random questions
What simulates aldosterone secretion from the adrenal cortex?
decreased Na & h2o
Aldosterone is a mineralocorticoid with strong sodium-retaining and potassium-excreting capabilities.
Decreased renal perfusion or decreased sodium in the distal part of the renal tubule activates the renin-angiotensin-aldosterone system (RAAS), resulting in aldosterone secretion.
In addition to the RAAS, increased serum potassium, decreased serum sodium, and adrenocorticotropic hormone (ACTH) stimulate aldosterone secretion.
Aldosterone increases sodium and water reabsorption in the renal distal tubules, decreasing plasma osmolality and restoring fluid volume.
In a pt with Na imbalances, the primary clinical manifestations are related to alterations in what body system?
Central Nervous System: think neuro changes with Na
hyponatremia: neuro: agitation, restless, ams, headache, seizures
hypernatremia: neuro: agitation, restless, ams
pH 7.50, PaCO2 30, HCO3 24
respiratory alkalosis, uncompensated
fully compensated: pH is normal, pH 7.35 - 7.45
partially compensated: pH, PCO2, & HCO3 (all of these values) are out of the normal range
uncompensated: pH and one other value is out of the normal range
With increased carbonic acid (H2CO3), what is the mechanism associated with this imbalance?
Respiratory acidosis
Respiratory acidosis (carbonic acid excess) occurs when a person has hypoventilation (Table 16.11 or table 17.12). Hypoventilation leads to a buildup of CO2, resulting in an accumulation of carbonic acid in the blood.
The amount of CO2 in the blood directly relates to carbonic acid and H+ concentration. With increased respirations, more CO2 is expelled and less stays in the blood. This leads to less carbonic acid and less H+. With decreased respirations, more CO2 stays in the blood. This leads to increased carbonic acid and more H+.
During acute respiratory acidosis, the renal compensatory mechanisms begin to work within 24 hours. The kidneys conserve HCO3− and secrete increased H+ into the urine. Until the renal mechanisms have an effect, the serum HCO3− level will usually be normal and then increase.
Tx respiratory acidosis: compensatory response is to increase HCO3 retention by the kidney & blow off excess CO2
What electrolyte imbalances are commonly seen with chronic kidney disease?
May see high, normal, or low levels of Na: with impaired sodium excretion from the kidney, will retain more water. if large quantities of water are retained = dilutional hyponatremia.
Hyperkalemia 2/2 decreased excretion by kidney; may also see metabolic acidosis
Hyperphosphatemia is usually seen in ckd 2/2 decreased excretion by kidney (Ca-Phos have inverse relationship)
Hypermagnesemia is usually not a problem in ckd unless the pt is ingesting Magnesium (e.g., Milk of Magnesia, magnesium citrate, antacids containing magnesium).
May see hypocalcemia bc kidney cannot activate vit D, which is essential for Ca reabsorption from the GI tract
What disorder is often associated with hyperkalemia?
a) hypoglycemia
b) metabolic acidosis
c) respiratory alkalosis
d) decreased urine potassium levels
b) metabolic acidosis
Hyperkalemia (high serum potassium) may result from impaired renal excretion, a shift of potassium from ICF to ECF, a massive intake of potassium, or a combination of these factors.
The most common cause of hyperkalemia is renal failure.
Adrenal insufficiency with subsequent aldosterone deficiency leads to potassium retention.
Factors that cause potassium to move from ICF to ECF include acidosis, massive cell destruction (as in burn or crush injury, tumor lysis, severe infections), and intense exercise.
In metabolic acidosis, potassium ions shift from ICF to ECF in exchange for hydrogen ions moving into the cell.
An older woman is admitted to the medical unit with GI bleeding. Assessment findings that indicate fluid volume deficit include (select all that apply)
a. weight loss.
b. dry oral mucosa.
c. full bounding pulse.
d. engorged neck veins.
e. decreased central venous pressure.
a. weight loss.
b. dry oral mucosa.
e. decreased central venous pressure.
Fluid and electrolyte imbalances are commonly classified as deficits or excesses. ECF volume deficit (hypovolemia) and ECF volume excess (hypervolemia) are common clinical conditions. ECF volume imbalances are usually accompanied by one or more electrolyte imbalances, particularly changes in the serum sodium level.
Fluid volume deficit can occur with abnormal loss of body fluids (e.g., diarrhea, vomiting, hemorrhage, polyuria), inadequate fluid intake, or a shift from plasma to interstitial fluid.
Managing fluid volume deficit involves correcting the underlying cause and replacing both water and any needed electrolytes. Replacement therapy depends on the severity and type of volume loss. In mild losses, we can use oral rehydration. If the deficit is more severe, we replace volume with blood products or balanced IV solutions, such as isotonic (0.9%) sodium chloride or lactated Ringer’s solution. The choice of fluid depends on the cause and patient’s electrolyte status. For rapid volume replacement, 0.9% sodium chloride is preferred. Blood is given when volume loss is due to blood loss.
pH 7.20, PaCO2 25, HCO3 15, PaO2 96
metabolic acidosis, partial compensation
fully compensated: pH is normal, pH 7.35 - 7.45
partially compensated: pH, PCO2, & HCO3 (all of these values) are out of the normal range
uncompensated: pH and one other value is out of the normal range
A client weighs 193.6 lbs.
Order: bolus with Heparin at 80 units/kg; initiate drip at 18 units/kg/hr.
Heparin infusion bag: 25,000 units in 500 ml 0.9% NaCl
a. Calculate the heparin bolus dosage
b. Determine the rate in ml/hr at which to set the infusion device; round to the nearest whole number
193.6 lbs x 1kg/2.2 lbs = 88 kg
a. 80 units/1kg x 88 kg = 7040 unit bolus
b. x ml/hr
= 25,000 units/500 ml = 18 units/kg/1 hr
= 25,000 units/500 ml = 1584 units/x ml
cross multiply, solve for x
= 792,000/25,000
= 31.68 ml/hr or 32 ml/hr
or
desired/have x volume of solution on hand
What electrolyte imbalances are associated with chronic alcoholism?
Per Lewis text: may see hypocalemia and hypomagnesemia
However, may see lower levels of other electrolytes 2/2 poor nutrition.
Acute alcohol intake will initially act as a diuretic... but with chronic use, it will increase ADH and cause retention of fluids.
With prolonged vomiting, the nurse might see what type of acid-base imbalance?
With prolonged diarrhea, the nurse might see what type of acid-base imbalance?
Vomit: losing fluids with vomit, and with that acid (K); pts often have a burning/acidic taste in mouth; what's left in the body is base; expect to see metabolic alkalosis
Diarrhea: Biliary, pancreatic, and duodenal secretions are alkaline and are capable of neutralizing the acidity of gastric secretions; therefore with diarrhea, losing HCO3, losing base = what's left in the body is acid; expect to see metabolic acidosis
What would be an example of an appropriate iv solution to treat an extracellular fluid volume deficit?
a) D5W
b) 3% saline
c) lactated ringers
d) D5W in 0.45% NS
c) lactated ringers
Isotonic solution ideal to keep fluid in extracellular compartment; ecf = icf osmolality
Hypotonic solution would cause fluid shift from extracellular space into intracellular space (cell would eventually get big & lyse)
D5W (dextrose 5% in water) is a crystalloid isotonic IV fluid with a serum osmolarity of 252 mOsm/L. D5W is initially an isotonic solution and provides free water when dextrose is metabolized (making it a hypotonic solution osmolality), expanding the ECF and the ICF. It is administered to supply water and to correct an increase in serum osmolality.
Infusion of hypertonic sodium chloride solution shifts fluids from the intracellular space into the intravascular and interstitial spaces.
pH 7.26, PaCO2 56, HCO3 24, PaO2 68
respiratory acidosis, uncompensated
fully compensated: pH is normal, pH 7.35 - 7.45
partially compensated: pH, PCO2, & HCO3 (all of these values) are out of the normal range
uncompensated: pH and one other value is out of the normal range
With increased base bicarbonate (HCO3), what is the mechanism associated with this imbalance?
Metabolic alkalosis
Metabolic alkalosis (base bicarbonate excess) occurs when a loss of acid (e.g., from prolonged vomiting or gastric suction) or a gain in HCO3− (e.g., from ingestion of baking soda) occurs (Table 16.11 or table 17.12).
Tx metabolic alkalosis: compensatory response is to increase CO2 retention by lungs or renal excretion of HCO3
In the geriatric pt, what is a normal change of aging regarding fluid & electrolyte balance?
Hyponatremia: decreased Na resorption & increased h2o retention by the kidney
Increased moisture loss thru thinning skin
Lack of protein intake affects plasma oncotic pressure
What are s/sx of hypermagnesemia?
What type of pt should never receive IV Magnesium Sulfate?
If the pt is symptomatic with hypermagnesemia, the provider may consider ordering what type of med?
• Lethargy, drowsiness
• Muscle weakness
• Urinary retention
• Nausea, vomiting
• Diminished or absent deep tendon reflexes
• Flushed, warm skin, especially facial
• ↓ Pulse, ↓ BP
Do NOT give IV Mg to pt with renal insufficiency or renal failure - Mg is excreted via urine
If Mg levels continue to be elevated, can cause muscle paralysis, coma, respiratory arrest, cardiac arrest.
Consider giving IV Calcium gluconate to oppose the effects of Mg on cardiac muscle.
To provide free water & intracellular fluid hydration for a pt with acute gastroenteritis who is NPO, the rn would expect to administer...
a) D5 in water
b) D10 in water
c) lactated ringers
d) D5 in normal saline
a) D5 in water
Allows water to move from the ECF to the ICF (free water shifts into cells)
D5W is an isotonic solution (osmolarity) and provides free water when dextrose is metabolized (making it a hypotonic solution osmolality), expanding the ECF and the ICF. It is administered to supply water and to correct an increase in serum osmolality.
Dextrose 10% in Water (D10W) is an hypertonic IV solution used in the treatment of ketosis of starvation and provides calories (380 kcal/L), free water, and no electrolytes. It should be administered using a central line if possible and should not be infused using the same line as blood products as it can cause RBC hemolysis.
Lactated Ringer’s Solution (also known as Ringer’s Lactate or Hartmann solution) is a crystalloid isotonic IV fluid designed to be the near-physiological solution of balanced electrolytes. It contains 130 mEq/L of sodium, 4 mEq/L of potassium, 3 mEq/L of calcium, and 109 mEq/L of chloride. It also contains bicarbonate precursors to prevent acidosis. It does not provide calories or magnesium and has limited potassium replacement. It is the most physiologically adaptable fluid because its electrolyte content is most closely related to the composition of the body’s blood serum and plasma.
choice d: would not choose D5NS because NS would expand ECF and not the ICF (as the question is asking to provide free water & intracellular fluid hydration)
pH 7.62, PaCO2 48, HCO3 45
metabolic alkalosis, partial compensation
fully compensated: pH is normal, pH 7.35 - 7.45
partially compensated: pH, PCO2, & HCO3 (all of these values) are out of the normal range
uncompensated: pH and one other value is out of the normal range
Infuse 500 ml D5NS with 20 meq KCL over 12 hrs.
Drop factor 20 gtts/ml
a. _ gtt/min
b. _ ml/hr
a. = 500 ml/12 hr x 1 hr/60 min x 20 gtt/1 ml
= 10,000/720
= 13.89 or 14 gtt/min
b. = 500 ml/12 hr
= 41.67 or 42 ml/hr
A common collaborative problem related to both hyperkalemia and hypokalemia is...
a) seizures
b) paralysis
c) cardiac dysrhythmias
d) acute kidney injury
c) cardiac dysrhythmias
K is essential for cardiac conduction, will be seen with early changes in K levels
hyperkalemia: wide flat P wave, prolonged PR interval, wide QRS, ST segment depression, peaked T wave
hypokalemia: peaked P wave, slightly prolonged PR interval, wide QRS, flat T wave, ST segment depression, prominent U wave (ventricular repolarization)
fig. 16.14 or fig. 17.14
With a pt response to anxiety, fear, and pain; the rn might see what type of acid-base imbalance?
Respiratory alkalosis or Respiratory acidosis
Pain, anxiety, and some CNS disorders can increase RR without a physiological need. They have successfully blown off excess CO2 and are now in respiratory alkalosis (too little CO2 in body, decreased carbonic acid concentration in blood)...
OR
they aren't breathing in a normal pattern and are accumulating CO2 in the body, causing respiratory acidosis.
What electrolyte imbalances is commonly seen with loop & thiazide diuretics?
Per Lewis: may see hyponatremia, hypokalemia, hypocalcemia, hypomagnesemia
from another source: may see hyperphosphatemia because diuretics may indirectly interfere with the kidney's ability to excrete phos
pH 7.44, PaCO2 54, HCO3 36, PaO2 90
compensated or chronic metabolic alkalosis indicated by the high PaCO2 and a pH within normal range
fully compensated: pH is normal, pH 7.35 - 7.45
partially compensated: pH, PCO2, & HCO3 (all of these values) are out of the normal range
uncompensated: pH and one other value is out of the normal range
What is the serum K value associated with in acidosis and alkalosis and why...
acidosis: hyperkalemia 2/2 K moving from ICF to ECF in exchange for H; thus increasing the K in the ECF
alkalosis: hypokalemia 2/2 shift of K back into ICF of cells in exchange for H; thus lowering the K in the ECF
A pt has chronic kidney disease and hyperphosphatemia. What is a commonly associated electrolyte imbalance?
a) hypokalemia
b) hyponatremia
c) hypocalcemia
d) hypomagnesemia
c) hypocalcemia
As kidney function deteriorates, less vitamin D is converted to its active form, resulting in decreased serum levels. Low levels of active vitamin D result in decreased serum calcium levels.
Serum calcium levels are regulated primarily by PTH. When hypocalcemia occurs, the parathyroid gland secretes PTH, which stimulates bone demineralization, releasing calcium from the bones. Phosphate is also released, leading to high serum phosphate levels. Hyperphosphatemia results from decreased phosphate excretion by the kidneys. It decreases serum calcium levels and further reduces the kidneys’ ability to activate vitamin D.
Low serum calcium, increased phosphate, and decreased vitamin D contribute to the stimulation of the parathyroid gland and excretion of PTH. PTH acts on the bone to increase remodeling and increase serum calcium levels. The accelerated rate of bone remodeling causes a weakened bone matrix and places the patient at a higher risk for fractures.
Ca-Phos inverse relationship