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Adam G. > Fluids & Electrolytes > Flashcards

Fluids & Electrolytes Flashcards

1
Q

Processes calcium is involved in:

A
  1. ) Bone formation
  2. ) Blood coagulation
  3. ) Contraction of cardiac and skeletal muscle
  4. ) Maintenance of muscle tone
  5. ) Conduction of nerve impulses
  6. ) Synthesis and regulation of endocrine and exocrine glands
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2
Q

Normal calcium ranges:

A

8.6 to 10 mg/dL

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3
Q

Processes magnesium is involved in:

A
  1. ) Needed for use of ATP as a source of energy
  2. ) Needed for the action of numerous enzyme systems:
    - Carbohydrate metabolism
    - Protein synthesis
    - Nucleic acid synthesis
    - Contraction of muscular tissue
  3. ) Regulates nerve activity
  4. ) Regulates the clotting mechanism
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4
Q

Normal magnesium ranges:

A

1.6 to 2.6 mg/dL

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5
Q

Processes potassium is involved in:

A
  1. ) Nerve conduction
  2. ) Muscle function
  3. ) Acid-base balance
  4. ) Osmotic pressure
  5. ) Controls rate and force of contraction of the heart (along with calcium and magnesium)
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6
Q

Normal potassium ranges:

A

3.5 to 5.1 mEq/L

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7
Q

Processes phosphorous is involved in:

A
  1. ) Generation of bony tissue
  2. ) Metabolism of glucose and lipids
  3. ) Maintenance of acid-base balance
    - Binds with H+
  4. ) Storage and transfer of energy from one body site to another
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8
Q

Normal phosphorous ranges:

A

2.7 to 4.5 mg/dL

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9
Q

Processes sodium is involved in:

A
  1. ) Regulates osmolality
  2. ) Fluid balance
  3. ) Promotes transmission of nerve impulses to muscles and tissues
  4. ) Helps maintain acid-base balance
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10
Q

Normal sodium ranges:

A

135 to 145 mEq/L

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11
Q

Causes of Hypernatremia:

A
  1. ) Dehydration (e.g. low fluid intake, increased metabolic rate, fever, hyperventilation, infection, excessive diaphoresis, watery diarrhea, diabetes insipidus [DI])
  2. ) Excessive sodium intake
  3. ) Decreased sodium output (e.g. Corticosteroids, Cushing’s Syndrome, Renal failure, Hyperaldosteronism)
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12
Q

S&S of Hypernatremia:

A
  1. ) Irritability, Restlessness, Confusion, Seizures, Lethargy, Coma
  2. ) Thirst, Dry mucous membranes
  3. ) Decreased urinary output
  4. ) Flushed skin
  5. ) Orthostatic hypotension (from fluid loss)
  6. ) Fever
  7. ) Pulmonary edema (if hypervolemia present)
  8. ) Muscle changes: (Early = Muscle twitches, irregular muscle contractions; Late = Skeletal muscle weakness, depressed/absent deep tendon reflexes)
  9. ) Possible edema (if hypervolemia present)
  10. ) Increased urinary specific gravity
  11. ) Increased BP
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13
Q

Interventions for Hypernatremia:

A
  1. ) Monitor cardiovascular, respiratory, neruomuscular, cerebral, renal, and integumentary status
  2. ) Monitory I&O
  3. ) Daily Weight (gain of 2 or more lbs in 4 days must be reported)
  4. ) Assess for edema
  5. ) Monitor for seizure risk
  6. ) Administer IV infusion (sodium-free isotonic fluids, e.g. D5W, followed by 0.45% NS) (if cause is fluid loss)
  7. ) Administer diuretics that promote sodium loss (if cause is inadequate renal excretion of sodium)
  8. ) Restrict sodium and fluid intake
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14
Q

Causes of Hyponatremia:

A
  1. ) Increased sodium excretion (excessive diaphoresis, diuretics, vomiting, diarrhea, wound drainage [especially GI], renal disease, decreased secretion of aldosterone)
  2. ) Inadequate sodium intake (NPO, Low-salt diet)
  3. ) Dilution of serum sodium (Excessive ingestion of hypotonic fluids or irrigation with hypotonic fluids, renal failure, freshwater drowning, SIADH, hyperglycemia, CHF)
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15
Q

S&S of Hyponatremia:

A

From Sodium loss:

  1. ) Irritability, apprehension, confusion
  2. ) Postural hypotension and tachycardia
  3. ) Decreased CVP and decreased jugular vein filling
  4. ) Weight loss and dry mucous membranes
  5. ) Tremors, seizures, and coma
  6. ) Cerebral edema (if <125 mEq/L)

From Fluid gain:

  1. ) Headache, apathy and confusion
  2. ) Weight gain, increased BP, elevated CVP
    * 3.) Hallmark signs: Nausea, vomiting, anorexia, lethargy, and weakness
  3. ) Increased urinary output
  4. ) Cerebral edema
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16
Q

Interventions for Hyponatremia:

A
  1. ) Closely monitor neurologic signs during sodium replacement
  2. ) Daily weights
  3. ) Monitor I&O (loss or gain of 4.4 lb is equal to 2 L of fluid)
  4. ) Check urine color, consistency, and amount
  5. ) Monitor vital signs
  6. ) Assess for intravascular overload during infusion of sodium solutions (tachypnea, tachycardia, and SOB)
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17
Q

Causes of Hyperkalemia:

A
  1. ) Excessive potassium intake (overingestion of K+ containing foods/medications, rapid infusion of potassium-containing IV solutions).
  2. ) Decreased potassium excretion (K+ sparing diuretics, renal failure, adrenal insufficiency [Addison’s disease])
  3. ) Movement of potassium from ICF to ECF (tissue damage, acidosis, hyperuricemia, hypercatabolism)
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18
Q

S&S of Hyperkalemia:

A
  1. ) Muscle cramps/Weakness in lower extremities
  2. ) Diarrhea and hyperactive bowel sounds
  3. ) Numbness and tingling in the extremities
  4. ) Lethargy and fatigue
  5. ) Bradycardia
  6. ) Hypotension
  7. ) Cardiac dysrhythmias (ectopic beats)
  8. ) ECG changes
    - Tall, peaked T waves and flat or absent P waves
    - Shortened QT intervals
    - ST segment depression, prolonged PR interval, widened QRS complex ( >8 mEq/L)
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19
Q

Interventions for Hyperkalemia:

A
  1. ) Monitor cardiovascular, respiratory, neuromuscular, renal, and gastrointestinal status (*Place on cardiac monitor)
  2. ) Discontinue IV potassium and hold oral potassium supplements
  3. ) Initiate potassium-restricted diet
  4. ) Prepare to administer K+ excreting diuretics if renal function is not impaired
  5. ) If renal function IS impaired, administer Kayexalate (a cation exchange resin that promotes gastrointestinal Na+ absorption and K+ excretion).
  6. ) Dialysis (if K+ level critically high)
  7. ) IV administration of hypertonic glucose with regular insulin to move excess K+ into the cells.
  8. ) Monitor renal function
  9. ) Teach pt to avoid foods high in potassium
  10. ) Teach pt to avoid use of salt substitutes or other K+ containing substances.
20
Q

Causes of Hypokalemia:

A
  1. ) Total K+ loss (Excessive use of medications such as diuretics or corticosteroids, increased secretion of aldosterone [such as in Cushing’s syndrome], vomiting, diarrhea, wound drainage [particularly GI], prolonged NG suction, excessive diaphoresis, renal disease impairing reabsorption of K+)
  2. ) Inadequate K+ intake
  3. ) Movement of K+ from ECF to ICF (alkalosis, hyperinsulinism)
  4. ) Dilution of serum K+ (water intoxication, IV therapy with K+ -poor solutions).
21
Q

S&S of Hypokalemia:

A
  1. ) Fatigue and weakness (early sign)
  2. ) Leg cramps (early sign)
  3. ) Weak, irregular pulse
  4. ) Hyperglycemia cause by the impaired release of insulin
  5. ) Decreased GI motility - Nausea, vomiting, and paralytic ileus
  6. ) Bradycardia
  7. ) ECG changes
    - Flattened T wave, eventual prominent U wave
    - ST segment depression, slightly peaked P wave
    - Frequent premature ventricular contractions (PVCs)
    - Inability to concentrate urine and diuresis
22
Q

Interventions for Hypokalemia:

A
  1. ) Monitor cardiovascular, respiratory, neuromuscular, GI, and renal status (*Place on cardiac monitor)
  2. ) Monitor electrolyte values
  3. ) Administer K+ supplements orally, IV
  4. ) Oral potassium supplements (should not be taken on empty stomach)
  5. ) IV administered K+
  6. ) If taking a K+ -losing diuretic, it may be d/c (may be replaced with a K+ -sparing diuretic)
  7. ) Instruct about foods high in K+ content.
23
Q

What is the recommended amount of Potassium to infuse through IV?

A

Recommended: A dilution of no more than 1 mEq/10 mL of solution

  • After adding K+ to the IV solution, rotate and invert the bag to distribute the K+.
  • The MAX recommended infusion rate is 5 to 10 mEq/hr, NEVER to exceed 20 mEq/hr
  • Potassium can cause irritation or phlebitis to blood vessels. Therefore, frequently check the site. Stop the infusion immediately if this occurs.
  • Monitor renal function before administering K+.
24
Q

Causes of Hypocalcemia:

A
  1. ) Inhibition of calcium absorption from the GI tract (inadequate oral intake of calcium, lactose intolerance, malabsorption syndromes [celiac sprue, Crohn’s disease], inadequate intake of vitamin D, End-stage renal disease)
  2. ) Increase calcium excretion (renal failure [polyuric phase], diarrhea, steatorrhea, wound drainage [especially GI]
  3. ) Conditions that decrease the ionized fraction of calcium (hyperproteinemia, alkalosis, medications such as calcium chelators or binders, acute pancreatitis, hyperphosphatemia, immobility, removal or destruction of the parathyroid glands)
25
Q

S&S of Hypocalcemia:

A
  1. ) Muscle spasms or cramps in calf muscles or foot during rest
  2. ) Tetany (numbness and tingling of nose, fingertips, and fingertips [paresthesias])
  3. ) Positive Chvostek sign
  4. ) Positive Toursseau sign
  5. ) Hyperreflexia
  6. ) Laryngospasm
  7. ) Dysrhythmias
    - Ventricular fibrillation
    - Prolonged QT interval >0.48 seconds
    - Elongation of ST segment
  8. ) Cardiac contractility and BP decreases
  9. ) Hypomagnesemia frequently occurs
26
Q

Interventions for Hypocalcemia:

A
  1. ) Monitor cardiovascular, respiratory, neuromuscular, and GI status; Place pt on cardiac monitor
  2. ) Administer calcium supplements orally or calcium IV
    - Warm the solution to body temperature before administering and administer slowly.
  3. ) Administer medications that increase calcium absorption (Vitamin D, Aluminum hydroxide [reduces serum phosphorous, thereby increasing calcium levels]).
  4. ) Reduce environmental stimuli
  5. ) Initiate seizure precautions
  6. )Move the client carefully, and monitor for signs of pathological Fx
  7. ) Keep 10% calcium gluconate available for treatment of acute calcium deficit
  8. ) Instruct the client to consume foods high in calcium.
27
Q

Causes of Hypercalcemia:

A
  1. ) Increased calcium absorption (Excessive oral intake or calcium, Excessive oral intake of vitamin D)
  2. ) Decreased calcium excretion (renal failure, use of thiazide diuretics)
  3. ) Increased bone resorption of calcium (hyperparathyroidism, hyperthyroidism, malignancy [bone destruction from metastatic tumors], immobility, use of glucocorticoids)
  4. ) Hemoconcentration (dehydration, use of lithium, adrenal insufficiency)
28
Q

S&S of Hypercalcemia:

A
  1. ) Anorexia, nausea, and fatigue
  2. ) Constipation
  3. ) Polyuria
  4. ) Dehydration
  5. ) ECG changes
    • Shortened QT interval and ST segment
    • Depressed T wave
    • Bradycardia
    • Heart block
29
Q

Interventions for Hypercalcemia:

A
  1. ) Monitor cardiovascular, respiratory, neuromuscular, renal, and GI status; Place pt on cardiac monitor.
  2. ) D/C IV infusions of solutions containing calcium and oral medications containing calcium or Vitamin D.
  3. ) D/C thiazide diuretics and replace with diuretics that enhance calcium excretion
  4. ) Administer prescribed medications that inhibit calcium resorption from the bone (such as phosphorous, calcitonin [Calcimar], bisphosphonates, and prostaglandin synthesis inhibitors [aspirin, NSAIDS])
  5. ) Dialysis (if severe)
  6. ) Monitor for urinary stone development
  7. ) Instruct pt to avoid foods high in calcium.
  8. ) Encourage increased oral fluid intake
  9. ) Assess for changes in neurologic status q4h.
  10. ) Encourage increased mobility
30
Q

Causes of Hypomagnesemia:

A
  1. ) Insufficient magnesium intake (malnutrition/starvation, vomiting or diarrhea, malabsorption syndrome, celiac disease, Crohn’s disease)
  2. ) Increased magnesium secretion (medications such as diuretics, chronic alcoholism)
  3. ) Intracellular movement of magnesium (hyperglycemia, insulin administration, sepsis)
31
Q

S&S of Hypomagnesemia:

A
  1. ) Increased neruomuscular ability (secondary to hypocalcemia)
    • Leg and foot cramping
    • Tremors and hyperactive deep tendon reflexes
    • Twitching (positive Chvostek and Trousseau signs)
  2. ) Cardiac dysrhythmias (atrial fibrillation and frequent PVCs)
  3. ) Dysphagia
  4. ) Paralytic ileus
32
Q

Interventions for Hypomagnesemia:

A
  1. ) Review pt’s medications for causes of low magnesium
  2. ) Assess for dysphagia
  3. ) Assess lab values for presence of hypokalemia and hypocalcemia
  4. ) Instruct about magnesium-rich foods
  5. ) Possible d/c of diuretics
  6. ) Replace magnesium either orally or parenterally.
    • For IV, use magnesium sulfate
    • Administer at a slow rate (<150 mg/min)
    • *Never give magnesium as an IV bolus, may cause cardiac arrest
  7. ) Seizure precautions
33
Q

Causes of Hypermagnesemia:

A
  1. ) Increased magnesium intake (magnesium-containing antacids and laxatives, excessive administration of magnesium intravenously)
  2. ) Decreased renal excretion of magnesium as a result of renal insufficiency
34
Q

S&S of Hypermagnesemia:

A
  1. ) Muscular weakness, lethargy, drowsiness
  2. ) Nausea, vomiting, and diaphoresis
  3. ) hypotension, bradypnea, and bradycardia
  4. ) Decreased deep tendon reflexes
  5. ) Decreased LOC
35
Q

Interventions for Hypermagnesemia:

A
  1. ) Assess neurologic status for mental status and reflex changes.
  2. ) Closely monitor I&O and kidney function
  3. ) Monitor vital signs; watch for bradycardia and hypotension
  4. ) Provide a list of foods and drugs containing magnesium that should be avoided
  5. ) Continuous cardiac monitoring for pts with elevated levels
    • Report a prolonged QT interval, a wide QRS complex, or presence of an atrioventricular (AV) block.
  6. ) Carefully monitor serum magnesium levels in obstetric clients receiving magenium sulfate for the Tx of preeclampsia and preterm labor.
  7. ) Evaluate the newborn’s magnesium levels if the mother received magnesium sulfate immediately before delivery.
  8. ) Administer IV solution containing calcium salts (calcium gluconate) for severe hypermagnesemia.
  9. ) Administer diuretics for clients with normal renal function
  10. ) D/C use of medications containing magnesium
  11. ) Dialysis (if have renal failure)
36
Q

Causes of Hypophosphatemia:

A
  1. ) Insufficient phosphorus intake (malnutrition, starvation)
  2. ) Increased phosphorus excretion (hyperparathyroidism, malignancy, use of magnesium-based or aluminum hydroxide-based antacids)
  3. ) Intracellular shift (hyperglycemia, respiratory alkalosis).
37
Q

S&S of Hypophosphatemia:

A
  1. ) Neurolgic symptoms:
    • Acute = confusion, seizures, coma
    • Chronic = memory loss, lethargy
  2. ) Decreased strength:
    • Acute = difficulty speaking, weakness of respiratory muscles
    • Chronic = lethargy, weakness, joint stiffness
  3. ) Decreased myocardial contractility with decreased cardiac output and BP

*Acute symptoms result from a sudden decrease in phosphate; chronic symptoms occur when the loss is gradual

38
Q

Interventions for Hypophatemia:

A
  1. ) Assess changes in LOC and orientation
    • Teach neurologic changes are temporary
  2. ) Closely monitor rate of infusion of IV phosphorous
  3. ) Monitor for sudden hypocalcemia, secondary to calcium phosphate binding, as a complication of IV phosphorus administration.
  4. ) Cardiac monitoring during infusion of phosphorus (because of increased risk of dysrhythmias).
  5. ) Assess for hypoxemia (because pts on ventilators are at higher risk for developing hypophosphatemia)
  6. ) Evaluate mobility and the presence of bone pain.
  7. ) (If Mild) Increase intake of foods high in phosphorus (dairy products).
  8. ) (If Moderate) Treat with oral phosphorus supplements (Neutra-Phos)
  9. ) (If Severe) Treat with IV infusion of phosphate.
39
Q

Causes of Hyperphosphatemia:

A
  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. ) Hypoparathyroidism
40
Q

S&S of Hyperphosphatemia:

A

Reciprocal relationship to calcium exists. High phosphorus level relates to a low calcium level, which leads to hypocalcemia

  1. ) Tetany and twitching of muscles, especially of the hands and feet
  2. ) Tingling, numbness, and cramps
  3. ) Nervousness, irritability, and apprehension
  4. ) Anorexia, nausea, and vomiting
  5. ) Tachycardia, dysrhythmias, and conduction problems
41
Q

Interventions for Hyperphosphatemia:

A
  1. ) Assess for constipation (caused by phosphate binders)
  2. ) Assess for signs of hypocalcemia (tetany)
  3. ) Monitor serum phosphate and calcium levels
  4. ) Teach client to limit foods and substances (e.g. laxatives, enemas) high in phosphate
42
Q

Common food sources for Sodium:

A

Bacon, Butter, Canned food, Cheese, Frankfurters, Ketchup, Lunch Meat, Milk, Mustard, Processed food, Snack food, Soy sauce, Table salt, White and whole-wheat bread

43
Q

Common food sources for Potassium:

A

Avocado, Bananas, Cantalope, Carrots, Fish, Mushrooms, Oranges, Potatoes, Pork, Beef, Veal, Raisin, Spinach, Strawberries, Tomatoes

44
Q

Common food sources for Calcium:

A

Cheese, Collard greens, Milk and soy milk, Rhubarb, Sardines, Spinach, Tofu, Yogurt

45
Q

Common food sources for Magnesium:

A

Avocado, Canned white tuna, Cauliflower, Green leafy vegetables (e.g. spinach, broccoli), Milk, Oatmeal, Peanut butter, Peas, Pork, Beef, Chicken, Potatoes, Raisins, Yogurt

46
Q

Common food sources for Phosphorus:

A

Fish, Organ meats, Nuts, Pork, Beef, Chicken, Whole-grain breads and cereals

Adam G. (12 decks)

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