D3 is specifically hydroxylated to form 1,25- dihydroxycholecalciferol (1,25-[OH]2-D3), the biologically active form. This active form of vitamin D increases Ca2_ absorption in the intestine and enhances the effect of PTH on bone resorption.  Calcitonin, which originates in the medullary cells of the thyroid gland, is secreted when the concentration of Ca2_ in blood increases.  Calcitonin exerts its Ca2+ lowering effect by inhibiting the actions of both PTH and vitamin D. it is secreted in response to a hypercalcemic stimulus. Causes  Primary hypoparathyroidism: ▪ Glandular aplasia ▪ Destruction or removal  Hypomagnesemia  Hypermagnesemia  Hypoalbuminemia ▪ chronic liver disease ▪ nephrotic syndrome ▪ malnutrition  Acute pancreatitis  Vitamin D deficiency  Renal disease  Rhabdomyolysis  Pseudohypoparathyroidism Causes  Primary hyperparathyroidism  hyperplasia  Hyperthyroidism  Benign familial hypocalciuria  Malignancy  Multiple myeloma  Increased vitamin D  Thiazide diuretics  Prolonged immobilization  Specimen ▪ serum or lithium heparin ▪ EDTA or oxalate are unacceptable for use. ▪ samples must be collected anaerobically. ▪ analysis of Ca in urine, timed urine collection is used ▪ The urine should be acidified with 6 mol/L HCl, with approximately 1 mL of the acid added for each 100 mL of urine.  Methods ▪ ortho-cresolphthalein complexone (CPC) or arsenzo III dye ▪ 8-hydroxyquinoline to prevent Mg interference. ▪ AAS remains the reference method for total Ca  Higher thru adolescence when bone growth is most active.  Ionized/free Ca2_ concentrations is unstable from day 1 to day 3 of life the stabilizes then declines gradually through adolescence  TOTAL CALCIUM—SERUM, PLASMA ▪ Child,