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Foundations > Fluid Volume > Flashcards

Fluid Volume Flashcards

1
Q

Fluid balance is influenced by which three hormones?

A 
antidiuretic hormone (ADH)-takes water from renal system and puts back into body
-Renin-angiotensin-aldosterone system (RAAS)-influences how much urine and output is excreted in the body, angiotensin2 is a powerful vasoconstrictor,

-Atrial natuiuretic peptides (ANPs)

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2
Q

Hypovolemia

A

Decreased intravascular volume

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3
Q

Dehydration

A

loss of water from the body without loss of electrolytes

Results in hemoconcentration INCREASESES in hematocrit, serum electrolytes and urine specific gravity.

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4
Q

Hypervolemia

A

can lead to heart failure or pulmonary edema, this is due to the extra strain and work put on both heart and lungs
-retention of water and sodium

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5
Q

Overhydration

A

Gain of more water than electrolytes

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6
Q

Clinical dehydration

A

EFC deficit and hypernatremia combined

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7
Q

Volume imbalances

A

Too much or too little fluids with the same solute concentration

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8
Q

osmolality imbalances

A

too much or too little solutes with the same concentration of water

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9
Q

Clinical manifestations of Fluid Volume Deficit (FVD)

A
  • Thirst
  • Weight loss (1kg=1L)
  • Dry Mucous membranes-sunken eyes,
  • Oliguria-decrease in urine output
  • weak, thready pulse,
  • Orthostatic hypotension: >15% increase in HR and >15mmHg drop in systolic bp (or >10 mmHg drop in diastolic bp) when rising from supine to stand
  • Confusion
  • Decreased turgor
  • decreased venous filling
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10
Q

Nursing assesments for FVD

A
  • assess Intake and output
  • assess cause of loss
  • daily weights
  • IV fluuids-requires an order
  • Asses vital signs
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11
Q

Hyponatremia

A

caused by too little Na+ in the body, too much water. This is an example of a osmolality imbalance.

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12
Q

Causes of Hyponatremia

A
  • gain of more salt than water by; excessive hypotonic IV fluids, tap water enemas, heart failure, SIADH-too much ADH
  • loss of more salt than water caused by salt wasting disease.
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13
Q

Symptoms of Hyponatremia

A

-Musculoskeletal(occurs early in presentation):fatigue, weakness, muscle cramps
-Gastrointestinal (occurs after musculoskeletal); anorexia, nausea, vomiting, cramping, diarrhea, hyperactive bowel sounds.
-CNS (only in sever cases mEq in 120’s or rapid onset);
lethargy, confusion, seizures.
-cardiovascular; r/t hypo, hypervolemia

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14
Q

Nursing interventions for Hyponatremia

A

Monitor- I&O, daily weights, lab values, neuro status, muscle tone and strength

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15
Q

Treatment for Hyponatremia

A
  • Administer PO Salt tabs, or Na+ containing fluids
  • Administer IV hypertonic saline such as 3-5% saline (only if Na+ dangerously low)
  • Restrict free water intake
  • Replace other electrolytes lost
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16
Q

Hypernatremia

A

Too much salt in body fluids

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17
Q

Causes of hypernatremia

A
  • loss of more water than salt caused by; osmotic diuresis (increased urination), and Diabetes insipidus
  • Gain of more salt than water caused by; difficulty swallowing fluids, dehydration, too much salt intake (salt tabs, hypertonic saline)
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18
Q

Symptoms of Hypernatremia

A

extreme thirst, dry flushed skin

-CNS (if onset is rapid);confusion, agitation, coma, seizures.

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19
Q

Treatment of Hypernatremia

A

Oral free water intake or IV replacement of fluids

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20
Q

Potassium

A

main component of IFC, constantly excreted by kidneys and replaced by diet. 40-60 mg needed daily.

  • aid in nerve impules conduction and muscle (cardiac, smooth, and skeletal) function.
  • main electrolyte available at renal tubules. so K+ loss is increased when pt is given a high loop diuretic.
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21
Q

Hypokalemia

A

Serum potassium is <3.5mEq/L

loss of potassium

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22
Q

Causes of hypokalemia

A
  • Diarrhea
  • Vomiting
  • NG tube drainage
  • Medications: diuretics (lasix), corticosteroids
  • Trauma: Burns, Wounds
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23
Q

Symptoms of hypokalemia

A
  • Skeletal muscle; fatigue, weakness, cramps, heaviness in legs.
  • Smooth muscle; decreased bowel motility, nausea/vomiting( secondary to abdominal distention), constipation.
  • Cardiac muscle; irregular pulse, ectopic beats, ECG changes-flat/depressed T-waves
  • Respiratory muscles; shallow, ineffective respirations.
  • CNS; vertigo, drowsiness, confusion, decreased deep tendon reflex, change in mental state.
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24
Q

What happens if hypokalemia is left untreated?

A
  • kidney damage
  • Paralytic ileus (absent bowel sounds)
  • Paralysis
  • Death secondary to cardiac and respiratory arrest (muscles cease to function)
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25
Q

Nursing implications of Hyopkalemia

A
  • Assess kidney function (kidnesy excrete 90% of K+); monitor output-watch for decrease in urine output
  • Impaired renal function may cause k+ intoxication
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26
Q

Treatment of Hypokalemia

A

Oral Potassium supplements: cost-effective, safest method
-Dosing – 40-80 mEq/day in equally divided doses
Major S/E of K+ replacement are GI – N/V/D, bad taste
dilute in full glass H2O, juice/take with meals
sip slowly-Don’t crush enteric coated/extended release tablets
-IV Potassium Replacement; K+ is a vesicant-burns vein pathway, may cause tissue damage, assess for phlebitis frequently
-change IV site if problems maintaining flow rate occur, skin above IV site is cool, taught, and painful
-administer slowly using IV pump, max 10mEq/1hr
**NEVER GIVE K+ IV BOLUS PUSH!!!!

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27
Q

Hyperkalemia

A

Too much K+ in fluids

>5 mEq/L

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28
Q

Causes of Hyperkalemia

A
  • large amounts of K+ admistration
  • acute or chronic Oliguria
  • potassium sparing diuretics
  • hemolysis of blood sample ( always re-draw to check)
29
Q

Symptoms of Hyperkalemia

A

Abdominal cramps
Diarrhea
CARDIAC DYSRHYTHMIAS, CARDIAC ARREST
(ski off the T—peaked T waves, early sign of hyperkalemia)

30
Q

Treatment of Hyperkalemia

A
  • IV calcium-stabilize myocardium by reducing threshold potential
  • Insulin-shifts K+ from EFC into IFC
  • Glucose- to avoid drop in blood sugar
  • Kayexalate-pull K+ into feces,
  • Potassium Wasting Diuretics
  • Dialysis (last resort)
31
Q

Calcium

A
  • essential for muscle contraction
  • regulates heart rate and BP
  • Necessary for synaptic release of neurotransmitters for transmission of nerve impulses
  • bone growth and function
  • Maintains cell membrane and capillary permeability
32
Q

Calcium regulation

A

Serum calcium level is regulated by parathyroid hormone (released from parathyroid) and calcitonin (released from thyroid)

  • Release of parathyroid hormone increases serum calcium
  • release of calcitonin decreases serum calcium
33
Q

Vitamin D

A

Necessary for calcium absorption from GI tract

34
Q

Hypocalcemia

A

<8.4 mg/dl
Too little Ca++
increases neuromuscular excitability

35
Q

Causes of Hypocalcemia

A

-Renal failure (CKD)
-Endocrine disorders
-Hypoparathyroidism, thyroid cancer, pancreatitis
-Surgery
-Parathyroidectomy – can be life-threatening
Any neck surgery w/ injury to thyroid or parathyroids
-Vit D deficiency
-Drugs

36
Q

Symptoms of Hypocalcemia

A
  • CNS; Seizures, Paresthesias, Tetany, Positive Chvostek’s sign (contraction of facial muscles when facial nerve is tapped), Positive Trousseau’s sign (carpal spasm with hypoxia-inflate bp cuff above systolic bp to create hypoxia and carpal spasm will occur)
  • CV; Cardiac dysrhythmias
  • GI; N&V, Increased peristalsis
  • Skeletal; Osteoporosis
37
Q

Nursing interventions for Hypocalcemia

A
  • Monitor Ca levels; report abnormals

- Observe for signs of hypocalcemia; notify MD

38
Q

Treatment for Hypocalcemia

A

-Oral calcium
-IV calcium replacement (if emergent); IV Ca gluconate or calcium chloride
Watch for phlebitis, can cause cardiac dysrhythmia

39
Q

Hypercalcemia

A

too much Ca++ in fluids

>10.5 mg/dl

40
Q

Causes of Hypercalcemia

A
  • Excessive intake of Vit D or calcium
  • Hyperparathyroidism
  • Malignancies (lymphoma, multiple myeloma)-Results in bone destruction and subsequent calcium release
41
Q

Symptoms of Hypercalcemia

A
  • CNS:Lethargy, Decreased LOC
  • MS; Decreased deep tendon reflexes
  • CV; Dysrhythmias,Cardiac arrest
  • Renal Stones
42
Q

Nursing interventions for Hypercalcemia

A

Implement measures to promote calcium excretion by kidneys

43
Q

Treatments for Hypercalcemia

A

-Emergency treatment w/ IV fluids and w/ loop diuretics
-Mild cases – increase fluid intake to 3-4L/day
-Drugs:
IV Calcitonin
IV Bisphosphonates
IV Glucocorticoids

44
Q

Magnesium

A
  • helps in transmission of nerve impulses and muscular excitability,
  • draws water into GI tract- stimulates peristalsis
45
Q

Uses for magnesium

A
  • treatment for eclampsia/ pre-eclampsia
  • used as a laxative
  • used to evacuate colon prior to procedures
46
Q

Hypomagnesemia

A

too little magnesium in fluids

<1.5 mg/dl

47
Q

Causes of Hypomagnesemia

A
  • inadequate dietary intake due to; alcoholism, malabsorption, inflammatory bowel disease.
  • excessive gastric or intestinal drainage
  • renal disease
  • rapid administration of blood from a blood bank
  • loop diuretics
48
Q

Hypomagnesemia Symptoms

A
  • Result from increased neuromuscular excitability (similar to calcium!)
  • CV: Tachycardia, Hypertension, Dysrhythmias
  • CNS: Tetany-like symptoms, Hyperactive reflexes, Positive Chvostek’s and Trousseau’s
  • GI: Anorexia, N&V-nausea and vomiting
49
Q

Nursing interventions for Hypomagnesemia

A 
Diet – encourage Mg in diet
Green, leafy vegetables
Whole grains
Fish
Nuts
50
Q

Treatment for Hypomagnesema

A

Administer Magnesium – p.o., IM, IV

-IV- monitor closely, test reflexes before administering, if reflexes absent hold does, high levels Mg depress reflexes

51
Q

Hypermagnesemia

A

Too much Mg
>2.5 mg/dl
rare!

52
Q

Causes of Hypermagnesemia

A
  • Usually R/T IV administration
  • Renal insufficiency or failure
  • Excessive intake of OTC antacids or laxatives containing Mg;Maalox, milk of magnesia, Mylanta, Di-Gel, epsom salts
53
Q

Hypermagnesemia Symptoms

A

Result from decreased neuromuscular excitability

  • CV; Cardiac arrest, Hypotension
  • Musculoskeletal; Muscular weakness, Decreased reflexes
  • CNS; Apprehension
  • Integumentary; Flushing, Excessive perspiration
54
Q

Nursing interventions for Hypermagnesemia

A

Administer IV calcium
IVF
Renal dialysis if dangerously high

55
Q

Phosphates/Phosphorus

A 
Inverse relationship to Calcium
Functions:
Metabolism of protein, calcium, and glucose
Muscle contraction
Conversion of glycogen to glucose
Transportation of fatty acids
Maintaining acid-base balance
Acidifying urine
Proper functioning of RBC’s
56
Q

Hypophosphatemia

A

PO deficiency

<2.7 mg/dl

57
Q

Causes of Hypophosphatemia

A
  • Inadequate intake due to; Alcoholism, Hyperalimentation, Eating disorders
  • Increased excretion due to; Diuresis w/ loop diuretics, Decreased absorption, Chronic diarrhea
  • Chronic use of phosphate-binding antacids (Amphogel, Alternagel)
58
Q

Symptoms of Hypophosphatemia

A
  • GI-anorexia
  • Musculoskeletal; weakness, bone pain
  • CNS; decreased reflexes, confusion
59
Q

Treatment of Hypophosphatemia

A

-Severe:IV potassium phosphate or sodium phosphate
-Mild;Increase dietary sources-Milk, cheese, egg yolk, meat, fish, fowl, nuts
Administer oral supplements-K-phosphate, Neutra-Phos K, Phospha-Soda

-Disadvantages of supplements
Diarrhea, volume overload, hyperkalemia

60
Q

Hyperphosphatemia

A

Too much PO

>4.5 mg/dl

61
Q

Causes of Hyperphosphatemia

A

-Renal insufficiency is the most common cause may also be caused by; overuse of laxatives or enemas containing PO, or increased cell breakdown caused by;Rhabdomyelosis, Trauma, burns, crush injuries,Severe infections, Cancer, Acidosis

62
Q

Symptoms of Hyperphosphatemia

A
  • CNS; twitching, tetany, Positive Chvostek’s and Trousseau’s, Confusion
  • Musculoskeletal; weakness, fatigue
  • CV- ECG changes, dysrhythmias, tachycardia
63
Q

Treatment of Hyperphosphatemia

A
  • Limit oral intake of foods high in phosphorus (Milk, cheese, egg yolk, meat, fish, fowl, nuts)
  • Administer aluminum-based antacids (binds w/ phosphorus in GI tract)ex;Amphogel, Alternagel
  • Administer diuretics
64
Q

Normal Aging Changes Affecting Fluid and electrolyte balance

A

Decreases in; total body weight, thirst mechanism, number of glomeruli in kidneys, ability to concentrate urine, aldosterone secretion, ability to correct acid/base balance, skin elasticity, sweat glands, cardiac output, renal plasma flow, elasticity of arteries, number of alveoli, lung elasticity, muscle strength, saliva, gastric juice, calcium absorption

65
Q

Possible nursing diagnoses for patients with fluid, electrolyte, and acid-base alterations

A
  • Decreased cardiac output
  • Impaired oral mucous membrane
  • impaired skin integrity
  • risk for injury
  • acute confusion
  • risk for electrolyte imbalance
  • deficient fluid volume
  • deficient knowledge regarding disease managment
  • impaired gas exchange
  • ineffective tissue perfusion
  • excess fluid volume
66
Q

ADH

A

Anti Diuretic Hormone
-released from posterior pituitary
Monitors serum osmolality and serum volume and then reabsorbs water or excretes water (urine) from kidneys based on these values
-Diuretic means to excrete or promote urine production, there fore anti-diuretic means the opposite (with holds/decreases urine production)

-Two pathologic variations can occur: SIADH and Diabetes Insipidus

67
Q

SIADH

A

Syndrome of Inappropriate Anti-diuretic Hormone=too much ADH

  • causes water which would normally be excreted by kidneys to be reabsorbed into circulation.
  • Results in; decreased serum osmolality, decreases serum Na+, increased urine specific gravity
  • Caused by; brain tumors, head injury, pituitary surgery
  • May lead to cerebral edema and death
68
Q

Diabetes Insipidus

A
  • too little ADH
  • water which would normally be reabsorbed into circulation is excreted,
  • results in; increased serum osmolality, increased serum Na+, decreased specific gravity of urine.
  • Caused by; transphenoidal pituitary resection for pituitary tumors
  • symptoms; Excessive thirst, severely diluted urine, LOTS of urine output

Foundations (11 decks)

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