Chapter 16 Fluid Electrolyte and Acid Base Imbalances Flashcards
1
Q
normal sodium ranges
A
135 to 145 mEq/L
2
Q
normal BUN ranges
A
7-20 mg/dL
3
Q
HCT normal levels
A
35-47% for women and 39-50% for men
4
Q
Many diseases and their treatments affect fluid and electrolyte balance. For example, a patient with metastatic colon cancer may develop?
A
hypercalcemia because of bone destruction from tumor invasion.
5
Q
Chemotherapy used to treat the cancer may result in nausea and vomiting and, subsequently?
A
dehydration and acid-base imbalances
6
Q
When correcting dehydration with IV fluids, the patient requires?
A
close monitoring to prevent fluid overload.
7
Q
The body is composed primarily of water. It accounts for about _______ of body weight in the adult.
A
50% to 60%
8
Q
Water content varies with?
A
body mass, gender, and age
9
Q
Lean body mass has a higher percentage of?
A
water, while adipose tissue has a lesser percentage of water.
10
Q
water content in women
A
Women generally have a lower percentage of body water because they tend to have less lean body mass than men
11
Q
Water content in older adults
A
Older adults also tend to have less lean body mass, resulting in a lower percentage of body water when compared to younger adults. In older adults, body water content 271averages 45% to 50% of body weight. This places them at a higher risk for fluid-related problems than young adults.
12
Q
The two fluid compartments in the body are the?
A
intracellular space (inside the cells) and the extracellular space (outside the cells)
13
Q
About two thirds of the body water is located?
A
within cells and is termed intracellular fluid (ICF). ICF makes up about 40% of body weight of an adult.
14
Q
The two main compartments containing ECF are the?
A
interstitial fluid, or the fluid in the spaces between cells, and the intravascular fluid or plasma, the liquid part of blood. Other ECF compartments include lymph and transcellular fluids.
15
Q
Electrolytes are substances whose?
A
molecules dissociate, or split, into ions when placed in water. Ions are electrically charged particles.
16
Q
Cations are?
A
positively charged ions. Examples include sodium (Na+), potassium (K+), calcium (Ca2+), and magnesium (Mg2+) ions
17
Q
Anions are?
A
negatively charged ions. Examples include bicarbonate (HCO3−), chloride (Cl−), and phosphate (PO43−) ions. Most proteins bear a negative charge and are thus anions.
18
Q
Electrolyte composition varies between ECF and ICF. The overall concentration of electrolytes is nearly the same in the two compartments. However, concentrations of specific ions differ greatly.
1) In ECF
2) In ICF
A
1) ECF the main cation is sodium, with small amounts of potassium, calcium, and magnesium. The primary ECF anion is chloride, with small amounts of bicarbonate, sulfate, and phosphate anions.
2) ICF the most prevalent cation is potassium, with small amounts of magnesium and sodium. The prevalent ICF anion is phosphate, with some protein and a small amount of bicarbonate. See Table 16-1 for normal serum electrolyte values.
19
Q
Bicarbonate (HCO3−) Levels
A
22-26 mEq/L (22-26 mmol/L)
20
Q
Chloride (Cl−) Levels
A
96-106 mEq/L (96-106 mmol/L)
21
Q
Phosphate (PO43−) Levels
A
2.4-4.4 mg/dL (0.78-1.42 mmol/L)
22
Q
Potassium (K+) Levels
A
3.5-5.0 mEq/L (3.5-5.0 mmol/L)
23
Q
Magnesium (Mg2+) Levels
A
1.5-2.5 mEq/L (0.75-1.25 mmol/L)
24
Q
Sodium (Na+) Levels
A
135-145 mEq/L (135-145 mmol/L)
25
Calcium (Ca2+) (total) Levels
8.6-10.2 mg/dL (2.15-2.55 mmol/L)
26
Calcium (ionized) Levels
4.6-5.3 mg/dL (1.16-1.32 mmol/L)
27
The movement of electrolytes and water between ICF and ECF to maintain homeostasis involves many different processes, including simple diffusion, facilitated diffusion, and active transport. Water moves as driven by two forces:
hydrostatic pressure and osmotic pressure.
28
Diffusion is the movement of molecules from?
an area of high concentration to low concentration. Net movement of molecules stops when the concentrations are equal in both areas. It occurs in liquids, gases, and solids. Simple diffusion requires no external energy.
29
Facilitated diffusion involves the use of a protein carrier in the cell membrane. The protein carrier combines with a molecule, especially one too large to pass easily through the cell membrane, and assists in moving the molecule across the membrane from?
an area of high to low concentration. Like simple diffusion, facilitated diffusion is passive and requires no energy. An example of facilitated diffusion is glucose transport into the cell. The large glucose molecule must combine with a carrier molecule to be able to cross the cell membrane and enter most cells.
30
Active transport is a process in which molecules move?
Against the concentration gradient. External energy is required for this process. An example is the sodium-potassium pump. The concentrations of sodium and potassium differ greatly intracellularly and extracellularly. To maintain this concentration difference, the cell uses active transport to move sodium out of the cell and potassium into the cell. The energy source for this movement is adenosine triphosphate (ATP), which is made in the cell's mitochondria.
31
Osmosis is the movement of water “down” a concentration gradient, that is, from a region of?
low solute concentration to one of high solute
* requires no outside energy sources
* stops when concentration differences disappear or when hydrostatic pressure builds and opposes any further movement of water
- Imagine a chamber with two compartments separated by a semipermeable membrane, one that allows only the movement of water. If you add albumin to one side, water will move from the less concentrated side (has more water) to the more concentrated side of the chamber water (has less water) until the concentrations are equal.
32
Whenever dissolved substances are contained in a space with a semipermeable membrane, they can pull water into the space by osmosis. The concentration of the solution determines the strength of the osmotic pull. The higher the concentration, the?
greater a solution's pull, or osmotic pressure
33
Osmotic pressure
* Amount of pressure required to stop osmotic flow of water
| * Determined by concentration of solutes in solution
34
Fluid tonicity
Isotonic, hypotonic, hypertonic
35
The osmolality of the fluid surrounding cells affects them. Fluids with the same osmolality as the cell interior are termed?
isotonic. Normally, ECF and ICF are isotonic to one another, so no net movement of water occurs.
36
Changes in the osmolality of ECF alter the volume of cells. Solutions in which the solutes are less concentrated than in the cells are termed?
hypotonic (hypoosmolar). If a cell is surrounded by hypotonic fluid, water moves into the cell, causing it to swell and possibly to burst.
37
Fluids with solutes more concentrated than in cells, or an increased osmolality, are termed?
hypertonic (hyperosmolar). If hypertonic fluid surrounds a cell, water leaves the cell to dilute ECF; the cell shrinks and may eventually die
38
Hydrostatic pressure is the?
force of fluid in a compartment pushing against a cell membrane or vessel wall. In the blood vessels, hydrostatic pressure is the BP generated by the contraction of the heart. Hydrostatic pressure in the vascular system gradually decreases as the blood moves through the arteries until it is about 30 mm Hg in the capillary bed. At the capillary level, hydrostatic pressure is the major force that pushes water out of the vascular system and into the interstitial space.
39
Oncotic pressure (colloidal osmotic pressure) is the osmotic pressure caused by plasma colloids in solution. The major colloids in the vascular system contributing to osmotic pressure are proteins, such as albumin. Plasma has?
substantial amounts of protein, while the interstitial space has very little. The plasma protein molecules attract water, pulling fluid from the tissue space to the vascular space. Under normal conditions, plasma oncotic pressure is about 25 mm Hg. The small amount of protein found in the interstitial space exerts an oncotic pressure of about 1 mm Hg
40
Osmotic pressure caused by plasma proteins
Oncotic pressure
41
Blood pressure generated by heart contraction
Hydrostatic pressure
42
As plasma flows through the capillary bed, four factors determine if fluid moves out of the capillary and into the interstitial space or if fluid moves back into the capillary from the interstitial space. The amount and direction of movement are determined by the interaction of
(1) capillary hydrostatic pressure
(2) plasma oncotic pressure
(3) interstitial hydrostatic pressure
(4) interstitial oncotic pressure
43
Capillary hydrostatic pressure and interstitial oncotic pressure move water?
out of the capillaries
44
Plasma oncotic pressure and interstitial hydrostatic pressure move fluid?
into the capillaries
45
At the arterial end of the capillary?
| At the venous end of the capillary?
- At the arterial end of the capillary, capillary hydrostatic pressure exceeds plasma oncotic pressure, and fluid moves into the interstitial space
- At the venous end of the capillary, the capillary hydrostatic pressure is lower than plasma oncotic pressure, drawing fluid back into the capillary by the oncotic pressure created by plasma proteins
46
Fluid Shifts
| If capillary or interstitial pressures change, fluid may?
abnormally shift from one compartment to another, resulting in edema or dehydration.
47
Shifts of Plasma to Interstitial Fluid.
| Edema, an accumulation of fluid in the interstitial space, occurs if?
venous hydrostatic pressure rises, plasma oncotic pressure decreases, or interstitial oncotic pressure rises. Edema may also develop if an obstruction of lymphatic outflow causes decreased removal of interstitial fluid.
48
Elevation of Venous Hydrostatic Pressure.
Increasing the pressure at the venous end of the capillary inhibits fluid movement back into the capillary, which results in edema. Causes of increased venous pressure include?
fluid overload, heart failure, liver failure, obstruction of venous return to the heart (e.g., tourniquets, restrictive clothing, venous thrombosis), and venous insufficiency (e.g., varicose veins)
49
Decrease in Plasma Oncotic Pressure.
Fluid remains in the interstitial space if the plasma oncotic pressure is too low to draw fluid back into the capillary. Low plasma protein content decreases oncotic pressure. This can result from?
excessive protein loss (renal disorders), deficient protein synthesis (liver disease), and deficient protein intake (malnutrition).
50
Plasma-to-interstitial fluid shift results in edema
| Interstitial fluid to plasma decreases edema
.
51
Elevation of Interstitial Oncotic Pressure.
Trauma, burns, and inflammation can damage capillary walls and allow plasma proteins to accumulate in the interstitial space. This?
increases interstitial oncotic pressure, draws fluid into the interstitial space, and holds it there.
52
Shifts of Interstitial Fluid to Plasma.
An increase in the plasma osmotic or oncotic pressure draws fluid into the plasma from the interstitial space. This could happen with administration of?
colloids, dextran, mannitol, or hypertonic solutions. Increasing the tissue hydrostatic pressure is another way of causing a shift of fluid into plasma. Wearing elastic compression gradient stockings or hose to decrease peripheral edema is a therapeutic application of this effect.
53
Fluid spacing is a term used to describe the distribution of body water.
1) First spacing describes?
2) Second spacing refers to an?
3) Third spacing occurs when?
1) First spacing describes the normal distribution of fluid in ICF and ECF compartments.
2) Second spacing refers to an abnormal accumulation of interstitial fluid (i.e., edema).
3) Third spacing occurs when excess fluid collects in the nonfunctional area between cells. This fluid is trapped where it is difficult or impossible for it to move back into the cells or blood vessels. Third spacing occurs with ascites; fluid leaking into the abdominal cavity with peritonitis or pancreatitis; and edema associated with burns, trauma, or sepsis.
54
Normal distribution
First spacing
55
Abnormal (edema)
Second spacing
56
Fluid accumulation in part of body where it is not easily exchanged with ECF
Third spacing
57
A number of factors are involved in maintaining the finely tuned balance among water intake, use, and excretion. For proper fluid balance, an average healthy adult requires a daily water intake between?
2000 and 3000 mL
This amount replaces what is lost from the body in urinary output and insensible losses. Oral fluid intake accounts for most of the water intake. Water intake also includes water from food metabolism and water present in solid foods.
58
```
Normal fluid balance in adults
Intake
Fluids
Solid food
Water from oxidation
Total
Output
Insensible loss (skin and lungs)
In feces
Urine
Total
```
```
Intake
Fluids 1200 mL
Solid food 1000 mL
Water from oxidation 300 mL
Total 2500 mL
Output
Insensible loss (skin and lungs) 900 mL
In feces 100 mL
Urine 1500 mL
Total 2500 mL
```
59
Insensible water loss, which is invisible vaporization from the lungs and skin, assists in regulating body temperature. Accelerated body metabolism, which occurs with increased body temperature and exercise, increases the amount of water lost and may result in the need for additional water replacement.
Do not confuse water loss through the skin with the vaporization of water excreted by sweat glands. Insensible perspiration causes only water loss. Excessive sweating (sensible perspiration) caused by exercise, fever, or high environmental temperatures may lead to?
large losses of water and electrolytes.
60
Hypothalamic-pituitary regulation
- Osmoreceptors in hypothalamus sense fluid deficit or increase
- Deficit stimulates thirst and antidiuretic hormone (ADH) release
- Decreased plasma osmolality (water excess) suppresses ADH release
61
The primary function of the kidneys is to regulate?
fluid and electrolyte balance by adjusting urine volume and the excretion of most electrolytes
62
Regulation of water balance: Renal regulation
- 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
63
Regulation of water balance: Adrenal Cortical Regulation
Glucocorticoids and mineralocorticoids secreted by the adrenal cortex help regulate water and electrolyte balance.
- The glucocorticoids (e.g., cortisol) primarily have what effect ?
- the mineralocorticoids (e.g., aldosterone) enhance?
- The glucocorticoids (e.g., cortisol) primarily have an antiinflammatory effect and increase serum glucose levels
- the mineralocorticoids (e.g., aldosterone) enhance sodium retention and potassium excretion. When sodium is reabsorbed, water follows because of osmotic changes.
64
Aldosterone is a mineralocorticoid with strong sodium-retaining and potassium-excreting capabilities. Decreased renal perfusion or decreased sodium in the distal portion of the renal tubule activates the renin-angiotensin-aldosterone system (RAAS), resulting in aldosterone secretion. In addition to the RAAS, increased serum potassium, decreased serum sodium, and adrenocorticotropic hormone (ACTH) stimulate aldosterone secretion. Aldosterone increases?
sodium and water reabsorption in the renal distal tubules, decreasing plasma osmolality and restoring fluid volume.
65
Cortisol is the most abundant glucocorticoid. In large doses, cortisol has both?
glucocorticoid (glucose-elevating and antiinflammatory) and mineralocorticoid (sodium-retention) effects. Normally cortisol secretion is in a diurnal or circadian pattern. Increased cortisol secretion occurs in response to physical and psychologic stress. This affects many body functions, including fluid and electrolyte balance
66
Adrenal cortical regulation main points
- Releases hormones to regulate water and electrolytes
1) Glucocorticoids
Cortisol
2) Mineralocorticoids
Aldosterone
67
Gastrointestinal Regulation
In addition to oral intake, the GI tract normally secretes around ____ mL of digestive fluids each day. The GI tract normally reabsorbs most of this fluid, with only a small amount eliminated in feces. This is why diarrhea and vomiting, which prevent GI reabsorption of?
8000 mL
| prevent GI reabsorption of secreted fluid, can lead to significant fluid and electrolyte loss.
68
Gastrointestinal regulation main points
- Oral intake accounts for most water
- Small amounts of water are eliminated by gastrointestinal tract in feces
- Diarrhea and vomiting can lead to significant fluid and electrolyte loss
69
Insensible water loss main points
- Invisible vaporization from lungs and skin
- Loss of approximately 600 to 900 mL/day
- No electrolyte loss
70
Two possible reasons for fluid and electrolyte imbalance
1) Directly caused by illness or disease (burns or heart failure)
2) Result of therapeutic measures (IV fluid replacement or diuretics)
71
Perioperative patients are at risk for developing fluid and electrolyte imbalances because of?
fluid restrictions, blood or fluid loss, and the stress of surgery
72
ECF volume deficit (hypovolemia) and ECF volume excess (hypervolemia) are common clinical conditions. ECF volume imbalances are usually accompanied by one or more electrolyte imbalances, particularly changes in the?
serum sodium level
73
ECF Volume Deficit
| Causes
* ↑ Insensible water loss or perspiration (high fever, heatstroke)
* Diabetes insipidus
* Osmotic diuresis
* Hemorrhage
* GI losses: vomiting, NG suction, diarrhea, fistula drainage
* Overuse of diuretics
* Inadequate fluid intake
* Third-space fluid shifts: burns, pancreatitis
74
ECF volume Deficit Manifestations
* Restlessness, drowsiness, lethargy, confusion
* Thirst, dry mucous membranes
* Cold clammy skin
* Decreased skin turgor, ↓ capillary refill
* Postural hypotension, ↑ pulse, ↓ CVP
* ↓ Urine output, concentrated urine
* ↑ Respiratory rate
* Weakness, dizziness
* Weight loss
* Seizures, coma
75
ECF Volume Excess Causes
* Excessive isotonic or hypotonic IV fluids
* Heart failure
* Renal failure
* Primary polydipsia
* SIADH
* Cushing syndrome
* Long-term use of corticosteroids
76
ECF Volume Excess Manifestations
* Headache, confusion, lethargy
* Peripheral edema
* Jugular venous distention
* S3 heart sound
* Bounding pulse, ↑ BP, ↑ CVP
* Polyuria (with normal renal function)
* Dyspnea, crackles, pulmonary edema
* Muscle spasms
* Weight gain
* Seizures, coma
77
ECF volume deficit (hypovolemia)
- Abnormal loss of?
- Clinical manifestations?
- Treatment?
- Abnormal loss of normal body fluids, inadequate intake, or plasma-to-interstitial fluid shift
- Clinical manifestations related to loss of vascular volume as well as CNS effects
- Treatment: Replace water and electrolytes with balanced IV solutions
78
Fluid Volume Deficeit Interprofessional Care
- Managing fluid volume deficit involves correcting the underlying cause and replacing both water and any needed electrolytes.
- Replacement therapy depends on the severity and type of volume loss. In mild losses, oral rehydration may be used. If the deficit is more severe, volume is replaced with blood products or balanced IV solutions, such as isotonic (0.9%) sodium chloride or lactated Ringer's solution. The choice of fluid depends on the cause and patient's electrolyte status. For rapid volume replacement, 0.9% sodium chloride is preferred. Blood is administered when volume loss is due to blood loss.
79
Fluid volume excess may result from?
- excess intake of fluids, abnormal retention of fluids (e.g., heart failure, renal failure), or a shift of fluid from interstitial fluid into plasma fluid. Weight gain is the most consistent manifestation of fluid volume excess.
80
Fluid volume excess may result from excess intake of?
Fluids, abnormal retention of fluids (e.g., heart failure, renal failure), or a shift of fluid from interstitial fluid into plasma fluid. Weight gain is the most consistent manifestation of fluid volume excess.
81
Fluid volume excess interprofessional care
Managing fluid volume excess involves treating the underlying cause and removing fluid without producing abnormal changes in the electrolyte composition or osmolality of ECF. Diuretics and fluid restriction are the primary forms of therapy. Some patients also need sodium restrictions. If the fluid excess leads to ascites or pleural effusion, an abdominal paracentesis or thoracentesis may be necessary.
82
Fluid volume excess (hypervolemia) main points
- Excessive intake of?
- Clinical manifestations related to?
- Treatment:
- Excessive intake of fluids, abnormal retention of fluids, or interstitial-to-plasma fluid shift
- Clinical manifestations related to excess volume
- Treatment: Remove fluid without changing electrolyte composition or osmolality of ECF
83
Nursing diagnosis for hypovolemia
- Deficient fluid volume
- Decreased cardiac output
- Risk for deficient fluid volume
- Potential complication: Hypovolemic shock
84
Nursing diagnosis for hypervolemia
- Excess fluid volume
- Impaired gas exchange
- Risk for impaired skin integrity
- Activity intolerance
- Disturbed body image
- Potential complications: Pulmonary edema, ascites
85
Nursing implementation
- Daily weights
- I&O
- Laboratory findings
- Cardiovascular care
- Respiratory care
- Patient safety
- Skin care
- Fluid therapy
86
Daily weights are the most accurate measure of volume status. An increase of 1 kg (2.2 lb) is equal to _______ of fluid retention, provided the person has maintained usual dietary intake or has not been on NPO status. Obtain the weight under standardized conditions. Weigh the patient at the same time every day, wearing the same garments and on the same carefully calibrated scale. Remove excess bedding and empty all drainage bags before the weighing. If items are present that are not there every day, such as bulky dressings or tubes, note this along with the weight.
1000 mL (1 L) of fluid retention
87
Intake and output records provide valuable information about fluid and electrolyte problems. An accurately recorded intake and output will identify sources of excessive intake or fluid losses.
1) Intake should include?
2) Estimate fluid loss from wounds and perspiration. Note the amount and color of the urine and measure the urine specific gravity. Readings greater than?
1) Intake should include oral, IV, and tube feedings and retained irrigants. Output includes urine, excess perspiration, wound or tube drainage, vomitus, and diarrhea.
2) Readings greater than 1.025 indicate concentrated urine, while readings less than 1.010 indicate dilute urine.
88
Laboratory Findings: Monitor laboratory results when available and calculate the serum osmolality. The patient with a fluid volume deficit often has increased?
- With fluid volume excess, the patient will have decreased?
- The patient with a fluid volume deficit often has increased BUN, sodium, and hematocrit levels with increased plasma and urine osmolality.
- With fluid volume excess, the patient will have decreased BUN, sodium, and hematocrit levels with decreased plasma and urine osmolality.
89
Cardiovascular Care
Monitor vital signs and perform a thorough cardiovascular assessment as needed. Changes in BP, central venous pressure, pulse force, and jugular venous distention reflect ECF volume imbalances.
- In fluid volume excess, the pulse is?
- In mild to moderate fluid volume deficit, sympathetic nervous system compensation increases the?
- pulse is full, bounding, and not easily obliterated. Increased volume causes distended neck veins (jugular venous distention), increased central venous pressure, and high BP. Auscultate heart sounds, being alert for the presence of an S3.
- heart rate and results in peripheral vasoconstriction in an effort to maintain BP within normal limits. Pulses may be weak and thready. Assess for orthostatic changes. A change in position from lying to sitting or standing may elicit a decrease in BP or a further increase in the heart rate (orthostatic hypotension). In more severe deficits, hypotension may be present.
90
Respiratory Care: What should the nurse monitor for?
- pulse oximetry and auscultate lung sounds as needed.
- ECF excess can result in pulmonary congestion and pulmonary edema, as increased hydrostatic pressure in the pulmonary vessels forces fluid into the alveoli. The patient will experience shortness of breath and moist crackles on auscultation.
- The patient with ECF deficit will demonstrate an increased respiratory rate because of decreased tissue perfusion and resultant hypoxia. Administer oxygen as ordered.
91
Skin Care
Examine the skin for turgor and mobility. Normally a fold of skin, when pinched, will readily move and, on release, rapidly return to its former position.
- In ECF volume deficit, skin turgor is?
Skin areas over the sternum, abdomen, and anterior forearm are the usual sites for evaluation of tissue turgor. In older people, decreased skin turgor is less predictive of fluid deficit because of the?
- skin turgor is diminished, and there is a lag in the
| - tissue elasticity
92
Administer IV fluids as ordered. Carefully monitor the rates of infusion of IV fluid solutions, especially when large volumes of fluid are being given. This is especially true in patients with?
cardiac, renal, or neurologic problems.
93
Sodium, the main cation of ECF, plays a major role in maintaining the concentration and volume of ECF and influencing water distribution between ECF and ICF. Sodium has an important role in the generation and transmission of?
nerve impulses, muscle contractility, and regulation of acid-base balance
94
The serum sodium level reflects the ratio of sodium to water, not necessarily the amount of sodium in the body. Changes in the serum sodium level can reflect a primary water imbalance, primary sodium imbalance, or combination of the two. Sodium imbalances are typically associated with imbalances in ECF volume. Because sodium is the primary determinant of ECF osmolality, sodium imbalances are typically associated with?
parallel changes in osmolality.
95
Sodium main points
- Imbalances typically associated with parallel changes in osmolality
- Plays a major role in
1) ECF volume and concentration
2) Generation and transmission of nerve impulses
3) Muscle contractility
4) Acid-base balance
96
The GI tract absorbs sodium from foods. Typically, daily intake of sodium far exceeds the body's daily requirements. Sodium leaves the body through urine, sweat, and feces. The kidneys primarily regulate sodium balance. The kidneys control ECF sodium concentration by?
excreting or retaining water under the influence of ADH. Aldosterone plays a smaller role in sodium regulation by promoting sodium reabsorption from the renal tubules.
97
Hypernatremia (elevated serum sodium) may occur with inadequate water intake, excess water loss or, rarely, sodium gain. Because sodium is the major determinant of ECF osmolality, hypernatremia causes hyperosmolality. ECF hyperosmolality causes water to move out of the cells to restore equilibrium, leading to cellular dehydration. As discussed earlier, the primary protection against the development of hyperosmolality is thirst. Hypernatremia is not a problem in an alert person who has access to water, can sense thirst, and is able to swallow. Hypernatremia secondary to water deficiency is often the result of an?
impaired level of consciousness or an inability to obtain fluids
98
Hypernatremia: Several clinical states can produce hypernatremia from water loss. A deficiency in the synthesis or release of ADH from the posterior pituitary gland (central diabetes insipidus) or a decrease in kidney responsiveness to ADH (nephrogenic diabetes insipidus) can result in profound diuresis, producing a water deficit and hypernatremia. Hyperosmolality with osmotic diuresis can result from?
hyperglycemia associated with uncontrolled diabetes mellitus or administering concentrated hyperosmolar tube feedings
99
Hypernatremia: Excess sodium intake with inadequate water intake can also lead to hypernatremia. Examples of sodium gain include?
IV administration of hypertonic saline or sodium bicarbonate, use of sodium-containing drugs, excessive oral intake of sodium (e.g., ingestion of seawater), and primary aldosteronism (hypersecretion of aldosterone) caused by a tumor of the adrenal glands.
100
Clinical Manifestations
| The manifestations of hypernatremia are primarily the result of water shifting out of cells into ECF with resultant?
dehydration and shrinkage of cells. Dehydration of brain cells results in alterations in mental status, ranging from agitation, restlessness, confusion, and lethargy to coma. If there is any accompanying ECF volume deficit, manifestations such as postural hypotension, tachycardia, and weakness occur.
101
Hypernatremia (Na+ >145 mEq) main points
- Elevated serum sodium occurring with water loss or sodium gain
- Causes hyperosmolality leading to cellular dehydration
- Primary protection is thirst from hypothalamus
102
Hypernatremia (Na+ >145 mEq) Manifestations main points
- Thirst, lethargy, agitation, seizures, and coma
- Impaired LOC
- Symptoms of fluid volume deficit
103
What diseases can cause hypernatremia (Na+ >145 mEq)?
* Diabetes insipidus
* Primary hyperaldosteronism
* Cushing syndrome
* Uncontrolled diabetes mellitus
104
Hypernatremia (Na+ >145 mEq) causes
1) Excessive Sodium Intake
• IV fluids: hypertonic NaCl, excessive isotonic NaCl, IV sodium bicarbonate
• Hypertonic tube feedings without water supplements
• Near-drowning in salt water
2) Inadequate Water Intake
• Unconscious or cognitively impaired individuals
3) Excessive Water Loss (↑ sodium concentration)
• ↑ Insensible water loss (high fever, heatstroke, prolonged hyperventilation)
• Osmotic diuretic therapy
• Diarrhea
4) Diseases
• Diabetes insipidus
• Primary hyperaldosteronism
• Cushing syndrome
• Uncontrolled diabetes mellitus
105
Manifestations for Hypernatremia (Na+ >145 mEq) With Decreased ECF Volume
* Restlessness, agitation, lethargy, seizures, coma
* Intense thirst, dry swollen tongue, sticky mucous membranes
* Postural hypotension, ↓ CVP, weight loss, ↑ pulse
* Weakness, muscle cramps
106
Manifestations for Hypernatremia (Na+ >145 mEq) With Normal or Increased ECF Volume
* Restlessness, agitation, twitching, seizures, coma
* Intense thirst, flushed skin
* Weight gain, peripheral and pulmonary edema, ↑ BP, ↑ CVP
107
Hyponatremia (Na+ <135 mEq/L [mmol/L]) Causes
```
1) Excessive sodium loss
• GI losses: diarrhea, vomiting, fistulas, NG suction
• Renal losses: diuretics, adrenal insufficiency, Na+ wasting renal disease
• Skin losses: burns, wound drainage
2) Inadequate sodium intake
• Fasting diets
3) Excessive water gain (↓ sodium concentration)
• Excessive hypotonic IV fluids
• Primary polydipsia
4) Diseases
• SIADH
• Heart failure
• Primary hypoaldosteronism
• Cirrhosis
```
108
Manifestations for Hyponatremia With Decreased ECF Volume
* Irritability, apprehension, confusion, dizziness, personality changes, tremors, seizures, coma
* Dry mucous membranes
* Postural hypotension, ↓ CVP, ↓ jugular venous filling, ↑ pulse, thready pulse
* Cold and clammy skin
109
Manifestations for Hyponatremia With Normal or Increased ECF Volume
* Headache, apathy, confusion, muscle spasms, seizures, coma
* Nausea, vomiting, diarrhea, abdominal cramps
* Weight gain, ↑ BP, ↑ CVP
110
Nursing Diagnoses for hypernatremia
Nursing diagnoses and collaborative problems for the patient with hypernatremia include, but are not limited to, the following:
* Risk for electrolyte imbalance related to inadequate water intake, excess sodium intake and/or water loss injury related to altered sensorium and seizures
* Risk for fluid volume deficit related to inadequate water intake and/or water loss
* Risk for injury related to altered sensorium and seizures
* Potential complications: seizures and coma
111
Nursing Implementation for hypernatremia
- depends on underlying cause and patient's volume status.
- primary water deficit, fluid replacement provided either orally or IV with isotonic such as 0.9% sodium chloride
- If it is sodium excess, expect diluting the high sodium concentration with sodium-free IV fluids, such as 5% dextrose in water, and promoting sodium excretion with diuretics.
- Dietary sodium intake restricted
- If patient has altered sensorium or is having seizures, initiate seizure precautions.
- Monitor serum sodium levels, serum osmolality, and the patient's response to therapy
- serum sodium level should not decrease by more than 8 to 15 mEq/L in an 8-hour period
- Quickly reducing levels can cause a rapid shift of water back into the cells, resulting in cerebral edema and neurologic complications, risk is greatest in patient who developed hypernatremia over several days or longer.
112
Hyponatremia (low serum sodium) may result from a?
- loss of sodium-containing fluids, water excess in relation to the amount of sodium (dilutional hyponatremia), or a combination of both
- usually associated with ECF hypoosmolality from excess water. To restore balance, fluid shifts out of the ECF and into the cells, leading to cellular edema.
113
Common causes of hyponatremia from loss of sodium-rich body fluids include?
- draining wounds, diarrhea, vomiting, and primary adrenal insufficiency
- Inappropriate use of sodium-free or hypotonic IV fluids causes hyponatremia from water excess. This may occur in patients after surgery or major trauma or administering fluids to patients with renal failure
- Patients with psychiatric disorders may have excessive water intake
- Syndrome of inappropriate antidiuretic hormone secretion (SIADH) results in dilutional hyponatremia caused by abnormal retention of water.
114
Hyponatremia
- results from
- manifestations
- Results from loss of sodium-containing fluids and/or from water excess
- Manifestations
Confusion, irritability, headache, seizures, and coma
115
Clinical Manifestations
| The manifestations of hyponatremia are due to?
cellular swelling and first appear in the central nervous system (CNS). Mild hyponatremia has minor, nonspecific neurologic symptoms including headache, irritability, and difficulty concentrating. More severe hyponatremia can cause confusion, vomiting, seizures, and even coma. If hyponatremia is severe and develops rapidly, irreversible neurologic damage or death from brain herniation can occur
116
Nursing Diagnoses
Nursing diagnoses and collaborative problems for the patient with hyponatremia include, but are not limited to, the following:
* Risk for electrolyte imbalance related to excess sodium loss and/or excess water intake or retention
* Risk for injury related to altered sensorium and decreased level of consciousness
* Risk for acute confusion related to electrolyte imbalance
* Potential complication: severe neurologic changes
117
Nursing Implementation
| Managing hyponatremia from fluid loss includes?
- replacing fluid using isotonic sodium-containing solutions, encouraging oral intake, and withholding all diuretics
- In mild hyponatremia caused by water excess, fluid restriction is often the only treatment
- aim of restriction is 500 mL less than previous 24-hour urine output
- Loop diuretics and demeclocycline may be given
- If hyponatremia is acute or more serious, small amounts of IV hypertonic saline solution (3% sodium chloride) can restore the serum sodium level while the body is returning to a normal water balance.
118
Hyponatremia: Vasopressor receptor antagonists (drugs that block the activity of ADH), are used to treat patients who cannot tolerate fluid restrictions or have more severe symptoms. These drugs include?
conivaptan (Vaprisol) and tolvaptan (Samsca). Conivaptan is given IV to hospitalized patients with severe hyponatremia from water excess. Tolvaptan is an oral preparation used to treat hyponatremia from heart failure and SIADH.
119
Nursing implementation for hyponatremia: Monitor serum sodium levels and the patient's response to therapy to avoid rapid or overcorrection. The level should not increase by more than?
8 to 12 mEq/L in the first 24 hours
- Quickly increasing levels of sodium can cause osmotic demyelination syndrome with permanent damage to nerve cells in the brain
- accurate urine output record is essential
- patient may need a urinary catheter placed if unable to assist with monitoring output
- If patient has altered sensorium or having seizures, initiate seizure precautions
120
Hyponatremia:
Caused by?
Severe symptoms?
- Caused by water excess
* Fluid restriction needed
- Severe symptoms (seizures)
* Give small amount of IV hypertonic saline solution (3% NaCl)
121
Hyponatremia
-Abnormal fluid loss
-Drugs that block vasopressin (ADH)
```
- Abnormal fluid loss
Fluid replacement with sodium-containing solution
- Drugs that block vasopressin (ADH)
1) Convaptan (Vaprisol)
2) Tolvaptan (Samsca)
```
122
Potassium is a:
- Major?
- Necessary for?
- Major ICF cation
- Necessary for
1) Transmission and conduction of nerve and muscle impulses
2) Cellular growth
3) Maintenance of cardiac rhythms
4) Acid-base balance
123
Potassium is the major ICF cation, with ___% of the body potassium being intracellular. For example, potassium concentration within muscle cells is around 140 mEq/L; potassium concentration in ECF is _______. The sodium-potassium pump in cell membranes maintains this concentration difference by pumping potassium into the cell and sodium out. Insulin helps by stimulating the?
98%
ECF is 3.5 to 5.0 mEq/L
Insulin helps by stimulating the sodium-potassium pump.
124
Because the ratio of ECF potassium to ICF potassium is the major factor in the resting membrane potential of ______ what function is affected by potassium imbalances?
- Potassium is involved with regulating?
- It is required for glycogen to be deposited in?
- Potassium also plays a role in _____ balance
- major factor in resting membrane potential of nerve and muscle cells, so neuromuscular and cardiac function are often affected by potassium imbalances.
- involved w/regulating intracellular osmolality and promoting cellular growth
- required for glycogen to be deposited in muscle and liver cells
- plays a role in acid-base balance
125
Main source of potassium
Diet is the source of potassium. The typical Western diet contains roughly 50 to 100 mEq of potassium daily, mainly from protein-rich foods and many fruits and vegetables. Many salt substitutes used in low-sodium diets contain substantial potassium. Patients may receive potassium from parenteral sources, including IV fluids; transfusions of stored, hemolyzed blood; and medications (e.g., potassium penicillin).
126
What is the route of potassium in the body?
The kidneys are the primary route for potassium loss, eliminating about 90% of the daily potassium intake. Potassium excretion depends on the serum potassium level, urine output, and renal function. When serum potassium is high, urine potassium excretion increases and when serum levels are low, excretion decreases. Large urine output can cause excess potassium loss. Impaired kidney function can cause potassium retention. There is an inverse relationship between sodium and potassium reabsorption in the kidneys. Factors that cause sodium retention (e.g., low blood volume, hyponatremia, aldosterone secretion) cause potassium excretion.
127
What is the relationship between potassium and sodium?
They have an inverse relationship
128
Potassium main points
-Sources
- Regulated by?
- Sources
1) Fruits and vegetables (bananas and oranges)
2) Salt substitutes
3) Potassium medications (PO, IV)
4) Stored blood
- Regulated by kidneys
129
Hyperkalemia
- High serum potassium caused by?
- Most common in?
- High serum potassium caused by
1) Impaired renal excretion
2) Shift from ICF to ECF
3) Massive intake
- Most common in renal failure
130
Hyperkalemia (high serum potassium) may result from? The most common cause of hyperkalemia is renal failure. Adrenal insufficiency with a subsequent aldosterone deficiency leads to?
- Factors that cause potassium to move from ICF to ECF include?
- impaired renal excretion, a shift of potassium from ICF to ECF, a massive intake of potassium, or a combination of these factors
- Adrenal insufficiency with a subsequent aldosterone deficiency leads to potassium retention
- Factors that cause potassium to move from ICF to ECF include acidosis, massive cell destruction (as in burn or crush injury, tumor lysis, severe infections), and intense exercise. In metabolic acidosis, potassium ions shift from ICF to ECF in exchange for hydrogen ions moving into the cell.
131
Hyperkalemia (K+ >5.0 mEq/L [mmol/L]) Causes
1) Excess potassium intake
• Excessive or rapid parenteral administration
• Potassium-containing drugs (e.g., potassium penicillin)
• Potassium-containing salt substitute
2) Shift of Potassium Out of Cells
• Acidosis
• Tissue catabolism (e.g., fever, crush injury, sepsis, burns)
• Intense exercise
• Tumor lysis syndrome
3) Failure to Eliminate Potassium
• Renal disease
• Adrenal insufficiency
• Medications: Angiotensin II receptor blockers, ACE inhibitors, heparin, potassium-sparing diuretics, NSAIDs
132
Hyperkalemia (K+ >5.0 mEq/L [mmol/L]) Manifestations (8)
* Fatigue, irritability
* Muscle weakness, cramps
* Loss of muscle tone
* Paresthesias, decreased reflexes
* Abdominal cramping, diarrhea, vomiting
* Confusion
* Irregular pulse
* Tetany
133
Hyperkalemia (K+ >5.0 mEq/L [mmol/L]) ECG Changes
* Tall, peaked T wave
* Prolonged PR interval
* ST segment depression
* Widening QRS
* Loss of P wave
* Ventricular fibrillation
* Ventricular standstill
134
Hypokalemia (K+ <3.5 mEq/L [mmol/L]) Causes
1) Potassium loss
• GI losses: diarrhea, vomiting, fistulas, NG suction, ileostomy drainage
• Renal losses: diuretics, hyperaldosteronism, magnesium depletion
• Skin losses: diaphoresis
• Dialysis
2) Shift of Potassium Into Cells
• Increased insulin release (e.g., IV dextrose load)
• Insulin therapy (e.g., with diabetic ketoacidosis)
• Alkalosis
• ↑ Epinephrine (e.g., stress)
3) Lack of Potassium Intake
• Starvation
• Diet low in potassium
• Failure to include potassium in parenteral fluids if NPO
135
Hypokalemia (K+ <3.5 mEq/L [mmol/L]) Clinical manifestations
* Fatigue
* Muscle weakness, leg cramps
* Soft, flabby muscles
* Paresthesias, decreased reflexes
* Constipation, nausea, paralytic ileus
* Shallow respirations
* Weak, irregular pulse
* Hyperglycemia
136
Hypokalemia (K+ <3.5 mEq/L [mmol/L]) ECG Changes
* Flattened T wave
* Presence of U wave
* ST segment depression
* Prolonged QRS
* Peaked P wave
* Ventricular dysrhythmias
* First- and second-degree heart block
137
What drugs can cause hyperkalemia?
- Digoxin-like drugs and β-adrenergic blockers (e.g., propranolol) can impair entry of potassium into cells, resulting in a higher ECF potassium concentration.
- Several drugs, such as heparin, potassium-sparing diuretics, angiotensin II receptor blockers (e.g., losartan), and angiotensin-converting enzyme (ACE) inhibitors (e.g., lisinopril), can contribute to hyperkalemia by reducing the kidney's ability to excrete potassium
138
Manifestations main points for hyperkalemia
- Cramping leg pain
- Weak or paralyzed skeletal muscles
- Abdominal cramping or diarrhea
- Cardiac dysrhythmias
139
Clinical Manifestations for hyperkalemia:
The increased potassium concentration outside the cell changes the normal ECF and ICF ratio, resulting in increased cell excitability and changes in impulse transmission to the nerves and muscles. The most clinically significant problems are the disturbances in?
The initial ECG finding is?
- As potassium increases, cardiac depolarization decreases, leading to?
- What else may occur?
- Elevated potassium may cause failure to capture in a patient who has a?
- disturbances in cardiac conduction
- initial ECG finding is tall, peaked T waves.
- As potassium increases, cardiac depolarization decreases, leading to loss of P waves, a prolonged PR interval, ST segment depression, and widening QRS complex
- Heart block, ventricular fibrillation, or cardiac standstill may occur
- patient who has a pacemaker
140
Hyperkalemia: The patient may experience?
- As potassium increases, loss of?
- What happens to GI smooth muscles
- fatigue, confusion, tetany, muscle cramps, paresthesias, and weakness
- loss of muscle tone and weakness or paralysis of other skeletal muscles, including the respiratory muscles can occur, leading to respiratory arrest
- Abdominal cramping, vomiting, and diarrhea occur from hyperactivity of gastrointestinal smooth muscles.
141
Nursing Diagnoses
Nursing diagnoses and collaborative problems for the patient with hyperkalemia include, but are not limited to, the following.
• Risk for electrolyte imbalance related to excessive retention or cellular release of potassium
• Risk for activity intolerance related to muscle weakness
• Risk for injury related to muscle weakness and seizures
• Potential complication: dysrhythmias
* Risk for electrolyte imbalance related to excessive retention or cellular release of potassium
* Risk for activity intolerance related to muscle weakness
* Risk for injury related to muscle weakness and seizures
* Potential complication: dysrhythmias
142
Management of hyperkalemia consists of the following:
1. Eliminate oral/parenteral potassium intake
2. Increase elimination potassium (loop or thiazide diuretics, dialysis, patiromer (Veltassa), and/or sodium polystyrene sulfonate (Kayexalate). You should not give it within 6 hours of other drugs.
3. Force potassium from ECF to ICF. A combination of IV regular insulin and a β-adrenergic agonist stimulates sodium-potassium pump, shifting potassium into cells. Both metered dose inhalers and nebulized β-adrenergic agonists (e.g., nebulized albuterol) are equally effective. IV sodium bicarbonate is an option if the patient is acidotic.
4. Stabilize cardiac membranes. IV calcium chloride or calcium gluconate reverse membrane potential effects of elevated ECF potassium and restore electrical gradient. This protects patient from life-threatening dysrhythmias
143
Hyperkalemia management: When the potassium elevation is mild and the kidneys are functioning, it may be sufficient to?
- Patients with severe hyperkalemia or symptomatic patients should receive?
(1) withhold potassium from the diet and IV sources
(2) increase renal potassium elimination by administering fluids and loop or thiazide diuretics.
- severe hyperkalemia or symptomatic patients should receive one of the treatments to force potassium into cells.
144
Hyperkalemia monitoring: Provide continuous ECG monitoring of all patients with clinically significant hyperkalemia to detect?
- The patient experiencing dangerous cardiac dysrhythmias should receive?
- Monitor BP because?
- When administering insulin, monitor for?
- ECG monitoring to detect dysrhythmias and monitor effects of therapy
- patient experiencing dangerous cardiac dysrhythmias should receive IV calcium immediately.
- Monitor BP because rapidly administering calcium can cause hypotension.
- When administering insulin, monitor for hypoglycemia and give glucose as needed.
145
Nursing Management: Nursing Implementation two main points
1) Eliminate oral and parenteral K intake
| 2) Increase elimination of K (diuretics, dialysis, Kayexalate)
146
Nursing Management: Nursing Implementation
- Force K from ECF to ICF by?
- Reverse membrane effects of elevated ECF potassium by administering?
- Force K from ECF to ICF by IV insulin or sodium bicarbonate
- Reverse membrane effects of elevated ECF potassium by administering calcium gluconate IV
147
Hypokalemia (low serum potassium) can result from an?
| - most common causes of hypokalemia are?
- result from an increased loss of potassium, an increased shift of potassium from ECF to ICF, or rarely from deficient dietary potassium intake
- most common causes are abnormal losses from either kidneys or GI tract. GI tract losses associated w/diarrhea, laxative misuse, vomiting, and ileostomy drainage. Renal losses occur when a patient is diuresing or has a low magnesium level. Low plasma magnesium levels stimulate renin and aldosterone release, resulting in potassium excretion.
148
Among the factors causing potassium to move from ECF to ICF are insulin therapy, especially in conjunction with?
- Alkalosis can cause a?
- conjunction with diabetic ketoacidosis, and β-adrenergic stimulation (catecholamine release in stress, coronary ischemia)
- Alkalosis can cause a shift of potassium into cells in exchange for hydrogen, lowering potassium in ECF and causing symptomatic hypokalemia
149
Hypokalemia alters the resting membrane potential, resulting in hyperpolarization (an increased negative charge within the cell) and impaired muscle contraction. Therefore the manifestations of hypokalemia involve changes in?
cardiac and muscle function
150
The most serious clinical problems for hypokalemia are?
cardiac changes, including impaired repolarization, resulting in a flattened T wave, depressed ST segment, and the presence of a U wave. The P waves peak and the QRS complex is prolonged. There is an increased incidence of heart block and potentially lethal ventricular dysrhythmias.
151
As with hyperkalemia, skeletal muscle weakness and paresthesias may occur. Severe hypokalemia can cause?
- Alterations in smooth muscle function may lead to?
- Severe hypokalemia can cause paralysis. This usually involves the extremities but can involve the respiratory muscles, leading to shallow respirations and respiratory arrest.
- Alterations in smooth muscle function may lead to decreased GI motility (e.g., constipation, paralytic ileus). Finally, hypokalemia impairs insulin secretion, leading to glucose intolerance and hyperglycemia.
152
Nursing Diagnoses
Nursing diagnoses and collaborative problems for the patient with hypokalemia include, but are not limited to, the following:
* Risk for electrolyte imbalance related to excess potassium loss
* Risk for activity intolerance related to muscle weakness
* Risk for injury related to muscle weakness and hyporeflexia
* Potential complication: dysrhythmias
153
Managing hypokalemia consists of?
* oral or IV potassium chloride (KCl) supplements and increased dietary intake of potassium
* Consuming potassium-rich foods usually correct mild hypokalemia
* Clinically significant hypokalemia requires administering oral or IV KCl
154
Administering IV KCl (Safety Alert)
* IV KCl must always be diluted and never given in concentrated amounts.
* Never give KCl via IV push or as a bolus.
* Invert IV bags containing KCl several times to ensure even distribution in the bag.
* Do not add KCl to a hanging IV bag to prevent giving a bolus dose.
155
- IV KCl infusion rates should not exceed?
- IV KCl must be given by?
- Patients who are critically ill and those at risk for hypokalemia should have continuous?
- IV KCl infusion rates should not exceed 10 mEq/hr unless the patient is in a critical care setting with continuous ECG monitoring and central line access for administration
- IV KCl must be given by infusion pump to ensure correct administration rate. Because KCl is irritating to the vein, assess IV sites at least hourly for phlebitis and infiltration. Infiltration can cause necrosis and sloughing of the surrounding tissue.
- Patients critically ill and those at risk for hypokalemia should have continuous ECG monitoring to detect cardiac changes. Monitor serum potassium levels and urine output as appropriate.
156
Hypokalemia
- KCl is usually given only if the urine output is at least?
- Because patients on digoxin therapy have an increased risk of toxicity if their serum potassium level is low, monitor the patient for?
- Teach patients ways to prevent hypokalemia. Patients at risk for hypokalemia should have?
- 0.5 mL/kg of body weight per hour.
- digitalis toxicity.
- regular serum potassium levels monitored. Teach the patient taking digitalis to report signs and symptoms of digoxin toxicity immediately to the HCP.
157
Prevention of Hypokalemia
Include the following instructions when teaching at-risk patients how to prevent hypokalemia:
1. For all patients at risk:
2. For patients taking oral potassium supplements:
1. For all patients at risk:
• Report the signs and symptoms of hypokalemia to the HCP.
• Have serum potassium levels checked regularly.
• Regularly include foods high in potassium in your diet
• Consume alcohol in moderation only.
• Avoid consuming large amounts of licorice.
2. For patients taking oral potassium supplements:
• Take the medication as prescribed to prevent overdosing.
• Take the supplement with a full glass of water. Do not crush or chew tablets.
158
Hypokalemia
| Low serum potassium caused by
- Increased loss of K+ via the kidneys or gastrointestinal tract
- Increased shift of K+ from ECF to ICF
- Dietary K+ deficiency (rare)
- Magnesium deficiency
- Metabolic alkalosis
159
Hypokalemia Manifestations 6 main points
- Cardiac most serious
- Skeletal muscle weakness (legs)
- Weakness of respiratory muscles
- Decreased gastrointestinal motility
- Impaired regulation of arteriolar blood flow
- Hyperglycemia
160
Nursing ManagementNursing Implementation 4 main points
1) KCl supplements orally or IV
2) Always dilute IV KCL
3) NEVER give KCL via IV push or as a bolus
4) Should not exceed 10 mEq/hr
- To prevent hyperkalemia and cardiac arrest
161
Calcium Functions
- Formation of teeth and bone
- Blood clotting
- Transmission of nerve impulses
- Myocardial contractions
- Muscle contractions
162
The source of calcium is?
| Calcium absorption require?
- The source of calcium is dietary intake.
- Calcium absorption requires the active form of vitamin D. Vitamin D is obtained from foods or made in the skin by the action of sunlight on cholesterol.
163
The total body content of calcium is about 1200 g. The bones contain 99% of the body's calcium; the remainder is in plasma and body cells. Of the calcium in plasma, 50% is bound to plasma proteins, primarily albumin; 40% is in a free or ionized form, and the remainder is found bound with phosphate, citrate, or carbonate. The ionized or free calcium is biologically active. The serum pH influences how much calcium is?
serum pH influences how much calcium is ionized or bound to albumin. A decreased plasma pH (acidosis) decreases calcium binding to albumin, leading to more ionized calcium. An increased plasma pH (alkalosis) increases calcium binding, leading to decreased ionized calcium.
164
```
Calcium:
Obtained from?
Need ____ to absorb
Present in three forms:
Changes in pH and serum albumin affect?
```
- ingested foods/diet
- Need vitamin D to absorb
- Present in three forms: Ionized calcium is biologically active
- calcium levels
165
Serum calcium levels reflect the total level of all forms of plasma calcium. Serum albumin levels affect the interpretation of total calcium levels. Total calcium values increase or decrease directly with?
Ionized calcium levels are measured using?
- serum albumin levels.
- Ionized calcium levels are measured using special laboratory techniques or calculated using a formula. Albumin levels do not affect ionized calcium levels.
166
```
Parathyroid hormone (PTH) and calcitonin regulate calcium levels. Since the bones serve as a readily available store of calcium, the body is usually able to maintain normal serum calcium levels by regulating the movement of calcium into or out of the bone. Low serum calcium levels stimulate the parathyroid glands to?
- High serum calcium levels stimulate the release of?
```
1) Low serum calcium levels stimulate the parathyroid glands to produce and release PTH. PTH increases bone resorption (movement of calcium out of bones), increases GI absorption of calcium, and increases renal tubule reabsorption of calcium.
2) High serum calcium levels stimulate the release of calcitonin from the thyroid gland. Calcitonin has the opposite effect of PTH. It lowers the serum calcium level by increasing calcium deposition into bone, increasing renal calcium excretion, and decreasing GI absorption.
167
Calcium Balance controlled by?
```
Parathyroid hormone (PTH)
Calcitonin
```
168
Hypercalcemia (high serum calcium) is caused by?
- hyperparathyroidism in two thirds of persons.
- Malignancies (hematologic, breast, and lung cancers) cause remaining third. Malignancies lead to hypercalcemia through bone destruction from tumor invasion or tumor secretion of parathyroid-related proteins, which stimulate calcium release from bones.
- rare causes include thiazide diuretic use, prolonged immobilization, and increased calcium intake (e.g., use of calcium-containing antacids).
169
Hypercalcemia: High levels of serum calcium caused by what 3 things?
1) Hyperparathyroidism (two thirds of cases)
2) Malignancy
3) Prolonged immobilization
170
Excess calcium acts like a sedative, leading to reduced?
- Neurologic manifestations begin with?
- Disturbances in cardiac conduction can lead to?
excitability of muscles and nerves.
- Neurologic manifestations begin with fatigue, lethargy, weakness, and confusion and progress to hallucinations, seizures, and coma.
- Disturbances in cardiac conduction can lead to dysrhythmias, including heart block and ventricular tachycardia.
171
Hypercalcemia (Ca2+ >10.2 mg/dL [2.55 mmol/L]) Causes
```
1) Increased Total Calcium
• Hyperparathyroidism
• Hematologic malignancy
• Malignancies with bone metastasis
• Prolonged immobilization
• Vitamin A or D overdose
• Paget's disease
• Adrenal insufficiency
• Thyrotoxicosis
• Thiazide diuretics
• Milk-alkali syndrome
• Calcium-containing antacids
• Mycobacterium infection
2) Increased Ionized Calcium
• Acidosis
```
172
Hypercalcemia Manifestations
```
Manifestations
• Lethargy, weakness, stupor, fatigue
• Decreased memory
• Depressed reflexes
• ↑ BP
• Confusion, personality changes, psychosis
• Anorexia, nausea, vomiting
• Bone pain, fractures
• Polyuria, dehydration
• Nephrolithiasis
• Seizures, coma
```
173
Hypercalcemia ECG Changes
* Shortened ST segment
* Shortened QT interval
* Ventricular dysrhythmias
* Increased digitalis effect
174
Hypocalcemia (Ca2+ <8.6 mg/dL [2.15 mmol/L]) Causes
```
1) Decreased Total Calcium
• Primary hypoparathyroidism
• Renal insufficiency
• Acute pancreatitis
• Elevated phosphorus
• Vitamin D deficiency, malnutrition
• Magnesium deficiency
• Bisphosphonates
• Tumor lysis syndrome
• Loop diuretics
• Chronic alcoholism
• Diarrhea
• ↓ Serum albumin
2) Decreased Ionized Calcium
• Alkalosis
• Excess administration of citrated blood
```
175
Hypocalcemia manifestations
* Weakness, fatigue
* Depression, irritability, confusion
* Hyperreflexia, muscle cramps
* ↓ BP
* Numbness and tingling in extremities and region around mouth
* Chvostek's sign
* Trousseau's sign
* Laryngeal and bronchial spasms
* Tetany, seizures
176
Hypocalcemia ECG Changes
* Elongation of ST segment
* Prolonged QT interval
* Ventricular tachycardia
177
Nursing Diagnoses
Nursing diagnoses and collaborative problems for the patient with hypercalcemia include, but are not limited to, the following:
* Risk for electrolyte imbalance related to excessive bone destruction
* Risk for activity intolerance related to generalized muscle weakness
* Risk for injury related to neuromuscular and sensorium changes
* Potential complication: dysrhythmias
178
Nursing Implementation for hypercalcemia
Management depends on the degree of hypercalcemia, patient's condition, and the underlying cause. Patients with mild hypercalcemia should?
- stop any medications related to hypercalcemia, start a diet low in calcium, increase weight-bearing activity, and maintain adequate hydration
- patient must drink 3000 to 4000 mL of fluid daily to promote renal excretion of calcium and decrease chance of kidney stone formation. Fluids that promote urine acidity (cranberry or prune juice) will help to prevent formation of stones.
179
Managing severe hypercalcemia includes administering?Begin with hydrating the patient with IV isotonic saline to maintain a urine output of 100 to 150 mL per hour.8 IV saline therapy requires careful monitoring. Fluid overload can occur in patients who cannot excrete the excess sodium because of impaired renal function.
-Bisphosphonates?
- severe means administering saline, a bisphosphonate, and calcitonin. hydrating patient with IV isotonic saline to maintain a urine output of 100 to 150 mL per hour. IV saline therapy requires careful monitoring. Fluid overload can occur in patients who cannot excrete the excess sodium because of impaired renal function.
- Bisphosphonates (e.g., pamidronate, zoledronic acid) are the most effective agents in treating hypercalcemia, particularly when caused by a malignancy. They interfere with the activity of osteoclasts, cells that break down bone. Because it takes 2 to 4 days for bisphosphonates to achieve maximum effect, patients receive IM or SC calcitonin for an immediate effect. Calcitonin rapidly increases renal calcium excretion. However, therapy is only effective for a few days and may cause tachycardia. Dialysis is an option in life-threatening situations.
180
Nursing management for hypercalcemia 6 main points
1) Excretion of Ca with loop diuretic
2) Hydration with isotonic saline infusion
3) Low calcium diet
4) Mobilization
5) Synthetic calcitonin
6) Bisphosphonates
181
Hypocalcemia (low serum calcium) can result from any condition associated with PTH deficiency. This may occur with?
- The patient who receives multiple blood transfusions can become hypocalcemic because?
- Sudden alkalosis may result in ?
- surgical removal of a portion of or injury to the parathyroid glands during thyroid or neck surgery or with neck radiation
- multiple blood transfusions can become hypocalcemic because the citrate used to anticoagulate the blood binds with calcium, decreasing ionized calcium levels.
- alkalosis may result in symptomatic hypocalcemia despite a normal total serum calcium level. The high pH increases calcium binding to protein, decreasing the amount of ionized calcium.
182
Hypocalcemia: Low ionized calcium levels decrease the threshold for activating the sodium channels that cause cell membrane depolarization. This results in increased nerve excitability and sustained muscle contraction, or tetany. Clinical signs of tetany include?
- Other manifestations of tetany are?
- Cardiac effects of hypocalcemia include?
- Clinical signs of tetany include Chvostek's sign and Trousseau's sign. Chvostek's sign is contraction of facial muscles in response to a tap over the facial nerve in front of the ear.
Trousseau's sign refers to carpal spasms induced by inflating a BP cuff on the arm. When the cuff is inflated above the systolic pressure, carpal spasms occur within 3 minutes if hypocalcemia is present. Other manifestations of tetany are laryngeal stridor, dysphagia, paresthesia, and numbness and tingling around the mouth or in the extremities.
- Cardiac effects of hypocalcemia include decreased cardiac contractility and ECG changes. A prolonged QT interval may develop into ventricular tachycardia
183
Tests for hypocalcemia
1) Chvostek's sign is contraction of facial muscles in response to a light tap over the facial nerve in front of the ear
2) Trousseau's sign is a carpal spasm induced by inflating a BP cuff above the systolic pressure for a few minutes. After 3 the spasms will occur
184
Low serum Ca levels caused by?
- Decreased production of PTH
- Acute pancreatitis
- Multiple blood transfusions
- Alkalosis
- Increased calcium loss
185
Hypocalcemia manifestations
- Positive Trousseau’s or Chvostek’s sign
- Laryngeal stridor
- Dysphagia
- Tingling around the mouth or in the extremities
- Cardiac dysrhythmias
186
Nursing Diagnoses
Nursing diagnoses and collaborative problems for the patient with hypocalcemia include, but are not limited to, the following:
* Risk for electrolyte imbalance related to decreased PTH level
* Ineffective breathing pattern related to laryngospasm
* Acute pain related to sustained muscle contractions
* Risk for injury related to tetany and seizures
* Potential complications: fracture, respiratory arrest
187
Managing hypocalcemia depends on the underlying cause and the presence of symptoms.
- Treating mild or asymptomatic hypocalcemia involves?
- Symptomatic hypocalcemia is treated with?
- Patients taking loop diuretics may need to change to?
- Closely observe any patient who had thyroid or neck surgery in the immediate postoperative period for?
- Adequately treat pain and anxiety because?
- mild or asymptomatic hypocalcemia involves a diet high in calcium-rich foods and calcium and vitamin D supplementation.
- Symptomatic hypocalcemia is treated with IV calcium gluconate. Measures to promote CO2 retention, such as breathing into a paper bag or sedating the patient, can control muscle spasm and other symptoms of tetany until the calcium level is corrected.
- Patients taking loop diuretics may need to change to thiazide diuretics to decrease urinary calcium excretion.
- Closely observe any patient who had thyroid or neck surgery in the immediate postoperative period for manifestations of hypocalcemia because of the proximity of the surgery to the parathyroid glands.
- Adequately treat pain and anxiety because hyperventilation-induced respiratory alkalosis can precipitate hypocalcemic symptoms.
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Hypocalcemia implementation 4 main points
1) Treat cause
2) Oral or IV calcium supplements
- Not IM to avoid local reactions
3) Rebreathe into paper bag
4) Treat pain and anxiety to prevent hyperventilation-induced respiratory alkalosis
189
Phosphorus is the primary anion in ____ and the second most abundant element in the body after calcium. Most phosphorus is in?
- The remaining phosphorus is metabolically active and essential to the function of?
- It is involved in the?
- primary anion in ICF
- Most is in bones and teeth as calcium phosphate
- remaining phosphorus is metabolically active and essential to the function of muscle, red blood cells, and the nervous system
- involved in acid-base buffering system; mitochondrial formation of ATP; cellular uptake and use of glucose; and carbohydrate, protein, and fat metabolism
190
Phosphate 3 main points
1) Primary anion in ICF
2) Essential to function of muscle, red blood cells, and nervous system
3) Involved in acid-base buffering system, ATP production, cellular uptake of glucose, and metabolism of carbohydrates, proteins, and fats
191
PTH maintains serum phosphorus levels and balance. Proper phosphate balance requires adequate renal functioning because?
- What happens when the phosphate level in the glomerular filtrate falls below normal or PTH levels are low?
- A reciprocal relationship exists between phosphorus and?
- adequate renal functioning because the kidneys are the major route of phosphate excretion.
- When the phosphate level in the glomerular filtrate falls below normal or PTH levels are low, the kidneys reabsorb additional phosphorus.
- A reciprocal relationship exists between phosphorus and calcium. This means a low serum calcium level stimulates the release of PTH, decreasing reabsorption of phosphorus and lowering phosphorus levels
192
Phosphate
1) Serum levels controlled by?
2) Maintenance requires?
3) Reciprocal relationship with?
1) Serum levels controlled by parathyroid hormone
2) Maintenance requires adequate renal functioning
3) Reciprocal relationship with calcium
193
Hyperphosphatemia (high serum phosphate) is common in patients with?
- Other causes include?
- common in patients with acute kidney injury or chronic kidney disease, which alters the kidney's ability to excrete phosphate.
- Other causes include
* excess phosphate intake from the use of phosphate-containing laxatives or enemas
* shift of phosphate from ICF to ECF (occur in patients with tumor lysis syndrome or rhabdomyolysis)
* Hypoparathyroidism and Vitamin D intoxication cause increased kidney phosphate reabsorption
194
Hyperphosphatemia: High serum PO43- caused by?
| 3 main points
1) Acute kidney injury or chronic kidney disease
2) Chemotherapy
3) Excessive ingestion of phosphate or vitamin D
195
Hyperphosphatemia (PO43− >4.4 mg/dL [1.42 mmol/L]) 9 Causes
* Renal failure
* Phosphate enemas (e.g., Fleet Enema)
* Excessive ingestion (e.g., phosphate-containing laxatives)
* Rhabdomyolysis
* Tumor lysis syndrome
* Thyrotoxicosis
* Hypoparathyroidism
* Sickle cell anemia, hemolytic anemia
* Hyperthermia
196
Hyperphosphatemia (PO43− >4.4 mg/dL [1.42 mmol/L]) 5 manifestations
* Hypocalcemia
* Numbness and tingling in extremities and region around mouth
* Hyperreflexia, muscle cramps
* Tetany, seizures
* Calcium-phosphate precipitates in skin, soft tissue, cornea, viscera, blood vessels
197
Hypophosphatemia (PO43− <2.4 mg/dL [0.78 mmol/L]) 10 Causes
* Malabsorption syndromes
* Chronic diarrhea
* Malnutrition, vitamin D deficiency
* Parenteral nutrition
* Chronic alcoholism
* Phosphate-binding antacids
* Diabetic ketoacidosis
* Hyperparathyroidism
* Refeeding syndrome
* Respiratory alkalosis
198
Hyperphosphatemia Manifestations 2 main points
1) Neuromuscular irritability and tetany (hypocalcemia)
2) Calcified deposition in soft tissue such as joints, arteries, skin, kidneys, and corneas (can cause organ dysfunction)
199
Hypophosphatemia (PO43− <2.4 mg/dL [0.78 mmol/L]) 6 manifestations
* CNS depression (confusion, coma)
* Muscle weakness, including respiratory muscle weakness
* Polyneuropathy, seizures
* Cardiac problems (dysrhythmias, heart failure)
* Osteomalacia, rickets
* Rhabdomyolysis
200
Hyperphosphatemia is often asymptomatic unless calcium binds with phosphate, leading to manifestations of?
Long term, increased phosphate levels result in the development of?
- leading to manifestations of hypocalcemia. These manifestations include tetany, muscle cramps, paresthesias, and seizures.
- Long term, increased phosphate levels result in the development of calcified deposits outside of the bones. These calcium deposits can be found in soft tissues such as joints, arteries, skin, corneas, and kidneys and produce organ dysfunction, notably renal failure.
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Hyperphosphatemia Management 5 main points
1) Identify and treat underlying cause
2) Restrict foods and fluids containing phosphorus
3) Phosphate-binding agents
4) Adequate hydration and correction of hypocalcemic conditions
5) Hemodialysis, IV insulin and glucose
202
Managing hyperphosphatemia involves identifying and treating the underlying cause.
1) Intake of foods and fluids high in phosphorus (e.g., dairy products) should be restricted.
2) Oral phosphate-binding agents (e.g., calcium carbonate) limit intestinal phosphate absorption and increase phosphate secretion in the intestine.
3) With severe hyperphosphatemia, hemodialysis may be used to rapidly decrease levels.
4) Volume expansion and forced diuresis with a loop diuretic may increase phosphate excretion.
5) If hypocalcemia is present, institute measures to correct calcium levels.
203
Hypophosphatemia (low serum phosphate) can result from?
| - Hypophosphatemia may occur in those who are?
- result from decreased intestinal absorption, increased urinary excretion, or from ECF to ICF shifts.
- Malabsorption, diarrhea, and phosphate-binding antacids lead to decreased absorption.
- Phosphate shifts occur in respiratory alkalosis, treatment of diabetic ketoacidosis, and refeeding syndrome (reinstitution of nutrition to patients who are severely malnourished).
- Hypophosphatemia may occur in those who are malnourished or receive parenteral nutrition with inadequate phosphorus replacement
204
Most of the manifestations of hypophosphatemia result from?
- Mild to moderate hypophosphatemia is often?
- Severe hypophosphatemia may be?
- Acute manifestations include?
- Chronic hypophosphatemia alters?
- result from impaired cellular energy and O2 delivery due to low levels of cellular ATP and 2,3-diphosphoglycerate (2,3-DPG), an enzyme in RBCs that facilitates O2 delivery to the tissues.
- Mild to moderate hypophosphatemia is often asymptomatic.
- Severe hypophosphatemia may be fatal because of decreased cellular function.
- Acute manifestations include CNS depression, muscle weakness and pain, respiratory failure, and heart failure.
- Chronic hypophosphatemia alters bone metabolism, resulting in rickets and osteomalacia.
205
Managing mild phosphorus deficiency involves?
- Symptomatic hypophosphatemia can be?
- Frequent monitoring is necessary during IV therapy as complications include?
- mild phosphorus deficiency involves increasing oral intake with dairy products or phosphate supplements. Dairy products are better tolerated because phosphate supplements are often associated with adverse GI effects.
- Symptomatic hypophosphatemia can be fatal and usually requires IV administration of sodium phosphate or potassium phosphate.
- Frequent monitoring is necessary during IV therapy as complications include hypocalcemia, hyperkalemia, hypotension, and dysrhythmias.
206
Hypophosphatemia manifestations 5 main points
1) CNS depression
2) Confusion
3) Muscle weakness and pain
4) Dysrhythmias
5) Cardiomyopathy
207
Hypophosphatemia management 3 main points
1) Oral supplementation
2) Ingestion of foods high in phosphorus
3) IV administration of sodium or potassium phosphate
208
Magnesium, the second most abundant intracellular cation, plays an important role in essential cellular processes. It is a cofactor in many enzyme systems, including those responsible for?
- Magnesium is required for the production and use of?
- What depends on magnesium?
- responsible for carbohydrate metabolism, DNA and protein synthesis, blood glucose control, and BP regulation
- required for production and use of adenosine triphosphate (ATP) (energy source for the sodium-potassium pump)
- Muscle contraction and relaxation, normal neurologic function, and neurotransmitter release depend on magnesium
209
Magnesium 4 main points
- Coenzyme in metabolism of protein and carbohydrates
- Required for nucleic acid and protein synthesis
- Helps maintain calcium and potassium balance
- Necessary for sodium-potassium pump
210
About 50% to 60% of the body's magnesium is stored in?
- 30% is in?
Only 1% is in?
- What regulates magnesium levels?
- 50% to 60% stored in muscle and bone
- 30% is in cells
- 1% is in ECF
- The intestines and kidneys regulate magnesium levels. GI absorption increases when magnesium levels are low. The kidney regulates serum magnesium by controlling the amount of magnesium reabsorbed in the ascending loop of Henle and distal tubules.
211
Magnesium
- Acts directly on?
- Important for normal?
- 50% to 60% contained in?
- Absorbed in?
- Excreted by?
- Acts directly on myoneural junction
- Important for normal cardiac function
- 50% to 60% contained in bone
- Absorbed in GI tract
- Excreted by kidneys
212
Hypermagnesemia (high serum magnesium level) usually occurs only with?
- A patient with chronic kidney disease who ingests products containing magnesium will have a problem with?
- Magnesium excess could develop in a pregnant woman receiving?
- occurs only with increased magnesium intake accompanied by renal insufficiency or failure
- patient with chronic kidney disease who ingests products containing magnesium (e.g., Maalox, milk of magnesia) will have a problem with excess magnesium.
- Magnesium excess could develop in a pregnant woman receiving magnesium sulfate for the treatment of eclampsia or in patients taking laxatives and antacids that contain magnesium
213
Hypermagnesemia High serum Mg two main causes
1) Increased intake or ingestion of products containing magnesium when renal insufficiency or failure is present
2) Excess intravenous magnesium administration
214
Hypermagnesemia (Mg+ >2.5 mEq/L [1.25 mmol/L]) Causes
* Renal failure
* IV administration of magnesium, especially for treatment of eclampsia
* Tumor lysis syndrome
* Hypothyroidism
* Metastatic bone disease
* Adrenal insufficiency
* Antacids, laxatives
215
Hypermagnesemia (Mg+ >2.5 mEq/L [1.25 mmol/L]) Manifestations (7)
* Lethargy, drowsiness
* Muscle weakness
* Urinary retention
* Nausea, vomiting
* Diminished deep tendon reflexes
* Flushed, warm skin, especially facial
* ↓ Pulse, ↓ BP
216
Hypomagnesemia (Mg+ <1.5 mEq/L [0.75 mmol/L]) Causes
* GI tract fluid losses (e.g., diarrhea, NG suction)
* Chronic alcoholism
* Malabsorption syndromes
* Prolonged malnutrition
* ↑ Urine output
* Hyperglycemia
* Proton pump inhibitor therapy
217
Hypomagnesemia (Mg+ <1.5 mEq/L [0.75 mmol/L])
| Manifestations
* Confusion
* Muscle cramps
* Tremors, seizures
* Vertigo
* Hyperactive deep tendon reflexes
* Chvostek's and Trousseau's signs
* ↑ Pulse, ↑ BP, dysrhythmias
218
Excess magnesium inhibits acetylcholine release at the?
- Initial manifestations include?
- As the serum magnesium level increases, what happens?
- inhibits acetylcholine release at the myoneural junction and calcium movement into cells, impairing nerve and muscle function.
- Initial manifestations include hypotension, facial flushing, lethargy, urinary retention, nausea, and vomiting.
- As the serum magnesium level increases, deep tendon reflexes are lost, followed by muscle paralysis and coma. Respiratory and cardiac arrest can occur.
219
Hypermagnesemia Management begins with avoiding?
- If renal function is adequate, increased?
- In the patient with impaired renal function?
- If hypermagnesemia is symptomatic, giving?
- avoiding magnesium-containing drugs and limiting diet intake of magnesium-containing foods (e.g., green vegetables, nuts, bananas, oranges, peanut butter, chocolate).
- If renal function is adequate, increased fluids and diuretics promote urinary excretion.
- In the patient with impaired renal function, dialysis is required.
- If hypermagnesemia is symptomatic, giving IV calcium gluconate will oppose the effects of the excess magnesium on cardiac muscle.
220
Hypermagnesemia 5 main manifestations
1) Lethargy
2) Nausea and vomiting
3) Impaired reflexes
4) Somnolence
5) Respiratory and cardiac arrest
221
Hypermagnesemia Management
1) Prevention first-
2) Emergency treatment-
3) Fluids and IV furosemide to promote-
4) Dialysis
1) Prevention first—restrict magnesium intake in high-risk patients
2) Emergency treatment
- IV CaCl or calcium gluconate
3) Fluids and IV furosemide to promote urinary excretion
4) Dialysis for impaired renal function
222
Hypomagnesemia (low serum magnesium level) occurs in patients with limited magnesium intake or increased gastrointestinal or renal losses. Causes of hypomagnesemia from insufficient food intake include?
- Another potential cause is prolonged?
- Fluid loss from the GI tract, inflammatory bowel disease, and proton pump inhibitors interfere with?
- Many diuretics and osmotic diuresis from high glucose levels may cause?
- insufficient food intake include prolonged fasting or starvation and chronic alcoholism.
- prolonged parenteral nutrition without magnesium supplementation.
- Fluid loss from the GI tract, inflammatory bowel disease, and proton pump inhibitors interfere with magnesium absorption.
- Many diuretics and osmotic diuresis from high glucose levels may cause magnesium loss through increased urinary excretion
223
Clinically, hypomagnesemia resembles hypocalcemia. Neuromuscular manifestations are common, such as?
muscle cramps, tremors, hyperactive deep tendon reflexes, Chvostek's sign, and Trousseau's sign. Neurologic manifestations include confusion, vertigo, and seizures.
224
Magnesium deficiency can lead to?
cardiac dysrhythmias, such as torsades de pointes and ventricular fibrillation.
225
Hypomagnesemia is associated with?
digitalis toxicity
226
Managing hypomagnesemia depends on the underlying cause and the patient's symptoms.
1) Mild magnesium deficiencies involve?
2) If hypomagnesemia is severe or if hypocalcemia is present, what is given?
1) Mild magnesium deficiencies involve oral supplements and increased dietary intake of foods high in magnesium. 2) If hypomagnesemia is severe or if hypocalcemia is present, IV magnesium (e.g., magnesium sulfate) is given. Monitor vital signs and use an infusion pump, since rapid administration can lead to hypotension and cardiac or respiratory arrest.
227
Hypomagnesemia Low serum Mg caused by? 6 main points
1) Prolonged fasting or starvation
2) Chronic alcoholism
3) Fluid loss from gastrointestinal tract
4) Prolonged parenteral nutrition without supplementation
5) Diuretics
6) Hyperglycemic osmotic diuresis
228
Hypomagnesemia manifestations 7 main points
1) Confusion
2) Hyperactive deep tendon reflexes
3) Muscle cramps
4) Tremors
5) Seizures
6) Cardiac dysrhythmias
7) Corresponding hypocalcemia and hypokalemia
229
Hypomagnesemia management 4 main points
1) Treat underlying cause
2) Oral supplements
3) Increase dietary intake
4) Parenteral IV or IM magnesium when severe
230
IV Fluids
1) Purposes
2) Types of fluids categorized by?
1) Purposes
- Maintenance
When oral intake is not adequate
- Replacement
When losses have occurred
2) Types of fluids categorized by tonicity
231
A hypotonic solution has more?
- Infusing a hypotonic solution? Osmosis then produces a movement of water from ECF to interstitial spaces and cells, causing cells to swell. After achieving equilibrium, ICF and ECF have the same osmolality.
- Hypotonic solutions (e.g., ______) are useful in treating patients with?
- They are not good for replacement because they can?
- Because hypotonic solutions have the potential to cause cellular swelling, monitor patients for changes in?
- more water than electrolytes, with an osmolality of less than 250 mOsm/kg
- Infusing a hypotonic solution dilutes ECF, lowering serum osmolality. Osmosis then produces a movement of water from ECF to interstitial spaces and cells, causing cells to swell. After achieving equilibrium, ICF and ECF have the same osmolality
- useful in treating patients with hypernatremia and are a good maintenance fluid because normal daily losses are hypotonic
- not good for replacement because they can deplete ECF and lower BP.
- Because hypotonic solutions have the potential to cause cellular swelling, monitor patients for changes in mentation that may indicate cerebral edema
232
Although 5% dextrose in water is technically an isotonic solution, the dextrose quickly metabolizes. The net result is the administration of?
- One liter of a 5% dextrose solution provides 50 g of dextrose, or 170 calories. While this amount of dextrose is not enough to meet caloric requirements, it helps prevent?
- administration of hypotonic free water with equal expansion of ECF and ICF.
- helps prevent ketosis associated with starvation
233
IV Fluids: Hypotonic main points
1) More water than electrolytes
- Pure water lyses RBCs
2) Water moves from ECF to ICF by osmosis
3) Usually maintenance fluids
4) Monitor for changes in mentation
234
IV Fluids: Isotonic --- “I so perfect” main points
1) Expands only ECF
2) No net loss or gain from ICF
3) Ideal to replace ECF volume deficit
235
An isotonic solution has a similar concentration of water and electrolytes to plasma, with an osmolality of 250 to 375 mOsm/L. Because of the similarity, administering an isotonic solution does what?
expands only ECF, and the fluid does not move into cells. This makes isotonic solutions the ideal fluid replacement for patients with ECF volume deficits. Examples of isotonic solutions include 0.9% NaCl and lactated Ringer's solution.
236
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Isotonic saline (0.9% NaCl) or normal saline has a sodium concentration (154 mEq/L) somewhat higher than that of plasma (135 to 145 mEq/L) and a chloride concentration (154 mEq/L) significantly higher than the plasma chloride level (96 to 106 mEq/L). Therefore excessive administration of isotonic saline has the potential to?
- Isotonic saline is used when?
```
- excessive administration of isotonic saline has the potential to increase sodium and chloride levels.
- Isotonic saline is used when a patient has experienced both fluid and sodium losses (e.g., diarrhea, vomiting). It is the fluid of choice for replacement
237
Lactated Ringer's solution contains?
- This makes it the ideal fluid in certain situations, such as?
- Patients with what should not receive lactated Ringer's solution?
- contains sodium, potassium, chloride, calcium, and lactate (the precursor of bicarbonate) in about the same concentrations as ECF.
- ideal fluid in certain situations, such as surgery, burns, or GI fluid losses.
- Patients with liver dysfunction, hyperkalemia, and severe hypovolemia should not receive lactated Ringer's because they have a decreased ability to convert lactate to bicarbonate.
238
Hypertonic main points
1) Initially expands and raises the osmolality of ECF
2) Require frequent monitoring of
- Blood pressure
- Lung sounds
- Serum sodium levels
239
A hypertonic solution initially raises the?
- The higher osmotic pressure does what?
- It is useful in the treatment of?
- Hypertonic solutions require frequent monitoring of?
- raises the osmolality of ECF and expands volume.
- higher osmotic pressure draws water out of the cells into ECF.
- useful in the treatment of hyponatremia and trauma patients with head injury.
- frequent monitoring of BP, lung sounds, and serum sodium levels because of the risk for intravascular fluid volume excess.
240
Although concentrated dextrose and water solutions (___% dextrose or greater) are hypertonic solutions, once the dextrose is metabolized, the net result is the administration of?
- The primary use of these solutions is?
- You may administer solutions containing ___% dextrose or less through a _______ line.
You must use a _____ line to administer solutions with dextrose concentrations greater than ___%
(10% dextrose or greater)
- administration of water. This free water ultimately expands ECF and ICF.
- The primary use providing calories as part of parenteral nutrition.
- You may administer solutions containing 10% dextrose or less through a peripheral line.
- You must use a central line to administer solutions with dextrose concentrations greater than 10%.
241
D5W (5% Dextrose in Water)
Tonicity
Indications and considerations
1) Tonicity: Isotonic, but physiologically hypotonic
2) Indications and considerations:
• Contains free water only, no electrolytes
• Provides 170 cal/L
• Used to replace water losses and treat hypernatremia
• Prevents ketosis associated with starvation
242
D5W
- Free water
- Used to replace?
- Does not provide?
- Free water
* Moves into ICF
* Increases renal solute excretion
- Used to replace water losses and treat hypernatremia
- Does not provide electrolytes
243
Normal Saline (NS or NSS)
- Isotonic
- More NaCl than ECF
- Expands IV volume
- Preferred fluid for immediate response
- Risk for fluid overload higher
- Also monitor for hyperchloremic acidosis
- No free water
- No calories
- No additional electrolytes
- Blood products
- Compatible with most medications
244
Lactated Ringer's (Hartmann's) solution
Tonicity
Indications and considerations
- Tonicity: Isotonic
- Indications and considerations:
• Similar in composition to normal plasma except does not contain Mg2+
• Does not provide free water or calories
• Used to treat hypovolemia, burns, and GI fluid losses
• Cannot be used in patients with alkalosis or lactic acidosis
245
D5 1/2 NS (5% dextrose in 0.45% NS)
- Tonicity: hypertonic
- Indications and considerations:
• Provides Na+, Cl−, and free water
• Used as a maintenance solution
• Replaces fluid loss
• KCl added for maintenance or replacement
246
D10W (10% dextrose in water)
-Tonicity: Hypertonic
- Indications and considerations
• Contains free water only, no electrolytes
• Provides 340 cal/L
• Used with parenteral nutrition
• Limit of dextrose concentration may be infused peripherally
247
Plasma expanders
- Stay in vascular space and increase osmotic pressure
- Colloids (protein solutions)
* Plasma, albumin, commercial plasmas
- Dextran
- Hetastarch
- Blood
248
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Dextrans are synthetic complex sugar solutions. There are two types: low-molecular-weight dextran (dextran 40) and high-molecular-weight dextran (dextran 70). Because dextran metabolizes slowly, it remains in the vascular system for a prolonged period. It pulls additional?
Hydroxylethyl starches (e.g., Hespan) are synthetic colloids that work similarly to dextran to expand plasma volume.
```
-pulls additional fluid into the intravascular space, expanding it by more volume than what is infused. Hydroxylethyl starches (e.g., Hespan) are synthetic colloids that work similarly to dextran to expand plasma volume.
249
In a patient with prolonged vomiting, the nurse monitors for fluid volume deficit because vomiting results in
A. Fluid movement from the cells into the interstitial space and the blood vessels
B. Excretion of large amounts of interstitial fluid with depletion of extracellular fluids
C. An overload of extracellular fluid with a significant increase in intracellular fluid volume
D. Fluid movement from the vascular system into the cells, causing cellular swelling and rupture
A. Fluid movement from the cells into the interstitial space and the blood vessels
Rationale: Fluid volume deficit occurs when there is loss of both sodium and water. Intracellular fluid moves into the interstitial spaces and blood vessels
250
The nurse is administering 3.0 % saline solution IV to a patient with severe hyponatremia. It is most important for the nurse to observe for what?
a. Decreased heart rate and blood pressure
b. Prolonged QT interval and facial flushing
c. Shortness of breath and increased respiratory rate
d. Increased urine output and decreased urine specific gravity
c
Rationale: Hypertonic solutions such as 3.0% saline must be administered with extreme caution because it may cause dangerous intravascular volume overload and pulmonary edema. Signs and symptoms of volume overload and pulmonary edema include shortness of breath and increased respiratory rate.
251
A patient is admitted with renal failure and an arterial blood pH level of 7.29. Which lab result would the nurse expect?
Serum sodium 138 mEq/L
Serum glucose 145 mg/dL
Serum creatinine 0.4 mg/dL
Serum potassium 5.9 mEq/L
Serum potassium 5.9 mEq/L
