Exam 2 Flashcards
Cardiac Biomarkers
Troponin I or T (cTnI or cTnT)
Creatinine Kinase-MB (CK-MB)
Myoglobin
Priorities of treatment in electrolyte imbalances
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).
Sodium Range:
135-145 mmol/L
Hyponatremia: 145 mmol/L
Potassium Range:
3.5-5.0 mmol/L
Hypokalemia: 5.0mmol/L
Magnesium Range:
0.75-.1.5 mmol/L
Hypomagnesemia: 1.5 mmol/L
Calcium Range:
8.5-10.5 mEq/L
Hypocalcemia: 10.5 mmol/L
Fasting Lipid Profile
Total Cholesterol
LDL
Triglycerides
HDL
Labs for cardiac profiles
Cardiac Biomarkers
Fasting Lipid Profile
Brain Natriuretic Peptide (BNP)
Pro-BNP
Body fluid intake
water enters the body through three sources:
- orally ingested liquids
- water in foods
- water formed by oxidation of foods
insensible (insensate) loss
water lost through the skin or lungs via expelled air that can not be measured.
Maintaining fluid and electrolyte balance
- 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)
Fluid volume deficit description
Dehydration occurs when the fluid intake of the body is not sufficient to meet the fluid needs of the body.
Goal of treatment for fluid volume deficit
restore fluid volume and replace electrolytes as needed and eliminate the cause of the fluid volume deficit.
Types of fluid volume deficits:
- isotonic dehydration
- Hypertonic dehydration
- Hypotonic dehydration
Isotonic dehydration
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)
Hypertonic dehydration
- 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
hypotonic dehydration
- 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
Interventions for fluid volume deficit
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.
Fluid volume excess description
Fluid intake or fluid retention exceeds the fluid needs of the body.
Also called overhydration or fluid overload.
Goal of treatment for fluid volume excess
restore fluid balance, correct electrolyte imbalances if present, and eliminate or control the underlying cause of the overload.
Types of fluid volume excess
- Isotonic overhydration
- Hypertonic overhydration
- Hypotonic overhydration
isotonic overhydration
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
Hypertonic overhydration
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
Hypotonic overhydration
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
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
Hyponatremia description
Severe sodium level lower than 135 mEq/L
Usually associated with fluid volume imbalances
Causes of hyponatremia
Increased sodium excretion:
Inadequate sodium intake
Dilution of serum sodium
increased sodium excretion causes
- excessive sweating
- diuretics
- vomiting
- diarrhea
- wound drainage, especially GI
- Kidney disease
- decreased secretion of aldosterone
Inadequate sodium intake causes
- fasting, NPO
- low salt diet
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
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
Hypernatremia description
Serum sodium level that exceeds 145 mEq/L
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
Causes of decreased sodium excretion
- corticosteroids
- cushing’s syndrome
- Kidney disease
- Hyperaldosteronism
Causes for increased water loss
- increased rate of metabolism
- fever
- hyperventilation
- infection
- excessive diaphoresis
- watery diarrhea
- diabetes insipidus
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
Hypokalemia description
Serum potassium lover than 3.5 mEq/L.
Potassium deficit is potentially life threatening because every body system is affected
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
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
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
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
Cause of inadequate potassium intake
fasting or NPO status
Causes of movement of potassium from the extracellular fluid to the intracellular fluid
Alkalosis
Hyperinsulinism
Causes of dilution of serum potassium
water intoxication
IV therapy with potassium deficient solutions
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.
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
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.
Electrocardiograph changes in hypocalcemia
prolonged ST segment
prolonged QT interval
ECT changes in hypercalcemia
Shortened ST segment
Widened T wave
ECT changes in hypokalemia
ST depression
Shallow or flat or inverted T wave
Prominent U wave
ECT changes in hyperkalemia
Tall peaked T wave
Flat P wave
Widened QRS complex
Prolonged PR interval
ECT changes in hypomagnesemia
Tall T waves
Depressed ST segment
ECT changes in hypermagnesemia
Prolonged PR interval
Widened QRS complex
Hyperkalemia description
serum potassium level that exceeds 145 mEq/L
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.
Causes of hyperkalemia
Excessive potassium intake
Decreased potassium excretion
Movement of potassium from the intracellular fluid to the extracellular fluid
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
Causes of decreased potassium excretion
potassium retaining diuretics
Kidney disease
Adrenal insufficiency, such as addison’s disease
Causes of movement of potassium from the intracellular fluid to the extracellular fluid
Tissue damage
Acidosis
Hyperuricemia
Hypercatabolism
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
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
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
Hypocalcemia description
serum calcium level lower than 8.6 mg/dL
Hypocalcemia causes
Inhibition of calcium absorption from the GI tract
Increased calcium excretion
Conditions that decrease the ionized fraction of calcium
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
Causes of increased calcium excretion
kidney disease
diarrhea
steatorrhea
wound drainage, especially GI
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
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
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
Hypercalcemia descriptions
serum calcium level that exceeds 10 mg/dL
Causes of hypercalcemia
Increased calcium absorption
Decreased calcium excretion
Increased bone resorption of calcium
Hemoconcentration
Causes of increased calcium absorption
excessive oral intake of calcium or vitamin D
Causes of decreased calcium excretion
Kidney disease
Use of thiazide diuretics
Causes of increased bone resorption of calcium
Hyperparathyroidism
Hyperthyroidism
Malignancy (bone destruction from metastic tumors)
Immobility
Use of glucocorticoids
Causes of hemoconcentration
Dehydration
Use of lithium
Adrenal insufficiency
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
Hypomagnesmia description
serum magnesium level lower than
Phosphate Range:
2.5-4.5 mmol/L
Hypophosphatemia: 4.5 mmol/
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
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
