ec cpr, llc © 2010-20110 fluids, electrolytes, and intravenous therapy brian mitu, fnp, pa-c, faapa...

EC CPR, LLC © 2010-2011 1

Fluids, Electrolytes, and Intravenous Therapy

Fluids, Electrolytes, and Intravenous Therapy

Brian Mitu, FNP, PA-C, FAAPA

Internal Medicine, Cardiology

Instructor Basic/Advance EKG

National/Community Speaker Chronic Hepatitis B

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Learning Objectives

Theory

1. Recall the various functions fluid performs in the body.

2. Identify the body’s mechanisms for fluid regulation.

3. Review three ways in which body fluids are continually being distributed among the fluid compartments.

4. Distinguish the signs and symptoms of various electrolyte imbalances.

5. Discuss why the elderly have more problems with fluid and electrolyte imbalances.

6. Recognize the disorders that cause specific fluid and electrolyte imbalances.

7. Compare the major causes of acid-base imbalances.

8. State correct interventions to correct an acid-base imbalance.

9. Discuss the steps in managing an intravenous infusion.

10. Describe the measures used to prevent the complications of intravenous therapy.

11. Identify intravenous fluids that are isotonic.12. Discuss the principles of intravenous

therapy.

Clinical Practice

1. Assess patients for signs of dehydration.

2. Correctly assess for and identify edema and signs of overhydration.

3. Apply knowledge of normal laboratory values in order to recognize electrolyte imbalances.

4. Carry out interventions to correct an electrolyte imbalance.

5. Determine if a patient has an acid-base imbalance.

6. Carry out measures to prevent the complications of Intravenous therapy.

7. Compare interventions for the care of a patient receiving total parenteral nutrition with one undergoing intravenous therapy.

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Basic Concepts of Fluid and Electrolytes

• So why do we care about fluid and electrolytes?– Lets start with the fluids

• Over half of our body weight is fluid material• Body weight of adult male 55-60%, female 50-

55%, newborn 75-80%• In adults, a loss of just 1/5 of your body fluid weight

can be fatal. • That is how marathon runners who are not

adequately hydrated die in mile 21

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• So why do we care about fluid and electrolytes?– Elderly patients are even more at risk. Why ?

• They have less muscle mass. This also means that a smaller amount of fluid loss can and will be detrimental

– The same can be said to infants. Why?• Because 80% of their body weight consist of fluids

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• So why do we care about fluid and electrolytes?– Electrolytes

• Are substances that become ions in solution and acquire the capacity to conduct electricity.

• Essential for normal function of our cells and our organs

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• So where are these fluids kept? – Body fluid compartments

• Each body fluid compartment has a particular composition of electrolytes/fluid, which differ from that of the other compartments

• Extracellular compartment ( 20% BW)– Tissue fluid (interstitial) ( 15% BW)– Intravascular compartment ( 4.5% BW)– Transcellular (1.5% BW)

• Intracellular compartment ( 40% of BW)– Refers to all the fluid inside the cell (most bodily fluid are

inside the cell)

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• Extracellular (ECF) compartment– 1/3 ( 20%) of body fluid– Comprised of 3 major components

• Intravascular– Fluid within the blood vessels. Plasma accounts for

about half of the total blood volume of the body

• Interstitial– Fluid that surrounds the cells – an example of

interstitial fluid is lymph

• Transcellular– Fluid found in the cerebrospinal column, pericardial

envelope, synovial joints, or intraocular space

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• Extracellular fluids provide– Nutrients for cell functioning

• Na• Ca• Cl• Glucose• Fatty acids• Amino Acids

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• Intravascular Component– Plasma

• Fluid portion of blood

– Made of:• Water• Plasma proteins

– Albumin– Clotting protein– Immunoglobulins (Antibodies)

• Small amount of other substances

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• Interstitial component– Made up of fluid between cells

• Surrounds cells • Transport medium for nutrients, gases, waste

products and other substances between blood and body cells

• Back-up fluid reservoir

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• Transcellular component– 1% of ECF– Located in joints, connective tissue, bones,

body cavities, CSF, and other tissues– Potential to increase significantly in abnormal

conditions • 3rd space

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• Intracellular (ICF)– Fluid within the cells themselves – 2/3 of body fluid (40%)– Located primarily in skeletal muscle mass– Provide nutrients for metabolism:

• High in K, Po4, protein• Moderate levels of Mg, So4

– Assists in cellular metabolism

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• Who are the major players of fluid and electrolyte balance?– Hypothalamus

• Thirst center – Stimulated by changes in water loss or increase

extracellular osmolality• Baroreceptors (carotid/ aortic) and stretch

receptors (atrial) as detectors – Impulses sent to the thirst control centers in the

hypothalamus


• Who are the major players of fluid and electrolyte balance?– Posterior Pituitary

• ADH ( Antidiuretic Hormone or Vasopressin)• Stimulated by changes in water loss or increase

extracellular osmolality– Heart

• ANP (Atrial Natriuretic Peptide)• In response to an increase in blood volume• Increase sodium excretion by increasing GFR and

inhibiting sodium reabsorption

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• Who are the major players of fluid and electrolyte balance?– Kidneys/Adrenal glands (RAAS)

• Renin– Is released in response to decreased blood flow or

decreased renal pressure (sensed by receptors in the nephrons)

• Aldosterone – Is produced by the adrenal cortex (in response to

stimulation by angiotensin II) causing the tubules to excrete K+ while retaining Na 2+, adding to the reabsorption of water back into the vascular system.

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Movement of Fluid and Electrolytes

• Water Steady State• Amount Ingested =

Amount Eliminated

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• Electrolyte (Na+, K+, Ca++) Steady State

• Amount Ingested = Amount Excreted.

• Normal entry: Mainly ingestion in food.

• Clinical entry: Can include parenteral administration

• Just a remember that each fluid compartment has constant amount of fluid, and constant amount of electrolytes

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• What is the exact mechanism of fluid and electrolyte shift?– Passive transport

• Diffusion• Osmosis• Filtration• Hydrostatic pressure• Oncotic pressure

– Active transport• Sodium pump and ATP

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• Passive transport– Diffusion

• Movement of solutes from an area of higher concentration to an area of lower concentration in a solution and/or across a permeable membrane (permeable for that solute)

• Movement occurs until near equal state

– Osmosis• Movement of water through a selectively permeable

membrane from an area of low solute concentration to a higher concentration until equilibrium occurs

• Movement occurs until near equal concentration found

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• Osmolality– Concentration of body fluids – affects

movement of fluid by osmosis– Reflects hydration status– Measured by serum and urine – Solutes measured - mainly urea, glucose,

and sodium– Measured as solute concentration/Kg

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• Osmolality– Serum Osm/L = (serum Na x 2) + BUN/3 +

Glucose/18– Normal serum value - 280-300 mOsm/Kg– Serum <240 or >320 is critically abnormal – Normal urine Osm – 250 – 900 mOsm / kg

• Increase means dehydrated• Decrease means excess fluid

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Osmolality of a Solution

• Isotonic solutions– Means the solutions on both sides of a selectively

permeable membrane have established equilibrium or are equal in concentration Examples

• 0.9% NaCl, 5% dextrose water, 5% dextrose in 0.225% saline, LR

• Hypotonic solutions– The solution contains lower concentration of salt or

solute than another solution or lower osmolality than body fluid

– Less salt or > water than isotonic– 0.45% NaCl, 0.226%, 0.33% Nacl

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Osmolality of a Solution

• Hypertonic solution– A solution has higher concentration of

solutes than another solution or higher osmolality than body fluids

– 3%, 5% NaCl, D10%w, D5% with 0.9% NaCl, D5% with 0.45% NaCl, D5% LR

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• Passive transport– Filtration

• Movement of solutes and solvents through semipermeable membrane

• Influenced by hydrostatic pressure– Hydrostatic pressure is created by the pumping action of the

heart– Think of arterial end of the capillary– Supplying fluid to tissue cells

– Oncotic /osmotic pressure • Think of the venous end • Getting back the excess fluid and solutes that are in the

tissue and returned to the vascular compartment via lymph

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• Active transport:– Ion moves through a membrane from an area

of lower to higher concentration– Sodium pump and ATP– Substances that are transported actively

through the cell membrane• Sodium• Potassium, calcium, iron• Hydrogen, sugars, amino acids

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Fluid Volume deficit

• Description– Dehydration

• Occurs when the fluid intake of the body is not sufficient to meet the fluid needs of the body

– Goal of treatment• Is to restore fluid volume, replace electrolytes PRN, find

the cause

• Types– Isotonic fluid deficit/dehydration

• Both water and electrolytes are lost equally• Known as hypovolemia → ↓circulating blood volume,

tissue perfusion• Stimulates ADH

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• Types– Hypertonic dehydration

• Water loss exceeds electrolyte loss• Fluid moves from the intracellular

compartment into the plasma and tissue fluid compartment → cellular dehydration and shrinkage

– Hypotonic dehydration• Electrolyte loss exceeds water loss• Fluids from the plasma and tissue

compartment moves into the cells → swelling

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• Causes of fluid volume deficits– Isotonic dehydration

• Third spacing – peritonitis, intestinal obstruction, ascites, burns

• Hemorrhage• Altered intake, such as nothing by mouth (NPO)

– Hypertonic dehydration• Excessive perspiration, Ketoacidosis• Prolonged fevers, Diarrhea• ESRD, Diabetes Insipidus• Diuretic therapy

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• Causes of fluid volume deficits– Hypotonic dehydration

• Chronic illness• Excessive fluid replacement (hypotonic)• RF, Chronic malnutrition• Gastrointestinal (GI) losses – vomiting,

nasogastric suctioning

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Fluid Volume Deficit: AssessmentFluid Volume Deficit: Assessment

• Cardiovascular– Thready, increase pulse rate– Decrease BP, Orthostatic hypotension– Flat neck and hand veins in dependent position– Diminished peripheral pulses

• Respiratory– Increase rate and depth of respiration

• Neuromuscular – Lethargy and coma– Fever

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• Renal– Decrease urine output, increase specific

gravity• Integumentary

– Dry skin, poor turgor, tenting– Dry mouth

• GI– Wt loss, thirst

• Hypotonic dehydration– Muscle weakness

• Hypertonic dehydration– Pitting edema, hyperactive DTR

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Fluid Volume Deficit: Nsg InterventionsFluid Volume Deficit: Nsg Interventions• Place client in shock position (on back with legs

elevated).• Fluid replacement

– Mild cases can be corrected via PO route– Significant losses (hemorrhage, anemia, 3rd space)

• Blood transfusion• Colloid solution ( albumin, dextran)• 0.9% NaCl or 154mEq/L Na+

– Solution of choice for normonatremic and mildly hyponatremic, hypotensive or shock pts

• Severe hyponatremia– Hypertonic saline (3.0% NaCl or 513 mEq/L)


Fluid Volume Deficit: Nsg InterventionsFluid Volume Deficit: Nsg Interventions

• Monitor I&O. – Alert the primary care provider to urine output

less than 30 mL/hr for 2 consecutive hr.• Monitor vital signs and heart rhythm.• Monitor level of consciousness and maintain

client safety.• Treat underlying cause of fluid volume deficit.• Encourage the client to change positions

slowly.

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Fluid Volume Deficit: ComplicationsFluid Volume Deficit: Complications

• Hypovolemic Shock– This can lead to vital organ hypoxia/anoxia

decreased hemoglobin, oxygen saturation, and pulse pressure (systolic-diastolic blood pressure).

– Administer oxygen.– Provide fluid replacement.– Perform hemodynamic monitoring.


Fluid Volume Deficit: ComplicationsFluid Volume Deficit: Complications

• Hypovolemic Shock– Administer vasoconstrictors, coronary

vasodilators, and/or positive inotropes• dopamine (Inotropin)• Epinephrine• dobutamine (Dobutrex)• norepinephrine (Levophed)• phenylephrine (Neo-Synephrine)

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Nausea and Vomiting• “Sick to my stomach"

• Pallor, mild diaphoresis, cold clammy skin, excessive salivation, and attempts to remain quiet and motionless

• Vomitus odor, color, contents (e.g., undigested food), and amount

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Medical Treatment• Antihistamines, sedative-hypnotics,

anticholinergics, and phenothiazines

• Complementary and alternative therapy

• NPO, then progressing slowly to a regular diet

• Carbonated drinks

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Diarrhea• Frequent watery bowel movements, abdominal

cramping, and general weakness • Watery stools often contain mucus and are

blood‑streaked; frequency could be as high as 15 to 20 liquid stools.

• Acute diarrhea and local irritation• Chronic and prolonged diarrhea in ulcerative

colitis, irritable bowel syndrome, allergies, lactose intolerance, and nontropical sprue

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Diarrhea• Dehydration, malnutrition, and anemia

• Bowel sounds likely to be loud gurgling and tinkling sounds that come in waves and are hyperactive

• Note and record the number of stools during the shift and the characteristics of each stool and associated pain

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Acute Diarrhea• Limit the intake of food• Progress to clear, bland liquids and to solids with

increased calories and high‑protein, high‑carbohydrate content

• Give rehydrating solutions containing glucose and electrolytes

• Avoid iced fluids, carbonated drinks, whole milk, roughage, raw fruits, and highly seasoned foods

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Medications for Diarrhea• Cause of the disorder and the length of time the

conditionMild cases:– Kaolin and bismuth preparations, (e.g., Kaopectate)

• Antispasmodic drugs such as belladonna or paregoric • Bismuth and "traveler's diarrhea" • Codeine, diphenoxylate (Lomotil), or loperamide

(Imodium)• Drugs and causative organisms• Metabolic acidosis and buffer solutions

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Nursing Management• Provide physical and mental rest, prevent

unnecessary loss of water and nutrients, protect the rectal mucosa, and replace fluids

• Maintain a calm and dignified manner, accept and understand the patient's behavior, and provide privacy and a restful environment

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Home Care: Fluid Volume Deficit

• Log of intake and output

• Small amounts of liquid every hour while awake

• Emergency department and intravenous fluids

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Fluid Volume Excess Fluid Volume Excess

• Description– Fluid intake or fluid retention exceeds the

fluid needs of the body or extracellular compartment

– Aka: fluid overload or overhydration

• Types– Isotonic overhydration

• Hypervolemia. Only the EC compartment expands

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Fluid Volume ExcessFluid Volume Excess

• Types– Isotonic overhydration

• Results in circulatory overload and tissue edema

• When severe it can worsen CHF and lead to pulmonary edema

– Hypertonic overhydration• Rare. Caused by excessive Na intake• Fluid is drawn from the ICF compartment and the

EC volume expands

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• Types– Hypotonic overhydration

• Water intoxication

• Causes– Isotonic overhydration

• Inadequate control of IV• RF

– ↓ excretion of sodium and water

• Long-term corticosteroid therapy

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• Causes– Hypertonic overhydration

• Excessive sodium ingestion• Rapid infusion of hypertonic solution• Excessive sodium bicarbonate therapy• Interstitial to plasma fluid shifts (hypertonic

fluids, burns)


• Causes– Hypotonic overhydration

• Early RF• CHF, SIADH

– Chronic stimulus to the kidney to conserve sodium and water (heart failure, cirrhosis, glucocorticosteroids)

• Irrigation of wounds and body cavities with hypotonic fluids

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Fluid Volume Excess: Risk Fluid Volume Excess: Risk FactorsFactors

• Overhydration– Water replacement without electrolyte

replacement such as strenuous exercise with profuse diaphoresis


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Fluid Volume Excess: AssessmentFluid Volume Excess: Assessment

• Cardiovascular– Bounding, increase pulse rate– ↑ BP, elevated JVP or distended neck vein, CVP

• Respiratory– Dyspnea, crackles

• Neuromuscular – ALOC, HA, visual disturbance, muscle weakness,

paresthesia• Integumentary

– Pitting edema in dependent areas

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Fluid Volume Excess: AssessmentFluid Volume Excess: Assessment

• GI– Hepatojugular reflux, ascites, liver

enlargement

• Labs– ↓ serum osmolality, hct, BUN, sodium,

urine specific gravity

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Fluid Volume Excess: Fluid Volume Excess: AssessmentAssessment


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Excess Fluid Volume• Hematocrit:

– 35% to 54%, depending on age and sex

• Urine concentration: – Specific gravity: 1.003 to 1.030 (average range

is 1.010 to 1.025)

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Fluid Volume Excess: Nsg Fluid Volume Excess: Nsg InterventionsInterventions

• Assess/monitor for signs of respiratory distress– including breath sounds and arterial blood gases

(ABGs).

• Position the client in semi-Fowler’s position.• Administer oxygen as needed.• Reduce IV flow rates.• Administer diuretics (osmotic, loop) as ordered.• Monitor daily I&O and weight.


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Fluid Volume Excess: Nsg Fluid Volume Excess: Nsg InterventionsInterventions

• Limit fluid and sodium intake as ordered.• Assess/monitor and document peripheral vascular

system including– skin color, presence of edema (pretibial, sacral,

periorbital), and circulation to extremities.

• Turn and position the client at least every 2 hr.• Support arms and legs to decrease dependent

edema and promote venous return as appropriate.• Monitor for/treat skin breakdown.

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Fluid Volume Excess: Fluid Volume Excess: ComplicationsComplications

• Pulmonary Edema– Signs and symptoms include ascending

crackles, dyspnea at rest, and confusion.– Position the client in Fowler’s position.– Administer IV morphine. Why?

• ↑ pulmonary venous capacitance, ↓ left atrial pressure and anxiety → better ventilation

– Administer IV diuretic.– Prepare for possible intubation and

mechanical ventilation.Mosby items and derived items © 2007 by Mosby, Inc., an affiliate of Elsevier, Inc.

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Edema• Localized edema and generalized edema

• General causes of edema:– An increase in capillary hydrostatic pressure– A loss of plasma proteins– An obstruction of lymphatic circulation– An increase in capillary permeability

• Dependent edema


Figure 17-3 Mechanisms of edema formation. Na+, Sodium; H2O, water. From Huether SE, McCance KL: Understanding pathophysiology, ed 3, St Louis, 2004, Mosby.

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Treatment• Correct the underlying cause • Assist the body to rebalance fluid content• Restrict fluids• Give diuretic drugs• Allow bed rest• Provide low-sodium diet• Use elastic stockings or sequential

compression devices

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Home Care: Fluid Excess• Weigh daily

• Assess edema

• Know when to notify physician

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ElectrolytesElectrolytes

• Electrolytes are minerals (sometimes called salts) that are present in all body fluids.

• They regulate fluid balance, hormone production, and strengthen skeletal structures, as well as act as catalysts in nerve response, muscle contraction, and the metabolism of nutrients.



ElectrolytesElectrolytes• Electrolytes are distributed between

intracellular (ICF) and extracellular (ECF) fluid compartments.

• When dissolved in fluids, separate in to ions and conduct either – Cations: Positively charged ions

• magnesium, potassium, sodium, calcium – Anions: Negatively charged ions

• phosphate, sulfate, chloride, bicarbonate

• Measured in milliequivalents (mEq)• Serum levels indicate extracellular

concentration not inside the cells

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Electrolytes• Creation of an electrical impulse:

– Transmission of nerve impulses– Contraction of muscles– Excretion of hormones and other substances

from glandular cells

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Osmolality • Concentration of the solution determined by

the number of solutes • Osmolality controls water movement and

the body fluid distribution in the intracellular and extracellular compartments

• Intracellular fluid and potassium• Extracellular fluid and sodium• Normal osmolality: 280 to 294 milliosmoles

per kilogram


Sodium is the predominant Sodium is the predominant electrolyte in ECF. electrolyte in ECF.

• Sodium imbalances are usually associated with parallel changes in osmolality.

• Sodium is essential for the maintenance of acid-base balance, active and passive transport mechanisms, and maintaining irritability and conduction of nerve and muscle tissue.

• Normal serum sodium levels are 135 to 145 mEq/L.

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Hyponatremia

• Plasma Na+ of < 135 mEq/L

• Causes– Increased sodium excretion

• Excessive diaphoresis• Diuretics • Vomiting• Diarrhea• Wound drainage ,especially GI; Renal disease• Burns , nasogastric suctioning

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Hyponatremia

• Causes– Inadequate sodium intake

• NPO• Low-salt diet

– Dilution of serum sodium• Excessive irrigation/ ingestion of hypotonic

fluids, tap water enemas • Renal failure• Freshwater drowning• SIADH

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Hyponatremia

• Causes– Dilution of serum sodium

• CHF– Due to ↓ forward flow by the failing heart, the kidney

senses hypoperfusion and tries to ↑ percieved diminished intravascular volume via RAAS

– Furthermore, ADH gets activated also

• Cirrhosis– Pooling of blood in the mesenteric veins which

leads to decrease amount of blood seen by the kidneys

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Hyponatremia

• Causes– Dilution of serum sodium

• Hyperglycemia– When BG becomes acutely elevate, water is drawn

from the cells into the extracellular space, diluting the serum sodium

– Plasma sodium falls by 2 meq/L for every 100 mg/dL rise of BG


Hyponatremia Hyponatremia

• Classification– Hypotonic hyponatremia < 280 mOsm/kg

• Fluid volume deficit (Hypovolemic) : Sodium loss greater than water loss

• Fluid volume excess (Hypervolemic): Water gain greater than sodium gain

• Normal fluid volume ( Euvolemic): Pure water gain

– Isotonic hyponatremia 280-290 mOsm/kg– Hyper hyponatremia > 290 mOsm/kg

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Hyponatremia: Assessment

• Manifestations– Asymptomatic to nonspecific

• Nausea, HA, seizure• Weakness

– Hyponatremia delays and slows the depolarization of membranes.

• Muscle cramps• Orthostatic hypotension, Decreased blood

pressure

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Hyponatremia: Assessment

• Manifestations– Symptoms are primarily neurologic (Na+

115 to 118 meq/L)• Mental status change, seizure• Lethargy• Disorientation• Obtundation,coma

– Water moves from ECF into the ICF, which causes cells to swell (e.g., cerebral edema).

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Hyponatremia

• Diagnosis – H&P– Plasma osmolality (decrease)– Urine osmolality and volume

• Specific gravity

– Urine Na+ concentration ( increase or decrease depending on the cause)

– CT scan of the brain is done if SIADH is suspected

– C-XRAY to r/o lung pathology

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Hyponatremia: AssessmentHyponatremia: Assessment


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Hyponatremia: Nsg Hyponatremia: Nsg InterventionsInterventions

• Fluid overload: Restrict water intake as ordered (Hypervolemic)

• Acute Hyponatremia– Administer hypertonic oral and IV fluids as ordered.– Encourage foods and fluids high in sodium (cheese,

milk)• If pt is taking lithium, check lithium level

because hyponatremia causes lithium toxicity

• Give demeclocycline (Declomycin) if the cause is d/t excess ADH


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Hyponatremia: Nsg InterventionsHyponatremia: Nsg Interventions

• Foods high in sodium– Bacon, butter, canned food, american/cottage

cheese– Frankfurters, ketchup, milk, soy sauce,

processed foods– White and whole-wheat bread

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Hyponatremia: Nsg Hyponatremia: Nsg InterventionsInterventions

• Restoration of normal ECF volume– Administer isotonic IV therapy (0.9% normal saline,

Ringer’s lactate solution). – If the cause is hypovolemic hypotonic hyponatremia

• Serum sodium level must be check hourly• Monitor I&O and daily weight.• Monitor vital signs and level of consciousness –

report abnormal findings.• Encourage the client to change positions slowly


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Hyponatremia: ComplicationsHyponatremia: Complications

• Seizures, Coma, and Respiratory Arrest– Seizure precautions and management– Life support interventions

• Note:– Avoid too rapid correction, because osmotic

imbalance may cause water to enter the brain cells → cerebral edema and potentially severe neurologic impairment (central pontine myelinolysis)


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Hypernatremia

• Serum sodium level of > 145 meq/L• Water content of body fluid is deficient in

relation to sodium content• Hypernatremia causes significant

neurological, endocrine, and cardiac disturbances.

• Increased sodium causes hypertonicity of the serum. This causes a shift of water out of the cells, making the cells dehydrated.

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Hypernatremia

• Causes– Decrease sodium excretion (hypervolemic

Hypenatremia)• Corticosteroid• Cushing’s syndrome• RF• Hyperaldosteronism

– Increase sodium intake (PO/IV), sodium bicarbonate intake

– Decrease water intake (NPO)

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Hypernatremia

• Causes– Increase water loss ( hypovolemic

Hypernatremia)• Insensible losses

– Fever– Exercise– Heat exposure– Severe burns– Mechanically ventilated pts

• Diarrhea

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Hypernatremia

• Causes ( Euvolemic Hypernatremia)– Central Diabetes Insipidus

• Impaired ADH– Causes: destruction of posterior pituitary from trauma,

neurosurgery, granulomatous dz, neoplasm, vascular accident, infxn, idiopathic, hereditary

– Nephrogenic Diabetes Insipidus• Resistance to the action of ADH

– Causes: acquired or inherited» Lithium toxicity, hypercalcemia, hypokalemia,

conditions that impair medullary hypertonicity

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Hypernatremia

• How to diagnose if DI is central or nephrogenic?– Administer IV DDAVP– If the urine becomes concentrated, then the

problem is central because the kidney responded to the vasopressin

– If the urine is still diluted, then the problem is the kidneys because it did not respond to vasopressin

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Hypernatremia

• Manifestations– Thirst, polyuria, polydipsia (likes ice-cold water for

CDI)– Dry mouth, mucous membranes, decrease tears,

salivation, oliguria– Orthostatic hypotension– Major sxs are neurologic

• AMS (altered mental status)• Weakness• Neuromuscular irritability• Focal neurologic deficits, coma, seizures

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Hypernatremia• Signs and symptoms:

– Decreased urine output if compensatory ADH is being secreted

– Increased thirst with dry mucous membranes– Weakness and agitation– Good tissue turgor and firm subcutaneous

tissues

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Hypernatremia: AssessmentHypernatremia: Assessment


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Hypernatremia

• Diagnostic studies– Check serum sodium level– Check serum osmolality– Check urine volume and osmolality

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Hypernatremia: Nsg Hypernatremia: Nsg InterventionsInterventions

• Based on serum osmolarity

– Fluid Loss (Hypernatremia with hypovolemia)• Isotonic (0.9%) saline, followed by 0.45% saline

– Decrease excretion of sodium (Hypernatremia with euvolemia)

• Water drinking or 5% dextrose in water → excretion of sodium in the urine


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Hypernatremia: Nsg Hypernatremia: Nsg InterventionsInterventions

Excess Sodium (Hypernatremia with hypervolemia)

• Encourage water intake and discourage sodium intake.

• Administer diuretics, such as loop diuretics.• Monitor level of consciousness and maintain

client safety.• Provide oral hygiene and other comfort

measures to decrease thirst.• Monitor I&O, and alert the primary care

provider of inadequate renal output.Mosby items and derived items © 2007 by Mosby, Inc., an affiliate of Elsevier, Inc.

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Hypernatremia: ComplicationsHypernatremia: Complications

• Cellular Dehydration, Convulsions, and Death– Seizure precautions and management– Life support interventions

• Note– Avoid rapid correction → pulmonary or

cerebral edema


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PotassiumPotassium• Major intracellular cation (150mEq/L)• Normal plasma 3.5 -5.3mEq/L

– Note: K+ concentration is higher inside the cells than the serum

• Na-K pump actively transports Na+ out of the cell and K+ into the cell

• The passive outward diffusion of K+ generates the resting of membrane potential

• Renal excretion is the major route of elimination of excess K+

• Vital role in cell metabolism, transmission of nerve impulses, functioning of cardiac, lung, and muscle tissues, and acid base balance.


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HypokalemiaHypokalemia

• Hypokalemia is a serum potassium less than 3.5 mEq/L.

• Causes– Inadequate potassium intake

• NPO• Rare cause because body has many mechanisms

of K+ regulation (aldosterone, insulin, catecholamine)


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• Causes– Increased loss

• Renal loss d/t ↑ flow rate (washing away K+ → ↑ secretion of the tubules)

– Diuretic therapy– Hyperaldosteronism (adrenal adenoma

or carcinomas)

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• Causes– Increased loss

• GI losses– Diarrhea– Vomiting/NGT suctioning

» Direct or indirect K+ loss» Indirect loss via kidneys. Why?» Vomiting →loss of acid from the stomach» Loss of acid will →alkalosis (excess HCO3-)» Excess HCO3- makes into the kidneys (more

negative)» To maintain normal balance, the kidneys will

secrete positively charge k+ which → excretion of K+

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Hypokalemia

• Etiology– Movement from the blood into the cells

• Insulin excess• Beta agonist treatment

– Albuterol

• Alkalosis– Not enough H+ in the blood, so cells release H+ into

the blood in exchange for K+


Causes and Effects of Hypokalemia

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Hypokalemia

• Manifestation– Cardiovascular

• Ventricular arrhythmias• Hypotension• Cardiac arrest• EKG

– Flattened T or inverted T wave– ST depression

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Hypokalemia

• Manifestation– Neuromuscular

• Malaise• Weakness, Flacid paralysis• Cramps• Smooth muscle involvement

– Ileus and constipation, abdominal pain, distention

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Hypokalemia: Nsg InterventionsHypokalemia: Nsg Interventions• Treat underlying cause. Usually not an

emergency unless cardiac manifestations are present

• Replacement of Potassium:– Encourage foods high in potassium (e.g.,

avocados, broccoli, dairy products, dried fruit, cantaloupe, bananas).

– Provide oral potassium supplementation• Liquid potassium chloride has an unpleasant taste• Should be taken with juice


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Common food source for potassium

• Avocado• Bananas• Cantaloupe• Carrots• Fish• Mushrooms• Oranges

• Potatoes• Pork• Beef, veal• Raisins• Spinach• Strawberries• tomatoes

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Hypokalemia: Nsg InterventionsHypokalemia: Nsg Interventions

• Precaution with IV potassium– Never give IV push, IM, SC– Ensure that IV bag containing potassium is

properly labeled– Can cause phlebitis

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Hypokalemia: Nsg InterventionsHypokalemia: Nsg Interventions

– IV potassium supplementation• Never IV push (high risk cardiac arrest).• Monitor for phlebitis (tissue irritant).• Monitor for and maintain adequate urine output.

• Monitor for shallow ineffective respirations and diminished breath sounds.

• Monitor the client’s cardiac rhythm, level of consciousness, and bowel function.


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Hypokalemia: ComplicationsHypokalemia: Complications

• Respiratory Failure– Monitor for hypoxemia and hypercapnia.– Intubation and mechanical ventilation may be

required.

• Cardiac Arrest– Perform continuous cardiac monitoring.– Treat life-threatening dysrhythmias.

• Hypokalemia potentiates digitalis intoxication


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Hyperkalemia

• Plasma K+ >5.3mEq/L

• 3 basic mechanism/Etiology– ↑ intake

• Iatrogenic infusion of K+• Ingestion via eating would be quite difficult

unless there is a problem with the kidneys

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Hyperkalemia

• 3 basic mechanism/Etiology– ↓ urinary excretion

• Renal failure• ↓ inflow rate in the distal nephron → a

perceived high concentration of K+ in the nephron, thus inhibiting further secretion of K+ in the nephron (CHF, cirrhosis)

• Hypoaldosteronism/Addison’s disease

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Hyperkalemia

• 3 basic mechanism/Etiology– ↑ movement of K+ from the cells into the

blood stream• Processes that → breakdown of cells will

cause the release of k+– CRUSHING INJURIES– Rhabdomyolysis– Tumor lysis after chemotherapy– Pseudohyperkalemia

» Due to improper blood drawing technique– Acidosis

» To maintain homeostasis the body will trade K+ for H+

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Hyperkalemia

• 3 basic mechanism/Etiology– ↑ movement of K+ from the cells into the

blood stream• Insulin deficiency or resistance

– Insulin causes k+ to move into cells

• Beta-blockers– Like insulin, catecholamines causes K+ entry into cells


Causes and Effects of Hyperkalemia

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Hyperkalemia

• Manifestation– Muscle weakness– Hypotension– Paresthesia– Paralysis– Cardiac dysrhythmia

• EKG > 6mEq/L– Peak T wave– Flattening of P wave– Prolongation of PR interval– Widening of QRS complex → V.tach, fib

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Hyperkalemia: Nsg Hyperkalemia: Nsg InterventionsInterventions

• Decrease potassium intake.– Stop infusion of IV potassium.– Withhold oral potassium.– Provide potassium-restricted diet. Avoid foods

high in potassium (e.g., avocados, broccoli, dairy products, dried fruit, cantaloupe, bananas).


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• Increase potassium excretion.– Administer potassium-losing diuretics, such

as furosemide (Lasix), if renal function is adequate.

– Administer cation exchange resins such as sodium polystyrene sulfonate (Kayexalate).

– Perform dialysis.


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• Promote movement of potassium from ECF to ICF.– Administer IV fluids with dextrose (glucose) and

regular insulin.– Administer sodium bicarbonate (reverse

acidosis).

• Monitor the client’s cardiac rhythm, and notify primary care provider of abnormal findings– Calcium gluconate to antagonize the effects of

hyperkalemia on the heart


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Hyperkalemia: ComplicationHyperkalemia: Complication

• Cardiac Arrest– Perform continuous cardiac monitoring.– Treat life-threatening dysrhythmias.


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Calcium

• Normal serum total Ca++ 9-10mg/dL• Essential for bone and neuromuscular

function• 99% of body ca++ is bone, 1% is in the ECF• 50% of serum Ca++ is ionized (free), remainder

is bound to albumin• Ca ++ metabolism is regulated by

parathyroid hormone (PTH), metabolites of vit.D, calcitonin– Parathyroid hormone serves to increase blood

concentrations of calcium. HOW?

Calcium

• Parathyroid hormone– Stimulates production of the biologically-active

form of vitamin D within the kidney.– Facilitates mobilization of calcium and phosphate

from bone.• Prevent detrimental increases in phosphate,

parathyroid hormone also has a potent effect on the kidney to eliminate phosphate (phosphaturic effect).

– Maximizes tubular reabsorption of calcium within the kidney, resulting in minimal losses of calcium in urine

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Calcium

• Ca ++ metabolism is regulated by parathyroid hormone (PTH) and metabolites of vit.D– Vit D is absorbed from food and synthesized

in skin after exposure to sunlight• Liver converts Vit. D to 25-hydroxyvitamin D3,

which in turn converted by the kidney to 1,25D3• 1,25D3 promotes intestinal Ca++ absorption,

phosphate absorption

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Calcium

• PTH– ↑s serum Ca++ but ↓s serum phosphate

• Vitamin D– ↑s both serum Ca++ and phosphate levels

• Calcitonin– Antagonistic hormone to PTH and Vit.D– Little/ minor effect

• Note:– Diseases that affect the bones or the kidneys

can cause hyper- or hypocalcemia

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Figure 37-9 Regulation and function of parathyroid hormone.

• Parathyroid gland: Increases blood calcium concentration.Calcium and Magnesium

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Calcium

Important in:

• building bones and teeth

• muscle contraction

• blood clotting

• maintenance of cell membranes

• nerve transmission

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Hypocalcemia • serum calcium level less than 9.0 mg/dL.• Etiology

– Decrease intake– Decrease PTH

• Hypoparathyroidism– DiGeorge syndrome (congenital absence of parathyroid)– Autoimmune destruction

» HAM (hypoparathyroid, adrenal insufficiency, mucocutaneous candidiasis)

» APECED (autoimmune polyendocrinopathy candidiasis,ectodermal dystrophy)

– Familial– Surgical damage/removal– Magnesium (hypo- or hypermagnesemia can→hypocalcemia– Metastases

• Pseudoparathyroidism (PTH resistance)

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Hypocalcemia• Etiology

– Vit D deficiency• Decrease intake, malabsorption, renal dz, liver dz)• Rickets (Children with Vit D deficiency)• Osteomalacia (adults with Vit D deficiency)

– Increase excretion• Fanconi syndrome

– Shift to bone (hungry bone syndrome)• Happens after surgical correction of the abn PTH

– Binding of ca++• Hyperphosphatemia (rhabdomyolosis)• Pancreatitis (fats releases from pancreas bind ca++)

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Hypocalcemia• Etiology

– Hypoalbumin• Recall that ca++ is bound to albumin “factitious

hypocalcemia”• Caused by

– Malnutrition– Liver dz

» Cirrhosis» Nephrotic syndrome

– Burns

– Hypercalciuric hypercalcemia• Increase ca++ excretion and decrease bone resorption

– Drugs ( ↓s ionized fraction of calcium)• Chemotherapy, phenytoin, foscarnet

– Sepsis


Causes and Effects of Hypocalcemia

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Hypocalcemia: AssessmentHypocalcemia: Assessment• Manifestation

– Neuromuscular• Muscle twitches/tetany, seizure• Frequent painful muscle spasms at rest• Hyperactive deep tendon reflexes• Positive Chvostek’s sign (tap on facial nerve

triggers facial twitching)• Positive Trousseau’s sign (hand/finger spasms

with sustained blood pressure cuff inflation)

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Hypocalcemia: AssessmentHypocalcemia: Assessment

• Cardiovascular– Decreased myocardial contractility –

decreased heart rate and hypotension– Dysrhythmias, prolonged QT interval

• GI – hyperactive bowel sounds, diarrhea, abdominal cramping

• Respiratory– Laryngospasm– Respiratory failure


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Hypocalcemia: Nsg InterventionsHypocalcemia: Nsg Interventions• Administer oral or IV calcium

supplements.– Aluminum hydroxide ↓s phosphorus levels →

↑calcium levels

– Vit. D to ↑ absorption calcium from the GI tract

• Encourage foods high in calcium including dairy products and dark green vegetables.

• Be aware of seizure precautions.Keep emergency equipment on standby.


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Hypocalcemia: Nsg InterventionsHypocalcemia: Nsg Interventions

• Calcium gluconate IV administration– Warm solution to body temperature prior to

administration– Give slowly– Monitor EKG– Watch for infiltration

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Food source for calcium

• Cheese• Collard greens• Milk and soy milk• Rhubarb• Sardines• Spinach• Tofu• yogurt

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Hypercalcemia

• Hypercalcemia > 10.6 mg/dL• Causes

– Increase calcium absorption• Excess ingestion from milk and calcium carbonate

antacids (milk-alkali syndrome)• Vit D

– Decrease excretion• Decrease renal excretion (thiazide diuretics, lithium)• Hypocalciuric hypercalcemia (which causes both ↓

excretion and ↑ bone resorption

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Hypercalcemia

• Causes– Increase bone resorption

• Elevated parathyroid (hyperparathyroidism)• Elevated vit D (lymphoma, granulomatous

disease, milk-alkali syndrome)• Bone breakdown (secondary to mets to bone,

primary bone tumor, multiple myeloma, immobilization, hyperthyroidism)

– Hemoconcentration• Dehydration• Adrenal insufficiency


Causes and Effects of Hypercalcemia

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Hypercalcemia

• Manifestation– “stones, bones, abdominal groans, moans,

and psychiatric overtones” means• Renal stones• Bone breakdown• Constipation/abdominal pain/ pancreatitis• Fatigue, weakness, arthralgia• Psychiatric disturbance

– Ekg: shorten QT interval • Mnemonic: Lots of Californians are short QTs

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Hypercalcemia: Nsg Interventions

• Calculate corrected calcium level if albumin is low– Serum calcium+0.8 (4-albumin)

• Monitor cardiac, respiratory status, neuromuscular, renal, GI status

• Place pt on cardiac monitor

• D/C IV or PO’s containing calcium, vit D, thiazide diuretic

• Prepare for dialysis if severe levels

• Position pt carefully due to risk of fracture

• Monitor for flank pain, strain urine

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• Treatment– Dilute blood Ca++

• 0.9% NaCl. Infuse 5-10 l over the 1st 24 hrs until dehydration is corrected

– Give furosemide IV (40-80mg q 2-4 hrs) to enhance excretion and prevent volume overload

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• Treatment– Metastatic bone dz

• Calcitonin (rapid, mild inhibition of bone resorption)• Pamidronate (delayed onset, but most potent than

calcitonin)

– Sarcoidosis, vit A or D intoxication, multiple myeloma, leukemia, breast ca

• Glucocorticoid (↑ ca++urinary excretion,↓ GI absorption of ca++

– Neoplasm• Resection, irridation

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Magnesium • Plays an important role in neuromuscular

function ( same as the effect of calcium )• 60% is in bone, and most of the remainder

is within cells• 1% is in ECF, serum levels do not reflect

total body Mg++ content; thus, levels have limited diagnostic value

• Normal 1.3-2.2 mEq/L• Excreted by the kidneys

Magnesium

• Imbalance of magnesium usually provokes alteration of calcium

• Hypermagnesemia can decrease PTH action ( hypocalcemia )– This is seen in pts being treated due to

preeclampsia

• Hypomagnesemia– Causes PTH resistance in end-organs and

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HypomagnesemiaHypomagnesemia

• Serum magnesium level less than 1.3 mg/dL.

• Hypomagnesemia and hypokalemia shares the same etiologies

• Causes– ↓ intestinal absorption/insufficient intake

• Malnutrition, alcoholism• Prolonged diarrhea, laxative abuse• NGT aspiration, small bowel bypass• Malabsorption syndrome, Celiac, Crohn’s

disease

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• Causes– ↑ renal excretion

• Hypercalcemia• Osmotic diuresis• Loop diuretics• Aminoglycosides• Amphothericin B• Cisplatin• Cyclosporine• Hyperparathryroidism

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• Causes– Intracellular movement

• Hyperglycemia• Insulin administration• Sepsis

– Other• Hypoparathyroidism


Causes and Effects of Hypomagnesemia

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• Manifestation– Hypokalemia and hypocalcemia– Neurologic abnormalities

• Lethargy, Confusion• Tremor, Fasciculations• Ataxia, Nystagmus• Tetany, Seizure

– EKG • Prolonged PR and QT interval →

atrial and ventricular arrhythmia (esp if on digoxin)

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Hypomagnesemia: AssessmentHypomagnesemia: Assessment

• Neuromuscular – increased nerve impulse transmission (hyperactive deep tendon reflexes, paresthesias, muscle tetany), positive Chvostek’s and Trousseau’s signs

• GI – hypoactive bowel sounds, constipation, abdominal distention, paralytic ileus


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Hypomagnesemia: Nsg Hypomagnesemia: Nsg InteventionsInteventions

• Discontinue magnesium-losing medications, such as loop diuretics.

• Administer oral or IV magnesium sulfate following safety protocols (check DTR for hyporeflexia)– Magoxide 250-500mg qd or bid– Mag sulfate 1-2 g IV, followed by 6g in 1liter/24hrs– Mag sulfate 200-800 mg/d IM in 4 divided doses

• Encourage foods high in magnesium, including dairy products and dark green vegetables


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Hypomagnesemia: Nsg Hypomagnesemia: Nsg InteventionsInteventions

• Monitor cardiac, respiratory, neuromuscular, GI status

• Place pt on cardiac monitor

• Implement seizure precaution

Hypermagnesemia

• Serum magnesium level of >2.1mEq/dL

• Etiology– Decrease renal excretion

• Renal failure

– Increase intake• After therapy with Antacid or laxatives

– Maalox, Mylanta, Camalox, and Riopan

• During preeclampsia treatment with magnesium• Aspiration of sea water

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Causes and Effects of Hypermagnesemia

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Hypermagnesemia

• Manifestation– s/sx on seen if Mg++ level is > 4 mEq/L– Impaired neuromuscular transmission

• Areflexia

– Lethargy, weakness, paralysis, respiratory failure

– Hypotension, bradycardia– EKG

• Prolonged PR, QRS widen, peaked T wave (hyperkalemia) , shorten QT → complete heart block, asystole

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Hypermagnesemia: Nsg InteventionsHypermagnesemia: Nsg Inteventions

• Teach pt to avoid abuse of laxatives and antacids

• Instruct pts with renal problems to avoid OTC meds that contain Mg++

• Judicious fluid intake• Monitor I/Os• Administer diuretics as ordered, calcium

gluconate 10-20ml IV over 10 minutes (antagonizes effects of magnesium)

• Dialysis

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Food sources for Mg++

• Avocado• Canned white tuna• Cauliflower• Green leafy

vegetables (spinach/broccoli)

• Milk• Oatmeal

• Peanut butter• Peas• Pork, beef, chicken• Potatoes• Raisins• Yogurt

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Phosphorus

• Critical for bone formation and cellular energy metabolism

• 85% of body phosphorus is in bone, remainder is within cells

• Only 1% is in ECF (do not reflect total body phosphorus stores)

• Phosphorus exists in the body as phosphate• Normal range 3.0-4.5 mg/dL• Must be drawn in fasting state (diurnal variation;

nadir in a.m.)

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Phosphorus

• Carbohydrate ingestion and glucose infusion lower serum phosphorus (do fasting), whereas high-phosphate meal raises it

• Major regulatory factors– PTH (lowers PO4 - via renal excretion)– Vit D ( increase PO4- by enhancing intestinal

absorption)– Insulin (lowers by shifting PO4- into cells– Dietary PO4- intake– Renal function (most important regulator)

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Hypophosphatemia

• Serum PO4- level of < 3mg/dL• Normal 2.7-4.5• Etiology

– Impaired intestinal absorption• Alcohol abuse and withdrawal ( beta

adrenergic effect )• Malabsorption• Oral phosphate binders• Refeeding after malnutrition,Hyperalimentation• Vit D deficiency

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Hypophosphatemia

• Etiology– Increased renal excretion

• Respiratory alkalosis• hyperPTH ( hypercalcemia; hypomagnesemia)

– Redistribution into cells• Severe burns• DKA therapy

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Hypophosphatemia

• Manifestation– Muscular abnormalities

• Weakness• Rhabdomyolysis• Impaired diaphragmatic function• Respiratory failure ( strong affinity of hgb to

oxygen d/t decrease of erythrocyte 2,3 diphosphoglycerate)

• Heart failure• Fractures, decrease reflex

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Hypophosphatemia

• Manifestation– Neurologic

• Paresthesia• Dysarthria• Confusion• Stupor• Sz• Coma

– Hemolysis, plt dysfunction, metabolic acidosis (rare)

– Rickets and osteomalacia in chronic hypophosphatemia

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Hypophosphatemia: Nsg InteventionsHypophosphatemia: Nsg Inteventions

• Assess for vit D deficiency, hyperPTH

• Assess for overuse of aluminum-containing antacids

• Elemental phosphorus 0.5-1.0 g bid or tid– Neutra-phos or neutra-phos K– Fleet phospho-Soda

• Check crt, phosphorus, ca++• SE: diarrhea, nausea

– Potasium phosphate or sodium phosphate IV TRO 6 hrs

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Hyperphosphatemia

• Serum PO4- > 4.5 mg/dL

• Etiology– Renal failure– hypoPTH– pseudohypoPTH– Rhabdomyolysis– Tumor lysis syndrome– Metabolic and respiratory acidosis– Excess phosphate administration

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Hyperphosphatemia• Manifestation

– s/sx are attributable to hypocalcemia and metastatic calcification of soft tissues

• BVs, cornea, skin, kidney, periarticular tissue

– Please refer to hypocalcemia for s/sx

• InterventionAdminister phosphate-binders that increase

fecal excretion of phosphorus• Calcium carbonate tid with meals• Sevelamer (avoids hypermag, calcemia, aluminum

toxicity)– Also lowers total chol– SE: GI complaints and metabolic acidosis

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Hyperphosphatemia

• Intervention– Aluminum hydroxide and aluminum carbonate

• No longer used in dialysis pts because of toxicity

– Calcium citrate should not be use with aluminum gels because it increases aluminum toxicity

– Instruct pt to avoid phosphate containing meds-laxatives and enemas

– Restrict dietary phosphate to 600-900mg/day

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Foods rich in phosphorus

• Fish

• Organ meats

• Nuts

• Pork, beef, chicken

• Whole-grain breads and cereals

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Anion ImbalancesImbalances of chloride, phosphate, and

bicarbonate accompany cation imbalances:

• Hypochloremia (below 95 mEq/L) and hyponatremia

• Hyperchloremia (above 103 mEq/L) with hypernatremia and metabolic acidosis

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Anion ImbalancesImbalances of chloride, phosphate, and

bicarbonate accompany cation imbalances

• Hypophosphatemia (below 3.0 mg/dL): – Aluminum-containing antacids that bind

phosphate– Vitamin D deficiency– Hyperparathyroidism

• Hyperphosphatemia (above 4.5 mg/dL) and renal failure

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Of all of the following patients, the nurse Of all of the following patients, the nurse recognizes that the individual who is most at recognizes that the individual who is most at

risk for a fluid volume deficit is a:risk for a fluid volume deficit is a:

• 6-month-old infant learning to drink from a cup

• 12-year-old child who is moderately active in 80° F weather

• 42-year-old patient with severe diarrhea

• 90-year-old patient with frequent headaches


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The nurse anticipates that the The nurse anticipates that the patient with a fluid volume patient with a fluid volume excess will manifest a(n):excess will manifest a(n):

• Increased urine specific gravityIncreased urine specific gravity

• Decreased body weightDecreased body weight

• Increased blood pressureIncreased blood pressure

• Decreased pulse strengthDecreased pulse strength


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