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Electrolytes Flashcards

1
Q

Describe the physiology behind fluid and electrolytes.

A

➢The body is composed of fluids and particles dissolved or suspended in water.
➢ The fluid portion is called a solvent.
➢ The particles dissolved or suspended in the water are called solutes.
➢ Solutes that express an overall electrical charge are called electrolytes.
➢ The fluids and particles are in different fluid compartments or spaces.

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2
Q

What are the fluid compartments?

A

➢ Extracellular compartment
• Contains extracellular fluids and electrolytes
• The fluid is outside the cell (40%)
• Extracellular fluid (ECF) is divided into:
o Blood Plasma – in the vascular space (arteries/veins) (7% total)
o Interstitial fluid - in between the cells of the body ➢ Intracellular compartment
• Contains intracellular fluid (ICF) and electrolytes
• The fluid is inside the cell (60%)
• Intracellular fluid constitutes most of the body’s fluid (app. 2/3)

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3
Q

How does homeostasis work to keep fluid and electrolytes balanced in the body?

A

➢ Fluid and electrolyte balance must be maintained at all times for the body to function properly.
➢ Electrolyte homeostasis is the balance between dietary intake of electrolytes and renal
excretion or reabsorption of electrolytes.
➢ Hormones like aldosterone, antidiuretic hormone (ADH), natriuretic peptide (NP), and renin-
angiotensin II pathway regulate fluid and electrolyte balance (for details – refer to hormonal
regulation… and renin-angiotensin II pathways on pp. 165-167).
➢ Regulatory processes are also in place to keep the internal environment stable. They determine
how, when, and where fluids and particles move across cell membranes.
➢ The regulatory processes are filtration, diffusion, and osmosis, and active transport.

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4
Q

What are the regulatory processes of homeostasis?

A
  1. Filtration
  2. Diffusion
  3. Osmosis
  4. Active transport
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5
Q

What is filtration?

A

➢ It is the movement of water molecules (solvents) through a cell or blood vessel membrane from
an area of higher hydrostatic pressure to lower hydrostatic pressure.
➢ Hydrostatic pressure – “Water-pushing pressure” – is the force that pushes water outward from a confined space through a membrane.
➢ The amount of water in any body fluid space determines pressure.

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6
Q

What is hydrostatic pressure?

A

“Water-pushing pressure” – is the force that pushes water outward from a confined space through a membrane.

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7
Q

What is the clinical significance of filtration?

A
  1. Blood pressure
    o Moves blood from the heart to the capillaries where the exchange of water, nutrients, wastes between blood and tissues occurs.
  2. Edema
    o It occurs with changes in hydrostatic pressure. Venous hydrostatic pressure
    increases, forcing fluids into the interstitial spaces.
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8
Q

What is diffusion?

A

➢ It is the movement of particles (solutes) across a permeable membrane from an area of higher solute to lower solute concentration.
➢ It does not require energy (passive).

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9
Q

What is the clinical significance of diffusion?

A

• Transports most electrolytes and other particles through cell membranes.

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10
Q

What is facilitated diffusion?

A

Allows diffusion of large, membrane insoluble compounds such as sugars and amino
acids by binding to a membrane-altering system for transport.

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11
Q

What is the clinical significance of facilitated diffusion?

A

Glucose binds with insulin to enter most cell membranes

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12
Q

What is active transport?

A

➢ Movement of particles (solutes) across a membrane against a concentration or electrochemical gradient
➢ Used to pump specific compounds
➢ Requires energy (active)

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13
Q

What is the clinical significance of active transport?

A

• Na+/K+ pump
o Pumps K+ into the cell; pumps Na+ out of the cell o This transport requires ATP energy

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14
Q

What is osmosis?

A

➢ It is the movement of water molecules (solvent) across a selectively permeable (semi-permeable) membrane from a less concentrated solution to a more concentrated solution.
➢ The particle (solute) concentration of a body fluid dictates the osmosis and diffusion.

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15
Q

What is osmotic pressure?

A

“Water-pulling pressure” – is the force that stops osmosis.

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16
Q

What is an osmotic solution’s concentration called?

A

Osmolality (per liter of solution) or osmolarity (per
kg of a solution. They are used interchangeably.

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17
Q

What is the osmolality of blood plasma? (ECF)

A

270-300 mOsm/L.

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18
Q

What is the clinical significance of osmosis?

A

IV fluid therapy is based on the plasma’s osmolality

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19
Q

Describe the basics of fluid balance.

A

➢ “Input” includes all fluids that enter the body orally or parenterally.
➢ “Output” includes all fluids that leave the body.
➢ Insensible water loss from the skin, lungs, and GI system is 500 to 1000 mL/day. It must be
replaced to avoid severe dehydration and electrolyte imbalances.
➢ Obligatory urine output to effectively excrete toxic waste products is 400-600 ml/day.

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20
Q

Which populations are most prone to fluid imbalances?

A

Older adults, obese, and women are prone to fluid imbalances because they have less body water.

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21
Q

What are the main functions of Na+?

A

➢ Major extracellular cation

➢ Maintains blood volume by regulating water.

➢ Generates electrical impulses for proper brain functioning and muscle contraction

➢ Maintains osmotic pressure

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22
Q

How is Na+ regulated?

A

➢ Regulated by the kidneys through aldosterone, antidiuretic hormone, and natriuretic peptide

➢ Regulated by the Na-K pump

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23
Q

Which Electrolytes are related to Na+?

A

➢ Cl- directly related

➢Na+ Increases kidney excretion of Ca++

➢Hypernatremia slows the flow of Ca++ into the cardiac cells

➢has an inverse relationship with K+

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24
Q

What are the main functions of K+?

A

➢ Major intracellular cation

➢ Essential for the depolarization and generation of action potentials to maintain cardiac, skeletal, and smooth muscle function

➢ Transmits nerve and cardiac impulses

➢ Regulates protein synthesis, glucose use and storage, and acid-base balance

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25
Q

How is K+ regulated?

A

➢Regulated by the kidneys through excretion and aldosterone

➢Regulated by the Na-K pump

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26
Q

Which electrolytes are related to K+?

A

➢Mg++, Ca++
usually decreased with hypokalemia (Mg++ more than Ca++)

➢Mg++ acts as a modulator facilitating the movement of Na+ and K+ through the Na+-K+ pump

inverse relationship with Na

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27
Q

What are the main functions of Ca++?

A

➢The most abundant cation in the body stored in the bones and teeth

➢Calcium enters the body by dietary intake, absorbed through the intestinal tract, and stored in the bones.

➢ Two forms: Bound – attached to albumin Ionized – free, active form that must be kept within range.

➢Maintains bone strength and density

➢Activates enzymes
Allows skeletal and cardiac muscle contraction

➢Controls nerve impulse transmission by regulating the movement of Na+ across membranes.

➢Membrane stabilizer (essential in stabilizing cardiac membrane)

➢Allows blood clotting

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28
Q

How is Ca++ regulated?

A

➢Regulated by parathyroid hormones (increases) and thyrocalcitonin (decreases)

➢Vitamin D needed for absorption

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29
Q

What electrolytes are related to Ca++?

A

➢Phos –inverse relationship

➢Mg++ - directly related

➢Bound Ca++ (which is commonly tested) is directly related to Protein

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30
Q

What are the main functions of Mg++?

A

➢Mostly stored in bones and cartilage

➢It has a vasodilatory effect on the cardiac system

➢It has a relaxing effect on the nerves

➢Essential for cardiac function

➢Carbohydrate metabolism and Vitamin activation

➢ATP (energy) formation and cell growth

➢Regulates blood coagulation, skeletal muscle contractility, and smooth muscle relaxation

➢Required for Ca++ and Vit. B12 absorption

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31
Q

How is Mg++ regulated?

A

Regulated by the kidneys and intestinal tract

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32
Q

What electrolytes are related to Mg++?

A

➢Mg++, Ca++
usually decreased with hypokalemia (Mg++ more than Ca++)

➢Mg++ acts as a modulator facilitating the movement of Na+ and K+ through the Na+-K+ pump

➢Ca++ directly related

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33
Q

What are the main functions of Phos (- -)?

A

➢Major intracellular anion

➢Mostly found in the bones (80%)

➢Nearly present in all foods and absorbed efficiently in the jejunum

➢Activates vitamins and enzymes

➢Forms adenosine triphosphate (ATP) for energy supplies

➢Assists in bone mineralization and cell growth

➢Acid-base balance Calcium homeostasis

➢Regulation of nerve impulses, HR, muscle contraction

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34
Q

How is Phos (- -) regulated?

A

➢Regulated by parathyroid hormones

➢Regulated by renal excretion

➢Na+-mediated transport mechanism

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35
Q

What electrolytes are related to Phos (- -)

A

Ca++ inverse relationship

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36
Q

What are the main functions of Cl-?

A

➢ Major extracellular anion

➢ Enters the body through dietary intake

➢Regulates acid-base balance

➢Produces HCl acid

➢Regulates ECF balance

➢Acts as a buffer in O2-CO2 exchange

➢Maintains osmotic pressure

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37
Q

How is Cl- regulated?

A

➢Regulated by the kidneys through aldosterone, antidiuretic hormone, and natriuretic peptide

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37
Q

How is Cl- regulated?

A

➢Regulated by the kidneys through aldosterone, antidiuretic hormone, and natriuretic peptide

38
Q

What electrolytes are related to Cl-?

A

Na++ direct relationship HCO- inverse relationship

39
Q

What is Fluid Volume Deficit (FVD)?

A

➢Dehydration or Hypovolemia

40
Q

What is fluid volume excess (FVE)?

A

Overhydration or Hypervolemia

41
Q

How is FVD managed?

A

➢Patient safety: Monitor VS, mental status, muscle strength, and gait

➢Drug therapy: anti-diarrheal, antibiotic, anti- emetic, anti-pyretic

➢Fluid therapy: Oral hydration; IV fluid (see IV Fluid Management of FVD below). Monitor for fluid overload and IV site, weigh daily, I&O

➢Patient Education: Adequate hydration throughout the day, avoid falls/injuries, identify risks

42
Q

How is FVE managed?

A

➢Patient safety: Monitor VS, peripheral edema, skin breakdown, respiratory status, mental status, cardiac status

➢Drug therapy: diuretics, conivaptan, or tolvaptan. Monitor response to therapy, weigh daily, I&O

➢Nutrition therapy: Fluid and diet restrictions

➢Patient Education: Identify risks, appropriate diet choices, weight gain

43
Q

Describe the IV management of FVD

A

RESUSCITATE FIRST, then MAINTAIN. REPLACE or REDISTRIBUTE as appropriate. ASSESS always!

If there are signs of hypotension and tissue hypoperfusion (SBP <100, HR >90, RR >20, capillary refill > 2 seconds, peripheries cold to touch, altered mental status) → give isotonic solutions

Note: Isotonic solutions do not shift between the compartments, which effectively expands intravascular (EFC) volume and improve BP.

Once BP has stabilized→maintain, replace, or redistribute to sustain cellular needs
• If hypernatremic, give hypotonic solutions or dextrose- containing crystalloids

Note: Hypotonic solutions hydrate the cells because they shift from EFC to IFC – watch for cerebral edema. Initially considered hypertonic, dextrose-containing solutions become isotonic or hypotonic once the dextrose is metabolized. For example, D5NS becomes isotonic, and D51/2NS becomes hypotonic.

If hyponatremic, give isotonic solutions

In symptomatic hyponatremia - give hypertonic solutions (3-5% Normal Saline) slowly to

prevent Central Pontine Myelinolysis (also known as Osmotic Demyelination Syndrome). Patients with chronic hyponatremia (occurring > 48 hours) are more prone to this condition with rapid correction than those with acute hyponatremia.

Note: Hypertonic solutions are used to treat symptomatic hyponatremia, volume resuscitation in critical care, and prevention of cerebral edema in Traumatic Brain Injury (TBI).

44
Q

What are the 3 types/categories of IV fluids and their osmolarity?

A
  1. Hypotonic solutions:
    1. < 270 mOsm/L
  2. Isotonic solutions
    1. 270-300 mOsm/L
  3. Hypertonic solutions
    1. > 300 mOsm/L
45
Q

What is a common hypotonic solution?

A

Crystalloid: 0.45% NaCl (½ normal saline)

46
Q

What are some common isotonic solutions?

A
  1. Crystalloid: 0.9% NaCl (normal saline/ NS)
  2. Balanced solution: Lactated Ringers (LR)
  3. Electrolyte-free (Dextrose) solutions: 5% Dextrose (D5W) *** once dextrose is metabolized, it becomes hypotnic****
47
Q

What are some common hypertonic solutions?

A
  1. Crystalloids: 3-5% NaCl
  2. Crystalloid containing Dextrose solutions:
    1. 10% Dextrose (D10W)
    2. 5% Dextrose in 0.9% sodium chloride (D5NS)
    3. 5% Dextrose in 0.45% NaCL (D5½NS)
    4. 5% Dextrose in lactated ringers (D5LR)

**Once dextrose is metabolized, the remaining crystalloid portion determines tonicity**

48
Q

What happens in Na+ imbalances?

A

Sodium imbalances occur with fluid imbalances because the same hormones regulate both sodium and water balance.

  • Hyponatremia can occur in the setting of FVD or FVE.*
  • Hypernatremia can occur in the setting of FVD or FVE.*

Cerebral changes are mainly seen in hyponatremia due to cerebral edema and increased intracranial

pressure.

Muscle weakness, spasms, and twitching occur due to a compromised transmission of nerve impulses. Assess respiratory status if muscle weakness is present.

49
Q

How is hyponatremia managed?

A
  • Patient safety: Monitor response to therapy; Skin protection; Seizure precaution if severe; Monitor for hypernatremia, fluid overload, neuro status, VS, and I&O
  • Nutrition therapy: High Na+ intake; Restrict fluid intake (if ass. with hypervolemia); Adequate fluid intake (if ass. with hypovolemia)
50
Q

Describe drug therapy for hyponatremia.

A
  • reduce diuretic doses
  • w/ hypervolemia: (dilutional hyponatremia)
    • Tolvaptan or conivaptan (removes water but keeps Na+)
  • w/hypovolemia: normal saline
  • with hypovolemia + neuro symptoms: hypertonic solution (3-5% normal saline)
51
Q

What pt education would you provide for hyponatremia

A

Patient Education: Identify risks; Appropriate diet choices; Monitor weight

52
Q

How is hypernatremia managed?

A

Patient safety: Monitor response to therapy; Skin protection; Seizure precaution if severe; Monitor for hyponatremia, dehydration, neuro status, VS, and I&O

Nutrition therapy: Na+ restriction; Restrict fluid intake (if ass. with hypervolemia); Adequate fluid intake (if ass. with hypovolemia)

53
Q

Describe potential drug therapies for hypernatremia.

A
  • with hypervolemia: loop diuretics
  • with hypovolemia: isotonic solution to resuscitate
    • Once BP is stable, hypotonic or D5W
54
Q

What pt education would you provide for hypernatremia

A

Identify risks; Appropriate diet choices; Monitor weight

55
Q

What happens in K+ imbalances?

A

K+ imbalances are life-threatening as K+ affects all body systems, particularly the heart.

Cardiac monitoring for dysrhythmias is critical: PVCs, conduction delays, ventricular fibrillation, and

heart blocks. Tall T waves (hyperkalemia) or presence of U wave (hypokalemia) on ECG.

In symptomatic hyperkalemia, giving calcium stabilizes the cardiac membrane to prevent lethal

dysrhythmias.

Patients at the highest risk for hyperkalemia include those with renal dysfunction, chronically ill,

debilitated patients, and older adults.

Patients at the highest risk for hypokalemia include those with CHF and on diuretics.

In hypokalemia,

o Assess respiratory status if muscle weakness is present.
o Monitor for common clinical complaints of leg cramps and constipation. o Watch for digoxin toxicity.

56
Q

Describe the management of hypokalemia

A

Patient safety: Adequate oxygenation; Fall prevention; Injury prevention from K+ administration; Monitor response to therapy; Monitor for hyperkalemia, metabolic alkalosis, cardiac status, respiratory status, muscle weakness, constipation, and VS

Drug therapy: K+ oral supplements; K+ IV infusion (essential to know proper administration); Discontinue medications causing the imbalance

Nutrition therapy: High K+ diet

Patient Education: Identify risk; Appropriate

food choices; Early detection of complications

57
Q

What are some important points to remember when treating hypokalemia?

A

Do not give intravenous potassium at a rate higher than 20 mEq per hour.

Never give potassium supplements by the intramuscular, subcutaneous, or IV push routes.

Use a pump or controller when giving intravenous potassium-containing solutions.

Assess the IV site hourly – stop infusion if infiltration or phlebitis is suspected.

Give oral potassium during or after a meal to avoid nausea and vomiting

58
Q

Describe the management of hyperkalemia.

A

Patient safety: Cardiac complications; Fall prevention; Monitor response to therapy; Monitor for hypokalemia, metabolic acidosis, cardiac status, and VS

Drug therapy: Discontinue medications causing the imbalance; IV Calcium (if cardiac symptoms are present); IV glucose and insulin; IV HCO3; Sodium Polystyrene Sulfonate; Loop Diuretics; Patiromer (a new drug that decreases absorption of K+ in the GI tract); Sodium Zirconium Cyclosilicate (a new drug that works on the GI tract to lower K+)

Hemodialysis

Nutrition therapy: Low K+ diet

Patient Education: Identify risks; Appropriate food choices; Early detection of complications

59
Q

Describe Ca+ imbalances

A

• Neuromuscular changes (paresthesia, tingling, numbness, and tetany) occur, particularly in hypocalcemia. These tests are also used in hypomagnesemia.

o Trousseau sign - carpopedal spasm when BP cuff inflated (Fig. 11.13) p. 180

o Chvostek’s sign – facial twitching when facial nerve tapped (Fig. 11.14) p. 180 • Hypocalcemia may cause laryngospasms – watch respiratory status.
• Hypercalcemia

o Cardiac dysrhythmias can occur – cardiac monitoring is essential.
o May further increase the risk of clotting in those who are predisposed to blood clots.

Patients with chronic renal failure will most likely have hypocalcemia due to hyperphosphatemia.

Hyperphosphatemia must be treated with hypocalcemia.

60
Q

What is chronic hypocalcemia?

A

o Postmenopausal women are at risk for chronic calcium loss due to reduced weight-bearing

activities and decreased estrogen levels.
o Patients with chronic hypocalcemia will have brittle, fragile bones – use lift sheets when

repositioning to prevent fractures.
o Chronic hypocalcemia may further increase the risk of bleeding related to delayed clotting.

61
Q

Describe the management of hypocalcemia.

A

Patient safety: Reduce environmental stimuli; Prevent injury – fractures from chronic hypocalcemia; Seizure precaution if severe; Monitor for hypercalcemia, K+, Mg++, Vit D, PTH levels, cardiac status, respiratory status, neuromuscular status, VS, skeletal – for chronic hypocalcemia, and delayed clotting

Drug therapy: Ca++ oral/IV replacements; Vit D supplement Aluminum hydroxide

Nutrition therapy: High calcium diet; Low phosphate diet

Patient Education: Identify risks; Appropriate food choices

62
Q

Describe the management of hypercalcemia.

A

Patient safety: Cardiac complications; Monitor for hypocalcemia, cardiac status, neuro status, intestinal status, VS, and blood clotting

Drug therapy: Discontinue medications causing the imbalance (lactated ringers, thiazide diuretics, Vit. D); Loop diuretics; Bisphosphonates (pamidronate) – for malignancy-associated hypercalcemia; Calcitonin – to inhibit bone resorption; IV fluid therapy

Hemodialysis

Nutrition therapy: Low Ca++ diet; High

phosphate diet

Patient Education: Identify risks; Appropriate food choices

63
Q

Describe Mg ++ imbalances

A

• Imbalances have a sedating effect on the nerves and a vasodilatory effect on the cardiac muscle. o Hypo – neuromuscular Irritability
o Hyper – neuromuscular depression

The key characteristic of hypermagnesemia is severe hypotension with nausea and sometimes vomiting.

With symptomatic hypermagnesemia, giving calcium stabilizes the cardiac membrane to prevent lethal dysrhythmias.

Hypomagnesemia is common in the critically ill and is associated with hypokalemia and hypocalcemia - treat all imbalances

Oral Mg++ can cause diarrhea and thereby increases Mg++ loss.

Avoid administering magnesium sulfate by the intramuscular route – it causes pain and tissue

damage.

Assess for depressed DTR, neuro status, and hypotension during the administration of IV Mg++.

64
Q

Describe the management of hypomagnesemia

A

Patient safety: Reducing environmental stimuli; Preventing injury; Seizure precaution if severe; Monitor for hypermagnesemia, K+, Ca++ levels, cardiac (torsades), neuromuscular status, intestinal status, and VS
• Drug therapy: Discontinue medications causing the imbalance; Oral Mg++ supplements (watch for diarrhea); IV MgSO4 (if severe); Ca++ replacement (if accompanied by hypocalcemia); K+ replacement (if accompanied by hypokalemia)
• Nutrition therapy: High Mg++ diet
• Patient Education: Identify risks, appropriate
food choices

65
Q

Describe the management of hypermagnesemia.

A

Patient safety: Cardiac complications; Monitor for hypomagnesemia, cardiac (bradycardia, hypotension), mental status, neuromuscular status, intestinal status, and VS

Drug therapy: Discontinue medications causing the imbalance; Loop Diuretics; IV fluid therapy

Hemodialysis

Nutrition therapy: Low Mg++ diet

Patient Education: Identify risks, appropriate food choices

66
Q

Describe Phos (- -) imbalances

A

Body functions are not usually affected by an acute imbalance.

Chronic hypophosphatemia is commonly seen in musculoskeletal changes

Issues associated with Phosphate imbalances are r/t Ca++ imbalances.

Management of one imbalance entails the management of the other.

67
Q

What are some common causes of hypophosphatemia?

A

Malnutrition

Starvation

Use of aluminum hydroxide-based antacids

Use of magnesium-based antacids

Hyperparathyroidism

Hypercalcemia

Kidney failure

Malignancy

Hyperglycemia

Hyperaliminetaion

Respiratory alkalosis

Uncontrolled DM

Alcohol abuse

68
Q

What assessment findings would you expect for someone with hypophosphatemia?

A

Cardiac: Weak contractility, decreased stroke volume, decreased cardiac output, weak peripheral pulses

Musculoskeletal: weakness leading to rhabdomyolysis, respiratory failure

Neuro status: Irritability and seizure (only if severe)

69
Q

How is hypophosphatemia managed?

A

Nutrition therapy: High phosphate diet; Low Ca++ diet

Patient Education: Identify risk, Appropriate food choices

  • Patient safety: Fall precaution; Monitor for hyperphosphatemia, hypocalcemia, neuro status, cardiac status, musculoskeletal, and VS
  • Drug therapy: Treat cause; Discontinue medications causing the imbalance; Oral phosphate with Vit D supplement; IV phosphates (for Phos < 1mg/dL); Cinacalcet
70
Q

What are common causes of hyperphosphatemia?

A
  • Decreased kidney excretion resulting from kidney disease
  • Tumor lysis syndrome
  • Increased intake of phosphorus
  • Hypoparathyroidism
71
Q

What assessment findings would you expect with someone with hyperphosphatemia?

A

• Consistent with the manifestations of hypocalcemia

72
Q

Describe the management of hyperphosphatemia.

A

Patient safety: Reduce environmental stimuli; prevent injury – fractures from chronic hypocalcemia; Seizure precaution if severe; monitor for hypercalcemia, K+, Mg++, Vit D, PTH levels, cardiac status, respiratory status, neuromuscular status, VS, skeletal – for chronic hypocalcemia, and delayed clotting

Drug therapy: Treat cause; Phosphate binders (sevelamer) – must be given with food; Ca++ oral/IV replacements; Vit D supplement; Aluminum hydroxide; IV fluid

therapy; Loop diuretic or acetazolamide

Hemodialysis

Nutrition therapy: Low phosphate diet; High Ca++ diet

Patient Education: Identify risks; Appropriate food choices

73
Q

Describe Cl - imbalances

A

Imbalances usually occur as a result of other electrolyte imbalances – correct other electrolyte or acid-base problems.

Hyperchloremia is associated with metabolic acidosis

Hypochloremia is associated with metabolic alkalosis

74
Q

What are common causes of hypochloremia?

A

Vomiting

Diarrhea

Gastrointestinal suction

Renal failure combined with salt deprivation

Overtreatment with diuretics

Chronic respiratory acidosis

Diabetic ketoacidosis

Excessive sweating

SIADH excretion

Salt-losing nephropathy

Acute intermittent porphyria

Water intoxication

Expansion of extracellular fluid volume

Adrenal insufficiency

Hyperaldosteronism

Metabolic alkalosis

Use of certain drugs like chronic laxative or

bicarbonate ingestion, corticosteroids, and diuretics

75
Q

What assessment findings would you expect with someone with hypochloremia?

A

• Hyperirritability

Tetany or muscular excitability

Slowed respiration

Hypotension secondary to fluid loss

76
Q

What are common causes of hyperchloremia?

A

Renal failure

Nephrotic syndrome

Dehydration

Overtreatment with normal saline

Hyperthyroidism

Diabetes insipidus

Metabolic acidosis from diarrhea (loss of HCO3–)

Respiratory alkalosis

Hyperadrenocorticism

Use of certain drugs -

acetazolamide (hyperchloremic acidosis), androgens, hydrochlorothiazide, salicylates (intoxication)

77
Q

What assessment findings would you expect with someone with hyperchloremia?

A

Weakness • Lethargy

Unconsciousness (usually a late sign)

Kussmaul respirations

78
Q

What are the nursing implications related to fluid and electrolyte imbalances?

A

➢ Assure patient safety.

➢ Use a gait belt when assisting a patient with muscle weakness to walk or transfer.

➢ Assess patient respiratory status if muscle weakness is present.

➢ Do not give oral fluids to an unconscious patient.

➢ Schedule offerings of feedings throughout the day if the patient has cognitive impairments or

limited mobility.

➢ Offer or perform oral care at least every 4 hours.

➢ Use a pump or controller to deliver intravenous fluids to patients with fluid overload.

79
Q

What patient teaching applies for fluid and electrolyte imbalances?

A

➢ Maintain adequate fluid intake (at least 2-3 L/day unless contraindicated).

➢ Increase fluid intake when exercising, in hot or dry environments, or during conditions

that increase metabolism, such as fever.

➢ Take daily weights on the same scale, close to the same time each day, and with about

the same amount of clothing each time - monitor for changes or trends.

➢ Caffeine and alcohol can cause dehydration.

➢ Read food labels to determine the electrolyte content of processed foods.

➢ Consider the patient’s food preferences/dislikes and the person preparing the food when

planning an electrolyte-restricted diet.

➢ Follow dietary restrictions and recommendations.

➢ Report changes in symptoms

80
Q

What foods are a source of sodium?

A

Worcestershire sauce, soy sauce, onion salt, garlic salt, bouillon cubes, processed meats like bacon, sausage, and ham, canned soups, canned vegetables, fast foods

81
Q

What foods provide potassium?

A

All meats (red meat and chicken) and fish, such as salmon, cod, flounder, sardines, soy products, veggie burgers., broccoli, peas, lima beans, tomatoes, potatoes (particularly their skins), sweet potatoes, winter squash, citrus fruits, cantaloupe, bananas, kiwi, prunes, and apricots, milk, yogurt, and nuts

82
Q

What foods provide calcium?

A

Yogurt, most cheeses, buttermilk, milk, green leafy vegetables such as broccoli, collards, kale, mustard greens, turnip greens, Chinese cabbage, salmon, and sardines canned with their soft bones, almonds, Brazil nuts, sunflower seeds, tahini, dried beans, blackstrap molasses, orange juice, soy milk, tofu, ready-to-eat cereals, and bread.

83
Q

What foods provide phosphorus?

A

Meat, milk, processed foods that contain sodium phosphate, whole-grain bread, cereals

84
Q

What foods provide magnesium?

A

Bananas, dried apricots, avocados, nuts, peas, beans, seeds, soy products, whole grains, milk

85
Q

Normal range for Na+

A

136-145

86
Q

Normal range for K+?

A

3.5-5.0

87
Q

Normal range for Ca ++

A

9.0-10.5

88
Q

Normal range for Phos - -

A

3.0-4.5

89
Q

Normal range for Magnesium Mg ++

A

1.3-2.1

90
Q

Normal range for Cl-

A

98-106

91
Q

Normal range for BUN

A

10-20

92
Q

Normal range for Creatinine

A

0.5-1.2

AH1 (6 decks)

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