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NSG 300 > Topic 6: Fluid Balance > Flashcards

Topic 6: Fluid Balance Flashcards

1
Q

where is fluid distributed in the body

A

fluid surrounds all cells in the body and is also inside cells

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2
Q

what are the characteristics of body fluids

A

-fluid amount (volume)
-concentration (osmolality)
-composition (electrolyte concentration)
-degree of acidity (pH)

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3
Q

what is the recommended fluid intake

A

~2300mL/day

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4
Q

when is the thirst mechanism in the hypothalamus activated?

A

when plasma osmolarity increases (osmoreceptor-mediated thirst) or the blood volume decreases (baroreceptor-mediated thirst and angiotensin II and III mediated thirst)

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5
Q

fluid distribution

A

the movement of fluid among its various compartments

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6
Q

extracellular and intracellular distribution occurs by

A

osmosis

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7
Q

vascular and interstitial distribution occurs

A

filtration

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8
Q

where does fluid ouput normally happen in the body

A

skin, lungs, GI tract, kidneys

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9
Q

insensible loss

A

Water lost thru the skin (individual is unaware of losing that water)

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10
Q

sensible loss

A

loss that is perceived or is measurable. (wound drainage, GI tract, urine)

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11
Q

fluid output is influenced by what hormonal influences

A

-ADH
-RAAS
-ANPs

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12
Q

When is ADH released?

A

when dehydrated and and body fluids are more concentrated

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13
Q

what factors increase ADH levels

A

o Decreased blood volume (dehydration, hemorrhage)
o Pain
o Stressors
o Some medications

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14
Q

what does the RAAS regulate

A

ECF volume by influencing how much sodium and water are excreted in urine.
it also contributes to regulation of BP

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15
Q

Atrial natriuretic peptides (ANPs)

A

regulates ECF volume by influencing how much sodium and water is excreted in urine
-Cells in the atria of the heart release ANP when they are stretched (e.g., by an increased ECV).

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16
Q

Volume imbalances

A

disturbances of the amount of fluid in the extracellular compartment

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17
Q

osmolarity imbalances

A

disturbances of the concentration of body fluids

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18
Q

When is ECV deficit present?

A

when isotonic fluid is insufficient in the extracellular compartment.
(With ECV deficit, output of isotonic fluid exceeds intake of sodium-containing fluid.)

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19
Q

When is ECV excess present?

A

occurs when too much isotonic fluid is found in the extracellular compartment.
(when you eat more salty foods than usual and drink water, ankles or feet may swell)

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20
Q

hypertonic

A

Water leaves cells by osmosis, and they shrivel (more solutes outside cell)

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21
Q

hypotonic

A

-The excessively dilute condition of interstitial fluid causes water to enter cells by osmosis, causing the cells to swell (more solute in cell)

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22
Q

hypernatremia

A

“water deficit”; hypertonic
loss of more water than salt or gain of salt

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23
Q

what are the s/s of hypernatremia

A

cerebral dysfunction (which arise when brain cells shrivel)

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24
Q

hyponatremia

A

“water excess/water intoxification”; hypotonic
(more water than salt or less salt than water)

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25
Q

what are the s/s of hyponatremia

A

cerebral dysfunction (occur when brain cells swell)

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26
Q

clinical dehydration

A

ECV deficit and hypernatremia often occur at the same time

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27
Q

what are some common causes of clinical dehydration

A

gastroenteritis or other causes of severe vomiting and diarrhea when people are not able to replace their fluid output with enough intake of dilute sodium-containing fluids.

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28
Q

hypokalemia

A

abnormally low potassium concentration in the blood.

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29
Q

hyperkalemia

A

abnormally high potassium concentration in the blood

30
Q

Hypercalcemia

A

abnormally high calcium concentration in the blood

31
Q

Hypomagnesemia

A

abnormally low magnesium concentration in the blood

32
Q

Hypermagnesemia

A

abnormally high magnesium concentration in the blood

33
Q

potassium function

A

Maintains resting membrane potential of skeletal, smooth, and cardiac muscle, allowing normal muscle function

34
Q

who are those at the greatest risk for hyperkalemia

A

-Chronically ill patients
-Debilitated patients
-Older adult
-Patients who have oliguria (decreased UO)

35
Q

what are s/s of hyperkalemia

A

o Bilateral muscle weakness in quadriceps
o Transient abdominal cramps
o Diarrhea
o Dysrhythmias
o Cardiac arrest if severe

36
Q

hypokalemia causes

A

o Decreased potassium intake and absorption, a shift of potassium from the ECF into cells, and an increased potassium output
o Increased potassium output include diarrhea, repeated vomiting, and use of potassium-wasting diuretics

37
Q

hypokalemia s/s

A

o Bilateral muscle weakness that begins in quadriceps and may ascend to respiratory muscles, abdominal distention, decreased bowel sounds, constipation, dysrhythmias

38
Q

calcium function

A

Influences excitability of nerve and muscle cells; necessary for muscle contraction

39
Q

hypercalcemia causes

A

o Increased calcium intake and absorption
o Shift of calcium from bones into the ECF
o Decreased calcium output

40
Q

hypercalcemia s/s

A

o Anorexia, nausea and vomiting, constipation, fatigue, diminished reflexes, lethargy, decreased level of consciousness, confusion, personality change, cardiac arrest if severe

41
Q

hypocalcemia causes

A

o Decrease absorption of dietary calcium and also increases calcium output by preventing resorption of calcium contained in GI fluid
o People who have acute pancreatitis frequently develop hypocalcemia because calcium binds to undigested fat in their feces and is excreted.

42
Q

hypocalcemia s/s

A

o Numbness and tingling of fingers, toes, and circumoral (around mouth) region, positive Chvostek’s sign (contraction of facial muscles when facial nerve is tapped), hyperactive reflexes, muscle twitching and cramping; carpal and pedal spasms, tetany, seizures, laryngospasm, dysrhythmias

43
Q

magnesium functions

A

o Influences function of neuromuscular junctions; is a cofactor for numerous enzymes

44
Q

hypermagnesemia causes

A

o Renal failure
o Diabetes Mellitus
o Clients who ingest large amounts of Mg-containing antacids such as Tums, Maalox, Mylanta, or laxatives such as MOM are also in ↑ risk for developing hypermagnesemia

45
Q

hypermagnesemia s/s

A

o Bradycardia and hypotension
o Severe hypermagnesemia: cardiac arrest
o Drowsy or lethargic
o Coma
o Deep tendon reflexes are reduced or absent
o Skeletal muscle contractions become progressively weaker and finally stop

46
Q

hypomagnesemia causes

A

o Decreased magnesium intake and absorption
o Shift of plasma magnesium to its inactive bound form
o Increased magnesium output

47
Q

hypomagnesemia s/s

A

o Positive Chvostek’s sign, hyperactive deep tendon reflexes, muscle cramps and twitching, grimacing, dysphagia, tetany, seizures, insomnia, tachycardia, hypertension, dysrhythmias

48
Q

Chronic alcohol abuse commonly causes…

A

hypomagnesemia, in part because it increases renal magnesium excretion

49
Q

what things in medical history are important to asses for fluid output

A

-recent surgery (excessive blood loss)
-GI output
-trauma (respiratory disorder, burns (increased exudate output) hemorrhage

50
Q

oliguria

A

Decreased urine output

51
Q

what is the most accurate indicator of fluid status?

A

daily weights

52
Q

each 2.2 lbs of weight gained or lost overnight is equal to _____

A

1 L of fluid retained or lost

53
Q

When taking daily weights it is impprtant to

A

use the same conditions (clothes, weight, scale, sheets etc)

54
Q

fluid intake and output

A

compare intake vs output

55
Q

if intake is substantially greater than output…

A

The patient may be gaining excessive fluid or may be returning to normal fluid status by replacing fluid lost previously from the body.

56
Q

if intake is substantially smaller than output…

A

The patient may be losing needed fluid from the body and developing ECV deficit and/or hypernatremia or may be returning to normal fluid status by excreting excessive fluid gained previously.

57
Q

Intake includes what?

A

all liquids eaten, drunk, or received through IV, NG tube

58
Q

output includes what?

A

Urine, diarrhea, vomitus, gastric suction, wound drainage, or other tubes

59
Q

health promotion and fluid balance

A

o Fluid replacement education
o Teach patients with chronic conditions about risk factors and signs and symptoms of imbalances.

60
Q

total parenteral nutrition

A

administered to patients who cannot, or should not, get their nutrition through eating

61
Q

crystalloids

A

electrolyte therapy

62
Q

colloids

A

Blood and blood components.

63
Q

what is the goal of IV fluid administration

A

to correct or prevent fluid and electrolyte disturbances. IVs allow direct access to the vascular system, permitting continuous infusion of fluids over a period of time.

64
Q

Isotonic solutions

A

have the same effective osmolality as body fluids. (normal saline)

65
Q

what is normal saline used for

A

ECV replacement to prevent or treat ECV deficit.

66
Q

Hypotonic solutions

A

have an effective osmolality less than body fluids, thus decreasing osmolality by diluting body fluids and moving water into cells.
*make body fluid less concentrated, forcing water into cells

67
Q

Hypertonic solutions

A

have an effective osmolality greater than body fluids. If they are hypertonic sodium-containing solutions, they increase osmolality rapidly and pull water out of cells, causing them to shrivel.

68
Q

Central catheters and implanted ports

A

Devices for long-term use, which empty into a central vein.

69
Q

Central catheters and implanted ports

A

Devices for long-term use, which empty into a central vein.

70
Q

Peripherally inserted central catheters (PICC lines)

A

enter a peripheral arm vein and extend through the venous system to the superior vena cava, where they terminate.

NSG 300 (13 decks)

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