Fluid and Electrolytes

Osmolality/Osmolarity:

Osmolality/Osmolarity measures the number of particles/osmoles/solutes in fluid and it affects the movement of water between fluid compartments (e.g. blood, urine, IV solutions). o Osmolality (mOsm/kg) is the concentration of solutes (particles) per Kg of H2O o Osmolarity (mOsm/L) is the concentration of solutes (particles) per Liter of solution/solvent (solution/solvent does not have to be H2O). o In the body, the osmolarity and osmolality are the same when discussing human fluid physiology. Examples of particles/osmoles/solutes in body: Na, protein, mannitol, glucose, urea and sorbitol Normal serum osmolality is 275 to 300 mOsm/kg (see IV fluids Brunner Table 14-5) Serum osmolality may be estimated by doubling the serum sodium level (e.g. 140 x 2 = 290). Urine osmolality (250-900 mOsm/kg) is determined by: urea (end product of protein metabolism). creatinine (end product of muscle metabolism) uric acid.

HCT

Measure of the percentage of RBCs in whole blood normally ranges from 42% to 52% (males) and 35-47% for (females) increase HCT with dehydration and polycythemia decrease HCT are overhydration and anemia

Cations Positive charged particles Sodium, potassium, calcium, magnesium, hydrogen ions Anions Negatively charged particles Chloride, bicarbonate, phosphate, sulfate, proteinate ions Major intracellular electrolytes K+ Mg ++ Na+ Total Cations 150 40 10 200 Phosphates and sulfates 150 Bicarbonate (HCO3-) 10 Organic Acids 5 Proteinate 40 Total Anions 200

Major extracellular electrolytes: Na+ 142 K+ 5 Ca++ 5 (useable form) (note: calcium is primarily in bone) Mg ++ 2 Total Cations 154 ClBicarbonate (HCO3-) Phosphate (HPO4--) Sulfate (SO4--) Organic Acids Proteinate Total Anions 103 26 2 1 5 17 154

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BODY FLUID COMPARTMENTS 1. 2. Body fluid is located in two fluid compartments Intracellular Fluid (2/3) Extracellular Fluid (1/3) - outside the cells 3 extracellular compartments: o Intravascular (plasma): 6L total of blood volume 3L plasma, 3L - erythrocytes, leukocytes, and thrombocytes o Interstitial: approximately 11-12L in the adult surrounds the cells e.g. lymph o transcellular: approximately 1L of fluid consists of cerebrospinal fluids, pericardial fluids, synovial fluids, intraocular fluids, pleural fluids, sweat, digestive secretions, peritoneal fluid Factors influencing body fluid younger have a higher percentage of body fluid Changes associated with aging (elderly):

Age

o o o

Decreased renal function decrease ability to concentrate urine - decreased ability to hold onto water, therefore more prone to fluid imbalances.. Decreased in muscle mass and total body water - therefore can dehydrate quickly. associated with increased body fat content (fat contains less water) Note: obese have less fluid than thin because fat cells contain little water Decreased muscle mass (less muscle to hold fluid reserve) Decreased skin turgor:

Skin turgor is less valid in elderly because their skin has lost elasticity and less able to hold interstitial fluid. Skin turgor is best tested over the forehead, sternum or inner aspect of the thighs because alteration in skin elasticity is less marked in these areas. Monitor skin turgor serially to detect subtle changes.

Normal Tongue turgor: Not affected by age, may be more valid than evaluating skin turgor. Normal only longitudinal furrow. Decreased additional longitudinal furrow and a smaller tongue, Wrinkles in tongue-cracked, rough, dry tongue Atypical symptom manifestations:

In elderly, the S&S of F&E disturbances may be subtle or atypical (e.g. fluid deficit may cause confusion in the elderly person, whereas, in the young person the first sign commonly is thirst) Elderly have a decreased ability to sense thirst.

Altered Fluid Response: Elderly reactions to IV fluid occur more quickly and with smaller volumes of fluids.

Capillary Permeability is the movement of fluid components (e.g. electrolytes, glucose, minerals) between organs and between cells.

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NORMAL FLUID LOSS Urine Output: The kidneys filter approximately 170-180 L of plasma daily BUT only excretes 1-2 L.

This is equal to approximately 1ml/kg/h in ALL age groups as daily urine output (UO). e.g. 150 = 68 kg, 68 x 1 = 68ml/hr, 68 x 24 = 1632ml/24hr Note: o 1 lb. = 450 ml

o 2.2 lbs. = 1000ml (1 liter) = 1 Kg Pediatrics : o weigh diapers: 1 Gm = 1 ml o

parents should expect approximately 6 wet diapers per day

GI tract: loss is 100-200ml per day even though 8L of fluid circulates through the GI system every 24 hours. Bulk of fluid (7,800 ml) is reabsorbed in the SMALL intestine. Diarrhea, ileostomies and fistulas can cause large losses (FVD). Lungs: Lungs remove approximately 300ml of water daily. Hyperpnea (abnormally deep respiration) or continuous coughing increase this loss.

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FLUID VOLUME DEFICIT FVD (Hypovolemia) Causes:

decreased fluid intake: o anorexia o nausea o swallowing problems o inability to gain access to fluid (elderly, children) o impaired thirst mechanism (elderly) o unconscious o excessive fluid restriction child abuse abnormal fluid losses: o GI suctioning o vomiting o Diarrhea: profuse watery diarrhea Crohns disease, ulcerative colitis hypertonic enteral feeding may cause diarrhea increased solutes in feeding formula are infused into the GI tract this can cause water to be pulled from the plasma into the intestine causing diarrhea. o ileostomy drainage that is not adequately replaced. o fistulas o draining wounds o increased insensible fluid loss excessive sweating without replacement infections - fever peritonitis pulls fluid into the peritoneal space (third spacing see below) hyperventilation with water vapor loss burns Excessive urination (polyuria)

NU-201 content - Diabetes Insipidus - decreased ADH from posterior pituitary gland causes renal excretion of water leads to hypernatremia because more water is lost with ADH.

NU-201 content - uncontrolled diabetes mellitus causes polyuria due to increase glucose particles in serum pulling water into vascular space. The excess fluid is excrete by kidney along with the excess glucose (glycosuria) Loss of Na and water: overuse of K sparing diuretics causes loss of Na and water. NU-201 content - adrenal insufficiency (decreased aldosterone) from adrenal cortex loss of Na and water via the kidney with increased retention of K+. hemorrhage blood loss coma Third spacing (see below)

o o o

Clinical Manifestations of FVD: (similar to shock) Cardiovascular/Blood

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Acute weight loss daily weights are monitored; (2.2 lbs. = 1000ml (1 liter) = 1 Kg ) Daily weights are the most reliable indicator of fluid loss/gain daily weights before breakfast using the same scale, same clothes. decreased BP - postural (orthostatic) hypotension a drop in systolic pressure exceeding 15 mmHg when the patient moves from a lying to a sitting or standing position. dizziness Decreased CVP (normal is 4 11mmH2O) Tachycardia - Weak, rapid (thready) heart rate (note: rapid bounding pulse with FVE) rapid and weak respirations in the initial stage of FVD due to decreased volume and Na-K pump imbalances

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o o o o o GI o o

If patient is in shock with metabolic acidosis, - Hyperventilation (Kussmauls breathing) - deep respiratory rate (increased inspiratory volume) - to blow off CO2. Flattened jugular neck, slowness of filling of feet and hand veins Weak peripheral pulses due to decrease volume Sunken eyes Infants depressed fontanel, irritability, no tears when crying Thirst, Anorexia, Nausea Hard stools (note: diarrhea with FVE)

Musculoskeletal o Muscle weakness and cramps related to sodium/potassium imbalances. These electrolytes are needed for normal muscle contraction. Neurological o Mental function is affected as a result of: decreasing cerebral perfusion and brain cell shrinkage (from Hypertonicity (e.g. hypernatremia) of the plasma which can cause cells to shrink. If this occurs in the brain cells, changes in mental status may result. (Confusion, irritability, dizziness, agitation, restlessness, seizures, and possible coma) Renal o increased specific gravity - Urine is concentrated (> 1.025) o early SX Oliguria (10-30ml/hr) - decreased urine output because the kidneys receive less blood and compensate by decreasing UO (less than 1 ml/kg/hr). Skin o Decreased (poor) skin tenting occurs o Decreased tongue turgor causes an additional longitudinal furrow and a smaller tongue Wrinkles in tongue-cracked, rough, dry tongue o Dry or sticky mucous membranes dry tongue o Decreased saliva white color o Crusted lips o Flakey, dry skin

o o
o o Labs: o o

Cool, clammy skin related to decreased peripheral perfusion (decreased capillary refill) and peripheral vasoconstriction from SNS stimulation. May have warm skin in early dehydration because SNS has not yet been stimulated. Cool, dry skin possible too due to dehydration. May have fever warm skin- especially is associated with infection. Prolonged (delayed) capillary filling time decreased volume and perfusion pressure HCT elevated - decreased plasma volume related to RBCs Increase serum osmolality normal 280 - 300 THIRD SPACING OR THIRD SPACE FLUID SHIFT

Indicates intravascular fluid volume deficit movement of fluid from the vascular system to other body spaces (cells, interstitial and transcellular). Causes: o Peritonitis, Pancreatitis inflammation of tissue causing increased capillary permeability with leaking of fluid into the peritoneal space. o Bowel obstruction increased intra-abdominal pressure and possible bowel rupture causing peritonitis

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o o

Bee sting increase capillary permeability causes proteins to leak into the interstitial space causing edema. Anaphylactic shock is a systemic increase in capillary permeability. Massive bleeding into a joint or body cavity Burns - increased capillary permeability causing leaking of fluid into interstitial spaces (edema depends on the severity of the burn) NU-202 content - Ascites associated with liver dysfunction and nephrotic syndrome. Ascites is a form of third-spacing edema in which fluid accumulates in the peritoneal cavity due to inadequate serum protein. Liver is not able to produce protein. Bulimia from extreme dieting and loss of protein causing decreased protein particles in vascular space resulting in plasma hypotonicity. This causes fluid to leak into tissues (edema).

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o

Symptoms of third spacing that differ from other causes of FVD due to fluid accumulation in body spaces: Cardiovascular/Blood

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o o

Edema diminished and weak pedal pulses due to edema (difficult to palpate) and decreased vascular volume Increased body weight fluid leaves the vascular space and collects in body spaces- creates vascular volume deficit with fluid weight gain. Abdominal distention and ascites ascites is a form of third-spacing edema in which fluid accumulates in the peritoneal cavity due to inadequate serum protein causing abdominal distention. Patients report SOB because of pressure on the diaphragm

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GI

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Medical Management of FVD Assessment I&O UO Daily weights before breakfast (same time), using the same scale, same clothes. A sudden weight change is the best indicator of FVE or FVD. Daily weights are the most reliable indicator of fluid loss/gain (1 L = 1 kg = 2.2 lbs.) VS CVP LOC (sensorium) vein filling Position:

Lower HOB or elevate lower extremities (foot of bed) to increase cerebral perfusion if vital signs show signs of shock.

Elevate extremity with third spacing to prevent skin breakdown from excess fluid in tissues. IV Fluids Replace fluids gradually over 48 hours assess symptoms of cerebral edema (cells swell)headache lethargy, irritability seizures, nausea/vomiting fluid overload, crackles in dependent lung fields related to excess Na fluid replacement over correct the fluid deficit with too much IV fluid.
Fluid Challenge Test with oliguria involves 100-200ml of NS over 15 minutes. Goal is to increase tissue perfusion without compromising the cardiovascular system. If kidneys are still functioning: UO increases and becomes more dilute B/P increases pulse will decrease *Assess for crackles in lungs, bounding pulse due to possible fluid overload especially in the elderly Types of solutions: o The infusion of an isotonic IV solution Lactated Ringers or 0.9% NS (isotonic) are frequently used to treat hypotensive patients with FVD to expand plasma volume. o Hypotonic solutions promote the movement of water into the cells- cells swell Examples:

D5W - If water loss without sodium loss (hypernatremia) give D5W (note the D5W is isotonic in bag but quickly becomes hypotonic in the plasma due to the metabolism of glucose), 0.45% NS ( NS) - As soon as the patient becomes normotensive, a hypotonic solution such as NS is used to provide electrolytes and water for renal excretion of metabolic wastes

Oral rehydration o Oral fluids containing Na and other substances H2O, sugar, K, Cl, and lactate.

Sugar facilitates the absorption of Na in oral rehydration fluids so do not give diet drinks. Do not use high sugar concentration (gelatin, soda, fruit juices) - cause diarrhea and worse dehydration.

o Avoid caffeine because acts a mild diuretic Medications Antidiarrheals as needed Anti emetics for nausea

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FLUID VOLUME EXCESS FVE (hypervolemia) Causes: More intake of water than Na water excess dilutional hyponatremia -cells swell - because the cell are more concentrated than plasma and pull fluid into cells. o Water intoxication, hypotonic solutions, excess tap water enemas, renal failure

NU-201 Content -SIADH Syndrome of Inappropriate ADH secretion - increase ADH causes an increased water retention by the kidney with dilution of Na and excessive loss of sodium in the urine

Isotonic expansion of ECF caused by the abnormal retention of water and sodium o Consumption of excessive amounts of PO sodium - table or other sodium salts causes fluid retention. o Overzealous administration of isotonic IV fluids 0.9% isotonic solutions o Prolonged corticosteroids, NSAIDs therapy increase Na and water retention

o o o

NU-201 Content Heart failure causes decrease renal excretion of fluid and sodium fluid overload NU-201 Content - Hyperaldosteronism - increased aldosterone retains Na+ and H2O NU-201 Content - Cushings Syndrome glucocorticoid excess - causes Na+ and H2O retention with K+ loss (hypokalemia may result)

Clinical Manifestations Cardiovascular/Blood o Distended neck, hand and feet veins

o
o o o o GI tract o

Tachycardia full bounding pulse related to SNS stimulation and increased volume headache Increased BP due to increased volume Elevated CVP (greater than 11 mm H2O) Acute increased weight (1L=1 kg = 2.2 lbs) NV

Liquid stools (Note: constipation with FVD) Renal o Increased UO only with functioning kidneys o SG less than 1.010 Respiratory o pulmonary edema/congestion - fluid in the pulmonary interstitium and alveoli increases. Manifestations include SOB, dyspnea, cough, increased respiratory rate, diaphoresis, and crackles (rales) and wheezing on auscultation of lungs Neurological/Muscular o Brain cells swell - causing confusion, coma, lethargy, seizures o Muscle weakness o Muscle cramps Skin o Edema pitting edema o Puffy eyelids o Severe generalized edema is called anasarca o Skin may be cool and edematous due to fluid accumulation and decreased perfusion Lab: o o o

HCT decreased because of plasma dilution Decreased serum osmolality - < 280 Na < 135

Management of FVE Fluids o o Discontinuing sodium containing fluids IV fluids:

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Nutrition/Diet o Restricting fluids and sodium: Restrict H2O if H2O excess only mild restriction (2 Gm Na) to a as little as 250mg per day seasoning substitutes to decrease Na intake i.e. Lemon juice, onions, and garlic Salt substitutes contain potassium and must be used with caution in conditions associated with potassium retention such as renal disease Medications o Diuretics when dietary restrictions of sodium alone is insufficient to reduce edema - cause loss of sodium and water by the kidneys Thiazide block Na reabsorption causes K+ retention Hydrochlorothiazide (HydroDIURIL)

If symptoms are severe and related to H2O intoxication, may give small amount of hypertonic saline to restore Na+. 3% NS 5%NS Avoid hypotonic IV solutions until Na rises otherwise may cause further dilutional hyponatremia

Other o o o o

Loop furosemide (Lasix) -Cause greater loss of Na and water Potassium sparing diuretics Aldactone - can cause hyperkalemia, especially with renal failure interventions: Hemodialysis or peritoneal dialysis to remove fluid and wastes Paracentesis drain fluid from the peritoneal cavity e.g. ascites third spacing Seizure precautions O2 therapy
NU-201 Content - Pulmonary edema treat with morphine, Nitroglycerine and digoxin Positioning: o Regular rest periods bedrest causes diuresis of edema fluid. o Elevate extremities o Apply elastic compression stockings o If dyspnea or orthopnea is present, place in the semi-fowlers position to promote lung expansion o Turn and position because edematous tissue is more prone to skin breakdown. Give good skin care Assess degree of edema in the most dependents parts of the body, (feet, ankles, sacrum and periorbital area). Measure circumference of the extremity with a tape measure.

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Sodium
Na regulates volume (along with Cl) o Retention of Na is associated with increased volume - fluid retention o Loss of Na associated with decreased volume fluid loss Na and Cl may deviate from normal independently or in combination When Na is reabsorbed by the kidneys, Cl usually goes along with it When the ratio of Cl to Na deviates from normal, it is reflected as an acid base imbalance Influences acid base balance because readily combines with Cl OR Bicarb. Cl- and Bicarb (HCO3) work opposite. If Na combines with bicarb, Cl- is lost through the kidneys. Inversely, if Na combines with Cl-, Bicarb is lost through the kidneys. Na K pump influences nerve and muscle irritability, nerve impulse conduction and muscle contraction

o
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An example of active transport is the Na-K pump. Active transport requires ATP to occur. (Phosphate is necessary for ATP production.) Without ATP (e.g. shock), the sodium and potassium pump fail to work efficiently, which leads to cellular swelling bursting- and eventual cell death.

Sodium-Potassium Pump - located on the cell membrane and actively moves Na from inside the cell to the outside of the cell (ECF) regulated by Phosphate level and the calcium channel calcium regulates the cell membrane permeability (See Calcium lecture notes) Decreased Ca (decreased guards at the gate) causes hyperexcitability (increased cell membrane permeability i.e. tetany). An increased Calcium (increased guards at the gate) causes decreased cell membrane permeability. NOTE: Calcium effects the heart muscle differently increased Ca causes increased contractility Sodium effects on Calcium:

o o

Increased Na (hypernatremia) prevents movement of calcium into the myocardium (Ca level may be normal) causes decreased myocardial contractility decreased cardiac output heart failure. Therefore, Na may be given to decrease Ca effects on the heart e.g. when hypercalcemia is present (see hypercalcemia notes). Na ALSO causes the excretion of Ca by the kidneys so Na can be given to treat Hypercalcemia. Avoid sodium IV solutions (e.g. 0.9% NS) with hypocalcemia

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Hyponatremia Na<135 decreased osmolality <280 - caused by: Inadequate intake of sodium Increased secretion or loss of Na:

Hypernatremia Na>145 increased osmolality > 300 caused by: Gain of Na: excessive PO Na (salt) intake - 1 tsp of table salt contain 2,300 mg of sodium)

Irrigation of body cavities with hypotonic solutions such as NGT irrigation with water water causes the diffusion of sodium into the stomach which is suctioned out and can lead to hyponatremia - NGT irrigation should be done with isotonic saline NOT water use of tap water enemas pulls Na into intestine

excess IV hypertonic saline (e.g. 3%, 5%) excess intake of IV normal saline

hypertonic enteral feedings and TPN without adequate water supplements leads to hypernatremia Near drowning in sea water which contains sodium Medications corticosteroids (cause retention of Na), antacids with Na bicarb., Kayexalate (Na+ exchange resin used to treat hyperkalemia)

fresh water drowning diuretics cause loss of Na+

Cystic fibrosis defective Cl- ion transport in cells causing excessive Na and Cl loss through exocrine glands such as sweat (perspiration), saliva, and mucus exocrine glands such as the pancreas, intestine and bronchi. Loss of GI fluids : vomiting, bulimia, diarrhea, sweating, fistulas, GI suctioning

NU-201 content - adrenal insufficiency (decreased aldosterone) from adrenal cortex loss of Na and water via the kidney with increased retention of K+. overuse of K sparing diuretics causes loss of Na and water.

NU-201 content - Hyperglycemia high glucose level dilutes the sodium, and the renal tubular flow rate is increased, causing further renal sodium loss in excess of water. Increased or gain water - dilutional hyponatremia:

Post op there is an increased release of ADH (vasopressin) in the post op period due to the stress response. Therefore, do not give D5W in the immediate (first 2-4 postoperative days) post-op period because it will add to the vascular H2O volume. Excessive use of hypotonic IV solutions e.g. D5W

water intoxication - compulsive water drinking (psychogenic polydypsia) infants fed too dilute formula with parents trying to save money water supplements for patients receiving hypotonic tube feedings Renal failure / Cardiac Failure (CHF) / Liver Failure: causes fluid overload as more water is gain in excess of sodium (volume excess)

decreased or lose water: fluid deprivation in unconscious patients who cannot perceive, respond to or communicate thirst - most often very old, young and cognitively impaired Water deprivation e.g. fluids are excessively restricted child abuse

fever colitis

hyperventilation (water vapor loss) sweating without fluid replacement, heat stroke, profuse, watery diarrhea- Crohns disease, ulcerative

SIADH (Syndrome of Inappropriate ADH secretion)increase ADH secretion causes excessive free water retention with dilution of Na and excessive loss of sodium in the urine

NU-201 content - Diabetes Insipidus - decreased ADH from posterior pituitary gland causes renal excretion of water leads to hypernatremia because more water is lost with ADH.

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Hyponatremia Na<135 Clinical manifestations If Na and H2O are lost together (isotonic dehydration) have symptoms of FVD hypovolemia shock type symptoms

Hypernatremia Na>145 Clinical manifestations

Decreased BP (also with decreased Cl) Orthostatic fall in blood pressure - a drop in systolic pressure exceeding 15 mmHg when the patient moves from a lying to a sitting or standing position. Increased pulse weak, rapid and thready with fluid deficit (see below bounding with hypervolemia

Decreased BP - Orthostatic hypotension (due to FVD from loss of H2O ) Hypertension, bounding pulse and dyspnea (FVE) if gain excess Na can cause increased vascular volume

Decreased jugular /hand/feet vein filling If SIADH occurs then - Oliguria (10-30ml/hr)

distended neck veins with excess fluid

Polyuria with Diabetes Insipidus oliguria, decreased urine output, increased S.G. (> 1.030) increased osmolarity of blood causes kidney to retain fluid.

o o

Skin Dry, cracked mucosa Decrease saliva production Poor skin turgor- shrunken tongue Low grade fever Clammy skin with hypovolemia Thirst with hypovolemia With Dilutional hyponatremia, can have signs of FVE:

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o o

o o o
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Skin Dry, swollen, red tongue Sticky mucous membranes Dry, warm, flushed skin from dehydration Decreased sweating Elevated body temperature from dehydration Intense thirst (polydispia)

N/V, anorexia and abdominal cramps

Altered mental status due to cell swelling and cerebral edema. This can cause headache, weakness, slurred speech, confusion, lethargy, anxiety, seizures, coma, and permanent neurological damage.

Primary manifestations are neurological Cellular dehydration (shrinkage) can cause altered sensorium, twitching/Seizures/convulsions, confusion, disorientation, decreased LOC, agitation, restless, lethargy. o In children, high pitched cry

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Symptoms due to hypervolemia (fluid overload)

Increased body weight edema causing fingerprint indentation over bony prominences o Increased urinary output Increased B/P Respiratory distress Rapid bounding pulse Distended neck veins

o dyspnea, puffy eyelids, dependent edema, and weight gain in 24 hours.

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Hyponatremia Na<135

Hypernatremia Na>145

Hypochloremic Metabolic Alkalosis - When decreased Na is associated with decreased Cl can develop Hypochloremic Metabolic Alkalosis. Alkalosis causes Ca to bind to protein causing Hypocalcemia this causes: o hyperexcitability of muscles tetany muscle twitching, muscle cramps (too few guards at the gate) o hyperactive bowel sounds o Anorexia, abdominal pain/cramps, N/V

Initially, increased Na causes loss of Calcium (hypocalcemia) through kidneys resulting in hypocalcemia (causing tetany (early sign) Hyperchloremic Metabolic Acidosis - As hypernatremia progresses, can develop Hyperchloremic Metabolic Acidosis. Acidosis causes Hypercalcemia. this causes: o Lethargy, muscle weakness, depressed reflexes calcium depresses neuromuscular excitability (too many guards at the gate)

Shallow respirations to retain CO2 (acid) to compensate for Hypochloremic metabolic alkalosis.

deep respirations to blow off CO2 to compensate for acidosis

crackles if have FVE with an increased Na intake crackles, rales is have FVE if increase fluid intake

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Hyponatremia Na<135 Management Assessment weights- same time, same scale, same amount of clothing each day for accuracy o neuro status o I&O o skin turgor o mucous membranes

Hypernatremia Na>145 Management o clothing o o o o o Assessment Weights- same time, same scale, same amount of each day for accuracy neuro status I&O Skin turgor Mucous membranes child abuse fluid deprivation Addition of Water Encourage P.O or IV water (see below)

o Assess finances if parents diluting formula to save money.

Water restriction: o Dilutional hyponatremia is treated by restriction of fluid to a total of 800ml in 24 hours Parent teach not to over-dilute formula. Teach how to mix powdered /liquid formulas

Parent teach not to under-dilute formula. Teach parents not to feed infants more concentrated formula. Teach how to mix powdered /liquid formulas Give water supplements with high osmolality (hypertonic) enteral feeding to decrease the concentration of the feeding

Avoid excess water supplements in patients receiving isotonic or hypotonic enteral feedings Do not replace diarrhea or vomiting with only tap water- use fluids containing Na

Irrigate GI and urinary tract with 0.9% NS not water

Sodium Replacement - encourage food and fluids high in sodium o For patients experiencing abnormal losses of sodium who can consume a diet, encourage Na rich foods e.g. broth, tomato juice, table salt, bacon, ham, processed cheese, corn flakes, crackers, IV Fluids: isotonic solutions for isotonic dehydration both Na and fluid loss give isotonic solutions - IV lactated Ringers or 0.9%NS o Severe hyponatremia (dilutional hyponatremia with FVE) - highly hypertonic solutions (3 or 5%Na Cl) to relieve acute manifestations of cerebral edema and prevent neurologic complications. These solutions should be infused with careful monitoring e.g. in the ICU on a pump

Sodium Restriction - restrict foods and fluids with high Na+ content

IV Fluids: hypotonic solutions - Gradual lowering of the serum Na by infusion of hypotonic solutions e.g. 0.3% NaCl, 0.45% NS, or an isotonic non-saline solution e.g. D5W (note: D5W becomes hypotonic as glucose is metabolized) o Hypotonic solutions are more dilute than normal body fluid they dilute body fluid back to normal concentration.

Note: Too rapid increase in the sodium causes Na may pull fluid from cells too rapidly (cell shrinkage) causing: o permanent neurologic damage due to osmotic cellular demyelination.

o o o

Note: Too rapid reduction in the serum sodium level causes the plasma to become hypo-osmotic causing movement of fluid into brain cells (cells swell) causing: cerebral edema Use pump to regulate flow gradually replace fluids

o o o

Prevent fluid overload Auscultate lungs for crackles Use pump to regulate flow gradually replace fluids

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Hyponatremia Na<135

Hypernatremia Na>145 Diuretics to cause increased Na loss - used to treat the sodium gain (lasix) Antidiarrheals if caused by diarrhea fluid loss.

Increase water excretion - Osmotic diuretics promote water excretion rather than Na loss i.e. mannitol

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Potassium

K greatest inside the cell (ICF) Release of large stores of intracellular K from the cells and tissues can be extremely dangerous e.g. trauma, burns Potassium influences all muscle contraction and transmission of nerve impulses. o Neuromuscular excitability is influenced by the Na-K pump which is regulated by Ca (the guard the gate). o An example of active transport is the Na-K pump. Active transport requires ATP to occur. (Phosphate is necessary for ATP production.) A decreased or increased K can lead to severe muscle weakness because K+ is glucose metabolism and energy production causes paralysis, ventilation problems, bradycardia and kidney problems o Regulates use of glucose by cells involved with energy production loss of K causes fatigue, lack of strength o Insulin decreases serum K: to treat excess serum K (hyperkalemia) give insulin (with glucose) to move K into cell. (note: Hyperalimentation (parenteral nutrition) can trigger a hypersecretion of insulin which can cause hypokalemia. The tissue build-up causes K+ to shift from the serum into the new cells) Influences acid base balance 1. K and H ions compete for exchange in renal tubules. 2. K exchanges with H in and out of cells in response to pH (compensatory mechanism).

1. 2.

In Acidosis, H goes into cell, K comes out. In acidosis, Ca increases (more guards at the gate) hypotonic muscles, decreased excitability.

In alkalosis, H comes out of cell, K goes into cell. In alkalosis, Ca decreases (less guards at the gate) tetany. Absorbed from intestine, excreted in urine (80%), feces (20%), sweat Potassium must be replaced every day as the kidneys do not conserve potassium and continue to excrete it even in the absence of any intake. o High urine output causes the excretion of K to increase

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Hypokalemia - K below 3.5 meq/L Causes: Excessive Output:

Hyperkalemia - K above 5 meq/L Causes: Decreased Renal excretion: Renal failure most common cause Potassium-sparing diuretics i.e. aldactone

Vomiting and gastric suction lose most K (approx. 30-50 meq/L

Diarrhea, Ileostomy drainage, overuse of laxatives Fistulas, wound drainage Heavy perspiration

In many instance, hypomagnesemia and hypokalemia occur together related to: o A decreased Mg cause the kidneys to excrete K

NU-201 Content Addisons Disease - adrenal insufficiency causes a decreased aldosterone which causes a loss of Na and water with the retention of K.

As cell are rebuilt, K+ and Mg go into cell together see Hyperalimentation below High doses of steroids causes retention of Na and loss of K Diuretics - Use of potassium-wasting diuretics (e.g. Loop diuretics Lasix and Thiazide diuretics -HCTZ)

NU-201 Content Urine output diabetes mellitus polyuria from excess glucose in urine causes loss of K through osmotic diuresis e.g. glucosuria in uncontrolled DM NU-201 Content Aldosterone is released by the adrenal cortex Na and water retention with K loss e.g. Stress, Cushings Syndrome (Hyperaldosteronism) Inadequate K+ intake: Anorexia nervosa & Bulimia loss of lean muscle releases K that is excreted by kidney and not replace in diet.

Excessive K+ intake:

Too rapid or excessive K+ replacement IV or P.O. excessive use of salt substitutes that have K+

starvation, malnutrition causes tissue wasting with loss of K NPO not taking in K must make sure IV K+ given if patient is NPO. Maintenance K+ is usually 20 40 meq/Liter of IV fluid.
Potassium shift into the cell from vascular space: Insulin causes K+ (and Mg) to go into the cell: NU-201 Content Treatment of Diabetic Ketoacidosis when insulin takes glucose into the cell, K+ goes with it. o Hyperalimentation (Parenteral Nutrition) often causes hypersecretion of insulin. Also, as cells and tissue builds up, K+ and Mg move into the cell. Stress response catecholamines such as epinephrine promote entry of K into the cell e.g. stress, surgery

Potassium shift out of cells into vascular space:

NU 201 Content - Diabetic Ketoacidosis - Lack of insulin (diabetic ketoacidosis) creates a hyperosmolar state that causes water to move out of cell, taking potassium with it

In Metabolic Alkalosis, a compensatory mechanism occurs. K shifts into the cell as H ions moves out of cells into blood vessel- causing Hypokalemia.

In Metabolic Acidosis, a compensatory mechanism occurs - K shifts out of cell as H ions move into cells - causing Hyperkalemia Blood transfusions K leaks out of RBCs that are stored the longer blood is stored, the more K leaks out of cells massive cell death Crush injury, infection, burns Sickle cell anemia (hemolytic crisis) Chemotherapy Pseudohyperkalemia - K+ is released from cells - Blood sample hemolysis, repeated fist clenching and unclenching with blood draws)

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Hypokalemia - K below 3.5 meq/L Clinical manifestations related to muscle dysfunction

Hyperkalemia - K above 5 meq/L Clinical manifestations related to muscle dysfunction

NU-201 Content - Cardiac arrhythmias a decreased K+ slows the conduction of heart causing: o bradycardia o can cause sudden cardiac death

NU-201 Content - Cardiac muscle weakness an increase in K+ causes weaker cardiac contraction (instability) results in bradycardia , heart block, and cardiac arrest

Note: decreased K+ causes an increased sensitivity to digoxin. Digoxin also slows heart rate too- predisposing to toxicity

In addition, a decreased K+ can be caused by an increased Na+ (hypernatremia). Increased Na prevents movement of calcium into the myocardium causing decreased myocardial contractility and decreased cardiac output resulting in heart failure.

**treat the instability with Calcium gluconate - Calcium stabilizes cell membranes and antagonizes the weak cardiac contraction that can occur from hyperkalemia.

Irritability, apathy, confusion, fatigue, drowsiness

Hypertension related to the retention of Na as K is lost. OR Postural hypotension is common. (A drop in systolic pressure exceeding 15 mmHg when the patient moves from a lying to a sitting or standing position.) GIdecreased bowel motility o anorexia o abdominal distention o nausea & vomiting o decreased bowel sounds o decreased bowel motility o constipation o paralytic ileus Depressed neuromuscular activity because 1) interferes with Na- K pump, and 2) K levels are insufficient to maintain cellular metabolism causing: o fatigue

GI increased bowel motility (hyperactivity) o Diarrhea o Nausea o Intestinal colic o Intestinal/abdominal cramping o Hyperactive bowel sounds

o o
o o

muscle weakness - usually first detected in the legs may progress to flaccid paralysis muscle/ leg cramps hypoactive reflexes respiratory muscle weakness respiratory arrest

An increased K depresses depolarization the nervous system and skeletal muscle contraction because 1) interferes with Na- K pump, and 2) K levels are insufficient to maintain cellular metabolism causing: o Muscle weakness and paralysis usually begins in legs. Muscle weakness mirrors hypokalemia. o hypoactive reflexes

Paresthesias in extremities, face and tongue usually first symptom. Paresthesia occurs more with increased K

If metabolic acidosis
o

If metabolic alkalosis is present as the cause

of hypokalemia, respiratory acidosis may develop as a compensatory mechanism for metabolic alkalosis. o shallow breathing to increase CO2 K+ depletion can lead to inability to concentrate urine Frequent urination (polyuria) Nocturia

is present as the cause of hyperkalemia, respiratory alkalosis may develop as a compensatory mechanism for metabolic acidosis deep breathing to decrease CO2

o o

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o o

Polydipsia Dilute urine

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Hypokalemia - K below 3.5 meq/L Management Assessment: Monitor heart rate and rhythm, resp status Place on cardiac monitor - ECG Must check K levels with ABGs to determine if the K imbalance is related to acid base disturbances. Assess I&O, GI status Prevent excessive loss of K from diuretics and laxatives.

Hyperkalemia - K above 5 meq/L Management Assessment: Monitor heart rate and rhythm, resp status Place on cardiac monitor - ECG Must check K levels with ABGs to determine if the K imbalance is related to acid base disturbances. Assess I&O, GI status Restrict Potassium intake Promote Potassium excretion:

Give K sparing diuretics i.e. aldactone

Administer K supplements Administer oral potassium as ordered with food or fluid (juice) to prevent gastric irritation and bad taste. Can cause ulcers check for abdomen pain, distention, N,V, diarrhea, GI bleed Do not crush or chew potassium tablets must swallow whole. for those on digoxin Teach to assess pulse for bradycardia check K+ levels before taking digoxin because hypokalemia increases risk of digitalis toxicity

oral:

Kayexalate PO or enema cation exchange

resin The resin binds with K in the intestine - in exchange for Na. The resin is then excreted in the feces. This can cause watery diarrhea.

Give K wasting diuretics e.g. Lasix (loop

diuretics) Hemodialysis if K remains high.

Increased Ca increases K excretion by kidneys

see calcium gluconate/chloride below Increase urine flow by IV Normal Saline AND Potassium-losing diuretics e.g. thiazides Lasix

IV:

Never administer undiluted potassium IV. Never give IV push can be fatal Make sure to mix IV solutions with K well turn several times to mix contents thoroughly Potassium Phosphate is used to keep potassium in the ICF during periods of tissue regeneration as during hyperalimentation, when treating diabetic ketoacidosis or when have both a phosphate and potassium deficit..

Promote K+ shift into the cells: Administer medications that drive K into cells o IV insulin WITH IV glucose e.g. 10 units of insulin in 500ml of D10W over 60 minutes o Insulin enhances the movement of K into the cell must give glucose with insulin to prevent hypoglycemia.

IV bicarb to treat metabolic acidosis if it is

present due to shock. This is done to stop the release of K+ from cells.

Potassium Acetate can be used to treat patients with potassium loss associated with metabolic acidosis Potassium chloride most common replacement Administer IV potassium solutions at a slow rate no faster than 10 20 meq/h use cardiac monitor and infusion pump o NPO for surgery give K maintenance of 2040meq/L o Bolus runs - 10meq/100ml of normal saline is administered at 100ml/hr o MAXIMUM 10meq/hour - check policy hospital policy Monitor for pain and inflammation at the injection site irritates vein - stop, slow or further dilute infusion. May use warm compress above the insertion site along the vein track throughout the infusion. Use large vein e.g. antecubital o Potassium is a vesicant and can cause tissue damage if infiltration occurs o If infiltration occurs, discontinue the IV, apply a COLD compress, (not heat) and notify the health care provider.

Beta-Adrenergic Agonists the most

frequently used high dose albuterol nebulization temporarily forces K+ into the cells Emergency Measures to protect the heart contractility:

Calcium Gluconate

Calcium Gluconate - Calcium stabilizes cell membranes and antagonizes the weak cardiac contraction that can occur from hyperkalemia. o Calcium can cause vein dilation - keep the patients lying down after administration to prevent postural hypotension. o Check for infiltration calcium infusions cause tissue necrosis o Calcium potentiates the effect of Digoxin on the heart give only if absolutely necessary Prevent Rapid Replacement of Potassium: Make sure to mix IV solutions with K well turn several times to mix contents thoroughly

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Assess urine output before giving K supplements. Never give KCL unless there is a UO of at least 30 ml/h In children, administer after the first void

Infuse K+ according to protocols

Nutrition: Teach about K rich foods: meats, dried fruits, bananas, tomatoes, melon, oranges, green leafy vegetables, potatoes, beans, fish, red meats, avocado, carrots, Juices esp OJ,

Other Interventions: Side rails and safety ROM for muscle weak Assisted ventilation for weak respiratory muscles

Nutrition: Teach to avoid: o foods high in K o salt substitutes. Salt substitutes are high in K+. Encourage: o foods low in K apples, pears, berries, corn, rice, noodles, bread Other Interventions: Make sure packed RBCs are fresh esp with multiple transfusions because stored blood breaks down cells and releases K Debride dead tissue so K is not released Assess urine output before giving K supplements. If kidneys are not producing urine, serum K+ levels may increase. Never give KCL unless there is a UO of at least 30 ml/h o In children, administer after the first void

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Chloride Facts: Normal total serum chloride level is 96-106 mEq/dL Imbalances usually linked to other electrolyte imbalances or acid-base imbalances Chloride is produced in the stomach as hydrochloric acid - which aids in the digestion of food Na and Cl determine osmotic pressure (osmolality) and Cl does so in direct proportion (along with) to sodium A high chloride level is usually accompanied by a high sodium level and fluid retention if there is not an acid base imbalance. Acid-Base Imbalances - With each Na ion reabsorbed by the kidney, a chloride OR bicarb ion is reabsorbed along with it. Depends on acid base balance. In acidosis, Na bonds with bicarb (Cl is excreted by the kidney), and the pH elevates. If the serum pH is normal, Na bonds with Cl (excretes bicarb), and the pH remains the same. Kidneys selectively secrete chloride or bicarb depending on acid-base balance:

Hypochloremic Metabolic Alkalosis - Increased bicarb resorption with Na+ causing a loss of Cl by the kidney causing hypochloremic metabolic alkalosis - as chloride decreases, bicarbonate ion are retained by the kidney causing alkalosis Chloride shift acidosis also causes bicarbonate to move from the RBCs to the plasma in exchange for chloride from the plasma to the red cells this results in hypochloremia. Hyperchloremic Metabolic Acidosis - There is a loss of bicarb by the kidneys with increased chloride retention . This causes a Hyperchloremic Metabolic Acidosis due to a loss of bicarb through the kidneys. Hyperchloremia - Cl above 106 meq/L Causes: Most common cause Dehydration due to loss of more water than Na and Cl Acid Base Imbalance: o loss of bicarbonate via the kidney causes Chloride gain- hyperchloremic metabolic acidosis - as bicarbonate ions are lost by the kidney, chloride increases causing acidosis o metabolic acidosis, shock, starvation, diabetic ketoacidosis, decreased ventilation, Ingestion of acids e.g. salicylate - As bicarb is used up to neutralize the excess acid in the body, Cl- is reabsorbed as a negative ion- to maintain electroneutrality- causing Hyperchloremia.

Hypochloremia - Cl below 96 meq/L Causes: vomiting causes loss of stomach HCl acid Fistula drainage Acid Base Imbalance: o loss of Cl- via the kidney causes bicarbonate gain: o hypochloremic metabolic alkalosis - as chloride decreases, bicarbonate ion are retained by the kidney causing alkalosis o Chloride shift a low serum ph (acidosis) causes the bicarbonate to move from the RBCs to the plasma in exchange for chloride from the plasma to the red cells. sweating diarrhea causes loss of Cl hyponatremia IV fluid without Chloride D5W salt restricted diets Cystic fibrosis defective Cl- ion transport in cells causing excessive Na and Cl loss through exocrine glands such as sweat (perspiration), saliva, and mucus exocrine glands, such of pancreas, intestine and bronchi.

Excessive GI tube drainage, diarrhea and severe

Steroids - cause retention of Na and Cl

hypernatremia- Cl increases with Na+ Excessive NaCl infusions

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Hypochloremia - Cl below 96 meq/L Clinical manifestations Are similar to metabolic alkalosis and hyponatremia: hypotension

Hyperchloremia - Cl above 106 meq/L

Clinical manifestations Are similar to metabolic acidosis, hypervolemia and hypernatremia. Mg and Potassium levels increase and decrease together Hypotension - Peripheral vasodilation ( see Hypermagnesemia) OR Hypertension due to increase Na and fluid retention Hyperchloremic metabolic acidosis increases the amount of useable Ca causing hypercalcemia (see hypercalcemia): o Muscle weakness - related to acidosis causing an increased Ca+ o confusion o Lethargy, Decreased LOC If metabolic Acidosis is present: o compensation can occur with deep respirations to blow off CO2 Kussmauls respirations

o o o o

Hypochloremic metabolic alkalosis causes Ca to bind to protein decreasing the amount of useable Ca causing hypocalcemia (see hypocalcemia): tetany Hyperexcitability of muscles, tetany Confusion Agitation, irritability, seizures

If metabolic alkalosis is present: o Compensation can occur with shallow respirations to retain CO2

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Hypochloremia - Cl below 96 meq/L Management IV Fluids Replace Cl- with IV NS 0.9% or 0.45% solutions

Hyperchloremia - Cl above 106 meq/L Management IV Fluids IV Lactated Ringers - the lactate is converted to bicarbonate in the liver, which will increase the bicarbonate level and cause renal excretion of Chloride. This helps to correct the acidosis and decrease Chloride.

Medications o May discontinue or change diuretics that cause loss of Na and Cl o Antiemetic for vomiting o Ammonium Chloride the ammonium ion is converted to urea in liver, liberating Hydrogen and Chloride. This help to correct alkalosis and increase Chloride. Foods high in chloride are encouraged: Tomato juice Salty broth Canned vegetables Processed meats Fruits

Medications Diuretics to eliminate chloride

o Na bicarbonate to increase bicarbonate levels, which leads to renal excretion of chloride

o o o o o

Chloride restricted foods Na foods and fluids are restricted

A person who drinks a lot of free water without

Use NS to flush NGT, not tap water

electrolytes will excrete large amounts of chloride; therefore this should be avoided

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Calcium Facts:

Normal total serum calcium level is 8.5 to 10.5mg/dL or 4.5 5.5meq/L (ionized) More than 90% of the bodys calcium is located in the skeletal system (bones) The small amount of calcium located outside the bone circulates in the serum, partly bound to protein, partly ionized or complexed. o Serum (plasma) calcium exists in three forms:

1.

ionized- about 50% of the serum calcium exists in an ionized form that is physiologically active (diffusible through capillary membrane) and important for neuromuscular activity and blood coagulation. The normal serum ionized calcium is 4.5-5.1 (1.1-1.3mmol/L) and is the only form that is clinically significant. Symptoms of Ca excess or deficit are correlated with free Ca (ionized). Bound- less than half of the plasma calcium is bound to serum proteins, primarily albumin therefore it is not diffusible through capillary membrane. PH levels affect calcium binding to albumin:

2.

a. b. 3.

Acidosis decreases calcium binding to protein , leading to increased ionized (free,useable) calcium Alkalosis increases Calcium binding to protein, leading to decreased ionized (free,usable) calcium

Complexed the remainder of serum calcium is combined with non-protein anions: i.e. phosphate, citrate (binds with this in blood transfusions), and carbonate

Note: Citrate is the anticoagulant used in blood products. It is usually rapidly metabolized by the liver if blood is infused slowly. Rapid administration of large quantities of stored blood may cause hypocalcemia and hypomagnesemia when citrate binds calcium and magnesium.

Function Major role in heart rhythm, transmitting nerve impulses, muscle contraction, bone formation and strength In skeletal muscles, Ca decreases cell membrane permeability (guards at the gate) prevents overcharge of cell membrane, therefore:

a decrease in Ca (decreased guards at the gate) causes hyperexcitability of nerve and muscles an increased calcium (increased guards at the gate) depresses nerve and muscle activity

Calcium has a positive inotropic effect on the heart (increased contractility) and reduces the heart rate similar to Digoxin so it potentiates effect of digoxin on heart. role in blood coagulation and secretion of hormones helps to convert prothrombin to thrombin Acid base balance see #2 above Factors that affect calcium regulation:

Calcium is absorbed from foods in the presence of normal gastric acidity and vitamin D. 30-40% of Calcium is primarily absorbed in the small intestine (duodenum and jejunum are the primary sites of absorption). Therefore ileostomies, fistulas, wound exudates, etc. can cause decreased Ca. Calcium and phosphorous have inverse relationship. Calcium balance depends on 3 hormones : C

V Vitamin D increases absorption of Ca from GI tract, most reliable source is sunlight

PTH is stimulated by decreased serum calcium level. PTH increases bone resorption (movement of Ca out of bones), GI absorption of Ca, renal excretion of phosphate, and decreases renal excretion of Ca. d Calcitonin Works opposite of PTH. When serum calcium increases, the thyroid gland secretes calcitonin to decrease serum calcium.

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Hypocalcemia - Ca below 8.5 meq/L Causes: Most common cause Renal Failure Vit D is not activated by the kidney Inadequate Vitamin D intake/activation

Hypercalcemia - Ca above 10.5 meq/L Causes: Excess is not common with functioning kidneys because kidneys excrete Ca. Vitamin D intoxication Malignancies of bone

Rapid administration of citrated blood:

Citrate is the anticoagulant used in blood products. Citrate can bind with ionized calcium causing a decrease calcium.

Alkalosis - With alkalosis, more calcium o

Hypoparathyroidism causes: Parathyriodectomy Decreased albumin

becomes bound to protein (unusable form of Ca).

Acidosis - With Acidosis, less calcium is bound

to protein resulting in more ionized (useable) calcium Hyperparathyroidism causes: Increased PTH release causes an increase release of calcium from the bones and o increased intestinal and renal absorption of calcium

Malabsorption (most calcium absorbed in the duodenum and jejunum)- caused by rapid peristalsis , small bowel resection, chronic diarrhea reduce Ca absorption from the GI tract Decreased stomach acid causes decreased absorption of calcium Associated electrolyte disturbances: o Increase Na causes increased Ca excretion by kidneys o Hyperphosphatemia (Phosphorus goes opposite calcium) o Hypomagnesium if Mg is low, parathyroid hormone (PTH) release is impaired, lowering serum Ca. Acute Pancreatitis: o Inflammation of the pancreas causes a release of fatty acids that bind to Ca o Ca is lost in fluid that is sequestered in the abdomen in pancreatitis Medications loss of Ca from bones caused by aluminumcontaining antacids, caffeine, nicotine, corticosteroids (can cause osteoporosis , o increase secretion of Ca caused by loop diuretics

Associated electrolyte disturbances: o Increased Ca increases Na and K excretion by kidneys

Medications o Increased intake calcium antacids and supplements

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Hypocalcemia - Ca below 8.5 meq/L Clinical manifestations Decreased myocardial contractility - weak heart muscle contraction leading to:

Hypercalcemia - Ca above 10.5 meq/L Clinical manifestations Increased myocardial contractility bradycardia, heart block Hypertension due to elevated serum epinephrine in patients with hypercalemia. bone pain spontaneous fractures with Hyperparathyroidism there is an increased PTH pulling Ca from the bone

Tachycardia (due to cardiac weakness) and Hypotension due to vasodilation

Osteoporosis Spontaneous fractures bone loss, osteoporosis

decreased cardiac output, bradycardia, asystole

excess calcium blocks the effect of sodium in skeletal muscles, increased neuromuscular (cell membrane) excitability (increased reduction excitation of muscles and nerves - reduces neuromuscular (cell membrane) excitability (decreased permeability): permeability: Repetitive uncontrolled impulses in peripheral (hypotonicity) nerves (increase in the Na-K pump which is Fatigue, lethargy uninhibited by a decreased Ca decreased guards at the gate) Muscle weakness/flaccid Tetany (hypertonicity / hyperreflexia.) depressed deep tendon reflexes muscle spasms (cramps, tremors, twitching) lethargy and confusion blurred vision Trousseaus sign - inflating a blood pressure cuff on the upper arm to about 20mmHg above systolic pressure for 2-5 minutes produces carpopedal spasm (an adducted thumb, flexed wrist and metacarpophalangeal joints, extended interphalangeal joints with fingers together - hands folded in) Will occur as ischemia of the ulnar nerve develops.

Chvosteks sign twitching of face muscles when

the facial nerve is tapped anterior to the ear. The corner of the mouth draws up due to muscle contraction- causes spasm of lip, nose or face facial grimacing

Convulsions, seizures laryngeal stridor/ spasms can occur- can lead to

resp. arrest, Paresthesias of extremities - sensations of tingling, numbness may occur in the tips of the fingers, around the mouth, and less commonly in the feet. confusion, anxiety irritability, restlessness, agitation, insomnia hoarse voice dysphagia (related to low Mg see Mg notes)

Abdominal distention and paralytic ileus with severe hypercalcemic crisis

Anorexia, N, V, constipation (are common sx)

Muscle cramps - Abdominal cramp, diarrhea,

hyperactive bowel sounds Skin Dry hair Sparse hair Scaly dry skin Brittle nails

due to decreased peristalsis and decreased contraction of GI tract from decreased muscle tone and decreased permeability. Renal Increased Ca excretion by kidneys due to diuresis from high solute loss urinary calculi causes flank pain Excessive urination - polyuria caused by the high solute (calcium) load - can lead to polydypsia, dehydration

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Hypocalcemia - Ca below8.5 meq/L Management Assessment: cardiovascular status airway for laryngeal spasms and respiratory arrest Teach:

Hypercalcemia - Ca above10.5 meq/L Management Assessment: cardiovascular status Decrease loss of Calcium from bone:

Prevent osteoporosis: Teach on reducing the risk for

falls adequate dietary calcium intake; regular weight-bearing exercise teach - alcohol, tobacco and caffeine inhibit calcium absorption and increases urinary calcium excretion. With chronic diarrhea or ileostomies encourage increased intake of Ca. Medications to reduce the rate of bone loss: biphosphonates calcitonin Calcium Supplements Ca antacids can cause constipation

Treating the underlying cause (eg

chemotherapy for malignancy or partial parathyroidectomy for hyperparathythroidism).

Calcium supplements - at least 1,000 to 1,500mg/day in the adult Proton pump inhibitors can interfere with Ca absorption Increase Ca absorption from Intestine with: o Acid environment (Vit C)-Ca supplements best absorbed in an acid environment. o Vit D e.g. Calcitrol increases Ca absorption from small intestine

Medications to reduce serum calcium: Calcitonin lowers the serum calcium levels by reducing bone resorption (loss of Ca from bone)

Bipisphosphonates obstruct calcium

release from the bone, thereby reducing bone resorption phosphate to induce Ca excretion via kidney Avoid Vit D & Ca supplements:

IV calcium
o o calcium gluconate. calcium chloride Encourage fluids - Encourage fluids to promote excretion by the kidneys:

infuse IV calcium slowly - too rapid IV administration of calcium can cause cardiac arrest, vasodilation, hypotension (should remain recumbent for 30-60 minutes after IV administration to prevent postural hypotension, bradycardia. Monitor EKG with VS o Check for infiltration calcium infusions cause tissue necrosis

Encourage patient to drink 3 to 4 quarts

Seizure precautions due to tetany: o Quiet environment to avoid overstimulation and neuromuscular excitability Avoid sodium IV solutions (e.g. 0.9% NS) with
Diet: dairy, milk products, green, leafy vegetables, canned salmon, sardines, fresh oysters, molasses, macaroni, nuts-almonds, whole grains, creamed soups fish, tofu. Blood Transfusions Give blood transfusions slowly so liver can metabolize citrate and prevent from binding to Ca Rapid administration of large quantities of stored blood may cause hypocalcemia and hypomagnesemia when citrate binds calcium and magnesium. hypocalcemia because sodium causes excretion of Ca by the kidneys

of fluid daily if tolerated by cardiac status - to promote excretion and formation of renal calculi Encourage fluids with sodium unless contraindicated. Na causes the excretion of Ca by the kidneys. E.g. 0.9% NS. Na decreases calcium effects on heart. Lasix to promote calcium excretion by kidneys. Diet: Low calcium diet High fiber and fluids to prevent the tendency for constipation

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Magnesium Facts: Normal serum magnesium level is 1.5 to 2.5meq/L The basic functions of magnesium are similar to the functions of potassium and calcium. The regulation of Mg, K and Ca are interrelated. Mg is an essential for ATP function which transports Na and K ions across cellular membranes. Regulated by Vit D and renal excretion In muscle contraction, Mg acts a relaxer. With HYPERmagnesemia, decreases muscle cell activity. Respiratory paralysis and delayed conduction in the myocardium may result.

Hypomagnesemia - Mg below 1.5 meq/L Causes: Magnesium deficiency can occur with decreased potassium, Mg and calcium.

Hypermagnesemia - Mg above 2.5 meq/L Causes: Renal Failure - Most common cause

Magnesium and K+ shift into cells with insulin therapy Mg deficiency is associated with decreased calcium
because decreased Mg inhibits release of PTH, lowering serum Ca. Chronic alcoholism is the most common cause magnesium shifts as glucose moves into the cell during the withdrawal period. Rapid administration of citrated blood. Mg becomes bound to citrate. Citrate is an anticoagulant in donated blood. ( also occurs with Ca) Acute Pancreatitis Mg gets sequestered in pancreatitis (also occurs with Ca) enteral feeding / IV solution deficient in Mg Mg loss or decreased absorption in the GI tract: prolonged nasogastric suction, vomiting diarrhea and intestinal fistulas intestinal malabsorption intestinal resection or inflammatory bowel disease, short bowel syndrome

Preeclampsia excessive treatment with Mg

infusion to relax contractions and decrease B/P

Excessive use of antacids that contain magnesium salts (eg, Maalox, Riopan, Mylanta) and laxatives (Milk of Magnesia) esp. in renal failure

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Hypomagnesemia - Mg below 1.5 meq/L Clinical manifestations (resembles hypocalcemia) Increased blood pressure o

Hypermagnesemia - Mg above 2.5 meq/L Clinical manifestations

hypotension because of peripheral vasodilation

Facial flushing

Diaphoresis o NOTE: Mg is used to Rx uncontrolled HTN (e.g. preeclampsia) Tetany (see Hypocalcemia) o Increased cell membrane activity - Frequently associated with hypocalcemia because decreased Mg inhibits release of PTH, lowering serum Ca dysphagiao test ability to swallow with water before oral medications or foods are offered

Anorexia, Constipation, Abdominal distention,

paralytic ileus o Decreased Mg causes decreased contractility of gut musculature

activity as a result of the blockage of acetylcholine release at the myoneural junction o delayed conduction in the myocardium may result bradycardia with cardiac arrest o Muscle weakness o Sedative effect- watch for decreased Level of sensorium - lethargic , coma o Paralysis- severe o Respiratory depression o Respiratory paralysis o Respiratory arrest

Mg depresses the CNS and muscle and nerve

Difficulty speaking (dysarthria)

Soft tissue calcifications (associated with increased

Ca) Mg excess is associated with increased calcium because increased Mg stimulates the release of PTH, lowering serum Ca.

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Hypomagnesemia - Mg below 1.5 meq/L Management Replace Mg: Oral magnesium SE of oral Mg is diarrhea give antidiarrheals if needed o IV Mg via pump. Too much or too rapidly infusion of Mg can produce HYPERmagnesemia: cardiac arrest (relaxing effect) flushing hypotension respiratory distress.

Hypermagnesemia - Mg above 2.5 meq/L Management Assess for: o Labored or depressed respirations may need ventilatory support o cardiac arrhythmias o hypotension (because decreased neuromuscular excitability with increased Mg)

Assess ability to swallow water prior to initiating oral

feedings or medications if dysphagia is present

Safety because of muscle weakness ROM to prevent complications of inactivity Decrease Mg level: IV calcium gluconate is a Mg antagonist may antagonizes the effects of magnesium. Ca increases contractility of heart muscle. o IV glucose and insulin promote Mg entry into cell o Remove Mg antacids and laxatives use Aluminum hydroxide o Avoid Mg containing foods

If hypocalcemia develops, o give IV Calcium together with Mg to treat tetany. (Decreased Mg inhibits release of PTH, lowering serum Ca) o Seizure precautions with severe Mg deficit due to decreased calcium

Treat alcoholism Patients receiving parenteral nutrition require magnesium in the solution to prevent hypomagnesemia because Mg goes into the cell as cells rebuild Mild Mg deficiency can be corrected by diet alone. Dietary sources of Mg are: whole grains - nuts, legumes Green leafy vegetables Fruits seafood Meat Milk products potatoes

Promote excretion of Mg Increase PO or IV fluids except in Renal failure o IV fluids (0.45% NS or LR) o diuretics to enhance Mg excretion o Dialysis in Renal failure

o o o o o o o

Increase fiber and fluids to promote bowel elimination

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Phosphorus Facts: Normal serum phosphorus level is 2.5 to 4.5mq/dL Primarily an intracellular anion and is a critical constituent of all body tissue. 85% is combined with calcium in teeth and bone, 14% intracellular Reciprocal relation to Ca Phosphorus circulated in the blood in three major forms Protein bound (12%), complexed (33%0, and ionized (55%) - **similar to Ca Similar to Ca in that it needs Vit D to be absorbed in the GI tract Regulated by: o PTH: stimulates Vit D to absorb phosphate by GI tract.

Necessary for:

Hypocalcemia stimulates PTH release - PTH causes kidneys to retain calcium and excrete Phosphorus normally, kidneys excrete 90% of phosphorus

o o o

Phosphorus is found in the body in ATP (adenosine triphosphate) which fuels muscle contractility, neuronal transmission, and electrolyte transport. ATP is required for substances to move into or out of a cell. e.g. NA-K pump. ATP interacts with Hgb in RBCs to release O2 release to tissues Metabolism of carbohydrates (CHO), proteins and fats Structural support to bones and teeth. Phosphorus acidifies urine. The acidic nature of urine minimizes urinary tract infections and helps prevent stone formation.

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Hypophosphatemia - Mg below 2.5 mq/dL Clinical manifestations

Hyperphosphatemia - Mg above 4.5 mq/dL Clinical manifestations Symptoms of hypocalcemia (see hypocalcemia notes)- result from: o in Ca. high phosphorus causes a reciprocal decrease

Symptoms due to deficiency of ATP and impaired

oxygen delivery. Phosphorus is essential for the production of cell energy (ATP). A deficiency of ATP results in muscle weakness manifested in: decreased hand grasp and difficulty speaking Muscle pain and tenderness

o o

Decreased cardiac contractility o hypotension o Weakness in breathing muscles acute respiratory failure o Dysphagia

soft tissue calcifications -

A complication of increased phosphorus is tissue (can occur in the kidneys, soft tissue, joints and arteries). This can lead to joint pain, loss of movement.

dysarthria - Changes in speech o Hypoactive bowel sounds, ileus, anorexia o Platelet dysfunction bruising, bleeding, pale skin and conjunctivae o Immunosuppression - due to depression of bacterial activity of granulocytes -Greater risk for infections because of changes in WBCs o Insulin resistance phosphorus is important in conversion of glycogen to glucose. results in hyperglycemia Neurological deficits: o Nystagmus o Seizures o Confusion o Paresthesias especially around the mouth o Peripheral neuropathy o neurological symptoms - apprehension (early signs), confusion, irritability, memory loss, diplopia, seizures, slurred speech o Involuntary movement of the eyeballs Nystagmus o disorientation o ataxia o tremor o disorientation Decreased bone density, bone pain, fractures because loss of Ca from bone due to decrease phosphorus

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Hypophosphatemia - Mg below 2.5 mq/dL Causes: Shift of phosphate from the extracellular fluid into the cells: o Debilitated states:

Hyperphosphatemia - Mg above 4.5 mq/dL Causes: Shift of phosphorus from the intracellular space into the ECF o Chemotherapy- causing cellular destruction as cells release phosphorus into serum. o acute cell hemolysis o infections / Sepsis

o
o o o

Alcoholic malnutrition/ alcohol withdrawal Eating disorders anorexia Debilitated elderly Child abuse - starvation

Diabetes diabetic ketoacidosis treatment with insulin causes intracellular transport of both glucose and phosphorus into the cells as the patient become anabolic o o Glucose administration (e.g. IV glucose) causes the pancreas to release more insulin, which in turn promotes he transport of both glucose and phosphorus into the cells as the patient become anabolic o Sepsis due to epinephrine release o Burns burn patients often hyperventilation causing resulting in the acceleration of glycolysis causing Hypophosphatemia or from anabolic process when burn patients start to build up tissue o Stress increases catecholamine release produces a shift of phosphate into the cell

Necrosis of muscle e.g. trauma, wounds o Blood transfusions the can leak phosphorus from blood cells during storage

Reduced renal excretion Renal insufficiency/failure most common decreased excretion

Increased phosphate loss:

Gastric suctioning o Chronic Diarrhea o laxative use Phosphate-binding antacids such as those that are aluminum or Magnesium based o loop diuretics cause increase Phosphorus loss

Increased phosphate intake

NU 201 Content - osmotic diuresis polyuria causes excessive loss of phosphate in urine e.g. glycosuria in uncontrolled diabetes Mellitus o Excessive IV glucose - can cause osmotic diuresis o Hyperparathyroidism - Increase PTH causes loss of phosphorus through kidneys (phosphaturia)

Medications -Overzealous administration of large amount of Fleets Phospho-Soda enema especially with slowed colonic motility e.g. elderly constipated client who received multiple enemas

Decreased absorption from GI tract - related to

o Vitamin D deficiency. Malnutrition Increased absorption from: GI tract - Large intake of Vitamin D causes increased absorption of phosphorus.

Medications that induce hypophosphatemia: o Diuretics o Anabolic steroids o Antacids - Phosphate-binding antacids o insulin promotes he transport of both glucose and phosphorus into the cells.
Prolonged , intense hyperventilation Inadequate addition of Phosphorous to nutrition sources - As cells are formed, phosphorus moves from serum into cells:

o Hypoparathyroidism causes decreased calcium with increased phosphate o Infant fed cows milk which contains more phosphate than human milk

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enteral feedings

Parenteral nutrition (TPN) TPN without phosphorus can lead to hypophosphatemia in the first 24 hours. o Overzealous infusion of calories (especially CHO) with severe malnutrition refeeding syndrome or nutritional recovery syndrome. This has a highmortality rate Associated electrolyte imbalances: o Hypokalemia - as K goes into cell, so does phosphorus o Hypomagnesemia fosters urinary loss of phosphorus o Hypocalcemia stimulates PTH release with loss of Phosphorus

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Hypophosphatemia - Mg below 2.5 mq/dL Management monitor cardiac, respiratory, neuro and hematologic status assess: hand grasp leg strength weak shakey voice gag swallow reflexes ability to perform ADLs

Hyperphosphatemia - Mg above 4.5 mq/dL Management Medications: Avoid: o phosphorus containing antacids Give: o Calcium antacids calcium carbonate or calcium citrate to replace Ca o Phosphate binding agents - gels or antacids Maalox o loop diuretics promote excretion o allopurinal (Zyloprim) to decrease uric acid production from use of cytotoxic drugs causing hyperphosphatemia o Administer glucose and insulin to move phosphorus from ECF to ICF Restrict diet phosphate Dialysis Surgery to remove large calcium phosphorus deposits. IV infusions of saline may promote renal phosphate excretion.

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IV phosphorus - caution: excess IV phosphorus can cause: o tetany from hypocalcemia calcium falls as phosphorus rises. o calcification in tissues o watch IV site for sloughing with infiltration administer slowly o diarrhea oral phosphorus o Neutra-Phos capsule or Fleets Phospho-soda asses for side effect of diarrhea risk for infections because of changes in WBCs take precautions to prevent infections esp. with central lines. Dietary sources milk products, eggs, meats, nuts, fish, poultry, whole grains.

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107379977.doc