Fluid & Electrolytes Flashcards

(127 cards)

1
Q

Calcium and its role in the body

A

“A mineral element needed for the process of bone formation, coagulation of blood, excitation of cardiac and skeletal muscle, maintenance of muscle tone, conduction of neuromuscular impulses, and the synthesis and regulation of the endocrine and exocrine glands. The normal adult level is 8.6 to 10mg/dL.”

    • It plays a huge role in bone & teeth, muscle/nerve function, cell function & blood clotting.
    • it’s absorbed in the GI system, stored in bone & excreted in the kidneys. Vitamin D helps play a role in calcium absorption.
    • Calcium and Phosphorus play affect each other in opposite ways.
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2
Q

Magnesium and its role in the body

A

“Concentrated in the bone, cartilage, and within the cell itself; required for the use of adenosine triphosphate as a source of energy. It is necessary for the action of numerous enzyme systems such as those involved in carbohydrate metabolism, protein synthesis, nucleic acid synthesis, and contraction of muscular tissue. It also regulates neuromuscular activity and the clotting mechanism. The normal adult level is 1.6 to 2.6mg/dL.”

  • –It plays a role in cell function (transferring & storing energy)
  • – regulates the parathyroid hormone (in turn plays a role in calcium levels; low Mag inhibits the release of low calcium)
  • – metabolizes carbs, lipids & proteins
  • – regulates blood pressure
  • – Mag is absorbed in the small intestine (any issues with GI system causes issues with Mag levels) and excreted by the kidneys
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3
Q

Phosphorus and its role in the body

A

“Needed for generation of bony tissue. It functions in the metabolism of glucose and lipids, in the maintenance of acid-base balance, and in the storage and transfer of energy from one site in the body to another. Phosphorus levels are evaluated in relation to calcium levels because of their inverse relationship; when calcium levels are decreased, phosphorus levels are increased, and when phosphorus levels are decreased, calcium levels are increased. The normal adult level is 2.7 to 4.5mg/dL.”

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4
Q

Potassium and its role in the body

A

“A principal electrolyte of intracellular fluid and the primary buffer within the cell itself. It is needed for nerve conduction, muscle function, acid-base balance, and osmotic pressure. Along with calcium and magnesium, potassium controls the rate and force of contraction of the heart and thus cardiac output. The normal adult level is 3.5 to 5.0mEq/L.”

—Its responsible for nerve impulse conduction and muscle contractility

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5
Q

Sodium and its role in the body

A

“An abundant electrolyte that maintains osmotic pressure and acid-base balance and transmits nerve impulses. The normal adult level is 135 to 145mEq/L.”

  • –It’s role is to help regulate H2O inside and outside the cell
  • – If too much H20 in the cells, especially brain cells, can cause confusion*** caused osmosis during hyponatremia
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6
Q

Metabolic Acidosis

A

“A total concentration of buffer base that is lower than normal, with a relative increase in the hydrogen ion concentration. This results from loss of buffer bases or retention of too many acids without sufficient bases, and occurs in conditions such as kidney failure and diabetic ketoacidosis, from the production of lactic acid, and from the ingestion of toxins, such as acetylsalicylic acid (aspirin).

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7
Q

Metabolic Alkalosis

A

“A deficit or loss of hydrogen ions or acids or an excess of base (bicarbonate) that results from the accumulation of base or from a loss of acid without a comparable loss of base in the body fluids. This occurs in conditions resulting in hypovolemia, the loss of gastric fluid, excessive bicarbonate intake, the massive transfusion of whole blood, and hyperaldosteronism.”

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8
Q

Respiratory Acidosis

A

“A total concentration of buffer base that is lower than normal, with a relative increase in hydrogen ion concentration; thus a greater number of hydrogen ions is circulating in the blood than the buffer system can absorb. This is caused by primary defects in the function of the lungs or by changes in normal respiratory patterns as a result of secondary problems. Any condition that causes an obstruction of the airway or depresses respiratory status can cause respiratory acidosis.

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9
Q

Respiratory Alkalosis

A

“A deficit of carbonic acid or a decrease in hydrogen ion concentration that results from the accumulation of base or from a loss of acid without a comparable loss of base in the body fluids. This occurs in conditions that cause overstimulation of the respiratory system.”

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10
Q

Phlebitis

A

“An inflammation of the vein that can occur from mechanical or chemical (medication) trauma or from a local infection.”

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11
Q

Infiltration

A

“Seepage of IV fluid out of the vein and into the surrounding interstitial spaces.”

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12
Q

Fresh-Frozen Plasma

A

“A blood product administered to increase the level of clotting factors in clients with such a deficiency.”

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13
Q

Packed Red Blood Cells

A

“A blood product used to replace erythrocytes lost as a result of trauma or surgical interventions or in clients with bone marrow suppression.”

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14
Q

Plasma

A

“The watery, straw-colored, fluid part of lymph and the blood in which the formed elements (blood cells) are suspended. Plasma is made up of water, electrolytes, protein, glucose, fats, bilirubin, and gases and is essential for carrying the cellular elements of the blood through the circulation.”

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15
Q

Platelet Transfusion

A

“A blood product administered to clients with low platelet counts and to thrombocytopenic clients who are bleeding actively or are scheduled for an invasive procedure.”

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16
Q

Isotonic solutions -
Ex: 0.9% sodium chloride (normal saline); (0.9% NS) & 5% dextrose in water (D5W) Isotonic (physiologically hypotonic) & 5% dextrose in 0.225% saline (D5W/¼ NS) & Lactated Ringer’s (LR)

A
  1. Have the same osmolality as body fluids
  2. Increase extracellular fluid volume
  3. Do not enter the cells because no osmotic force exists to shift the fluids

A.When the solutions on both sides of a selectively permeable membrane have established equilibrium or are equal in concentration, they are isotonic.
B.Isotonic solutions are isotonic to human cells, and thus very little osmosis occurs; isotonic solutions have the same osmolality as body fluids.

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17
Q

Hypotonic solutions -
Ex: 0.45% sodium chloride (normal saline); (½ NS) & 0.225% sodium chloride (normal saline); (¼ NS) & 0.33% sodium chloride (normal saline); (⅓ NS)

A
  1. Are more dilute solutions and have a lower osmolality than body fluids
  2. Cause the movement of water into cells by osmosis
  3. Should be administered slowly to prevent cellular edema

A. When a solution contains a lower concentration of salt or solute than another, more concentrated solution, it is considered hypotonic.
B.A hypotonic solution has less salt or more water than an isotonic solution; these solutions have lower osmolality than body fluids.
C.Hypotonic solutions are hypotonic to the cells; therefore osmosis would continue in an attempt to bring about balance or equality.

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18
Q

Hypertonic solutions -
Ex: 3% sodium chloride (normal saline); (3% NS) & 5% sodium chloride (normal saline); (5% NS) & 10% dextrose in water (D10W) & 5% dextrose in 0.9% sodium chloride (normal saline); D5W/NS & 5% dextrose in 0.45% sodium chloride (normal saline); (D5W/½ NS) & 5% dextrose in lactated Ringer’s (D5LR)

A
  1. Are more concentrated solutions and have a higher osmolality than body fluids
  2. Cause movement of water from cells into the extracellular fluid by osmosis

A. A solution that has a higher concentration of solutes than another, less concentrated solution is hypertonic; these solutions have a higher osmolality than body fluids.

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19
Q

Colloids solution-

Ex: Dextran & Albumin

A
  1. Also called plasma expanders

2. Pull fluid from the interstitial compartment into the vascular compartment

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20
Q

Isotonic dehydration (fluid volume deficit)

A

a. Water and dissolved electrolytes are lost in equal proportions.
b. Known as HYPOVOLEMIA, isotonic dehydration is the most common type of dehydration.
c. Isotonic dehydration results in decreased circulating blood volume and inadequate tissue perfusion.”

Cause -

a. Inadequate intake of fluids and solutes
b. Fluid shifts between compartments
c. Excessive losses of isotonic body fluids

Treatment - Use isotonic solutions

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21
Q

Hypertonic dehydration (fluid volume deficit)

A

a. Water loss exceeds electrolyte loss.
b. The clinical problems that occur result from alterations in the concentrations of specific plasma electrolytes.
c. Fluid moves from the intracellular compartment into the plasma and interstitial fluid spaces, causing cellular dehydration and shrinkage.”

Cause - “conditions that increase fluid loss, such as excessive perspiration, hyperventilation, ketoacidosis, prolonged fevers, diarrhea, early-stage kidney disease, and diabetes insipidus”

Treatment - Us hypertonic solution

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22
Q

Hypotonic dehydration (fluid volume deficit)

A

a. Electrolyte loss exceeds water loss.
b. The clinical problems that occur result from fluid shifts between compartments, causing a decrease in plasma volume.
c. Fluid moves from the plasma and interstitial fluid spaces into the cells, causing a plasma volume deficit and causing the cells to swell.”

Cause -

a. Chronic illness
b. Excessive fluid replacement (hypotonic)
c. Kidney disease
d. Chronic malnutrition

Treatment - Use Hypotonic solutions

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23
Q

Isotonic overhydration (fluid volume overload)

A

“1.Isotonic overhydration

a. Known as HYPERVOLEMIA, isotonic overhydration results from excessive fluid in the extracellular fluid compartment.
b. Only the extracellular fluid compartment is expanded, and fluid does not shift between the extracellular and intracellular compartments.
c. Isotonic overhydration causes circulatory overload and interstitial edema; when severe or when it occurs in a client with poor cardiac function, heart failure and pulmonary edema can result. ”

CAUSES-

a. Inadequately controlled IV therapy
b. Kidney disease
c. Long-term corticosteroid therapy

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24
Q

Hypertonic overhydration (fluid volume overload)

A

a. The occurrence of hypertonic overhydration is RARE and is caused by an excessive sodium intake.
b. Fluid is drawn from the intracellular fluid compartment; the extracellular fluid volume expands, and the intracellular fluid volume contracts.

CAUSES-

a. Excessive sodium ingestion
b. Rapid infusion of hypertonic saline
c. Excessive sodium bicarbonate therapy

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25
Hypotonic overhydration (fluid volume overload)
a.  Hypotonic overhydration is known as WATER INTOXICATION. b.  The excessive fluid moves into the intracellular space, and all body fluid compartments expand. c.  Electrolyte imbalances occur as a result of dilution. ” CAUSES- a.  Early kidney disease b.  Heart failure c.  Syndrome of inappropriate antidiuretic hormone secretion d.  Inadequately controlled IV therapy e.  Replacement of isotonic fluid loss with hypotonic fluids f.  Irrigation of wounds and body cavities with hypotonic fluids”
26
Fluid Volume Deficit interventions:
1.  Monitor cardiovascular, respiratory, neuromuscular, renal, integumentary, and gastrointestinal status. 2.  Prevent further fluid losses and increase fluid compartment volumes to normal ranges. 3.  PROVIDE oral rehydration therapy if possible and IV fluid replacement if the dehydration is severe; monitor intake and output. 4.  In general, isotonic dehydration is treated with isotonic fluid solutions, hypertonic dehydration with hypotonic fluid solutions, and hypotonic dehydration with hypertonic fluid solutions. 5.  ADMINISTER medications as prescribed, such as antidiarrheal, antimicrobial, antiemetic, and antipyretic medications, to correct the cause and treat any symptoms. 6.  ADMINISTER oxygen as prescribed.” 7.  MONITOR electrolyte values and prepare to ADMINISTER medication to treat an imbalance, if present.
27
Fluid Volume Excess (overload) interventions:
1.  Monitor cardiovascular, respiratory, neuromuscular, renal, integumentary, and gastrointestinal status. 2.  Prevent further fluid overload and restore normal fluid balance. 3.  ADMINISTER diuretics; osmotic diuretics typically are prescribed first to prevent severe electrolyte imbalances. 4.  RESTRICT fluid and sodium intake as prescribed. 5.  MONITOR intake and output; monitor WEIGHT. 6.  MONITOR electrolyte values, and prepare to ADMINISTER medication to treat an imbalance if present. * **A client with acute kidney injury or chronic kidney disease is at high risk for fluid volume excess.
28
Hyponatremia (sodium below 135 mEq/L) | Causes: Sodium imbalances usually are associated with fluid volume imbalances.
1.  Increased sodium excretion a.  Excessive diaphoresis b.  Diuretics c.  Vomiting d.  Diarrhea e.  Wound drainage, especially gastrointestinal f.  Kidney disease g.  Decreased secretion of aldosterone 2.  Inadequate sodium intake a.  Fasting; nothing by mouth status b.  Low-salt diet 3.  Dilution of serum sodium a.  Excessive ingestion of hypotonic fluids or irrigation with hypotonic fluids b.  Kidney disease c.  Freshwater drowning d.  Syndrome of inappropriate antidiuretic hormone secretion e.  Hyperglycemia f.  Heart failure
29
Hyponatremia interventions:
1.  Monitor cardiovascular, respiratory, neuromuscular, cerebral, renal, and gastrointestinal status. 2.  If hyponatremia is accompanied by a fluid volume deficit (hypovolemia), IV sodium chloride infusions (3% NS-Hypertonic solution) are administered to restore sodium content and fluid volume 3.  If hyponatremia is accompanied by fluid volume excess (hypervolemia), osmotic diuretics are administered to promote the excretion of water rather than sodium. 4.  If caused by inappropriate or excessive secretion of antidiuretic hormone (SIADH), medications that antagonize antidiuretic hormone may be administered. 5.  Instruct the client to increase oral sodium intake and inform the client about the foods to include in the diet 6.  If the client is taking lithium (Lithobid), monitor the lithium level, because hyponatremia can cause diminished lithium excretion, resulting in toxicity. ****Hyponatremia precipitates lithium toxicity in a client taking lithium (Lithobid).”
30
Hypernatremia (sodium above 145 mEq/L) Causes: Sodium imbalances usually are associated with fluid volume imbalances.
1.  Decreased sodium excretion a.  Corticosteroids b.  Cushing’s syndrome (Aldosterone problem) c.  Kidney disease d.  Hyperaldosteronism (Aldosterone retains sodium) 2.  Increased sodium intake: Excessive oral sodium ingestion or excessive administration of sodium-containing IV fluids 3.  Decreased water intake: Fasting; nothing by mouth status 4.  Increased water loss: Increased rate of metabolism, fever, hyperventilation, infection, excessive diaphoresis, watery diarrhea, diabetes insipidus
31
Hypernatremia (sodium above 145 mEq/L) Interventions:
1.  Monitor cardiovascular, respiratory, neuromuscular, cerebral, renal, and integumentary status. 2.  If the cause is fluid loss (dehydration), prepare to administer IV infusions. MD may order isotonic or hypotonic solutions (0.45%NS) to rehydrate the cells that have lost NA+ to ECF. 3.  If the cause is inadequate renal excretion of sodium, prepare to administer diuretics that promote sodium loss 4.  Restrict sodium and fluid intake as prescribed ****Monitor the client closely for signs of a potassium imbalance. A potassium imbalance can cause cardiac dysrhythmias that can be life-threatening!
32
Hyponatremia (Cardiovascular assessment)
■ Symptoms vary with changes in vascular volume ■ Normovolemic: Rapid pulse rate; normal blood pressure ■ Hypovolemic: Thready, weak, rapid pulse rate; hypotension; flat neck veins; normal or low central venous pressure ■ Hypervolemic: Rapid, bounding pulse; blood pressure normal or elevated; normal or elevated central venous pressure
33
Hypernatremia (Cardiovascular assessment)
■ Heart rate and blood pressure respond to vascular volume status
34
Hyponatremia (Respiratory assessment)
■ Shallow, ineffective respiratory movement is a late manifestation related to skeletal muscle weakness***
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Hypernatremia (Respiratory assessment)
■ Pulmonary edema if hypervolemia is present
36
Hyponatremia (Neuromuscular assessment)
■ Generalized skeletal muscle weakness that is worse in the extremities ■ Diminished deep tendon reflexes ■ Lethargy
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Hypernatremia (Neuromuscular assessment)
■ Early: Spontaneous muscle twitches; irregular muscle contractions ■ Late: Skeletal muscle weakness; deep tendon reflexes diminished or absent
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Hyponatremia (Central Nervous System assessment)
``` ■ Headache ■ Personality changes ■ Confusion*** ■ Seizures*** ■ Coma ```
39
Hypernatremia (Central Nervous System assessment)
■ Altered cerebral function is the most common manifestation of hypernatremia*** ■ Normovolemia or hypovolemia: Agitation, confusion, seizures*** ■ Hypervolemia: Lethargy, stupor, coma
40
Hyponatremia (Gastrointestinal assessment)
■ Increased motility and hyperactive bowel sounds ■ Nausea ■ Abdominal cramping and diarrhea
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Hypernatremia (Gastrointestinal assessment)
■ Extreme thirst
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Hyponatremia (Renal assessment)
■ Increased urinary output
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Hypernatremia (Renal assessment)
■ Decreased urinary output
44
Hyponatremia (Integumentary assessment)
■ Dry mucous membrane
45
Hypernatremia (Integumentary assessment)
■ Dry and flushed skin ■ Dry and sticky tongue and mucous membranes ■ Presence or absence of edema, depending on fluid volume changes
46
Fluid Volume Overload (Cardiovascular assessment)
``` ■ Bounding, increased pulse rate ■ Elevated blood pressure ■ Distended neck and hand veins ■ Elevated central venous pressure ■ Dysrhythmias ```
47
Fluid Volume Deficit (Cardiovascular assessment)
■ Thready, increased pulse rate ■ Decreased blood pressure and orthostatic (postural) hypotension ■ Flat neck and hand veins in dependent positions ■ Diminished peripheral pulses ■ Decreased central venous pressure ■ Dysrhythmias
48
Fluid Volume Overload (Respiratory assessment)
■ Increased respiratory rate (shallow respirations) ■ Dyspnea ■ Moist crackles on auscultation”
49
Fluid Volume Deficit (Respiratory assessment)
■ Increased rate and depth of respirations | ■ Dyspnea
50
Fluid Volume Overload (Neuromuscular assessment)
``` ■ Altered level of consciousness ■ Headache ■ Visual disturbances ■ Skeletal muscle weakness ■ Paresthesias ```
51
Fluid Volume Deficit (Neuromuscular assessment)
■ Decreased central nervous system activity, from lethargy to coma ■ Fever, depending on the amount of fluid loss ■ Skeletal muscle weakness
52
Fluid Volume Overload (Renal assessment)
■ Increased urine output if kidneys can compensate; decreased urine output if kidney damage is the cause
53
Fluid Volume Deficit (Renal assessment)
■ Decreased urine output
54
Fluid Volume Overload (Integumentary assessment)
■ Pitting edema in dependent areas | ■ Pale, cool skin
55
Fluid Volume Deficit (Integumentary assessment)
■ Dry skin ■ Poor turgor, tenting ■ Dry mouth
56
Fluid Volume Overload (Gastrointestinal assessment)
``` ■ Increased motility in the gastrointestinal tract ■ Diarrhea ■ Increased body weight ■ Liver enlargement ■ Ascites ```
57
Fluid Volume Deficit (Gastrointestinal assessment)
■ Decreased motility and diminished bowel sounds ■ Constipation ■ Thirst ■ Decreased body weight
58
Fluid Volume Overload (Laboratory Findings)
``` ■ Decreased serum osmolality ■ Decreased hematocrit ■ Decreased BUN level ■ Decreased serum sodium level ■ Decreased urine specific gravity ```
59
Fluid Volume Deficit (Laboratory Findings)
``` ■ Increased serum osmolality ■ Increased hematocrit ■ Increased blood urea nitrogen (BUN) level ■ Increased serum sodium level Increased urinary specific gravity ```
60
Osmosis (Body fluid transport)
a. Osmotic pressure is the force that draws the solvent (water) from a less concentrated solute through a selectively permeable membrane into a more concentrated solute, thus tending to equalize the concentration of the solvent. b.  If a membrane is permeable to water but not to all the solutes present, the membrane is a selective or semipermeable membrane. c.  Osmosis is the movement of solvent molecules (H2O) across a membrane in response to a concentration gradient, usually from a solution of lower to one of higher solute concentration. d.  When a more concentrated solution is on one side of a selectively permeable membrane and a less concentrated solution is on the other side, a pull called osmotic pressure draws the water through the membrane to the more concentrated side, or the side with more solute.
61
Diffusion (Body fluid transport)
a.  Diffusion is the process whereby a solute (substance that is dissolved) may spread through a solution or solvent (solution in which the solute is dissolved). b.  Diffusion of a solute spreads the molecules from an area of higher concentration to an area of lower concentration. c.  A permeable membrane allows substances to pass through it without restriction. d.  A selectively permeable membrane allows some solutes to pass through without restriction but prevents other solutes from passing freely. e.  Diffusion occurs within fluid compartments and from one compartment to another if the barrier between the compartments is permeable to the diffusing substances.”
62
Filtration (Body fluid transport)
a.  Filtration is the movement of solutes and solvents by hydrostatic pressure. b.  The movement is from an area of higher pressure to an area of lower pressure.
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Hydrostatic pressure (Body fluid transport)
a. Hydrostatic pressure is the force exerted by the weight of a solution. b.  When a difference exists in the hydrostatic pressure on two sides of a membrane, water and diffusible solutes move out of the solution that has the higher hydrostatic pressure by the process of filtration. c.  At the arterial end of the capillary, the hydrostatic pressure is higher than the osmotic pressure; therefore fluids and diffusible solutes move out of the capillary. d.  At the venous end, the osmotic pressure, or pull, is higher than the hydrostatic pressure, and fluids and some solutes move into the capillary. e.  The excess fluid and solutes remaining in the interstitial spaces are returned to the intravascular compartment by the lymph channels.”
64
Osmolality (Body fluid transportation)
a.  Osmolality refers to the number of osmotically active particles per kilogram of water; it is the concentration of a solution. b.  In the body, osmotic pressure is measured in milliosmoles (mOsm). c.  The normal osmolality of plasma is 270 to 300 milliosmoles/kilogram (mOsm/kg) water.
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Hypokalemia (Potassium below 3.5 mEq/L) - “Potassium deficit is potentially life-threatening because every body system is affected.” Causes:
1.  Actual total body potassium loss a.  Excessive use of medications such as diuretics or corticosteroids b.  Increased secretion of aldosterone, such as in Cushing’s syndrome c.  Vomiting, diarrhea, anorexia d.  Wound drainage, particularly gastrointestinal e.  Prolonged nasogastric suction f.  Excessive diaphoresis g.  Kidney disease impairing reabsorption of potassium 2. Inadequate potassium intake: Fasting; nothing by mouth status 3.  Movement of potassium from the extracellular fluid to the intracellular fluid a.  Alkalosis b.  Hyperinsulinism (too much insulin in the blood, in turn, causing hypoglycemia. 4.  Dilution of serum potassium a.  Water intoxication b.  IV therapy with potassium-deficient solutions
66
Hypokalemia (Cardiovascular assessment)
■ Thready, weak, irregular pulse ■ Weak peripheral pulses ■ Orthostatic hypotension
67
Hypokalemia (Respiratory assessment)
■ Shallow, ineffective respirations that result from profound weakness of the skeletal muscles of respiration ■ Diminished breath sounds
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Hypokalemia (Neuromuscular assessment)
``` ■ Anxiety, lethargy, confusion, coma ■ Skeletal muscle weakness, eventual flaccid paralysis ■ Loss of tactile discrimination ■ Paresthesias ■ Deep tendon hyporeflexia ```
69
Hypokalemia (Gastrointestinal assessment)
■ Decreased motility, hypoactive to absent bowel sounds ■ Nausea, vomiting, constipation, abdominal distention ■ Paralytic ileus
70
Hypokalemia (Laboratory assessment)
■ Serum potassium level lower than 3.5 mEq/L | ■ Electrocardiogram changes: ST depression; shallow, flat, or inverted T wave; and prominent U wave
71
Hypokalemia - Interventions:
1.  Monitor cardiovascular, respiratory, neuromuscular, gastrointestinal, and renal status, and place the client on a cardiac monitor. 2.  Monitor electrolyte values. 3.  Administer potassium supplements orally or intravenously, as prescribed. 4.  Oral potassium supplements a.  Oral potassium supplements may cause nausea and vomiting and they should not be taken on an empty stomach; if the client complains of abdominal pain, distention, nausea, vomiting, diarrhea, or gastrointestinal bleeding, the supplement may need to be discontinued. b.  Liquid potassium chloride has an unpleasant taste and should be taken with juice or another liquid. 5.  Intravenously administered potassium 6.  Institute safety measures for the client experiencing muscle weakness. 7.  If the client is taking a potassium-depleting diuretic, it may be discontinued; a potassium-retaining diuretic may be prescribed (Spironolactone, Aldactone, Dyazide, Maxide, Triamterene). 8.  Instruct the client about foods that are high in potassium content ****Potassium is never administered by IV push, intramuscular, or subcutaneous routes. IV potassium is always diluted and administered using an infusion device!
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Precautions with Intravenously Administered Potassium”
■ Potassium is never given by intravenous (IV) push or by the intramuscular or subcutaneous route. ■ A dilution of no more than 1 mEq/10 mL of solution is recommended. ■ Many healthcare agencies supply prepared IV solutions containing potassium; before administering and frequently during infusion of the IV solution, rotate and invert the bag to ensure that the potassium is distributed evenly throughout the IV solution. ■ Ensure that the IV bag containing potassium is properly labeled. ■ The maximum recommended infusion rate is 5 to 10 mEq/hour, never to exceed 20 mEq/hour under any circumstances. ■ A client receiving more than 10 mEq/hour should be placed on a cardiac monitor and monitored for cardiac changes, and the infusion should be controlled by an infusion device. ■ Potassium infusion can cause phlebitis; therefore the nurse should assess the IV site frequently for signs of phlebitis or infiltration. If either occurs, the infusion should be stopped immediately. ■ The nurse should assess renal function before administering potassium, and monitor intake and output during administration.
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Hyperkalemia (Potassium above 5.0 mEq/L) - Causes:
1.  Excessive potassium intake a.  Overingestion of potassium-containing foods or medications, such as potassium chloride or salt substitutes b.  Rapid infusion of potassium-containing IV solutions 2.  Decreased potassium excretion a.  Potassium-retaining diuretics b.  Kidney disease c.  Adrenal insufficiency, such as in Addison’s disease 3.  Movement of potassium from the intracellular fluid to the extracellular fluid a.  Tissue damage b.  Acidosis c.  Hyperuricemia d.  Hypercatabolism
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Sodium (Common Food Sources)
``` Bacon Butter Canned food Cheese Frankfurters Ketchup Lunch meat Milk Mustard Processed food Snack food Soy sauce Table salt White & wheat bread ```
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Potassium (Common Food Sources)
``` Avocado Bananas Cantaloupe Carrots Fish Mushrooms Oranges Potatoes Pork, beef, veal Raisins Spinach Strawberries Tomatoes ```
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Hyperkalemia - Interventions:
1.  Monitor cardiovascular, respiratory, neuromuscular, renal, and gastrointestinal status; place the client on a cardiac monitor. 2.  Discontinue IV potassium (keep the IV catheter patent), and hold oral potassium supplements. 3.  Initiate a potassium-restricted diet. 4.  Prepare to administer potassium-excreting diuretics if renal function is not impaired. 5.  If renal function is impaired, prepare to administer sodium polystyrene sulfonate (Kayexalate), a cation-exchange resin that promotes gastrointestinal sodium absorption and potassium excretion. 6.  Prepare the client for dialysis if potassium levels are critically high. 7.  Prepare for the administration of intravenous calcium if hyperkalemia is severe to avert myocardial excitability. 8.  Prepare for the IV administration of hypertonic glucose with regular insulin to move excess potassium into the cells. 9.  Monitor renal function. 10.  When blood transfusions are prescribed for a client with a potassium imbalance, the client should receive fresh blood, if possible; transfusions of stored blood may elevate the potassium level because the breakdown of older blood cells releases potassium. 11.  Teach the client to avoid foods high in potassium 12.  Instruct the client to avoid the use of salt substitutes or other potassium-containing substances. ****Monitor the serum potassium level closely when a client is receiving a potassium-retaining diuretic!
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Hyperkalemia (Cardiovascular assessment)
■ Slow, weak, irregular heart rate (dysrhythmias) | ■ Decreased blood pressure
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Hyperkalemia (Respiratory assessment)
■ Profound weakness of the skeletal muscles leading to respiratory failure
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Hyperkalemia (Neuromuscular assessment)
■ Early: Muscle twitches, cramps, paresthesias (tingling and burning followed by numbness in the hands and feet and around the mouth) ■ Late: Profound weakness, ascending flaccid paralysis in the arms and legs (trunk, head, and respiratory muscles become affected when the serum potassium level reaches a lethal level)******
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Hyperkalemia (Gastrointestinal assessment)
■ Increased motility, hyperactive bowel sounds | ■ Diarrhea
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Hyperkalemia (Laboratory findings assessment)
■ Serum potassium level that exceeds 5.0 mEq/L ■ Electrocardiographic changes: Tall peaked T waves, flat P waves, widened QRS complexes, and prolonged PR intervals****s
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“Electrocardiographic Changes in Electrolyte Imbalances” Hypocalcemia
Prolonged ST segment   Prolonged QT interval
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“Electrocardiographic Changes in Electrolyte Imbalances” Hypercalcemia
Shortened ST segment   Widened T wave
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“Electrocardiographic Changes in Electrolyte Imbalances” Hypokalemia
``` ST depression   Shallow, flat, or inverted T wave   Prominent U wave ```
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“Electrocardiographic Changes in Electrolyte Imbalances” Hyperkalemia
``` Tall peaked T waves   Flat P waves   Widened QRS complex   Prolonged PR interval ```
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“Electrocardiographic Changes in Electrolyte Imbalances” Hypomagnesemia
Tall T waves   Depressed ST segment
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“Electrocardiographic Changes in Electrolyte Imbalances” Hypermagnesemia
Prolonged PR interval   Widened QRS complexes
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Hypocalcemia (Calcium lower than 9.0 mg/dL) Causes:
1.  Inhibition of calcium absorption from the gastrointestinal tract a.  Inadequate oral intake of calcium b.  Lactose intolerance c.  Malabsorption syndromes such as celiac sprue or Crohn’s disease d.  Inadequate intake of vitamin D (helps calcium be reabsorbed) e.  End-stage kidney disease 2.  Increased calcium excretion a.  Kidney disease, polyuric phase b.  Diarrhea c.  Steatorrhea d.  Wound drainage, especially gastrointestinal 3.  Conditions that decrease the ionized fraction of calcium a.  Hyperproteinemia b.  Alkalosis c.  Medications such as calcium chelators or binders d.  Acute pancreatitis e.  Hyperphosphatemia f.  Immobility g.  Removal or destruction of the parathyroid glands
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Calcium (Common Food Sources)
Young Sally Calcium Serum Continues To Randomly Mess-up! ``` Cheese Collard greens Milk and soy milk Rhubarb Sardines Spinach Tofu Yogurt ```
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Hypocalcemia (Cardiovascular assessment)
■ Decreased heart rate ■ Hypotension ■ Diminished peripheral pulses
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Hypocalcemia (Respiratory assessment)
■ Not directly affected; however, respiratory failure or arrest can result from decreased respiratory movement because of muscle tetany or seizures
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Hypocalcemia (Neuromuscular assessment)
■ Irritable skeletal muscles: Twitches, cramps, tetany, seizures ■ Painful muscle spasms in the calf or foot during periods of inactivity ■ Paresthesias followed by numbness that may affect the lips, nose, and ears in addition to the limbs ■ Positive Trousseau’s and Chvostek’s signs ■ Hyperactive deep tendon reflexes ■ Anxiety, irritability
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Hypocalcemia (Renal assessment)
■ Urinary output varies depending on the cause
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Hypocalcemia (Gastrointestinal assessment)
■ Increased gastric motility; hyperactive bowel sounds | ■ Cramping, diarrhea
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Hypocalcemia (Laboratory findings)
■ Serum calcium level less than 8.6 mg/dL | ■ Electrocardiographic changes: Prolonged ST interval, prolonged QT interval
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Hypercalcemia (Cardiovascular assessment)
■ Increased heart rate in the early phase; bradycardia that can lead to cardiac arrest in late phases ■ Increased blood pressure ■ Bounding, full peripheral pulses
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Hypercalcemia (Respiratory assessment)
■ Ineffective respiratory movement as a result of profound skeletal muscle weakness
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Hypercalcemia (Neuromuscular assessment)
■ Profound muscle weakness ■ Diminished or absent deep tendon reflexes ■ Disorientation, lethargy, coma
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Hypercalcemia (Renal assessment)
■ Urinary output varies depending on the cause | ■ Formation of renal calculi; flank pain
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Hypercalcemia (Gastrointestinal assessment)
■ Decreased motility and hypoactive bowel sounds | ■ Anorexia, nausea, abdominal distention, constipation
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Hypercalcemia (Laboratory findings)
■ Serum calcium level that exceeds 10.5 mg/dL | ■ Electrocardiographic changes: Shortened ST segment, widened T wave
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Hypocalcemia (Calcium lower than 9.0 mg/dL) Interventions:
1.  Monitor cardiovascular, respiratory, neuromuscular, and gastrointestinal status; place the client on a cardiac monitor. 2.  Administer calcium supplements orally or calcium intravenously. - - after a meal or at bedtime with a full glass of water 3.  When administering calcium intravenously (ex: 10% calcium gluconate), warm the injection solution to body temperature before administration and administer slowly; monitor for electrocardiographic changes, observe for infiltration and monitor for hypercalcemia. - -also, watch pt's on digoxin because calcium may increase digoxin toxicity. 4.  Administer medications that increase calcium absorption. a.  Aluminum hydroxide reduces phosphorus levels, causing the countereffect of increasing calcium levels. b.  Vitamin D aids in the absorption of calcium from the intestinal tract. 5.  Provide a quiet environment to reduce environmental stimuli. 6.  Initiate seizure precautions. 7.  Move the client carefully, and monitor for signs of a pathological fracture. 8.  Keep 10% calcium gluconate available for treatment of acute calcium deficit. 9.  Instruct the client to consume foods high in calcium
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Diagnostic Tests for Hypocalcemia
A, Chvostek’s sign is contraction of facial muscles in response to a light tap over the facial nerve in front of the ear. B, Trousseau’s sign is a carpal spasm induced by inflating a blood pressure cuff (C) above the systolic pressure for a few minutes.
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Hypercalcemia (Calcium above 10.5 mg/dL) Causes:
1.  Increased calcium absorption a.  Excessive oral intake of calcium b.  Excessive oral intake of vitamin D 2.  Decreased calcium excretion a.  Kidney disease b.  Use of thiazide diuretics (calcium excretion decreased) 3.  Increased bone resorption of calcium a.  Hyperparathyroidism (causes too much calcium to be released in the blood) b.  Hyperthyroidism c.  Malignancy (bone destruction from metastatic tumors) d.  Immobility e.  Use of glucocorticoids (suppresses calcium absorption which leaves too much in the blood) 4.  Hemoconcentration a.  Dehydration b.  Use of lithium (affects parathyroid & causes phos increase and calcium increase) c.  Adrenal insufficiency (Addison's disease)
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Hypercalcemia Interventions:
1.  Monitor cardiovascular, respiratory, neuromuscular, renal, and gastrointestinal status; place the client on a cardiac monitor. 2.  Discontinue IV infusions of solutions containing calcium and oral medications containing calcium or vitamin D. 3.  Discontinue thiazide diuretics and replace with diuretics that enhance the excretion of calcium. 4.  Administer medications as prescribed that inhibit calcium resorption from the bone, such as phosphorus, calcitonin (Calcimar), bisphosphonates, and prostaglandin synthesis inhibitors (aspirin, nonsteroidal anti-inflammatory drugs). 5.  Prepare the client with severe hypercalcemia for dialysis if medications fail to reduce the serum calcium level. 6.  Move the client carefully and monitor for signs of a pathological fracture. 7.  Monitor for flank or abdominal pain, and strain the urine to check for the presence of urinary stones. (Too much calcium increases stone formation) ***A client with a calcium imbalance is at risk for a pathological fracture. Move the client carefully and slowly; assist the client with ambulation.
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Hypomagnesemia (Magnesium lower than 1.3 mEq/L) Causes:
1.  Insufficient magnesium intake a.  Malnutrition and starvation b.  Vomiting or diarrhea c.  Malabsorption syndrome (plus, proton pump inhibitors i.e. Protonix, Prilosec, Nexium and & GI drugs ending in "Prazole") d.  Celiac disease e.  Crohn’s disease f. Hypokalemia & hypocalcemia can cause hypomagnesemia 2.  Increased magnesium secretion a.  Medications such as diuretics (loop & thiazides) b.  ***Chronic alcoholism (ETOH stimulates kidneys to waste Mag, acute pancreatitis c. Cyclosporines (stimulates kidney to waste mag) 3.  Intracellular movement of magnesium a.  Hyperglycemia b.  Insulin administration c.  Sepsis
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Hypomagnesemia (Magnesium lower than 1.3 mEq/L) Interventions:
1.  Monitor cardiovascular, respiratory, gastrointestinal, neuromuscular, and central nervous system status; place the client on a cardiac monitor. 2.  Because hypocalcemia frequently accompanies hypomagnesemia, interventions also aim to restore normal serum calcium levels. 3.  Oral preparations of magnesium may cause diarrhea and increase magnesium loss. 4.  Magnesium sulfate by the IV route may be prescribed in severe cases (intramuscular injections cause pain and tissue damage); initiate seizure precautions, monitor serum magnesium levels frequently, and monitor for diminished deep tendon reflexes, suggesting hypermagnesemia, during the administration of magnesium. 5.  Instruct the client to increase the intake of foods that contain magnesium
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Hypermagnesemia (Magnesium above 2.1 mEq/L) Causes:
1.  Increased magnesium intake a.  Magnesium-containing antacids and laxatives (Mylanta, Maalox) b.  Excessive administration of magnesium intravenously (correcting hypomagnesemia with mag sulfate) 2.  Decreased renal excretion of magnesium as a result of renal insufficiency
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Hypermagnesemia (Magnesium above 2.1 mEq/L) Interventions:
1.  Monitor cardiovascular, respiratory, neuromuscular, and central nervous system status; place the client on a cardiac monitor. 2.  Diuretics are prescribed to increase renal excretion of magnesium. 3.  Intravenously administered calcium chloride or calcium gluconate may be prescribed to reverse the effects of magnesium on cardiac muscle. 4.  Instruct the client to restrict dietary intake of magnesium-containing foods 5.  Instruct the client to avoid the use of laxatives and antacids containing magnesium. ****Calcium gluconate is the antidote for magnesium overdose!
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Magnesium (Common Food Sources)
``` Avacado Canned white tuna Green leafy vegetables, such as spinach and broccoli Milk Nuts Oatmeal, wheat bran Peanut butter, almonds Peas Pork, beef, chicken, soybeans Potatoes Raisins Yogurt ```
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Hypomagnesemia (Cardiovascular assessment)
■ Tachycardia ■ Hypertension ■ **Torsades de pointes (lethal abnormal rhythm seen in ETOH abuse)
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Hypermagnesemia (Cardiovascular assessment)
■ Bradycardia, dysrhythmias (heart blocks) | ■ Hypotension
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Hypomagnesemia (Respiratory assessment)
■ Shallow respirations (weak)
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Hypermagnesemia (Respiratory assessment)
■ Respiratory insufficiency when the skeletal muscles of respiration are involved
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Hypomagnesemia (Neuromucular assessment)
■ Twitches; paresthesias ■ Positive Trousseau’s and Chvostek’s signs ■ Hyperreflexia ■ Tetany (abnormal twtiching), seizures
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Hypermagnesemia (Neuromuscular assessment)
■ Diminished or absent deep tendon reflexes | ■ Skeletal muscle weakness
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Hypomagnesemia (Central nervous system)
■ Irritability | ■ Confusion
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Hypermagnesemia (Central nervous system)
■ Drowsiness and lethargy that progresses to coma
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Hypomagnesemia (Laboratory findings)
■ Serum magnesium level less than 1.6 mg/dL | ■ Electrocardiographic changes: Tall T waves, depressed ST segments***
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Hypermagnesemia (Laboratory findings)
■ Serum magnesium level that exceeds 2.6 mg/dL | ■ Electrocardiographic changes: Prolonged PR interval, widened QRS complexes
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Hypophosphatemia (phosphorus lower than 3.0 mg/dL) Causes:
1.  Insufficient phosphorus intake: Malnutrition and starvation 2.  Increased phosphorus excretion a.  Hyperparathyroidism b.  Malignancy c.  Use of magnesium-based or aluminum hydroxide–based antacids 3.  Intracellular shift a.  Hyperglycemia b.  Respiratory alkalosis
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Hypophosphatemia (phosphorus lower than 3.0 mg/dL) Assessments:
1.  Cardiovascular a.  Decreased contractility and cardiac output b.  Slowed peripheral pulses 2.  Respiratory: Shallow respirations 3.  Neuromuscular a.  Weakness b.  Decreased deep tendon reflexes c.  Decreased bone density that can cause fractures and alterations in bone shape d.  Rhabdomyolysis (breakdown of muscle tissue that causes the release of myoglobin that's harmful to the kidneys) 4.  Central nervous system a.  Irritability b.  Confusion c.  Seizures 5.  Hematological a.  Decreased platelet aggregation and increased bleeding b.  Immunosuppression
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Hypophosphatemia (phosphorus lower than 3.0 mg/dL) Interventions:
1.  Monitor cardiovascular, respiratory, neuromuscular, central nervous system, and hematological status. 2.  Discontinue medications that contribute to hypophosphatemia. 3.  Administer phosphorus orally along with a vitamin D supplement. 4.  Prepare to administer phosphorus intravenously when serum phosphorus levels fall below 1 mg/dL and when the client experiences critical clinical manifestations. 5.  Administer IV phosphorus slowly because of the risks associated with hyperphosphatemia. 6.  Assess the renal system before administering phosphorus. 7.  Move the client carefully, and monitor for signs of a pathological fracture. 8.  Instruct the client to increase the intake of the phosphorus-containing foods while decreasing the intake of any calcium-containing foods. ***A decrease in the serum phosphorus level is accompanied by an increase in the serum calcium level, and an increase in the serum phosphorus level is accompanied by a decrease in the serum calcium level.
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Hyperphosphatemia (phosphorus above 4.5 mg/dL) Causes:
1.  Decreased renal excretion resulting from renal insufficiency 2.  Tumor lysis syndrome 3.  Increased intake of phosphorus, including dietary intake or overuse of phosphate-containing laxatives or enemas 4.  Hypoparathyroidis
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Hyperphosphatemia (phosphorus above 4.5 mg/dL) Assessments:
Refer to the assessment of hypocalcemia
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Hyperphosphatemia (phosphorus above 4.5 mg/dL) Interventions:
1.  Interventions entail the management of hypocalcemia. 2.  Administer phosphate-binding medications that increase fecal excretion of phosphorus by binding phosphorus from food in the gastrointestinal tract. 3.  Instruct the client to avoid phosphate-containing medications, including laxatives and enemas. 4.  Instruct the client to decrease the intake of food that is high in phosphorus 5.  Instruct the client in medication administration: Take phosphate-binding medications, emphasizing that they should be taken with meals or immediately after meals.
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Phosphorus (Common Food Sources)
``` Dairy products Fish Nuts Pork, beef chicken, organ meats Pumpkin, squash Whole-grain breads and cereals ```