fall 2012 fluid electrolytes notes

7/31/2019 Fall 2012 Fluid Electrolytes Notes

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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 H2Oo 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+ 150Mg ++ 40

Na+ 10

Phosphates and sulfates 150Bicarbonate (HCO3-) 10

Organic Acids 5Proteinate 40

Total Cations 200 Total Anions 200

Major extracellularelectrolytes:

Na+ 142

K+ 5Ca++ 5 (useable form) (note:calcium is primarily in bone)Mg ++ 2

Cl- 103

Bicarbonate (HCO3-) 26Phosphate (HPO4--) 2Sulfate (SO4--) 1Organic Acids 5Proteinate 17

Total Cations 154 Total Anions 154

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BODY FLUID COMPARTMENTS

Body fluid is located in two fluid compartments1. Intracellular Fluid (2/3)

2. Extracellular Fluid (1/3) - outside the cells

3 extracellular compartments:o Intravascular (plasma):

6L total of blood volume 3L plasma, 3L - erythrocytes, leukocytes, andthrombocytes

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 fluidAge

younger have a higher percentage of body fluid

Changes associated with aging (elderly):o Decreased renal function

decrease ability to concentrate urine - decreased ability to hold onto water, thereforemore prone to fluid imbalances..

o 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)

o Decreased skin turgor:

Skin turgor is less valid in elderly because their skin has lost elasticity and less able tohold 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.

o 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

o Atypical symptom manifestations:

In elderly, the S&S of F&E disturbances may be subtle or atypical (e.g. fluid deficitmay cause confusion in the elderly person, whereas, in the young person the firstsign commonly is thirst)

Elderly have a decreased ability to sense thirst.

o 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 DEFICITFVD (Hypovolemia)

Causes:

decreased fluid intake:o anorexia

o nauseao swallowing problemso inability to gain access to fluid (elderly, children)o impaired thirst mechanism (elderly)o unconsciouso excessive fluid restriction child abuse

abnormal fluid losses:o GI suctioningo vomitingo 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 intothe intestine causing diarrhea.

o ileostomy drainage that is not adequately replaced.o

fistulaso draining woundso 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

o Excessive urination (polyuria)

NU-201 content - Diabetes Insipidus - decreasedADH from posterior pituitary gland

causes renal excretion of water leads to hypernatremia because more water is lostwith ADH.

NU-201 content - uncontrolled diabetes mellitus causes polyuria due to increaseglucose particles in serum pulling water into vascular space. The excess fluid isexcrete by kidney along with the excess glucose (glycosuria)

o 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+.

o hemorrhage blood losso comao Third spacing (see below)

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

o Acute weight loss daily weights are monitored; (2.2 lbs. = 1000ml (1 liter) = 1 Kg) Dailyweights are the most reliable indicator of fluid loss/gain daily weights before breakfast usingthe same scale, same clothes.

o decreased BP - postural (orthostatic) hypotension a drop in systolic pressure exceeding 15mmHg when the patient moves from a lying to a sitting or standing position.

o dizzinesso Decreased CVP (normal is 4 11mmH2O)

o Tachycardia - Weak, rapid (thready) heart rate (note: rapid bounding pulse with FVE)o rapid and weak respirations in the initial stage of FVD due to decreased volume and Na-K

pump imbalances

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o If patient is in shock with metabolic acidosis, - Hyperventilation (Kussmauls breathing) - deeprespiratory rate (increased inspiratory volume) - to blow off CO2.

o Flattened jugular neck, slowness of filling of feet and hand veinso Weak peripheral pulses due to decrease volumeo Sunken eyeso Infants depressed fontanel, irritability, no tears when crying

GIo Thirst, Anorexia, Nausea

o Hard stools (note: diarrhea with FVE)

Musculoskeletalo 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 mayresult.(Confusion, irritability, dizziness, agitation, restlessness, seizures, and possible coma)

Renalo 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). Skino Decreased (poor) skin tenting occurso Decreased tongue turgor causes an additional longitudinal furrow and a smaller tongue

Wrinkles in tongue-cracked, rough, dry tongueo Dry or sticky mucous membranes dry tongueo Decreased saliva white coloro Crusted lipso Flakey, dry skin

o Cool, clammy skin related to decreased peripheral perfusion (decreased capillary refill) and

peripheral vasoconstriction from SNS stimulation. May have warm skin in early dehydrationbecause SNS has not yet been stimulated.

o Cool, dry skin possible too due to dehydration.o May have fever warm skin- especially is associated with infection.o Prolonged (delayed) capillary filling time decreased volume and perfusion pressure

Labs:o HCT elevated - decreased plasma volume related to RBCso 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 withleaking of fluid into the peritoneal space.

o Bowel obstruction increased intra-abdominal pressure and possible bowel rupture causingperitonitis

o Bee sting increase capillary permeability causes proteins to leak into the interstitial spacecausing edema. Anaphylactic shock is a systemic increase in capillary permeability.

o Massive bleeding into a joint or body cavityo Burns - increased capillary permeability causing leaking of fluid into interstitial spaces (edema

depends on the severity of the burn)

o NU-202 content - Ascites associated with liver dysfunction and nephrotic syndrome. Ascitesis 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.o 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).

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 Edemao diminished and weak pedal pulses due to edema (difficult to palpate) and decreased vascular

volume

o Increased body weight fluid leaves the vascular space and collects in body spaces- creates

vascular volume deficit with fluid weight gain. GI

o 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 abdominaldistention. Patients report SOB because of pressure on the diaphragm

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Medical Management of FVDAssessment

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 fluidloss/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 lungfields 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 stillfunctioning:

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 - Ifwater loss without sodium loss (hypernatremia) giveD5W (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 andwater for renal excretion of metabolic wastes

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

o 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 andworse dehydration.

o Avoid caffeine because acts a mild diuretic

Medications Antidiarrheals as needed Anti emetics for nausea

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FLUID VOLUME EXCESSFVE (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

o 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 theurine

Isotonic expansion of ECF caused by the abnormal retention of water and sodiumo 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 solutionso Prolonged corticosteroids, NSAIDs therapy increase Na and water retention

o NU-201 Content Heart failure causes decrease renal excretion of fluid and sodium fluidoverload

o NU-201 Content - Hyperaldosteronism - increased aldosterone retains Na+ and H2O

o NU-201 Content - Cushings Syndrome glucocorticoid excess - causes Na+ and H2Oretention with K+ loss (hypokalemia may result)

Clinical Manifestations Cardiovascular/Blood

o Distended neck, hand and feet veins

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

GI tracto NV

o Liquid stools (Note: constipation with FVD) Renal

o Increased UO only with functioning kidneyso SG less than 1.010

Respiratoryo pulmonary edema/congestion - fluid in the pulmonary interstitium and alveoli increases.

Manifestations include SOB, dyspnea, cough, increased respiratory rate, diaphoresis, andcrackles (rales) and wheezing on auscultation of lungs

Neurological/Muscularo Brain cells swell - causing confusion, coma, lethargy, seizureso Muscle weaknesso Muscle cramps

Skino Edema pitting edemao Puffy eyelidso Severe generalized edema is called anasarcao Skin may be cool and edematous due to fluid accumulation and decreased perfusion

Lab:

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

Management of FVE

Fluidso Discontinuing sodium containing fluidso IV fluids:

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If symptoms are severe and related to H2O intoxication, may give small amount ofhypertonic saline to restore Na+.

3% NS 5%NS

Avoid hypotonic IV solutions until Na rises otherwise may cause further dilutionalhyponatremia

Nutrition/Dieto

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 - causeloss of sodium and water by the kidneys

Thiazide block Na reabsorption causes K+ retention Hydrochlorothiazide (HydroDIURIL)

Loop furosemide (Lasix) -Cause greater loss of Na and water Potassium sparing diuretics

Aldactone - can cause hyperkalemia, especially with renal failure Other interventions:

o Hemodialysis or peritoneal dialysis to remove fluid and wasteso Paracentesis drain fluid from the peritoneal cavity e.g. ascites third spacingo Seizure precautionso O2 therapy

o NU-201 Content - Pulmonary edema treat with morphine, Nitroglycerine and digoxino Positioning:

o Regular rest periods bedrest causes diuresis of edema fluid.o Elevate extremitieso Apply elastic compression stockingso If dyspnea or orthopnea is present, place in the semi-fowlers position to promote lung

expansiono Turn and position because edematous tissue is more prone to skin breakdown. Give good

skin careo 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 retentiono 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 ORBicarb. Cl- and Bicarb (HCO3)work opposite. If Na combines with bicarb, Cl- is lost through the kidneys. Inversely, if Nacombines with Cl-, Bicarb is lost through the kidneys.

Na K pump influences nerve and muscle irritability, nerve impulse conduction and muscle

contraction

o An example of active transport is the Na-K pump. Active transport requires ATP to occur.(Phosphate is necessary for ATP production.)

o Without ATP (e.g. shock), the sodium and potassium pump fail to work efficiently, whichleads to cellular swelling bursting- and eventual cell death.

o Sodium-Potassium Pump - located on the cell membrane and actively moves Na frominside the cell to the outside of the cell (ECF) regulated by Phosphate level and thecalcium 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 causesincreased contractility

Sodium effects on Calcium:

o Increased Na (hypernatremia) prevents movement of calcium into the myocardium (Calevel may be normal) causes decreased myocardial contractility decreased cardiac

output heart failure. Therefore, Na may be given to decrease Ca effects on the hearte.g. when hypercalcemia is present (see hypercalcemia notes).

o 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 Na145

decreased osmolality 300 caused by:

Gain of Na: excessive PO Na (salt) intake - 1 tsp of table salt

contain 2,300 mg of sodium) 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 waterwhich contains sodium

Medications corticosteroids (cause retention of

Na), antacids with Na bicarb., Kayexalate (Na+ exchangeresin used to treat hyperkalemia)

decreased or lose water:

fluid deprivation in unconscious patients who cannotperceive, respond to or communicate thirst - most often very

old, young and cognitively impaired Water deprivation e.g. fluids are excessivelyrestricted child abuse

hyperventilation (water vapor loss)

sweating without fluid replacement, heat stroke,fever

profuse, watery diarrhea- Crohns disease, ulcerative

colitis

NU-201 content - Diabetes Insipidus - decreased

ADHfrom posterior pituitary gland causes renal excretion of

water leads to hypernatremia because more water is lostwith ADH.

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Hyponatremia Na145

Clinical manifestations Clinical manifestations

If Na and H2O are lost together (isotonicdehydration) have symptoms of FVD hypovolemia shock type symptoms

Decreased BP (also with decreased Cl)

Orthostatic fall in blood pressure - a drop in systolic

pressure exceeding 15 mmHg when the patient moves from alying to a sitting or standing position.

Increased pulse weak, rapid and thready withfluid 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

Decreasedjugular /hand/feet vein filling distended neck veins with excess fluid

If SIADH occurs then - Oliguria (10-30ml/hr) Polyuria with Diabetes Insipidus

oliguria, decreased urine output, increased S.G.(> 1.030) increased osmolarity of blood causes kidney

to retain fluid.

Skino Dry, cracked mucosa

o Decrease saliva production

o Poor skin turgor- shrunken tongue

o Low grade fever

o Clammy skin with hypovolemia

Skino Dry, swollen, red tongue

o Sticky mucous membranes

o Dry, warm, flushed skin from dehydration

o Decreased sweating

o Elevated body temperature from dehydration

Thirst with hypovolemia Intense thirst (polydispia)

With Dilutional hyponatremia, can have signs of FVE:

N/V, anorexia and abdominal cramps

Altered mental status due to cell swelling and

cerebral edema. This can cause headache, weakness, slurredspeech, confusion, lethargy, anxiety, seizures, coma, andpermanent 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

Symptoms due to hypervolemia (fluid overload)

o Increased body weight edema causing fingerprint

indentation over bony prominenceso Increased urinary output

o Increased B/P

o Respiratory distress

o Rapid bounding pulse

o Distended neck veins

o dyspnea, puffy eyelids, dependent edema, and weight

gain in 24 hours.

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Hyponatremia Na145

Hypochloremic Metabolic Alkalosis - When

decreased Na is associated with decreased Cl can developHypochloremic Metabolic Alkalosis. Alkalosis causes Ca tobind 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

Shallow respirations to retain CO2 (acid) to

compensatefor Hypochloremic metabolic alkalosis.

Initially, increased Na causes loss of Calcium

(hypocalcemia) through kidneys resulting inhypocalcemia (causing tetany (early sign)

Hyperchloremic Metabolic Acidosis - As

hypernatremia progresses, can develop HyperchloremicMetabolic Acidosis. Acidosis causes Hypercalcemia. this causes:o Lethargy, muscle weakness, depressed reflexes

calcium depresses neuromuscular excitability (too manyguards at the gate)

deep respirations to blow off CO2 to

compensateforacidosis

crackles, rales is have FVE if increase fluid intake

crackles if have FVE with an increased Na intake

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Hyponatremia Na145

Management Management

Assessment

o weights- same time, same scale, same amount of

clothing each day for accuracyo neuro status

o I&O

o skin turgor

o mucous membranes

Assessmento Weights- same time, same scale, same amount of

clothing each day for accuracyo neuro status

o I&O

o Skin turgor

o Mucous membranes

o Assess finances if parents diluting formula to save

money.

o child abuse fluid deprivation

Water restriction:

o Dilutional hyponatremia is treated by restriction of

fluid to a total of 800ml in 24 hours

Addition of Water

o Encourage P.O or IV water (see below)

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

Avoid excess water supplements in patients receiving

isotonic or hypotonic enteral feedings

Give water supplements with high osmolality

(hypertonic) enteral feeding to decrease theconcentration of the feeding

Do not replace diarrhea or vomiting with only tapwater- use fluids containing Na

Irrigate GI and urinary tract with 0.9% NS not water

Sodium Replacement - encourage food and fluids

high in sodiumo 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, cornflakes, crackers,

Sodium Restriction - restrict foods and fluids

with high Na+ content

IV Fluids:

o isotonic solutions for isotonic dehydration both

Na and fluid loss give isotonic solutions - IV lactatedRingers or 0.9%NS

o Severe hyponatremia (dilutional hyponatremia with

FVE) - highly hypertonic solutions (3 or 5%Na Cl) to relieveacute manifestations of cerebral edema and preventneurologic complications. These solutions should be infusedwith careful monitoring e.g. in the ICU on a pump

IV Fluids:

o hypotonic solutions - Gradual lowering of the

serum Na by infusion ofhypotonic solutions e.g. 0.3%NaCl, 0.45% NS, or an isotonic non-saline solution e.g.D5W (note: D5W becomes hypotonic as glucose ismetabolized)o Hypotonic solutions are more dilute than normal

body fluid they dilute body fluid back to normalconcentration.

Note: Too rapid increase in the sodium causes Namay pull fluid from cells too rapidly (cell shrinkage)

causing:

o permanent neurologic damage due to osmotic cellular

demyelination.

Note: Too rapid reduction in the serum sodiumlevel causes the plasma to become hypo-osmotic

causing movement of fluid into brain cells (cellsswell) causing:

o cerebral edema

Prevent fluid overload

o Auscultate lungs for crackles

o Use pump to regulate flow

o gradually replace fluids

o Use pump to regulate flow

o gradually replace fluids

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Hyponatremia Na145

Increase water excretion - Osmotic diuretics -

promote water excretion rather than Na loss i.e. mannitol

Diuretics to cause increased Na loss - used to treatthe sodium gain (lasix) Antidiarrheals if caused by diarrhea fluid loss.

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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.)

o A decreased or increased K can lead to severe muscle weakness because K+ is glucose

metabolism and energy production causes paralysis, ventilation problems, bradycardiaand kidney problems

o Regulates use of glucose by cells involved with energy production loss of K causesfatigue, lack of strength

o Insulin decreases serum K: to treat excess serum K (hyperkalemia) give insulin (withglucose) to move K into cell. (note: Hyperalimentation (parenteral nutrition) can trigger ahypersecretion of insulin which can cause hypokalemia. The tissue build-up causes K+ toshift from the serum into the new cells)

Influences acid base balance1. 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. In Acidosis, H goes into cell, K comes out. In acidosis, Ca increases (moreguards at the gate) hypotonic muscles, decreased excitability.

2. 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 Hyperkalemia - K above 5 meq/L

Causes:Excessive Output:

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

o As cell are rebuilt, K+ and Mg go into cell together see

Hyperalimentation below

High doses of steroids causes retention of Na and lossof K

Diuretics - Use of potassium-wasting diuretics (e.g. Loopdiuretics 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, CushingsSyndrome (Hyperaldosteronism)

Inadequate K+ intake:

Anorexia nervosa & Bulimia loss of lean muscle releases K that is excreted by kidney and not replace in diet.

starvation, malnutrition causes tissue wasting withloss of K

NPO not taking in K must make sure IV K+ given ifpatient 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:

o 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 epinephrinepromote entry of K into the cell e.g. stress, surgery

In Metabolic Alkalosis, a compensatory mechanism

occurs. K shifts into the cell as H ions moves out of cells into bloodvessel- causing Hypokalemia.

Causes:

Decreased Renal excretion: Renal failure most common cause

Potassium-sparing diuretics i.e. aldactone NU-201 Content Addisons Disease - adrenal

insufficiency causes a decreased aldosterone whichcauses a loss of Na and water with the retention of K.

Excessive K+ intake:

Too rapid or excessive K+ replacement IV or P.O.

excessive use of salt substitutes that have K+

Potassium shift out of cells into vascular space:

NU 201 Content - Diabetic Ketoacidosis - Lack of

insulin (diabetic ketoacidosis) creates a hyperosmolar statethat causes water to move out of cell, taking potassium withit

In Metabolic Acidosis, a compensatory mechanismoccurs - K shifts out of cell as H ions move into cells - causingHyperkalemia

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 - Bloodsample hemolysis, repeated fist clenching and unclenchingwith blood draws)

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Clinical manifestations related to muscledysfunction

NU-201 Content - Cardiac arrhythmias a

decreased K+ slows the conduction of heartcausing:

o bradycardia

o can cause sudden cardiac death

o Note: decreased K+ causes an increased

sensitivity to digoxin. Digoxin also slowsheart rate too- predisposing to toxicity

In addition, a decreased K+ can be caused by anincreased Na+ (hypernatremia). Increased Naprevents movement of calcium into themyocardium causing decreased myocardialcontractility and decreased cardiac outputresulting in heart failure.

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 thepatient 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 constipationo paralytic ileus

Depressed neuromuscular activity because 1)

interferes with Na- K pump, and 2) K levels are

insufficient to maintain cellular metabolismcausing:

o fatigue

o muscle weakness - usually first detected

in the legs may progress to flaccidparalysis

o muscle/ leg cramps

o hypoactive reflexes

o respiratory muscle weakness

respiratory arrest

If metabolic alkalosis is present as the cause

of hypokalemia, respiratory acidosis maydevelop as a compensatory mechanism formetabolic alkalosis.

o shallow breathing to increase CO2

K+ depletion can lead to inability toconcentrate urine

o Frequent urination (polyuria)

o Nocturia

Clinical manifestations related tomuscle dysfunction

NU-201 Content - Cardiac muscle weakness an

increase in K+ causes weaker cardiac contraction(instability) results in bradycardia , heartblock, and cardiac arrest

o **treat the instability with Calcium

gluconate - Calcium stabilizes cellmembranes and antagonizes the weakcardiac contraction that can occur fromhyperkalemia.

Irritability, apathy, confusion, fatigue, drowsiness

GI increased bowel motility (hyperactivity)

o Diarrhea

o Nausea

o Intestinal colic

o Intestinal/abdominal cramping

o Hyperactive bowel sounds

An increased K depresses depolarization the

nervous system and skeletal muscle contractionbecause 1) interferes with Na- K pump, and 2) Klevels are insufficient to maintain cellularmetabolism causing:

o Muscle weakness and paralysis

usually begins in legs. Muscle weaknessmirrors hypokalemia.

o hypoactive reflexes

o Paresthesias in extremities, face and

tongue usually first symptom.

Paresthesia occurs more with increased K

If metabolic acidosis is present as the cause

of hyperkalemia, respiratory alkalosis may

develop as a compensatory mechanism formetabolic acidosis

o deep breathing to decrease CO2

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o Polydipsia

o Dilute urine

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ManagementAssessment:

Monitor heart rate and rhythm, resp status

Place on cardiac monitor - ECG

Must check K levels with ABGs to determine ifthe K imbalance is related to acid basedisturbances. Assess I&O, GI status

Prevent excessive loss of K from diuretics and laxatives.

Give K sparing diuretics i.e. aldactone

Administer K supplements

oral:

Administer oral potassium as ordered with foodor 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 mustswallow whole.

for those on digoxin Teach to assess pulse forbradycardia

check K+ levels before taking digoxin because

hypokalemia increases risk of digitalis toxicity

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 regenerationas during hyperalimentation, when treating diabeticketoacidosis or when have both a phosphate andpotassium deficit..

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 andinfusion pumpo NPO for surgery give K maintenance of 20-

40meq/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 theinjection site irritates vein - stop, slow or further diluteinfusion. May use warm compress above the insertion sitealong the vein track throughout the infusion. Use largevein e.g. antecubitalo Potassium is a vesicant and can cause tissue

damage if infiltration occurso If infiltration occurs, discontinue the IV, apply a

COLD compress, (not heat) and notify the health careprovider.

Management

Assessment: Monitor heart rate and rhythm, resp status

Place on cardiac monitor - ECG Must check K levels with ABGs to determine ifthe K imbalance is related to acid basedisturbances.

Assess I&O, GI status

Restrict Potassium intake

Promote Potassium excretion:

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 thefeces. This can cause watery diarrhea.

Give K wasting diuretics e.g. Lasix (loopdiuretics) Hemodialysis if K remains high.

Increased Ca increases K excretion by kidneys -

see calcium gluconate/chloride below

Increase urine flow by IV Normal Saline ANDPotassium-losing diuretics e.g. thiazides Lasix

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 minuteso 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 therelease of K+ from cells.

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

o Calcium Gluconate - Calcium stabilizes cell

membranes and antagonizes the weak cardiac contraction

that can occur from hyperkalemia.

o Calcium can cause vein dilation - keep thepatients lying down after administration to prevent

postural hypotension.

o Check for infiltration calcium infusions cause

tissue necrosiso 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 turnseveral times to mix contents thoroughly

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o Assess urine output before giving K

supplements. Never give KCL unless there is a UO of atleast 30 ml/h

In children, administer after the first void

Nutrition: Teach about K rich foods: meats, dried fruits,bananas, tomatoes, melon, oranges, green leafyvegetables, 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

Infuse K+ according to protocols

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, breadOther Interventions:

Make sure packed RBCs are fresh esp with

multiple transfusions because stored blood breaksdown cells and releases K

Debride dead tissue so K is not released Assess urine output before giving Ksupplements. If kidneys are not producing urine,serum K+ levels may increase. Never give KCL

unless there is a UO of at least 30 ml/ho 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) tosodium

A high chloride level is usually accompanied by a high sodium level and fluid retention ifthere is not anacid base imbalance.

Acid-Base Imbalances - With each Na ion reabsorbed by the kidney, a chloride ORbicarb ion isreabsorbed 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 pHremains 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 - aschloride decreases, bicarbonate ion are retained by the kidney causing alkalosis

Chloride shift acidosis also causes bicarbonate to move from the RBCs to theplasma in exchange for chloride from the plasma to the red cells this results inhypochloremia.

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.

Hypochloremia - Cl below 96 meq/L Hyperchloremia - Cl above 106 meq/L

Causes:

Excessive GI tube drainage, diarrhea and severe

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 kidneycausing alkalosis

o Chloride shift a low serum ph (acidosis) causes

the bicarbonate to move from the RBCs to the plasma inexchange 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 cellscausing excessive Na and Cl loss through exocrineglands such as sweat (perspiration), saliva, andmucus exocrine glands, such of pancreas, intestineand bronchi.

Causes: Most common cause Dehydration due to lossof more water than Na and Cl

Acid Base Imbalance:

o loss of bicarbonate via the kidney causes

Chloride gain- hyperchloremic metabolic acidosis - asbicarbonate ions are lost by the kidney, chloride increasescausing acidosis

o metabolic acidosis, shock, starvation, diabetic

ketoacidosis, decreased ventilation, Ingestion of acids

e.g. salicylate - As bicarb is used up to neutralize theexcess acid in the body, Cl- is reabsorbed as a negativeion- to maintain electroneutrality- causingHyperchloremia.

Steroids - cause retention of Na and Cl

hypernatremia- Cl increases with Na+

Excessive NaCl infusions

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Clinical manifestations

Are similar to metabolic alkalosis and hyponatremia:

hypotension

Hypochloremic metabolic alkalosis causes Ca tobind to protein decreasing the amount of useable Cacausing hypocalcemia (see hypocalcemia):

o tetany

o Hyperexcitability of muscles, tetany

o Confusion

o Agitation, irritability, seizures

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

to retain CO2

Clinical manifestationsAre similar to metabolic acidosis, hypervolemia andhypernatremia.

Mg and Potassium levels increase and decreasetogether

Hypotension - Peripheral vasodilation ( seeHypermagnesemia)

OR

Hypertension due to increase Na and fluid

retention

Hyperchloremic metabolic acidosis increasesthe amount of useable Ca causing hypercalcemia(see hypercalcemia):

o Muscle weakness - related to acidosis causing an

increased Ca+

o confusiono Lethargy, Decreased LOC

If metabolic Acidosis is present:o compensation can occur with deep respirations

to blow off CO2 Kussmauls respirations

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Management

IV Fluidso Replace Cl- with IV NS 0.9% or 0.45% solutions

Medicationso May discontinue or change diuretics that cause loss

of Na and Clo 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:o Tomato juice

o Salty broth

o Canned vegetables

o Processed meats

o Fruits

A person who drinks a lot of free water without

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

Use NS to flush NGT, not tap water

Management

IV Fluids

o IVLactated Ringers - the lactate is converted to

bicarbonate in the liver, which will increase thebicarbonate level and cause renal excretion of Chloride.This helps to correct the acidosis and decrease Chloride.

Medicationso Diuretics to eliminate chloride

o Na bicarbonate to increase bicarbonate levels,

which leads to renal excretion of chloride

Chloride restricted foodso Na foods and fluids are restricted

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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 physiologicallyactive (diffusible through capillary membrane) and important for neuromuscular activityand 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 arecorrelated with free Ca (ionized).

2. 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 bindingto albumin:

a. Acidosis decreases calcium binding to protein , leading to increased ionized(free,useable) calcium

b. Alkalosis increases Calcium binding to protein, leading to decreased ionized

(free,usable) calcium

3. 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 largequantities 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) preventsovercharge 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 ofabsorption). Therefore ileostomies, fistulas, wound exudates, etc. can cause decreased Ca.

Calcium and phosphorous have inverse relationship. Calcium balance depends on 3 hormones :C

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

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, anddecreases renal excretion of Ca.dCalcitonin 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 Hypercalcemia - Ca above 10.5 meq/L

Causes:

Most common cause Renal Failure Vit D is

not activated by the kidney

Inadequate Vitamin D intake/activation

Rapid administration of citrated blood:

o Citrate is the anticoagulant used in blood

products. Citrate can bind with ionized calcium causing adecrease calcium.

Alkalosis - With alkalosis, more calcium

becomes bound to protein (unusable form of Ca).

Hypoparathyroidism causes:

o Parathyriodectomy

Decreased albumin

Malabsorption (most calcium absorbed in theduodenum and jejunum)- caused by rapidperistalsis , small bowel resection, chronicdiarrhea reduce Ca absorption from the GI tract

Decreased stomach acid causes decreasedabsorption of calcium

Associated electrolyte disturbances:o Increase Na causes increased Ca excretion by

kidneyso 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 Cao Ca is lost in fluid that is sequestered in the

abdomen in pancreatitis

Medications

o loss of Ca from bones caused by aluminum-

containing antacids, caffeine, nicotine, corticosteroids

(can cause osteoporosis ,o increase secretion of Ca caused by loop

diuretics

Causes:

Excess is not common with functioning

kidneys because kidneys excrete Ca.

Vitamin D intoxication

Malignancies of bone

Acidosis - With Acidosis, less calcium is bound

to protein resulting in more ionized (useable)calcium

Hyperparathyroidism causes:o Increased PTH release causes an increase

release of calcium from the bones ando increased intestinal and renal absorption of

calcium

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

kidneys

Medications

o Increased intake calcium antacids andsupplements

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Hypocalcemia - Ca below 8.5 meq/L Hypercalcemia - Ca above 10.5 meq/L


Decreased myocardial contractility - weak heart muscle

contraction leading to:Tachycardia (due to cardiac weakness) and

decreased cardiac output, bradycardia, asystole

Hypotension due to vasodilation

Osteoporosis

Spontaneous fractures bone loss, osteoporosis

increased neuromuscular (cell membrane) excitability (increasedpermeability):

Repetitive uncontrolled impulses in peripheralnerves (increase in the Na-K pump which isuninhibited by a decreased Ca decreased guards

at the gate) Tetany (hypertonicity / hyperreflexia.) muscle spasms (cramps, tremors, twitching)

Trousseaus sign - inflating a blood pressure cuff

on the upper arm to about 20mmHg above systolicpressure for 2-5 minutes produces carpopedalspasm (an adducted thumb, flexed wrist andmetacarpophalangeal joints, extendedinterphalangeal joints with fingers together - hands

folded in) Will occur as ischemia of the ulnar nervedevelops.

Chvosteks sign twitchingof face muscles when

the facialnerve is tapped anterior to the ear. Thecorner 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 oftingling, numbness may occur in the tips of thefingers, around the mouth, and less commonly inthe feet.

confusion, anxiety irritability, restlessness,agitation, insomnia

hoarse voice

dysphagia (related to low Mg see Mg notes)

Muscle cramps - Abdominal cramp, diarrhea,

hyperactive bowel sounds

Skin

Dry hair Sparse hair

Scaly dry skin

Brittle nails


Increased myocardial contractility bradycardia, heart

block

Hypertension due to elevated serum epinephrine inpatients with hypercalemia.

bone pain

spontaneous fractures with Hyperparathyroidism there is anincreased PTH pulling Ca from the bone

excess calcium blocks the effect of sodium in skeletal muscles,reduction excitation of muscles and nerves - reducesneuromuscular (cell membrane) excitability (decreasedpermeability:

(hypotonicity) Fatigue, lethargy

Muscle weakness/flaccid depressed deep tendon reflexes

lethargy and confusion blurred vision

Abdominal distention and paralytic ileus withsevere hypercalcemic crisis

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

due to decreased peristalsis and decreasedcontraction of GI tract from decreased muscle tone

and decreased permeability.

Renal

Increased Ca excretion by kidneys due todiuresis from high solute loss

urinary calculi causes flank pain

Excessive urination - polyuria caused by the highsolute (calcium) load - can lead to polydypsia,dehydration

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Hypocalcemia - Ca below8.5 meq/L Hypercalcemia - Ca above10.5 meq/L


cardiovascular status

airway for laryngeal spasms and respiratory arrest

Teach: Prevent osteoporosis: Teach on reducing the risk for

falls

adequate dietary calcium intake;

regular weight-bearing exercise teach - alcohol, tobacco and caffeine inhibit calciumabsorption and increases urinary calcium excretion. With chronic diarrhea or ileostomies encourageincreased intake of Ca.

Medications to reduce the rate of bone loss: biphosphonates

calcitonin

Calcium Supplements

Ca antacids can cause constipation

Calcium supplements - at least 1,000 to 1,500mg/dayin the adult Proton pump inhibitors can interfere with Caabsorption 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

IV calcium

o calcium gluconate.

o calcium chloride

o infuse IV calcium slowly - too rapid IV administration

of calcium can cause cardiac arrest, vasodilation, hypotension(should remain recumbent for 30-60 minutes after IVadministration to prevent postural hypotension, bradycardia.Monitor EKG with VSo Check for infiltration calcium infusions cause tissue

necrosis

Seizure precautions due to tetany:

o Quiet environment to avoid overstimulation and

neuromuscular excitability

Avoid sodium IV solutions (e.g. 0.9% NS) with

hypocalcemia because sodium causes excretion of Ca

by the kidneys

Diet:

dairy, milk products, green, leafy vegetables, cannedsalmon, sardines, fresh oysters, molasses, macaroni,nuts-almonds, whole grains, creamed soups fish, tofu.

Blood Transfusions

Give blood transfusions slowly so liver can metabolizecitrate and prevent from binding to Ca

Rapid administration of large quantities of storedblood may cause hypocalcemia and hypomagnesemiawhen citrate binds calcium and magnesium.


cardiovascular status

Decrease loss of Calcium from bone: Treating the underlying cause (eg

chemotherapy for malignancy or partialparathyroidectomy forhyperparathythroidism).

Medications to reduce serum calcium:

Calcitonin lowers the serum calciumlevels by reducing bone resorption (loss ofCa from bone)

Bipisphosphonates obstruct calcium

release from the bone, thereby reducing

bone resorption phosphate to induce Ca excretion viakidney

Avoid Vit D & Ca supplements:

Encourage fluids - Encourage fluids to promote

excretion by the kidneys:

Encourage patient to drink 3 to 4 quarts

of fluid daily if tolerated by cardiacstatus - to promote excretion andformation of renal calculi Encourage fluidswith sodium unless contraindicated. Nacauses 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 thetendency 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 Hypermagnesemia - Mg above 2.5 meq/L

Causes:

Magnesium deficiency can occur with decreasedpotassium, Mg and calcium.

Magnesium and K+ shift into cells with insulin therapy

Mg deficiency is associated with decreased calciumbecause 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 withCa)

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

Causes:

Renal Failure - Most common cause

Preeclampsia excessive treatment with Mginfusion to relax contractions and decrease B/P

Excessive use of antacids that contain magnesiumsalts (eg, Maalox, Riopan, Mylanta) andlaxatives (Milk of Magnesia) esp. in renal failure

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Clinical manifestations (resembles hypocalcemia)

Increased blood pressure

Tetany (see Hypocalcemia)o Increased cell membrane activity - Frequently

associated with hypocalcemia because decreased Mginhibits release of PTH, lowering serum Ca

dysphagia-o test ability to swallow with water before oral

medications or foods are offered

Anorexia, Constipation, Abdominal distention,

paralytic ileuso Decreased Mg causes decreased contractility of gut

musculature


hypotension because of peripheral vasodilationo Facial flushing

o Diaphoresis

o NOTE: Mg is used to Rx uncontrolled HTN (e.g.

preeclampsia)

Mg depresses the CNS and muscle and nerveactivity as a result of the blockage of

acetylcholine release at the myoneural junction

o delayed conduction in the myocardium may

result bradycardia with cardiac arresto Muscle weakness

o Sedative effect- watch for decreased Level of

sensorium - lethargic , comao Paralysis- severe

o Respiratory depressiono Respiratory paralysis

o Respiratory arrest

o Difficulty speaking (dysarthria)

Soft tissue calcifications (associated with increasedCa) Mg excess is associated with increasedcalcium because increased Mg stimulates therelease of PTH, lowering serum Ca.

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Management

Replace Mg:

o Oral magnesium SE of oral Mg is diarrhea giveantidiarrheals if neededo IV Mg via pump. Too much or too rapidly infusion

of Mg can produce HYPERmagnesemia:

cardiac arrest (relaxing effect)

flushing

hypotension

respiratory distress.

Assess ability to swallow water prior to initiating oral

feedings or medications if dysphagia is present

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 requiremagnesium in the solution to preventhypomagnesemia because Mg goes into the cellas cells rebuild

Mild Mg deficiency can be corrected by diet alone.Dietary sources of Mg are:

o whole grains - nuts, legumes

o Green leafy vegetables

o Fruits

o seafood

o Meat

o Milk products

o potatoes

Management

Assess for:

o Labored or depressed respirations may needventilatory supporto cardiac arrhythmias

o hypotension (because decreased neuromuscular

excitability with increased Mg)

Safety because of muscle weakness ROM to prevent complications of inactivity

Decrease Mg level:

o

IV calcium gluconate is a Mg antagonist mayantagonizes the effects of magnesium. Ca increases

contractility of heart muscle.o IV glucose and insulin promote Mg entry into

cello Remove Mg antacids and laxatives use

Aluminum hydroxideo Avoid Mg containing foods

Promote excretion of Mg

o 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

Increase fiber and fluids to promote bowelelimination

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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.

Hypocalcemia stimulates PTH release - PTH causes kidneys to retain calcium and

excrete Phosphorus normally, kidneys excrete 90% of phosphorus Necessary for:

o Phosphorus is found in the body in ATP (adenosine triphosphate) which fuels muscle

contractility, neuronal transmission, and electrolyte transport. ATP is required for substancesto move into or out of a cell. e.g. NA-K pump. ATP interacts with Hgb in RBCs to release O2release to tissues

o Metabolism of carbohydrates (CHO), proteins and fatso Structural support to bones and teeth.o 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 Hyperphosphatemia - Mg above 4.5 mq/dL


Symptoms due to deficiency of ATP and impaired

oxygen delivery. Phosphorus is essential for the

production of cell energy (ATP). A deficiency ofATP results in muscle weakness manifested in:

o decreased hand grasp and difficulty speaking

o Muscle pain and tenderness

o Decreased cardiac contractility

o hypotension

o Weakness in breathing muscles acute

respiratory failureo Dysphagia

o 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 forinfections because of changes in WBCso Insulin resistance phosphorus is important in

conversion of glycogen to glucose. results inhyperglycemia

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 -Nystagmuso disorientation

o ataxia

o tremor

o disorientation

Decreased bone density, bone pain, fracturesbecause loss of Ca from bone due to decreasephosphorus


Symptoms of hypocalcemia (see hypocalcemianotes)- result from:

o high phosphorus causes a reciprocal decrease

in Ca.

soft tissue calcifications - A complication ofincreased phosphorus is tissue (can occur in

the kidneys, soft tissue, joints and arteries).This can lead to joint pain, loss of movement.

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Causes:

Shift of phosphate from the extracellular fluid into

the cells:

o Debilitated states:o Alcoholic malnutrition/ alcohol withdrawal

o Eating disorders anorexia

o Debilitated elderly

o Child abuse - starvation

o Diabetes diabetic ketoacidosis treatment

with insulin causes intracellular transport of both glucoseand phosphorus into the cells as the patient becomeanabolico

o Glucose administration (e.g. IV glucose) causes

the pancreas to release more insulin, which in turnpromotes he transport of both glucose and phosphorusinto the cells as the patient become anabolico

Sepsis due to epinephrine releaseo Burns burn patients often hyperventilation

causing resulting in the acceleration of glycolysis causingHypophosphatemia or from anabolic process when burnpatients start to build up tissueo Stress increases catecholamine release

produces a shift of phosphate into the cell

Increasedphosphate loss:

Gastric suctioningo Chronic Diarrhea

o laxative use Phosphate-binding antacids such

as those that are aluminum or Magnesium basedo loop diuretics cause increase Phosphorus loss

o NU 201 Content - osmotic diuresis polyuria

causes excessive loss of phosphate in urine e.g.

glycosuria in uncontrolled diabetes Mellituso Excessive IV glucose - can cause osmotic

diuresiso Hyperparathyroidism - Increase PTH causes

loss of phosphorus through kidneys (phosphaturia)

Decreased absorption from GI tract - related to

Vitamin D deficiency.o Malnutrition

Medications that induce hypophosphatemia:o Diuretics

o

Anabolic steroidso 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 nutritionsources - As cells are formed, phosphorus movesfrom serum into cells:

Causes:

Shift of phosphorus from the intracellular

space into the ECF

o Chemotherapy- causing cellular destruction ascells release phosphorus into serum.o acute cell hemolysis

o infections / Sepsis

o Necrosis of muscle e.g. trauma,wounds

o Blood transfusions the can leak phosphorus

from blood cells during storage

Reduced renal excretion

o Renal insufficiency/failure most common

decreased excretion

Increased phosphate intake

o Medications -Overzealous administration of

large amount of Fleets Phospho-Soda enema especiallywith slowed colonic motility e.g. elderly constipatedclient who received multiple enemas

Increased absorption from:

o GI tract - Large intake of Vitamin D causes

increased absorption of phosphorus.

o Hypoparathyroidism causes decreasedcalcium with increased phosphate

o Infant fed cows milk which contains more

phosphate than human milk

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o enteral feedings

o Parenteral nutrition (TPN) TPN without

phosphorus can lead to hypophosphatemia in the first 24hours.

o Overzealous infusion of calories (especially

CHO) with severe malnutrition refeeding syndromeor nutritional recovery syndrome. This has a

highmortality rate

Associated electrolyte imbalances:o Hypokalemia - as K goes into cell, so does

phosphoruso Hypomagnesemia fosters urinary loss of

phosphoruso Hypocalcemia stimulates PTH release with

loss of Phosphorus

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Management

monitor cardiac, respiratory, neuro and hematologicstatus

assess:o hand grasp

o leg strength

o weak shakey voice

o gag swallow reflexes

o ability to perform ADLs

IV phosphorus - caution: excess IV phosphorus cancause:

o tetany from hypocalcemia calcium falls as

phosphorus rises.o calcification in tissues

o watch IV site for sloughing with infiltration

administer slowlyo diarrhea

oral phosphoruso Neutra-Phos capsule or Fleets Phospho-soda

asses for side effect ofdiarrhea

risk for infections because of changes in WBCs takeprecautions to prevent infections esp. with central lines.

Dietary sources milk products, eggs, meats, nuts, fish,poultry, whole grains.

Management

Medications:Avoid:

o

phosphorus containing antacidsGive:

o Calcium antacids calcium carbonate or calcium

citrate to replace Cao Phosphate binding agents - gels or antacids

Maaloxo loop diuretics promote excretion

o allopurinal (Zyloprim) to decrease uric acid

production from use of cytotoxic drugs causinghyperphosphatemiao 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 phosphateexcretion.

fall 2012 fluid electrolytes notes

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