Exam 2 Flashcards

(80 cards)

1
Q

Cardiac Biomarkers

A

Troponin I or T (cTnI or cTnT)
Creatinine Kinase-MB (CK-MB)
Myoglobin

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2
Q

Priorities of treatment in electrolyte imbalances

A

The priority goals of treatment are to:

  • restore balance
  • correct the underlying condition
  • prevent further complications

Also keep in mind that the treatment will be based upon the instigating cause. Make sure you understand the difference between electrolyte imbalances that stem from dehydration (low blood volume) or solute imbalance (hypervolemia or hypovolemia- either too many/few solutes or too much/few water volume content in the blood).

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3
Q

Sodium Range:

A

135-145 mmol/L

Hyponatremia: 145 mmol/L
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4
Q

Potassium Range:

A

3.5-5.0 mmol/L

Hypokalemia: 5.0mmol/L
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5
Q

Magnesium Range:

A

0.75-.1.5 mmol/L

Hypomagnesemia: 1.5 mmol/L
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6
Q

Calcium Range:

A

8.5-10.5 mEq/L

Hypocalcemia: 10.5 mmol/L
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7
Q

Fasting Lipid Profile

A

Total Cholesterol
LDL
Triglycerides
HDL

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8
Q

Labs for cardiac profiles

A

Cardiac Biomarkers

Fasting Lipid Profile

Brain Natriuretic Peptide (BNP)

Pro-BNP

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9
Q

Body fluid intake

A

water enters the body through three sources:

  1. orally ingested liquids
  2. water in foods
  3. water formed by oxidation of foods
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10
Q

insensible (insensate) loss

A

water lost through the skin or lungs via expelled air that can not be measured.

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11
Q

Maintaining fluid and electrolyte balance

A
  • Kidneys
  • Adrenal glands through the secretion of aldosterone (controls the amount of sodium reabsorbed by the kidneys. RAAS.)
  • Pituitary gland through the secretion of antidiuretic hormone (regulates the amount of water reabsorbed by the kidneys)
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12
Q

Fluid volume deficit description

A

Dehydration occurs when the fluid intake of the body is not sufficient to meet the fluid needs of the body.

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13
Q

Goal of treatment for fluid volume deficit

A

restore fluid volume and replace electrolytes as needed and eliminate the cause of the fluid volume deficit.

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14
Q

Types of fluid volume deficits:

A
  1. isotonic dehydration
  2. Hypertonic dehydration
  3. Hypotonic dehydration
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15
Q

Isotonic dehydration

A

water and dissolved electrolytes are lost in equal proportions. Known as hypovolemia. Results in decreased circulating blood volume and inadequate tissue perfusion.

Caused by:

  • inadequate intake of fluids (thirst mechanism disruption or inability to feed ones self)
  • fluid shifts between compartments
  • excessive losses of body fluids (blood loss)
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16
Q

Hypertonic dehydration

A
  • water loss exceeds electrolyte loss
  • clinical problems that occur result from alterations in electrolyte concentrations
  • cellular dehydration and shrinkage
Caused by:
-conditions that increase fluid loss:
excessive perspiration
hyperventilation
ketoacidosis
prolonged fevers
diarrhea
early stage kidney disease
diabetes insipidus
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17
Q

hypotonic dehydration

A
  • electrolyte loss exceeds water loss
  • clinical problems that occur result from fluid shifts between compartments, causing a decrease in plasma volume
  • cells swell
Caused by: 
Chronic illness
excessive fluid replacement
kidney disease
chronic malnutrition
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18
Q

Interventions for fluid volume deficit

A

monitor:

  • Cardiovascular
  • Respiratory
  • Neuromuscular
  • Renal
  • Integumentary
  • Gastrointestinal status

Prevent further fluid losses and increase fluid compartment volumes to normal ranges

Provide oral rehydration if possible and IV fluid replacement if the dehydration is severe. Fluids used depends on type of dehydration.

Monitor intake and output

administer medications as prescribed (antidiarrheal, antimicrobial, etc)

Administer O2 as prescribed

Monitor electrolyte values and prepare to administer medication to treat an imbalance if present.

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19
Q

Fluid volume excess description

A

Fluid intake or fluid retention exceeds the fluid needs of the body.

Also called overhydration or fluid overload.

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20
Q

Goal of treatment for fluid volume excess

A

restore fluid balance, correct electrolyte imbalances if present, and eliminate or control the underlying cause of the overload.

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21
Q

Types of fluid volume excess

A
  1. Isotonic overhydration
  2. Hypertonic overhydration
  3. Hypotonic overhydration
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22
Q

isotonic overhydration

A

Hypervolemia. results from excessive fluid in the extracellular space that does not shift between the extracellular and intracellular compartments.

leads to:
circulatory overload
interstitial edema

Caused by:
inadequately controlled IV therapy
Kidney disease
Long term corticosteroid therapy

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23
Q

Hypertonic overhydration

A

Rare. Caused by excessive sodium intake.

Fluid is drawn from the intercellular fluid compartment, the extra cellular fluid volume expands, and the intracellular fluid volume contracts.

Caused by:
Excessive sodium injestion
Rapid infusion of hypertonic saline
Excessive sodium bicarbonate therapy

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24
Q

Hypotonic overhydration

A

Water intoxication.

Excessive fluid moves into the intracellular space and all body fluid compartments expand.

Results in electrolyte imbalances=over dilution

Caused by:
Early kidney disease
Heart failure
Syndrome of inappropriate antidiuretic hormone secretion
inadequately controlled IV therapy
Replacement isotonic fluid loss with hypertonic fluids

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25
Interventions for fluid volume excess
Monitor: - cardiovascular - respiratory - neuromuscular - renal - integumentary - GI status Prevent further fluid overload and restore normal fluid balance. Administer diuretics; osmotic diuretics typically are prescribed first to prevent severe electrolyte imbalances Restrict fluid and sodium intake as prescribed Monitor intake and output/weight Monitor electrolyte values and prepare to administer medication to treat an imbalance if present
26
Hyponatremia description
Severe sodium level lower than 135 mEq/L Usually associated with fluid volume imbalances
27
Causes of hyponatremia
Increased sodium excretion: Inadequate sodium intake Dilution of serum sodium
28
increased sodium excretion causes
- excessive sweating - diuretics - vomiting - diarrhea - wound drainage, especially GI - Kidney disease - decreased secretion of aldosterone
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Inadequate sodium intake causes
- fasting, NPO | - low salt diet
30
Dilution of serum sodium causes
- excessive injestion of hypotonic fluids or irrigation with hypotonic fluids - kidney disease - freshwater drowning - syndrome of inappropriate antidiuretic hormone secretion - hyperglycemia - heart failure
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Interventions for hyponatremia
Monitor: - cardiovascular - respiratory - neuromuscular - cerebral - renal - GI status If accompanied by a fluid volume deficit, IV saline infusions are administered to restore sodium content and fluid volume If accompanied by fluid volume overload, osmotic diuretics are administered to promote the excretion of water rather than sodium If caused by excessive secretion of antidiuretic hormone, medications that antagonize ADH may be administered Instruct the client to increase oral sodium intake and inform the client about the foods to include in the diet If the client is taking lithium, monitor the lithium level, because hyponatremia can cause diminished lithium excretion, resulting in toxicity
32
Hypernatremia description
Serum sodium level that exceeds 145 mEq/L
33
Causes of hypernatremia
Decreased sodium excretion Increased sodium intake: excessive oral sodium injestion or excessive administration of sodium containing IV fluids Decreased water intake: fasting, NPO status Increased water loss
34
Causes of decreased sodium excretion
- corticosteroids - cushing's syndrome - Kidney disease - Hyperaldosteronism
35
Causes for increased water loss
- increased rate of metabolism - fever - hyperventilation - infection - excessive diaphoresis - watery diarrhea - diabetes insipidus
36
Interventions for hypernatremia
Monitor: - cardiovascular - respiratory - neuromuscular - cerebral - renal - integumentary If caused by fluid loss, prepare to administer IV infusions If caused by inadequate renal excretion of sodium, prepare to administer diuretics that promote sodium loss Restrict sodium and fluid intake as prescribed
37
Hypokalemia description
Serum potassium lover than 3.5 mEq/L. Potassium deficit is potentially life threatening because every body system is affected
38
Assessment findings of hyponatremia
CV: vary with changes in vascular volume - normovolemic: rapid pulse rate, normal bp - hypovolemic: thready, weak pulse rate. Hypotension, flat neck veins, normal or low central venous pressure - hypervolemic: rapid, bounding pulse. blood pressure normal or elevated, elevated central venous pressure Respiratory: shallow ineffective respiratory movements is a late manifestation related to skeletal muscle weakness Neuromuscular: Generalized skeletal muscle weakness that is worse in the extremeties. Diminished deep tendon reflexes. Central Nervous System: Headache, personality changes, confusion, seizures, coma GI: Increased motility and hyperactive bowel sounds, nausea, abdominal cramping and diarrhea renal: increased urinary output Integumentary: dry mucus membranes Labs: serum sodium less than 135 mEq/L and decreased urinary specific gravity
39
Assessment findings of hypernatremia
CV: heart rate and blood pressure respond to vascular volume status Respiratory: pulmonary edema is hypervolemia is present Neuromuscular: Early-spontaneous muscle twitches, irregular muscle contractions. Late-skeletal muscle weakness; deep tendon reflexes diminished or absent CNS: altered cerebral function is the most common manifestation of hypernatremia. Normovolemia or hypovolemia: aggitation, confusion, seizures. Hypervolemia- lethargy, stupor, coma GI: extreme thirst Renal: decreased urinary output Integumentary: dry and flushed skin, Dry and sticky tongue and mucus membranes. Presence or absense of edema, depending on fluid volume changes. Labs: serum sodium level that exceeds 145 mEq/L and increased urine specific gravity
40
Causes of hypokalemia
Actual total body potassium loss Inadequate potassium intake Movement of potassium from the extracellular fluid to the intracellular fluid Dilution of serum potassium
41
causes of total body potassium loss
excessive use of medications such as diuretics or corticosteroids Increased secretion of aldosterone (cushing's syndrome) vomiting/diarrhea wound drainage, particularly GI prolonged nasogastric suctioning excessive sweating kidney disease impairing reabsorption of potassium
42
Cause of inadequate potassium intake
fasting or NPO status
43
Causes of movement of potassium from the extracellular fluid to the intracellular fluid
Alkalosis | Hyperinsulinism
44
Causes of dilution of serum potassium
water intoxication IV therapy with potassium deficient solutions
45
Assessment findings of hypokalemia
CV: Thready, weak, irregular pulse. Weak peripheral pulses. Orthostatic hypotension Respiratory: shallow, ineffective respirations that result from profound weakness of the skeletal muscles of respirations. Diminished breath sounds. Neuromuscular: anxiety, lethargy, confusion, coma. Skeletal muscle weakness, leg cramps. Loss of tactile discrimination. Parethesias. deep tendon hyporeflexia. GI: decreased motility, hypoactive or absent bowel sounds. Nausea/vomiting, constipation, abdominal distension, paralytic ileus. Lab findings: serum potassium level lower than 3.5 mEq/L. electrocardiogram changes: ST depression, shallow, flat, or inverted T wave, and prominent U wave.
46
Interventions for hypokalemia
Moniter - cardiovascular - respiratory - neuromuscular - GI - renal Place client on cardiac monitor Monitor electrolyte values Administer potassium supplements orally or IV as prescribed Institute safety measures for the client experiencing muscle weakness If the client is taking a potassium depleting diuretic, it may be discontinued. A potassium retaining diuretic may be prescribed Instruct the patient about foods that are high in potassium content
47
Notes on potassium suppliments
Oral K supplients may cause nausea and vomiting so they should not be taken on an empty stomach. If the client complains of abdominal pain, distention, nausea, vomiting, diarrhea, or GI bleeding, the supplement may need to be discontinued. Liquid potassium chloride has an unpleasant taste and should be taken with juice or another liquid.
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Electrocardiograph changes in hypocalcemia
prolonged ST segment | prolonged QT interval
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ECT changes in hypercalcemia
Shortened ST segment | Widened T wave
50
ECT changes in hypokalemia
ST depression Shallow or flat or inverted T wave Prominent U wave
51
ECT changes in hyperkalemia
Tall peaked T wave Flat P wave Widened QRS complex Prolonged PR interval
52
ECT changes in hypomagnesemia
Tall T waves | Depressed ST segment
53
ECT changes in hypermagnesemia
Prolonged PR interval | Widened QRS complex
54
Hyperkalemia description
serum potassium level that exceeds 145 mEq/L
55
pseudohyperkalemia
a condition that can occur due to methods of blood specimen collection and cell lysis. If an increased serum value is obtained in the absence of clinical symptoms, the specimen should be redrawn and evaluated.
56
Causes of hyperkalemia
Excessive potassium intake Decreased potassium excretion Movement of potassium from the intracellular fluid to the extracellular fluid
57
Causes of excessive potassium intake
Over ingestion of potassium containing foods or medications such as potassium chloride or salt substitutes. Rapid infusion of potassium containing IV solutions
58
Causes of decreased potassium excretion
potassium retaining diuretics Kidney disease Adrenal insufficiency, such as addison's disease
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Causes of movement of potassium from the intracellular fluid to the extracellular fluid
Tissue damage Acidosis Hyperuricemia Hypercatabolism
60
Assessment findings of hypercalcemia:
CV: Increased heart rate in the early phase, bradycardia that can lead to cardiac arrest in late phase. Increased blood pressure. Bounding, full peripheral pulses. Respiratory: Ineffective respiratory movements as a result of profound skeletal muscle weakness. Neuromuscular: Profound muscle weakness. Diminished or absent deep tendon reflexes. Disorientation, lethargy, coma. Renal: urinary output varies depending on the cause. Formation of renal calculi, flank pain. GI: Decreased motility and hypoactive bowel sounds. Anorexia, nausea, abdominal distention, constipation. Labs: Serum calcium that exceeds 10 mg/dL. Electrocardiogram changes: shortened ST segment, widened T wave
61
Assessment findings of hyperkalemia
CV: slow, weak, irregular heart rate. Decreased blood pressure. Respiratory: profound weakness of the skeletal muscles leading to respiratory failure Neuromuscular: Early-muscle twitches, cramps, parethesias (tingling and burning followed numbness in the hands and feet and around the mouth) Late-profound weakness ascending flaccid paralysis in the arms and legs. (trunk, head, and respiratory muscles become affected when the serum potassium level reaches a lethal level) GI: Increased motility, hyperactive bowel sounds. Diarrhea Labs: serum potassium level that exceeds 5.0 mEq/L. ECG changes: tall peaked T waves, flat P waves, widened QRS complex, and prolonged PR intervals
62
Interventions for hyperkalemia
Monitor: - cardiovascular - respiratory - neuromuscular - renal - GI status Place patient on cardiac monitor Discontinue IV potassium and hold potassium supplements Initiate a potassium restricted diet Prepare to administer potassium excreting diuretics if renal function is not impaired If renal function is impaired prepare to administer sodium polystyrene sulfonate Prepare the client for dialysis if potassium levels are critically high Prepare for the administration of IV calcium if hyperkalemia is severe to avert myocardial excitability Monitor renal function when blood transfusions are prescribed, the client should receive fresh blood Teach to avoid potassium in foods
63
Hypocalcemia description
serum calcium level lower than 8.6 mg/dL
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Hypocalcemia causes
Inhibition of calcium absorption from the GI tract Increased calcium excretion Conditions that decrease the ionized fraction of calcium
65
Causes of inhibition of calcium absorption from the GI tract
Inadequate oral intake of calcium Lactose intolerance Malabsorption syndromes such as celiac or crohn's Inadequate intake of vitamin D End stage kidney disease
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Causes of increased calcium excretion
kidney disease diarrhea steatorrhea wound drainage, especially GI
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Conditions that decrease the ionized fraction of calcium
Hyperproteinemia Alkalosis Medications such as calcium chelators or binders Acute pancreatitis Hyperphosphatemia Immobility Removal or destruction of the parathyroid glands
68
Assessment findings of hypocalcemia
CV: decreased heart rate, hypotension, diminished peripheral pulses Respiratory: Not directly affected , however respiratory failure or arrest can result from decreased respiratory movement because of respiratory muscle tetany or seizures Neuromuscular: Irritable skeletal muscles. Twitches, cramps, tetany, seizures. Painful muscle spasms in the calf or foot during periods of inactivity. Paresthesia followed by numbness that may affect the lips, nose, and ears in addition to the limbs. Positive trousseaus and chvostek's signs. Hyperactive deep tendon reflexes. Anxiety, irritability. Renal: urinary output varies depending on the cause GI: Increased gastric motility, hyperactive bowel sounds. Cramping diarrhea Labs: serum calcium levels less than 8.6 mg/dL ECG changes: prolonged ST intervals, prolonged QT interval
69
Interventions of hypocalcemia
Monitor: - cardiovascular - respiratory - neuromuscular - GI status Place client on a cardiac monitor Administer calcium suppliments orally or calcium intravenously When administering IV, warm the injection solution to body temperature and administer slowly. Monitor for ECG changes observe for infiltration, monitor for hypercalcemia administer medications that increase calcium absorption/vitamin D Provide a quiet environment to reduce environmental stimuli Initiate seizure precautions move the client carefully and monitor for signs of a pathological fracture Keep 10% calcium gluconate available for treatment of acute calcium deficit Instruct the client to consume foods high in calcium
70
Hypercalcemia descriptions
serum calcium level that exceeds 10 mg/dL
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Causes of hypercalcemia
Increased calcium absorption Decreased calcium excretion Increased bone resorption of calcium Hemoconcentration
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Causes of increased calcium absorption
excessive oral intake of calcium or vitamin D
73
Causes of decreased calcium excretion
Kidney disease Use of thiazide diuretics
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Causes of increased bone resorption of calcium
Hyperparathyroidism Hyperthyroidism Malignancy (bone destruction from metastic tumors) Immobility Use of glucocorticoids
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Causes of hemoconcentration
Dehydration Use of lithium Adrenal insufficiency
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Interventions of hypercalcemia
Monitor: - Cardiovascular - Respiratory - Neuromuscular - renal - GI status Place client on a cardiac monitor Discontinue IV infusions of solutions containing calcium and oral medications containing calcium or vitamin D Discontinue thiazide diuretics and replace with diuretics that enhance the excretion of calcium administer medications as prescribed that inhibit calcium resorption Prepare the client with severe hypercalcemia for dialysis if medications do not work Move the client carefully and monitor for signs of a pathological fracture Monitor for flank or abdominal pain and urinary stones Instruct the client to avoid foods high in calcium
77
Hypomagnesmia description
serum magnesium level lower than
78
Phosphate Range:
2.5-4.5 mmol/L Hypophosphatemia: 4.5 mmol/
79
Clinical Manifestations of Hyponatremia
Tachycardia, thready pulse Fatigue Muscle cramps, especially abdominal, and muscle weakness Nausea, vomiting, dizziness Postural hypotension (possibly from hypovolemia) or hypertension Headache, confusion, or seizures (from swelling of brain cells) Weight changes Personality changes Dry mucous membranes and cool, clammy skin
80
Clinical Manifestations of Hypernatremia
Restlessness, agitation, twitching, coma, seizures Decreased central venous pressure Weight loss or changes in weight Intense thirst with dry, rough mucous membranes Flushed skin