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10-23-23 Fluids and electrolytes (1)

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Fluid Compartments of the Body
Fig. 16-2
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1
Electrolytes
● Substances whose molecules dissociate into ions
when placed in water
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Cations: positively charged
Anions: negatively charged
● Concentration of electrolytes is expressed in
milliequivalents (mEq)/L
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2
Electrolyte Composition
● ICF
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Prevalent cation is K+
Prevalent anion is PO43−
● ECF
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Prevalent cation is Na+
Prevalent anion is Cl−
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3
Concentrations of Cations and Anions in ICF and Plasma
Fig. 16-3
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4
Sodium-Potassium Pump
Fig. 16-5
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5
Osmotic Movement of Fluids
● The osmolality of the fluid surrounding cells affects
them
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Isotonic—same as cell interior
Hypotonic—solutes less concentrated than in cells/ hypoosmolar
Hypertonic—solutes more concentrated than in cells/ hyperosmolar
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6
Regulation of Water Balance
(1 of 5)
● Hypothalamic-pituitary regulation
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Osmoreceptors in hypothalamus sense fluid deficit or increase
Deficit stimulates thirst and antidiuretic hormone (ADH) release
Decreased plasma osmolality (water excess) suppresses ADH release
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7
Regulation of Water Balance
(2 of 5)
● Renal regulation
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Primary organs for regulating fluid and electrolyte balance
Adjusting urine volume
■ Selective reabsorption of water and electrolytes
■ Renal tubules are sites of action of ADH and aldosterone
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8
Regulation of Water Balance
(3 of 5)
● Adrenal cortical regulation
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Releases hormones to regulate water and electrolytes
Glucocorticoids
■ Cortisol
Mineralocorticoids
■ Aldosterone
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9
Regulation of Water Balance
(4 of 5)
● Cardiac regulation
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Natriuretic peptides are antagonists to the RAAS
Hormones made by cardiomyocytes in response to increased atrial pressure
They suppress secretion of aldosterone, renin, and ADH to decrease blood volume and pressure
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10
Regulation of Water Balance
(5 of 5)
● GI regulation
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Oral intake accounts for most water
Small amounts of water are eliminated by GI tract in feces
Diarrhea and vomiting can lead to significant fluid and electrolyte loss
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11
Gerontologic Considerations
● Structural changes in kidneys decrease ability to conserve water
● Hormonal changes include a decrease in renin and aldosterone and increase in
ADH and ANP
● Subcutaneous tissue loss leads to increased moisture lost
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12
Fluid and Electrolyte Imbalances
● Directly caused by illness or disease (burns or heart failure)
● Result of therapeutic measures
(colonoscopy preparation, diuretics)
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13
Sodium
● Imbalances typically associated with parallel changes
in osmolality
● Plays a major role in
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ECF volume and concentration
Generating and transmitting nerve impulses
Muscle contractility
Regulating acid-base balance
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14
Hypernatremia
● High serum sodium may occur with inadequate water intake, excess water loss
or sodium gain
● Causes hyperosmolality leading to cellular dehydration
● Primary protection is thirst
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15
Hypernatremia: Causes
● Model
● Medications, meals
● Osmotic diuretics
● Diabetes insipidus
● Excessive water loss
● Low water intake
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Hypernatremia
● Manifestations
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Thirst
Changes in mental status, ranging from drowsiness, restlessness, confusion and lethargy to
seizures and coma
Symptoms of fluid volume deficit
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17
Hypernatremia: Signs & Symptoms
● Fried
● Fever (low grade), flushed skin
● Restless and irritable
● Increased fluid retention and increased BP
● Edema (peripheral and pitting)
● Decreased urinary output, dry mouth
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Nursing Diagnoses
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Electrolyte imbalance
Fluid imbalance
Risk for injury
Potential complication: Seizures and coma
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19
Nursing Implementation
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Treat underlying cause
Primary water deficit—replace fluid orally or IV with isotonic or hypotonic fluids
Excess sodium—dilute with sodium-free IV fluids and promote sodium excretion with diuretics
Reduce level gradually
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20
Hyponatremia
● Results from loss of sodium-containing fluids and/or
from water excess
● Clinical manifestations
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Mild—headache, irritability, difficulty concentrating.
More severe—confusion, vomiting, seizures, coma
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21
Hyponatremia: Signs & Symptoms
●
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Salt Loss
Stupor and coma
Anorexia, N&V
Lethargy
Tendon reflexes decreased
Limp muscles (weakness)
Orthostatic hypotension
Seizures and headaches
Stomach cramping
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Nursing Implementation
If the cause is water excess,
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Fluid restriction may be only treatment
Loop diuretics and demeclocycline
Severe symptoms (seizures)
■
Give
small amount of IV hypertonic saline solution (3%
NaCl)
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23
Nursing Implementation
● If the cause is abnormal fluid loss,
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Fluid replacement with isotonic sodium-containing solution
Encouraging oral intake
Withholding diuretics
Drugs that block vasopressin (ADH)
■ Convaptan (Vaprisol)
■ Tolvaptan (Samsca)
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24
Chloride
● Primary anion in ECF (nl: 95-108 mEq/L)
● Combines w/Na to create neutrality
● Assists in reabsorption of Na in kidney
● Essential for reabsorbing hydrogen ion to buffer alkalosis
● Lost through vomiting, excessive sweating
● Normally excreted in urine
Potassium (1 of 2)
● Major ICF cation
● Necessary for
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Resting membrane potential of nerve and muscle cells
Cellular growth
Maintenance of cardiac rhythms
Acid-base balance
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26
Potassium (2 of 2)
● Sources
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Protein-rich foods
Fruits and vegetables
Salt substitutes
Potassium medications (PO, IV)
Stored blood
● Regulated by kidneys
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27
Hyperkalemia
● High serum potassium caused by
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Impaired renal excretion
Shift from ICF to ECF
Massive intake of potassium
Some drugs
● Most common in renal failure
● Common
in massive cell destruction
– Burn, crush injury, tumor lysis
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28
Hyperkalemia: Causes
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Machine
Medications - ACE inhibitors, NSAIDS
Acidosis – metabolic & respiratory
Cellular destruction – burns, traumatic injury
Hypoaldosteronism, hemolysis
Intake – excessive
Nephrons, renal failure
Excretion – impaired
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Hyperkalemia
● Manifestations
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Dysrhythmias
Fatigue, confusion
Tetany, muscle cramps
Weak or paralyzed skeletal muscles
Abdominal cramping or diarrhea
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30
Hyperkalemia: Manifestations
● Murder
● Muscle weakness
● Urine, oliguria, anuria
● Respiratory distress
● Decreased cardiac contractility
● ECG changes
● Reflexes, hyperreflexia, or areflexia (flaccid)
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ECG Effects of Hyperkalemia
Fig. 16-14
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32
Potassium Imbalances: Hyperkalemia
Clinical manifestations
Hyperkalemia in Acidosis
• As blood [H+] rises in
cases of acidosis, more
H+ ions are pumped
intracellularly in
exchange for K+ ions
that are pumped
extracellularly to
maintain electrical
neutrality.
Nursing Implementation
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Stop oral and parenteral K+ intake
Increase K+ excretion (diuretics, dialysis, Veltessa and/or Kayexalate)
Force K+ from ECF to ICF by IV insulin with dextrose and a β-adrenergic agonist or sodium
bicarbonate
Stabilize cardiac cell membrane by administering calcium gluconate IV
Use continuous ECG monitoring
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35
Nursing Implication
Hyperkalemia
● CBIGKD “see big kid”
● Calcium chloride or gluconate
● Bicarbonate
● Insulin
● Glucose
● Kayexalate
● Dialysis/Diuretics
Hypokalemia (1 of 2)
● Low serum potassium caused by
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Increased loss of K+ via the kidneys or gastrointestinal tract
Increased shift of K+ from ECF to ICF
Dietary K+ deficiency (rare)
Renal losses from diuresis
Magnesium deficiency
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37
Hypokalemia (2 of 2)
● Manifestations
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Cardiac most serious
Skeletal muscle weakness (legs)
Weakness of respiratory muscles
Decreased GI motility
Hyperglycemia
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38
Hypokalemia: Signs & Symptoms
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6 L’s
Lethargy
Leg cramps
Limp muscles
Low, shallow respirations
Lethal cardiac dysrhythmias
Lots of urine (polyuria)
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ECG Effects of Hypokalemia
Fig. 16-14
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40
Potassium Imbalances
Hypokalemia
● Clinical Manifestations:
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“SUCTION”
● Skeletal muscle weakness
● U wave
● Constipation
● Toxic effects of digoxin
● Irregular, weak pulse
● Orthostatic hypotension
● Numbness (paresthesia)
Nursing Implementation
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KCl supplements orally or IV
Always dilute IV KCl
NEVER give KCl via IV push or as
a bolus
Should not exceed 10 mEq/hr
Use an infusion pump
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42
ECG changes associated with alterations in potassium status
Calcium
● Functions
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Formation of teeth and bone
Blood clotting
Transmission of nerve impulses
Myocardial contractions
Muscle contractions
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44
Calcium
● Obtained from dietary intake
● Need vitamin D to absorb
● Present in bones and plasma
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Ionized calcium is biologically active
● Changes in pH and serum albumin affect levels
● Inverse relationship with phosphorus
● Blocks sodium transport
● Stabilizes cell membrane
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45
Calcium
● Balance controlled by
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Parathyroid hormone
■ Increases bone resorption, GI absorption, and renal
tubule reabsorption of calcium
Calcitonin
■ Increases calcium deposition into bone, increases renal
calcium excretion, and decreases GI absorption
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46
Calcium
●
Balance controlled by
–
–
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Parathyroid hormone
Calcitonin
Vitamin D
Hypercalcemia (1 of 2)
● High levels of serum calcium
caused by
○ Hyperparathyroidism (two-thirds
of cases)
– Malignancy
– Vitamin D overdose
– Prolonged immobilization
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48
Hypercalcemia (2 of 2) - Manifestations
● Dec. excitability
– Skeletal muscle
– Cardiac muscle
– Nervous system
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Fatigue, lethargy, weakness, confusion
Hallucinations, seizures, coma
Dysrhythmias
Bone pain, fractures, nephrolithiasis
Polyuria, dehydration
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49
Hypercalcemia: Signs & Symptoms
● Groans, Moans, Bones, Stones, and Overtones
● Groans: constipation
● Moans: pain – joint aches
● Bones: loss of calcium from bones, bone metastasis
● Stones: kidney stones
● Overtones: psychiatric overtones – depression, confusion
●
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Nursing Implementation
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Excretion of Ca with loop diuretic
Low calcium diet
Increased weight-bearing activity
Increased fluid intake
Hydration with isotonic saline infusion
Bisphosphonates—gold standard
Synthetic calcitonin (IM or SC)
Mobilization
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51
Hypocalcemia (1 of 2)
● Low serum Ca levels caused by
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Decreased production of PTH
Multiple blood transfusions
Alkalosis
Increased calcium loss
Acute pancreatitis
Multiple blood transfusions
Decreased intake
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52
Hypocalcemia (2 of 2)
● Manifestations
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Positive Trousseau’s or Chvostek’s sign
Laryngeal stridor
Dysphagia
Numbness and tingling around the mouth or in the extremities
Dysrhythmias
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53
Hypocalcemia: Signs & Symptoms
● Cats
● Convulsions
● Arrhythmias
● Tetany
● Spasms and stridor
●
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Tests for Hypocalcemia
Fig. 16-15
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55
Nursing Implementation
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Treat cause
Calcium and Vitamin D supplements
Not IM to avoid local reactions
IV calcium gluconate
Rebreathe into paper bag
Treat pain and anxiety to prevent hyperventilation-induced respiratory alkalosis
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56
Phosphate
● Primary anion in ICF
● Essential to function of muscle, red blood cells, and nervous system
● Deposited with calcium for bone and tooth structure
● Involved in acid-base buffering system, ATP production, cellular uptake of
glucose, and metabolism of carbohydrates, proteins, and fats
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57
Phosphate
● Serum levels controlled by parathyroid hormone
● Maintenance requires adequate renal functioning
● Reciprocal relationship with calcium
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58
Hyperphosphatemia (1 of 3)
● High serum PO43− caused by
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Acute kidney injury or chronic kidney disease
Chemotherapy
Excess intake of phosphate or vitamin D
Hypoparathyroidism
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59
Hyperphosphatemia (2 of 3)
● Manifestations
○ Tetany, muscle cramps, paresthesias,
hypotension, dysrhythmias, seizures
(hypocalcemia)
○ Calcified deposition in soft tissue such as
joints, arteries, skin, kidneys, and corneas
(cause organ dysfunction)
○ Neuromuscular irritability and tetany (hypocalcemia)
○ Calcified
deposition in soft tissue such as joints, arteries, skin, kidneys, and corneas (can cause
organ dysfunction)
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60
Hyperphosphatemia (3 of 3)
● Management
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Identify and treat underlying cause
Restrict intake of foods and fluids containing phosphorus
Oral phosphate-binding agents
Hemodialysis
Volume expansion and forced diuresis
Correct any hypocalcemia
Adequate hydration and correction of hypocalcemic conditions
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61
Hypophosphatemia (1 of 3)
● Low serum PO43− caused by
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Malnourishment/malabsorption
Diarrhea
Use of phosphate-binding antacids
Inadequate replacement during parenteral nutrition
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62
Hypophosphatemia (2 of 3)
● Manifestations
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CNS depression
Muscle weakness and pain
Respiratory and heart failure
Rickets and osteomalacia
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63
Hypophosphatemia (3 of 3)
● Management
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Oral supplementation
Ingestion of foods high in phosphorus
IV administration of sodium or potassium phosphate
■ Monitor serum calcium and phosphorus levels every 6 to
12 hours
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64
Self Assessment
● The nurse anticipates that the patient with hyperphosphatemia secondary to
renal failure will require
a.
calcium supplements.
b.
potassium supplements.
c.
magnesium supplements.
d.
fluid replacement therapy.
Magnesium (1 of 2)
● Second most abundant intracellular cation
● Essential for proper neuromuscular function
● Levels controlled by kidneys
● Cofactor in enzyme for metabolism of carbohydrates
● Required for DNA and protein synthesis
● Blood glucose control
● BP regulation
● Needed for ATP production
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66
Magnesium (2 of 2)
● Acts directly on myoneural junction
● Important for normal cardiac function
● 50% to 60% contained in bone
○
● Absorbed in GI tract
● Excreted by kidneys
Only 1% in ECF
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67
Hypermagnesemia (1 of 3)
● High serum Mg caused by
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Increased intake of products containing magnesium when renal insufficiency or failure is present
Excess IV magnesium administration
Advanced CKD
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68
Hypermagnesemia (2 of 3)
● Manifestations
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Hypotension, facial flushing
Lethargy
Nausea and vomiting
Impaired deep tendon reflexes
Muscle paralysis
Respiratory and cardiac arrest
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69
Hypermagnesemia (3 of 3)
● Management
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Prevention first—restrict magnesium intake in high-risk patients
IV CaCl or calcium gluconate if symptomatic
Fluids and IV furosemide to promote urinary excretion
Dialysis
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70
Hypomagnesemia
● Low serum Mg caused by
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Prolonged fasting or starvation
Chronic alcoholism
Fluid loss from GI tract
Prolonged parenteral nutrition without supplementation
Diuretics, proton-pump inhibitors
Hyperglycemic osmotic diuresis
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71
Hypomagnesemia
● Manifestations
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Resembles hypocalcemia
■ Muscle cramps, tremors
■ Hyperactive deep tendon reflexes
■ Chvostek’s and Trousseau’s signs
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■ Confusion, vertigo, seizures
Dysrhythmias
Corresponding hypocalcemia and hypokalemia
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72
Hypomagnesemia
Manifestations
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3 T’s
Tremors
Twitching
Tetany
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STARVED
SZ
Tetany
Anorexia & Arrhythmias
Rapid HR
Vomiting
Emotional lability
DTRs (hyperactive)
Hypomagnesemia
● Management
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Treat underlying cause
Oral supplements
Increase dietary intake
Parenteral IV or IM magnesium when severe
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74
Audience Response Question (1 of 2)
A patient is admitted with renal failure and an arterial blood pH level of 7.29. Which
lab result would the nurse expect?
a. Serum sodium 138 mEq/L
b. Serum glucose 145 mg/dL
c. Serum potassium 5.9 mEq/L
d. Serum magnesium 0.4 mg/dL
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75
Audience Response Question (2 of 2)
Answer: C
Serum potassium 5.9 mEq/L
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76
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