NursingCrib.com Fluids and Electrolytes

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Fluids and ElectrolytesWater, water everywhere… but not a drop to drink…

WALT WHITMAN

FLUID BALANCE Water and its electrolytes are distributed in two major compartments: 63% of the total body water is found within cells across the age groups. 37% of the total body water is found outside the cells, mainly in tissue spaces, plasma of blood, and lymph. The intracellular and extracellular fluid compartments are maintained in a steady state to ensure proper physiologic functioning. Water and its electrolytes are distributed in two major compartments: 63% of the total body water is found within cells across the age groups. 37% of the total body water is found outside the cells, mainly in tissue spaces, plasma of blood, and lymph. The intracellular and extracellular fluid compartments are maintained in a steady state to ensure proper physiologic functioning.TOTAL BODY WATER (AS PERCENTAGE OF BODY WEIGHT) IN RELATION TO AGE AND SEXAGE MALE FEMALEUNDER 18 65% 55%

18-40 60% 50%40-60 50-60% 40-50%

OVER 60 50% 40%

Intracellular Fluid Compartment Includes all the water and electrolytes inside the cells of the body. Approximately 63% of the total body water is contained within cell membranes. Contains high concentrations of potassium, phosphate, magnesium and sulfate ions, along with most of the proteins in the body.EXAMPLE: How much water is in the intracellular fluid compartment of a 25-year old male patient who weighs 60 kg?

Step #1: Compute the total body water (TBW) based on age and sex.TBW = (60 kg) (0.6)

= 36 kg weight of water= 36 liters volume of water

Step #2: Compute for the intracellular fluid volume (usually 63% of the total body water is intracellular fluid)

ICF = (36 liters) (0.63) = 22.7 liters

Extracellular Fluid Compartment Includes all the fluid outside the cells: interstitial fluid, plasma, lymph, secretions of glands, fluid within subcompartments separated by epithelial membranes.

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Constitutes approximately 37% of the total body water. Contains high concentrations of sodium, chloride and bicarbonate. One-third of the ECF is in plasma.

EXAMPLE: How much water is in the circulatory system of a 32-year old female patient who weighs 52 kg?Step #1: Compute for the total body water based on age and sex.

TBW = (52 kg) (0.5)= 26 kg weight of water= 26 liters volume of water

Step #2: Compute for the extracellular fluid volume (usually 37% of the total body water).ECF = (26 liters) (0.37) = 9.6 liters

Step #3: Compute for the plasma volume.Plasma = (9.6 liters)/3

= 3.2 litersTranscellular Exchange Mechanisms: ACTIVE TRANSPORT PASSIVE TRANSPORT Diffusion Osmosis Filtration Facilitated diffusion

Serum Osmolality Reflects the amount of solute particles in a solution and is a measure of the concentration of a given solution. Can be calculated using the formula:

Osmserum = 2 (Na) + BUN + glucoseNormal value = 285 – 295 mosm/kg

Sodium is the most active determinant of serum osmolality and is therefore actively moved across membranes to ensure normal osmolality.

Hence, if too much salt is used in food, the pulse hardens.

HUANG TI (THE YELLOW EMPEROR), 2697-2597 B.C.

Ions

NORMAL VALUES AND MASS CONVERSION FACTORSNormal Plasma Values

Mass Conversion

Sodium (Na+) 135 – 145 meq/L 23 mg = 1 meqPotassium (K+) 3.5 – 5.0 meq/L 39 mg = 1 meq

Chloride (Cl-) 98 – 107 meq/L 35 mg = 1 meqBicarbonate (HCO3-) 22 – 26 meq/L 61 mg = 1 meq

Calcium (Ca2+) 8.5 – 10.5 mg/dL 40 mg = 1 mmolPhosphorus 2.5 – 4.5 mg/dL 31 mg = 1 mmolMagnesium (Mg2+) 1.8 – 3.0 mg/dL 24 mg = 1 mmol

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Osmolality 285 – 295 mosm/kg265 - 305 mosm/kg

-

Sodium Dominant extracellular ion. About 90 to 95% of the osmotic pressure of the extracellular fluid results from sodium ions and the negative ions associated with them. Recommended dietary intake is less than 2.5 grams per day. Kidneys provide the major route by which the excess sodium ions are excreted.Sodium In the presence of aldosterone, the reabsorption of sodium ions in the loop of Henle is very efficient. When aldosterone is absent, the reabsorption of sodium in the nephron is greatly reduced and the amount of sodium lost in the urine increases. Also excreted from the body through the sweat mechanism. Primary mechanisms that regulate the sodium ion concentration in the extracellular fluid: Changes in the blood pressure Changes in the osmolality of the extracellular fluid

Sodium Regulation

Potassium Electrically excitable tissue such as muscle and nerves are highly sensitive to slight changes in extracellular potassium concentration. The ECF concentration of potassium must be maintained within a narrow range for tissues to function normally. Aldosterone also plays a major role in regulating the concentration of potassium ions in the ECF. Circulatory system shock resulting from plasma loss, dehydration, and tissue damage causes extracellular potassium ions to become more concentrated than normal. In response, aldosterone secretion increases and causes potassium secretion to increase.Potassium regulation

NORMAL Na+

INCREASED SODIUM

Increased ADH secretion, Decreased urine volume and increased plasma volume

Decreased aldosterone secretion, decreased sodium reabsorption

DECREASED SODIUM

Decreased ADH secretion, Increased urine volume and decreased plasma

volume

Increased aldosterone secretion, increased sodium reabsorption

INCREASED SODIUM

DECREASED SODIUM

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Calcium Extracellular concentration of calcium ions is maintained within a narrow range. Increases and decreases in ECF concentration of calcium ions have dramatic effects on the electrical properties of excitable tissues. Parathyroid hormone (PTH) secreted by the parathyroid glands increases extracellular calcium levels. Calcitonin is secreted by the thyroid gland. It reduces blood levels of calcium when they are too high. Calcium Regulation

Phosphate and Sulfate Phosphate and sulfate are reabsorbed by active transport in the kidneys. Rate of reabsorption is slow, so that if the concentration of these ions in the filtrate exceeds the ability of the nephron to reabsorb them, the excess is excreted in the urine.

NORMAL K+

INCREASED POTASSIUM

Increased aldosterone secretion with increased potassium secretion by the

kidneys and increased potassium in urine

DECREASED POTASSIUM Decreased aldosterone secretion with

decreased potassium secretion by the kidney and decreased potassium in the

urine

INCREASED POTASSIUM

DECREASED POTASSIUM

NORMAL Ca++

INCREASED CALCIUM DECREASED

CALCIUM

Increased Calcitonin secretion with decreased bone resorption

Decreased parathyroid hormone secretion with decreased bone resorption, decreased intestinal

calcium absorption, and decreased kidney calcium reabsorption

DECREASED CALCIUM

INCREASEDCALCIUM

Increased parathyroid hormone secretion with increased bone resorption, increased intestinal

calcium absorption, and increased renal calcium reabsorption

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Fluid and Electrolyte ManagementGeneral Management of FluidsMaintenance Therapy:Minimum Water Requirements Can be estimated from the sum of the urine output necessary to excrete the daily solute load (500 mL per day if the urine concentrating ability is normal) plus the insensible water losses from the skin and respiratory system (500 to 1000 mL per day), minus the amount of water produced from endogenous metabolism (300 mL per day) Two to three liters of water are needed to produce a urine volume of 1 to 1.5 liters daily.

Fluid / Electrolyte Replacement:Insensible Water Losses Usually average 500 to 1000 mL daily, and depend on respiratory rate, ambient temperature, humidity and body temperature. Water losses increase by 100 ml daily for each degree of body temperature over 37°C. Fluid losses from sweating can vary enormously and depend on physical activity and body and ambient temperature. Mechanical ventilation accentuate losses from the respiratory tract.A 72-year old female was admitted for pneumonia in the elderly, community-acquired.

Previous day’s profile:Total urine output: 1,700 ml3 episodes of loose stools, approximately 250 per episodeHighest temperature: 39.7 degrees CelsiusOn mechanical ventilator for the past three days

Today’s Orders:NGT feeding with the following:

TCR: 1700 kcal/day6 equal feedings, 2:1 dilutionFlush with 100 ml plain water after every feeding

Compute for the IVF rate for today if the patient is to be connected to an adult venoset.What would be your choice of IVF?Maintenance Therapy:Minimum Water Requirements Weighing the patient daily is the best means of assessing net gain or loss of fluid, since the gastrointestinal, renal and insensible fluid losses of the hospitalized patient are unpredictable.

ECF Volume Depletion Occurs with losses of both sodium and water. The character of the fluid loss will dictate the clinical picture. If the loss is isotonic, the osmolality is unaffected and intracellular volume will change minimally. Loss of hypotonic fluid will lead to an increase in serum or plasma osmolality.

ECF Volume Depletion

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TYPE OTHER NAME RESULTING SERUM OSMOLALITY

Hypotonic volume loss Hypertonic or hyperosmolar dehydration

Elevated serum osmolality

Hypertonic volume loss Hypotonic or hypoosmolar dehydration

Decreased serum osmolality

Isotonic volume loss Isotoniic or normoosmolar dehydration

Normal serum osmolality

TYPE CLASSIC EXAMPLES MANAGEMENT

Hypotonic volume loss Diabetes insipidus (predominant water loss)

Hypotonic fluid replacement

Hypertonic volume loss Burns, Nephrotic syndrome

Hypertonic fluid replacement

Isotonic volume loss Most usual types of dehydration (gastrointestinal losses, etc.)

Isotonic fluid replacement(goal: restore volume)

Manifestations of ECF volume depletion depend on the magnitude and on serum osmolality.

Symptoms:

Anorexia Nausea Vomiting Apathy Weakness Orthostatic lightheadedness Syncope Weight loss is an important sign and provides an estimate of the magnitude of the volume deficit. Other physical findings: Orthostatic hypotension Poor skin turgor Sunken eyes Absence of axillary sweat Oliguria Tachycardia Shock and coma (severe volume depletion)

ECF Volume Depletion: Treatment Should be directed at restoration of the ECF volume with solutions containing the lost water and electrolytes. Daily assessment of weight, ongoing fluid losses and serum electrolyte concentrations. Mild degrees of volume depletion can be corrected orally.

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More severe deficits accompanied by circulatory compromise should be treated initially through intravenous isotonic fluid replacement until hemodynamic stability has been restored. One to two liters of fluid should be given over the first hour.

Parenteral Solutions

Further therapy should be guided by the symptoms and signs. Used in reference to fluids administered via extra-enteric routes, usually intravenous. May either be colloidal solutions or crystalline solutions.

Parenteral Solution

Osmolality Contents Indications

Colloidal solutions

May be isotonic, although most are hypertonic

Water and organic solutes

Hypertonic volume loss, parenteral nutrition, volume expanders

Crystalloids Variable, depending on the electrolyte contents

Water and mostly electrolytes

Volume replacement

Parenteral Solutions(Crystalloids)COMMONLY USED PARENTERAL SOLUTIONS

IV Solutions Osmolality(mosm/kg)

Glucose(g/liter)

Sodium(meq/liter)

Chloride(meq/liter)

5% D/W 252 50 - -

10% D/W 505 100 - -

50% D/W 2525 500 - -

0.45% NaCl 154 - 77 77

0.9% NaCl 308 - 154 154

3% NaCl 1026 - 513 513

Ringer’s lactate

282 - 130 109

5% D/NR 294 50 147 147

5% D/NM 290 50 77 77

ECF Volume ExcessManifestations: Weight gain is the most sensitive and consistent sign of ECF volume excess. Edema is usually not apparent until 2 to 4 kg of fluid have been retained. Dyspnea Tachycardia Jugular venous distention Hepatojugular reflux

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Rales on pulmonary auscultation

Causes: Heart, liver or renal failure Excessive renal sodium and water retention Unnecessary salt administration

Treatment Must address not only the ECF volume excess but also the underlying pathologic process. Treatment of the nephrotic syndrome and the cardiovascular volume overload associated with renal failure. Treatment of heart failure and cirrhosis

.Fluid and Electrolyte ManagementSodium The primary extracellular cation. Always accompanies water in the extracellular fluid compartment.Hyponatremia Defined as serum concentration less than 135 meq/L. Most common electrolyte abnormality observed in a general hospitalized population. Initial approach is the determination of serum osmolality.

HyponatremiaHyponatremia

SERUM OSMOLALITY

Normal Low High

ISOTONICHyponatremia

HyperproteinemiaHyperlipidemia

HYPERTONICHyponatremiaHyperglycemia

Mannitol, sorbitol,Glycerol, maltose

HYPOTONICHyponatremia

VOLUME STATUS

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Treatment Hypertonic (3%) saline with furosemide is indicated for symptomatic hyponatremic patients. For asymptomatic patients, approach includes water restriction, isotonic saline infusion and administration of demeclocycline.Hypernatremia Serum sodium > 145 meq/L Develops from excess water loss, frequently accompanied by an impaired thirst mechanism.Hypernatremia: Treatment Directed toward correcting the cause of the fluid loss and replacing water and, as needed, electrolytes. Calculation of water deficit: When calculating fluid replacement, both the deficit and the maintenance requirement should be added to each 24-hour replacement regimen.

Calculation of water deficit (cont’d)Water deficit = current TBW x ([Na] – 140)

140where [Na] is the measured serum sodium andTBW is the total body water (as percentage of the total body weight based on age and

sex. Given a 38/F with a body weight of 50 kg and a serum sodium level of 160 meq/L:What is the total water deficit?How much water should you give your patient during the first 24 hours?Hypernatremia: TreatmentWater deficit = TBW x ([Na] - 140)

140 = (50 kg)(0.5) (160-140)

140 = 25 liters (20)

140 = 25 liters (0.14)

= 3.5 litersVolume to be replaced in 24 hours =

TBW x (160 – 148)

HyponatremiaHyponatremia

VOLUME STATUS

HypovolemicEuvolemic

HypervolemicUna <10 meq/LExtrarenal saltDehydrationDiarrheaVomiting

Edematous states:Congestive heart failureHepatic diseaseNephrotic syndromeAdvanced CHF

SIADHPostop HypoNaHypothyroidismPsychogenic polydipsiaBeer potomaniaDrug reactions

Una >20 meq/LRenal salt lossDiureticsACE-inhibitorsNephropathiesMineralo-Corticoid lack

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148= 25 liters (12)

148= 25 liters (0.08)= 2 liters

Fluid and Electrolyte ManagementPotassium

Hypokalemia A total body deficit of about 350 meq occurs for each 1 meq/L decrement in serum potassium concentration. Changes in blood pH and hormones (insulin, aldosterone, and β-adrenergic agonists) independently affect serum potassium levels.Hypokalemia: Clinical Findings Symptoms and Signs: Muscular weakness Fatigue Muscle cramps Constipation or ileus Flaccid paralysis, hyporeflexia, and rhabdomyolysis

Laboratory Findings: Decreased amplitude and broadening of the T waves Prominent U waves Depressed ST segments T wave inversion Atrioventricular block (1st, 2nd, 3rd degree AV blocks) Cardiac arrest

Note: Hypokalemia also increases the likelihood of digitalis toxicityHypokalemia: Treatment Safest way is with oral potassium. Intravenous replacement is indicated for patients with severe hypokalemia. If serum potassium is > 2.5 meq/L, and there are ECG abnormalities, potassium can be given at a rate of 10 meq/L/hr in concentration that should never exceed 80 meq/L. For severe deficiency, potassium may be given through a intravenous cutdown. Occasionally, hypokalemia may be refractory to potassium replacement. Magnesium deficiency may make potassium correction more difficult. Concomitant magnesium repletion avoids this problem.

Hypokalemia: Treatment SEVERITY RECOGNITION MANAGEMENTMild Low serum potassium levels

Rarely symptomatic+/- EKG manifestationsNo arrhythmia orhemodynamic instability

Dietary potassium replacement

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Moderate Low serum potassium, usually symptomatic with EKG abnormalities+/- arrhythmia, but hemodynamically stable

Intravenous potassium replacement, maximum dilution of 40 meq/L, running at max rate of 5 meq/hr

Severe With arrhythmia and evidence of hemodynamic instability

IV potassium replacement, maximum dilution of 100 meq/L, max rate of 10 meq/hr

ORAL POTASSIUM REPLACEMENTS

AMOUNT meq OF K ANION NAMES

LIQUIDS 15 ml 10 Cl 5% Potassium chloride

15 ml 20 Cl 10% Potassium chloride

15 ml 40 Cl 20% Potassium chloride

15 ml 20 Gluconate

Potassium gluconate

POWDERS Packet 15 Cl K-lor

Packet 20 Cl Potassium chloride

Packet 25 Cl K-lyte

TABLETS 1 8 Cl Slow-K

1 8 Cl Micro-K extencaps

1 10 Cl K-dur 10

1 20 Cl K-dur 20

POTASSIUM CONTENT OF FOODSVERY HIGH(12-20 meq)

HIGH(5-12 meq)

BEANS Garbanzo beansSoy beans

Kidney beans Navy beansLima beans Pinto beans

FRUIT (1/2 cup or as stated)

Papaya (one medium) Apricots (3 halves)Banana (6”)Cantaloupe (1/4”)Honeydew melon (1/4”)Orange (3”) and orange juicePear (one large)Prunes (4) and prune juiceRhubarb

POTASSIUM CONTENT OF FOODS

VERY HIGH(12-20 meq)

HIGH(5-12 meq)

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VEGETABLES (1/2 cup or as stated)

Artichoke (one)Avocado (1/4)Brussel sproutsCarrot (7 ½”) and chardKetchup (1 tbsp)Potato (one baked, one broiled, 10 fries, ½ cup mashed)Pumpkin and spinachTomato (one) and tomato juice

Hyperkalemia Many are spurious or associated with acidosis Common practice of repeatedly clenching and unclenching the fist during venipuncture may raise the potassium concentration by 1-2 meq/L by causing local release of potassium from forearm muscles.

CAUSES OF HYPERKALEMIA

SPURIOUS Leakage from erythrocytes if separation of serum from clot is delayed.

Thrombocytosis

Marked leukocytosis

Repeated fist clenching during phlebotomy

Specimen drawn from arm with infusion

DECREASED EXCRETION Renal failure, acute and chronic

Severe oliguria

Renal secretory defects

Adrenocortical insufficiency

Hyporeninemic hypoaldosteronism

Spironolactone, triamterene, ACE-I, trimethoprim, NSAIDs

CAUSES OF HYPERKALEMIA

SHIFT FROM TISSUES Burns, rhabdomyolysis, hemolysis

Metabolic acidosis

Hyperosmolality

Insulin deficiency

Hyperkalemic periodic paralysis

Succinylcholine, arginine, digitalis toxicity, beta-adrenergic blockers

EXCESSIVE INTAKE Over treatment, orally or parenterally

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Hyperkalemia: Clinical Findings Weakness and flaccid paralysis Abdominal distention and diarrhea ECG is not a sensitive method, but if abnormalities are present, the most common findings are: Peaked T waves ST segment elevation Tachyarrhythmia / supraventricular tachycardia Ventricular tachycardia Ventricular fibrillation Cardiac arrest

Hyperkalemia: Treatment Confirm that the elevated level of serum potassium is genuine. Measure plasma potassium. Withholding of potassium. Giving cation exchange resins by mouth or enema: polystyrene sulfate, 40-80 g/day in divided doses. Emergent treatment is indicated if cardiac toxicity or muscular paralysis is present, or if hyperkalemia is severe (> 6.5-7 meq/L) even in the absence of ECG changes. Insulin plus 10-50% glucose may be employed to deposit potassium with glycogen in the liver. Calcium may be given intravenously as an antagonist ion. Stimulate transcellular shifts by giving beta-adrenergic agonist drugs. Sodium bicarbonate as an emergency measure. Hemodialysis or peritoneal dialysis.

EMERGENCY TREATMENT OF HYPERKALEMIA

MODALITY MECHANISM OF ACTION

ONSET DURATION

PRESCRIPTION K REMOVED FROM BODY

Calcium Antagonizes cardiac conduction abnormalities

0-5 min

1 hour Ca gluconate 10%, 5-30 ml IV;CaCl 5%, 5-30 ml IV

None

Bicarbonate

Shifts K into cells

15-30 min

1-2 hours NaHCO3 44-88 meq IV

None

Insulin Shifts K into cells

15-60 min

4-6 hours SAI, 5-10 u IV, plus glucose 50%, 25 g IV

None

Albuterol Shifts K into cells

15-30 min

2-4 hours Nebulized albuterol, 10-20 mg in 4 ml saline

None

NON-EMERGENCY TREATMENT OF HYPERKALEMIA

MODALITY MECHANISM OF ACTION

DURATION OF TREATMEN

PRESCRIPTION K REMOVED FROM

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T BODYLoop diuretic

Increased renal K excretion

0.5-2 hours Furosemide 40-160 mg IV or orally with or without NaHCO3, 0.5-3 meq/kg daily

Variable

Sodium polystyrene sulfonate (Kayexalate

Ion exchange resin binds K

1-3 hours Oral: 15-30 g in 20% sorbitol (50-100 ml)Rectal: 50 g in 20% sorbitol

0.5-1 meq/g

Hemodialysis

Extracorporeal K removal

48 hours Blood flow > 200-300 ml/min; Dialysate K = 0

200-300 meq

Peritoneal dialysis

Peritoneal K removal

48 hours Fast exchange, 3-4 L/hr 200-300 meq

POTASSIUM EXCRETION

TRANSCELLULAR SHIFTING CARDIAC STABILIZER

Dialysis Diuretics Ion-

exchange resins administered orally or transrectally

Glucose and insulin infusion every 6 hours

Sodium bicarbonate infusion every 6 hours

Beta-adrenergic agonist nebulization every 6 hours

Calcium gluconate 10% via slow IV push every 15 minutes for a maximum of three doses

Fluid and Electrolyte ManagementCalcium Constitute 2% of body weight, but only 1% of the total body calcium is in solution in body fluid. In plasma, calcium is present as a non-diffusible complex with protein (33%); as a diffusible but undissociated complex with anions like citrate, bicarbonate, and phosphate (12%); and as ionized calcium (55%). Normal total plasma (or serum) calcium concentration is 8.5 to 10.5 mg/dL. It is the ionized calcium that is necessary for muscle contraction and nerve function (normal: 4.7 to 5.3 mg/dL).Hypocalcemia Seen commonly in critically ill patients due to acquired defects in parathyroid-vitamin D axis. Results occasionally in hypotension which responds to calcium replacement therapy.

CAUSES OF HYPOCALCEMIA

DECREASED INTAKE OR ABSORPTION

Malabsorption

Small bowel bypass, short bowel

Vitamin D deficit

INCREASED IONS Alcoholism

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Chronic renal insufficiency

Diuretic therapy (furosemide or bumetanide)

ENDOCRINE DISEASES True and pseudohypoparathyroidism

Calcitonin hypersecretion

PHYSIOLOGIC CAUSES Alkalosis and decreased response to vit. D

Decreased serum albumin

Hyperphosphatemia

Aminoglycosides, loop diuretics, foscarnet

Hypocalcemia: Clinical Findings Symptoms and Signs: Extensive spasm of skeletal muscle causing cramps and tetany Laryngospasm with stridor Convulsions with paresthesias of the lips and extremities Abdominal pain Chvostek’s sign Trousseau’s sign Laboratory Findings: Low serum calcium Elevated serum phosphorus Low serum magnesium Prolonged QT interval on the ECG

Hypocalcemia: Treatment Severe symptomatic hypocalcemia: In the presence of tetany, arrhythmias or seizures, calcium gluconate 10% is administered intravenously for 10-15 minutes or via calcium infusion. 10-15 mg of calcium per kilogram body weight, or 6-8 10-ml vials of 10% calcium gluconate (558-744 mg of calcium) is added to 1 liter of D5W and infused over 4 to 6 hours. Asymptomatic hypocalcemia: Oral calcium and vitamin D preparations Calcium carbonate is well tolerated and inexpensive.

TREATMENT OF HYPOCALCEMIA

MODALITY AMOUNT OF CALCIUM ONSET DOSE

Intravenous calcium (Calcium gluconate)

93 mg (4.7 meq) per 10 ml

Immediate

93-186 mg over 10-15 mins; then 10-15 mg/kg over 4-6 hours.

Oral calcium (calcium carbonate)

40% elemental calcium;250 mg/624 mg tablet or500 mg/1250 mg tablet or500 mg/1500 mg tablet

< 1 hour 250-500 mg calcium 3 to 5 times a day.

CAUSES OF HYPERCALCEMIA

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INCREASED INTAKE OR ABSORPTION

Milk-alkali syndrome

Vitamin D or vitamin A excess

ENDOCRINE DISORDERS Primary and secondary hyperparathyroidism

Acromegaly

Adrenal insufficiency

NEOPLASTIC DISEASES Tumors producing PTH-related proteins

Metastases to bone

Lymphoproliferative disease

Secretion of prostaglandins and osteolytic factors

MISCELLANEOUS CAUSES

Thiazide diuretics and renal transplant complicationsSarcoidosis and Paget’s disease of the bone

Hypophosphatasia, immobilization, iatrogenic

Hypercalcemia: Clinical Findings Symptoms and Signs: Polyuria and constipation Stupor, coma and azotemia Ventricular extrasystoles and idioventricular rhythm Laboratory Findings: Significant elevation of serum calcium Serum phosphorus may or may not be elevated Shortened QT interval on the ECGHypercalcemia: Treatment Renal excretion of calcium is promoted by giving saline with furosemide. Treatment of underlying condition.Fluid and Electrolyte Management

Magnesium About 50% of total body magnesium exists in the insoluble state in bone. Only 5% is present as extracellular cation; the remaining 45% is contained in cells as intracellular cation. Normal plasma concentration is 1.5-2.5 meq/L, with about one-third bound to protein and two-thirds existing as free cation. Excretion is via the kidney

Hypomagnesemia Nearly half of hospitalized patients have unrecognized hypomagnesemia. In critically ill patients, arrhythmias and sudden death may be complications. CAUSES OF HYPOMAGNESEMIA

DIMINISHED ABSORPTION OR INTAKE

Malabsorption, chronic diarrhea, laxative abuseProlonged gastrointestinal suction

Small bowel bypass, malnutrition

Alcoholism, parenteral alimentation

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INCREASED LOSS DKA, diuretic therapy, diarrhea

Hyperaldosteronism, Bartter’s syndrome

Hypercalciuria

Renal magnesium wasting

UNEXPLAINED Hyperparathyroidism

Postparathyroidectomy

Vitamin D therapy

Aminoglycoside antibiotics, cisplatin, amphotericin B

Clinical FindingsSymptoms and Signs: Weakness Muscle cramps CNS hyperexcitability with tremors Athetoid movements Jerking, nystagmus Positive Babinski response Hypertension, tachycardia and ventricular arrhythmias Confusion and disorientation

Laboratory Findings: Decreased serum magnesium levels Hypocalcemia and hypokalemia Prolonged QT interval on the ECG Lengthening of the ST segment on the ECG

Hypomagnesemia: Treatment Use of IVF containing magnesium as chloride or sulfate, 240-1200 mg/day (10-50 mmol/day) during the period of severe deficit, followed by 120 mg/day (5 mmol/day) for maintenance. MgSO4 may also be given intramuscularly in a dosage of 200-800 mg/day (8-33 mmol/day) in four divided doses. Serum levels must be monitored.

Hypermagnesemia Almost always the result of renal insufficiency and the inability to excrete what has been taken in from food or drugs, especially antacids and laxatives. Potentially life-threatening as it impairs both central nervous system and muscular function.Clinical Findings Symptoms and Signs: Muscle weakness Mental obtundation and confusion Hypotension Respiratory muscle paralysis or cardiac arrest

Laboratory Findings: Elevated serum magnesium, BUN, creatinine, K Decreased serum calcium

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Increased PR interval on the ECG Broadened QRS complex with elevated T waves

Hypermagnesemia: Treatment Alleviating renal insufficiency Administration of calcium Hemodialysis or peritoneal dialysis

In all things, you shall find everywhere the Acid and the Alcaly.

OTTO TACHENIUS (1620)

Fluid and Electrolyte ManagementAcid-Base DisturbancesArterial Blood Gases Regulation of pH is accomplished by: Kidneys Lungs Buffer systems Information obtained from the arterial blood gas measurements: pH Partial pressure of carbon dioxide (pCO2) Partial pressure of oxygen (pO2) HCO3 level Oxygen saturation (O2Sat)

Arterial Blood GasesNormal values: pH = 7.35 – 7.45 pCO2 = 35 – 45 mmHg pO2 = 80 – 100 mmHg HCO3 = 22 – 26 meqs/L O2Sat > 95%

Steps in obtaining an ABG specimen: Check the bleeding parameters of the patient. Prepare the following: Glass syringe Heparin (1,000 units/mL) Alcohol Cotton balls (soaked with alcohol AND dry) Container with ice water Aspirate 1 mL of heparin using a glass syringe Coat the inner surface of the syringe with heparin, taking care to pull and push the plunger to make sure heparin evenly coats the syringe. Expel the excess heparin from the syringe. Palpate for the radial pulse. With the needle directed at a slight angle from the vertical, and pointed cephalad, gradually puncture the site and wait for arterial blood to rush in. After obtaining the specimen, secure the needle and place the syringe with the specimen in ice water.

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Apply direct pressure on the puncture site for at least one minute, or until bleeding stops using a dry sterile cotton ball. Send the specimen directly to the laboratory. A sample is allowed to stand for a maximum of two hours only.

ABG Interpretation

SUMMARY OF EXPECTED COMPENSATION FOR SIMPLE ACID-BASE DISORDERSDISORDER INITIAL CHANGE COMPENSATORY RESPONSE

Metabolic Acidosis

Decrease in HCO3-

Decrease in pCO2:Δ pCO2 = 1.1 – 1.3 (ΔHCO3-)

Metabolic Alkalosis

Increase in HCO3-

Increase in pCO2:Δ pCO2 = 0.6 – 0.7 (ΔHCO3-)

Respiratory Acidosis

Increase in pCO2 Increase in HCO3-ACUTE: ΔHCO3-= 0.1 Δ pCO2 + 2CHRONIC: ΔHCO3-= 0.3 – 0.35 Δ pCO2

Respiratory Alkalosis

Decrease in pCO2

Decrease in HCO3-ACUTE: ΔHCO3-= 0.2 – 0.25 Δ pCO2CHRONIC: ΔHCO3-= 0.4 – 0.5 Δ pCO2

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