Electrolytes & Fluids Flashcards
If it is **bolded** then highly important Review Intro to Fluids flashcards especially Hypo., Iso., and Hypertonic fluids
Hydrostatic = _________ force
pushing
Hydrostatic pushes fluid out of
capillaries
Hydrostatic pressure is exerted by
pumping of heart
Oncotic is the __________ force
pulling
Oncotic pulls fluid out of
tissues and into capillaries
Oncotic pressure is exerted by
non-diffusible plasma proteins … albumin
Albumin def
protein that is soluble in water and coagulable by heat
What does the body use to maintain fluid balance in the body?
- Kidneys
- ADH
- RAAS
- Aldosterone
- ANP
Kidneys
adjust urine volume and excrete electrolytes
ADH medication form and controls what?
vasopressin; controls retention
RAAS system hormone order
Renin
Angiotensinogen
Angiotensin 1
Angiotensin 2
Aldosterone
Aldosterone is a
water regulator
ANP _______ ________ volume.
reduces fluid
ANP stands for
Atrial natriuretic peptide
Kidneys are considered
Hint: Royal
King
ALWAYS check _____ __________ before med admin.
- What lab value do you check?
renal function
- creatinine
High BUN but low Creatinine
Dehydrated
High Creatinine and High BUN
renal failure
Calcium is related to what vitamin
D
What are the 7 functions of the kidneys?
- control ACID-base balance
- control WATER balance
- maintaining ELECTROLYTE balance
- removing TOXINS and waste products out
- controlling BLOOD PRESSURE
- producing ERYTHOPOIETIN
- activating VITAMIN D
ADH medication
Vasopressin
Vasopressin controls
water retention
In the nephron, water is reabsorbed where
distal tubule
If the patient’s body is dehydrated, then what chain of events occurs?
RAAS
Where fluid flows
electrolytes go
What is the difference between ADH and aldosterone
ADH retains water
Aldosterone retains sodium and water
Aldosterone causes kidneys to
retain sodium and water
Aldosterone causes the body to excrete
potassium
Low aldosterone, potassium
high (hyperkalemia)
High aldosterone, potassium
low (hypokalemia)
Aldosterone increases
fluid volume (sodium and water)
BP
Ultimate goal of Aldosterone and RAAS
increases reabsorption of sodium and water
excretion of potassium
RAAS is activated by
low serum sodium
decreased cardiac output due to decreased ECF
ischemia in kidneys
Low sodium, decreased cardiac output, and kidney ischemia can cause what to be released
renin
RAAS system’s ultimate goal
bp elevation
increased fluid
Angiotensinogen is a
glycoprotein made in the liver
What converts Angiotensin 1 to Angiotensin 2?
an enzyme from the pulmonary bed
Angiotensin 2 is a powerful/POTENT
vasoconstrictor
- elevates BP through peripheral vasoconstriction
- Stimulation of aldosterone secretion
ACE inhibitors stop
Angiotensin 1 from converting Angiotensin 2 emzyme from working
Aldosterone is a
mineralocorticoid that helps control sodium utilization
Aldosterone is released by the
adrenal cortex
What does Aldosterone do?
reabsorbs water with sodium following
- increases plasma volume
ANP is produced and stored where?
in atria
BNP is released
when the heart can’t pump the way it should
- heart failure and severity ( > 100 )
BNP is what type of lab test?
blood test
ANP does what?
- stops RAAS
- decreases BP by vasodilation
- reduces fluid volume by increasing the secretion of sodium and water
Hypovolemia vs Dehydration
Hypovolemia = loss of ECF including water and sodium
Dehydration = water loss alone
What is perfusion?
Oxygen to the bloodstream
Dehydration is common in the
elderly
- because they are less thirsty
S/S of Dehydration
red and dry mouth
Thirst
Oliguria
less and more concentrated urine
dizzy, confused
decreased skin turgor
Hypovolemia
ECF volume is reduced
- results in decreased tissue perfusion
Dehydration is
pure water loss from total body water
ECF 1/3
Dehydration is ALWAYS
hypernatremic
Treatment of dehydration
free water administration
Electrolytes are
separate into ions (changed particles) when dissolved in water
Electrolyte purposes
- ions found in our body fluids
- conduct electricity and energy
- control body fluids
- maintain homeostasis
- communicate cell to cell, nerve to nerve, organ to organ
Cations are a ________ charge
positive
Anions are a ________ charge
negative
Cation electrolyte
Na+
K+
Ca++
Mg+
Potassium is more common in the
intracellular
Sodium is more common in
extracellular
Anion electrolytes
Cl
HCO3 (Bicarbonate)
Phosphate
Depletion of electrolytes
Vomiting
Peeing (urination)
Pooping (BM)
Sweating
Magnesium (Mg+) normal levels
1.5-2.5
Calcium and phosphorus have a/an __________ relationship
inverse
Phosphorus normal levels
2.4-4.5**
Potassium (K+) normal levels**
3.5-5.0
Calcium (Ca+) normal levels
8.5-10.5**
Chloride (Cl-) normal levels
95-105
Sodium (Na+)**
135-145
What foods are rich in Potassium?
fruits, green leafy vegetables, spinach, salt substitutes
- bananas and berry families
What foods are rich in Sodium?
table salt, cheese, spices, canned, processed foods (lunchmeat)
What foods are rich in Magnesium?
spinach, almonds, yogurt, green vegetables
Dark chocolate = excellent Mg+ source
What foods are rich in Calcium?
milk, cheese, green vegetables
What foods are rich in phosphorus?
dairy, meats and beans
What foods are rich in Chloride?
salty foods and salt substitutes, canned foods,
Vegetables such as tomatoes, lettuce, celery and olives
Sodium functions
maintain blood pressure
blood volume
pH balance (acid-base)
controlling nerve impulses
stimulating muscle contractions
Sodium key items
big impact on body’s fluid balance
major electrolyte in extracellular fluid
controls water balance
regulated by ADH & aldosterone, Na+ K+ pump
If the patient has a low or high sodium level, what assessment would you do? Possible intervention?
Neurological
Safety and fall bundle
With sodium think
Brain, Neuro checks, Safety
Hyponatremia Causes
dilution on sodium
- SIADH**
- water intoxication**
- psychogenic polydipsia
- hypotonic fluids**
- inadequate sodium intake
- increased Na diet
SIADH
impaired water excretion caused by an inability to suppress the secretion of ADH
water retention causes dilution sodium
Water intoxication
retaining fluid & sodium causing hemodilution of Na+
Psychogenic polydipsia
excessive fluid intake without physiologic stimuli
Hypotonic fluids
shifts solutes into the cells
Inadequate sodium intake types
fasting
NPO status
low Na+ diet
What is the 4 D’s
diarrhea
diuretics
drainage
diaphoresis (sweating)
What device is famous for depleting sodium and other electrolytes?
NG tube
Increased Na+ excretion
4D’s - diarrhea, diuretics, drainage, diaphoresis
Vomiting
Kidney disease
Hypoaldosteronism (Addison’s)
sodium loss and water retention
3 Flavors of Hyponatremia
Euvolemic
Hypovolemic
Hypervolemic
Euvolemic Hyponatremia
Low Na+ with (ECF) volume normal
Hypovolemic Hyponatremia
Na+ loss with ECF volume depletion
Hypervolemic Hyponatremia
Na+ loss with increased ECF volume
What is the mild S/S of hyponatremia?
Mild = headache, nausea/vomiting, fatigue
What are the moderate S/S of hyponatremia?
lethargy, weakness, altered LOC
What are the severe S/S of hyponatremia? (Below 120)
seizures, respiratory arrest, death
brainstem herniation
What can a nurse do when suspecting Hyponatremia
Replace Sodium slowly
Stop Sodium Wasting Diuretics
Provide IV Fluids/medications
Every time you give an electrolyte, you give it
SLOWLY and recommended rate
Why do you Replace Sodium slowly
avoid fluid overload due to fluid shifting with sodium
can lead to neuro damage if given too rapidly
0.5 mEq/L per hour MAXIMUM
6 - 12 pts in a 24-hour period
Check Na+ levels every 2-4 hours
Stop Sodium Wasting Diuretics
loop diuretics; thiazides
may need to switch to spironolactone
Spironolactone is a
potassium sparing
The thiazide and loop diuretics need to have strict monitoring of
electrolytes
What fluid would you give to someone with mild to moderate hypovolemic hyponatremia?
0.9% Normal saline to correct fluid volume status & Na+
What fluid would you give to someone with severe
hypovolemic hyponatremia?
3% normal saline (hypertonic solution)
- give through a central line = highly caustic on veins
- gets rid of cell swelling away from the brain
What medication would you give to someone with hypervolemic hyponatremia?
give osmotic diuretics and fluid restriction
- Mannitol – excretes water but not Na+
What fluid would you use for SIADH?
EUVOLEMIC (normal volume with low Na)
- restrict fluid intake
Severe hyponatremia is
less than 120
- not increase by more than 6-12 mEq/L in first 24 hours
What is the order of interventions during severe hyponatremia?
administer 3% saline IV slowly - 6 to12 pts in a 24-hour period
Plan for CVAD
Insert indwelling catheter for strict I&Os
Perform neurologic checks every 2-4 hours
Keep on bedrest
What is key when dealing with cerebral involvement?
safety
When administering 3% saline why go through a CVAD?
highly caustic to veins
- But can be given through peripheral veins
If hyponatremia is overcorrected too quickly,
demyelination syndrome causing damage to nerve cells in the brain
- Locked-in syndrome
SIADH full name
Syndrome of Inappropriate Anti-diuretic hormone
SIADH-euvolemic hyponatremia
TOO MUCH ADH
high levels of ADH = retain water
upsets electrolytes, especially SODIUM
Increased water retention
Diluted sodium
Mnemonic for SIADH
SIADH
- Soaked Inside
- Stop Urination
Causes (3 Ss) of SIADH: Most common
Small cell lung cancer
Severe brain trauma
Sepsis infections of the brain
ADH is created in
pituitary gland
Mnemonic for ADH
Adds Da H2O
What are the different types of Synthetic ADH?
Desmopressin, Vasopressin
** Pressin the BP up**
ADH ________ urine output
decreases
If SIADH or low Na, what is the priority problem?
Headaches
Low Na = seizures, DEATH
What is the best/accurate way to monitor fluid changes?
Daily weight (I&Os, then BP)
Treatment for SIADH
Fluid restriction = 800-1000 mL/day
Demeclocycline
Diuretics
Increase oral sodium intake
Daily weight
I&O
Demeclocycline
blocks the effect of ADH resulting in more dilute urine
T/F: caffeine is a diuretic used in the treatment of SIADH.
True
Types of oral sodium intake
salt tablets
bacon
processed foods
Causes of Hypernatremia
Decreased sodium excretion
- corticosteroids - retain sodium
- Cushing’s syndrome
- kidney disease
Increased sodium intake
Decrease Water intake
Increased water loss (hemoconcentration)
If the patient had Hypernatremia what should the nurse be most concerned about?
cerebral hemorrhage
Hypernatremia level
greater then 145
Corticosteroids causes
kidneys to retain sodium
Cushing’s syndrome
occurs due to prolonged exposure to glucocorticoids (prednisone) or a tumor producing excessive cortisol by adrenals
Hyperaldosteronism
high sodium and water retention
Severe hypernatremia level
greater then 160
Hypernatremia Cause
Increased sodium intake
excessive oral sodium ingestion
too many processed foods
Hypertonic solutions (3% NS or 5%NS)
Alka seltzer, aspirin
Decreased water intake due to
fasting; NPO status
Hemoconcentration is caused by
dehydration
too much water loss & Na+ gain
Infection
Diabetes Insipidus
Hypernatremia Interventions
- Bring sodium levels down slowly
- Provide IV/Meds of hypotonic solutions in case of fluid loss
- Diuretics
- Avoid high sodium meds
- Restrict sodium and fluid intake as prescribed
- Free water intake to help with hemodilution
- pt safety: confused and agitated
- Daily weight I&Os
- Neurologic precautions (checks)
Why do you bring a sodium level down slowly?
rapid correction can lead to seizures due to rapid
fluid shifts in the brain
What solutions would you give a hypernatremic patient?
hypotonic
- 1/2 NS, D5W
If inadequate renal excretion of sodium, administer
diuretics
-thiazides; loop diuretics
Patient S/S of mild hypernatremia
faint feeling
muscle fatigue
weakness
Patient S/S of moderate hypernatremia
(monitor closely)
confusion, irritability,
swollen and dry red tongue
hyperreflexia
muscle twitching
edema
thirst
Patient S/S of severe hypernatremia
nausea & vomiting
increased muscle tone
seizures
coma
Diabetes Inspidus =
hypernatremia
Diabetes Insipidus is when the
the pituitary gland produces insufficient ADH (vasopressin)
- ADH deficiency
S/S of diabetes insipidus
polydipsia
polyuria
dry inside = labs high
- increased sodium and diluted urine
**Dehydrated (DIE ADH)
Causes of ADH
damage to brain
tumors
trauma
Polydipsia
extreme thirst
Polyuria
excrete dilute urine, greater than 200 mL
If the patient is having their pitcher refilled every 15-20 mins and peeing constantly, what would you suspect and intervention?
Diabetes Insipidus
- record I&Os
What are the differences between DI and SIADH
DI
-low AD and water in the body
- High UO, polyuria
- High sodium
- High H&H and osmolality from dehydration
- Risk of hypovolemic shock
- Tx: ADH
SIADH
- high ADH, water intoxication
- Low UO, oliguria
- low sodium (dilutional)
- low osmolality
- weight gain
- Risk: seizures
- Tx: hypertonic saline
Potassium is the king of
hearts
What is the major electrolyte in intracellular fluid?
Potassium
Potassium purposes
Maintains heart & muscle contraction
Regulated by kidneys and aldosterone
Acid-Base balance
- Increased K+ in the cell——H+ moves out
- Increased H+ in the cell——K+ moves out
Diet is the main source of K+
Hypokalemia
potassium loss
Inadequate potassium intake
Alkalosis, metabolic
Potassium loss can occur from what
Diuretics - furosemide and digoxin
Corticosteroids
Inadequate intake of Potassium ( NPO, anorexia, nausea)
Increased secretion of aldosterone (Cushing’s)
GI loss
Excessive diaphoresis
Kidney disease
Digoxin toxicity
– low K+ causes dig toxicity;
caution using diuretics with digoxin = increased risk for hypokalemia
How do corticosteroids cause potassium loss?
water retention causing hemodilution
Aldosterone causes potassium loss
K+ excretion through kidneys; higher levels of aldosterone cause more K+ excretion
Ways of Potassium GI loss
Vomiting
diarrhea
prolonged NG suction
Inadequate Potassium Intake causes
movement of K+ from ECF to ICF
excess insulin – moves K+ into the cell
What happens during Metabolic Alkalosis
in alkalosis, there is less H+ in the blood—–causes H+ to shift out of cells and K+ to shift into cells
excess insulin – moves K+ into the cell
Severe Potassium level
less than 2.5
When remembering S/S of hypokalemia, what do you remember?
SLOW AND LOW
Hypokalemia S/S Cardiovascular
torsades de pointes- twisting of points
irregular apical HR
lethal dysrhythmias
bradycardia
Hypokalemia S/S Neuromuscular
confusion, lethargy
muscle weakness
diminished DTRs
Hypokalemia S/S GI
Constipation - paralytic ileus
If bowel sounds are absent, think
paralytic ileus – portion of bowel not moving and can lead to small bowel obstruction
What other electrolyte should you check with hypokalemia? If low?
Magnesium
if Mg+ is low, it exacerbates K+ losses;
correct Mg+ first to correct K+
torsades de pointes is also known as
Long QT Interval
If the patient faints, then what do you think?
cardiac, and neurological
Long QT Interval means
heart is taking longer to electrically charge for the next heartbeat
Congenital Long QT Syndrome
born with altered DNA that causes long QT syndrome
Why is Long QT syndrome bad?
This electrical glitch sets up the potential for something to catch the heart off guard and electrically trip it up, causing a spinning rhythm out of control
acquired long QT syndrome
occur later in life due to some medical conditions, certain drugs, or mineral imbalances.
Irregular QRS complexes
appearing to wrap around the EKG baseline
Torsades de Pointes in hypokalemia Tx
IV Mg+ is treatment (slow 2G IVP)
EKG in Hypokalemia
increased amplitude and width of P wave, T wave flattening and inversion, prominent U waves and apparent long QT intervals due to merging of the T and U wave.
Comparison of Hypokalaemia and Hyperkalaemia EKG
Hypokalaemia: T wave inversion ST depression Prominent U wave
Hyperkalaemia: Peaked T waves, P wave flattening, PR prolongation, Wide QRS complex
Hypokalemia Interventions
Monitor Cardiac and respiratory status
Administer K+ supplements orally or IV
administer K+ SLOWLY – can be lethal when given too fast
If patient in taking a diuretic may need to stop
Spironolactone (K+ sparing diuretic)
K+ rich foods
if taking orally, must take with food – never give
on an empty stomach
Monitor for digoxin toxicity
Potassium is never administered IV push, potassium is always diluted
and administered using an infusion pump.
How do you give potassium?
IV, intramuscular, or subcutaneous routes, PO
IV potassium is always diluted
and administered
using an infusion pump
Causes of Hyperkalemia
Excess Potassium intake
Decreased Potassium secretion
Adrenal insufficiency
Renal failure - #1 cause
Traumatic burns
- Metabolic Acidosis
ACE inhibitors drugs end in
pril
What are the reasons for decreased potassium excretion?
K+ sparing diuretics (spironolactone)
Ace inhibitors
NSAIDs (decrease renal perfusion)
Adrenal insufficiency causes
- Addisons = low aldosterone = retention of K+
- hypoaldosteronism causes large amounts of sodium excretion and retains K+ (Addison’s = destruction of adrenal gland)
Metabolic Acidosis
there is more H+ in blood
causes H+ to shift into the cells and K+ to shift out in the cells
- Excretion of H+ ions by kidneys is accomplished by conserving bicarbonate, secretion of ammonia, and excretion of hydrogen in exchange for sodium.
S/S of Hyperkalemia
Cardiovascular
bradycardia
dysrhythmias – V-fib and cardiac standstill
GI increased motility = hyperactive bowel sounds
diarrhea
Muscle weakness
can result in paralysis and respiratory arrest
Severe potassium level high
greater than 6.5
Lethal high level of potassium
greater than 8.5
EKG and High Potassium
peaked narrow T wave,
ST segment depressed,
prolonged PR interval
Mild Hyperkalemia Interventions
Monitor cardiac rhythm changes
Restrict K+ in diet
Diuretics
Cation exchange resins
sodium polystyrene sulfate (Kayexalate)
**PO or rectal = explosive diarrhea **
Stop medication causing an increase in K+
Dialysis for renal failure
When do you stop Ca Gluconate 10% IV?
bradycardia
Ca+ Gluconate 10% IV
Purpose?
Monitor?
protects heart from myocardial irritability
= DOES NOT LOWER potassium
- dysrhythmias, BP and HR
If the patient has a potassium level of 6.5 or higher, what emergency medical tx would occur
Ca+ Gluconate 10% IV - must be given over 3-5 minutes
Hypertonic glucose & insulin = Moves excess K+ into the cells
NaHCO3 if acidosis = K+ shifts into the cell and raises pH
What is the most abundant cation in the body?
Calcium
Calcium and Magnesium levels are
best friends (One goes up the other follows
Calcium functions
Calcium will help with function of Mg+ when Mg+ is low
Keeps the 3 B’s strong
= Bone – 90% of body’s calcium - fractures
= Blood clotting - bleeding
= Beat (heart rate) myocardial contraction
What 3 hormones regulate Calcium?
Parathyroid
Calcitonin
Calcitrol
Parathyroid hormone and Calcium relationship
the parathyroid gland makes it
- releases when Ca+ levels are low
- stops if Calcium is too high
Where are the parathyroid and thyroid glands located?
Neck
Calcitonin and Calcium relationship
– regulated by thyroid;
released when Ca+ levels are high to lower Ca+ and put back into the bone
____ increases blood calcium levels; __________ decreases blood calcium levels
PTH; Calcitonin
calcitriol
– Vitamin D analog; controls blood calcium by suppressing the release of PTH
Calcium normal levels
8.5-10.5
Ionized Calcium
NOT TESTED
Calcium in blood not attached to proteins (free calcium)
Most accurate test for assessing true calcium status
Important if abnormal levels of proteins
May be drawn if signs of bone, kidney, liver, or parathyroid disease
Ionized Calcium normal levels
NOT TESTED
4.8-5.6
Calcium and phosphorus relationship
inverse
Hypocalcemia Causes
Vitamin D deficiency - required for the absorption of Ca+
Long-term corticosteroids
Hypoparathyroidism - decrease in parathyroid hormone, removal of parathyroid glands
Renal disease
Massive diarrhea
Hyperphosphatemia – inverse relationship with calcium
Medications – diuretics; laxatives; corticosteroids (contribute to bone loss)
Thyroidectomy or any neck surgery can inadvertently irritate or remove
parathyroid glands
S/S of hypocalcemia
Cardiovascular
hypotension
dysrhythmias (V Tach)
decreased HR
Neuromuscular
irritable skeletal muscles – twitching, cramps, tetany, seizures, paresthesias
painful muscle spasms in calf or foot
positive Trousseau’s and Chvostek’s signs
hyperactive deep tendon reflexes (DTRs)
osteoporosis – body trying to get more calcium
GI
hyperactive bowel sounds
diarrhea
Chvostek and Trouseau Signs hypocalcemia
ouch the face near the ear and if they flinch then positive
contraction of hand after bp
Hypocalcemia Interventions
Replace Calcium (IV or PO)
IV calcium gluconate 10% over 10 – 20 minutes
monitor BP, HR & place patient on heart monitor
Vitamin D if giving PO
Aluminum hydroxide (Tums) calcium supplements
Initiate seizure precautions & bleeding precautions
Move patient carefully
Educate on calcium-rich foods
dairy, cheese, milk, yogurt
collard greens, broccoli
Hypercalcemia Causes
Hyperparathyroidism
Antacids
Excessive oral intake of calcium & vitamin D
Malignancies – of the bone; bone destruction = calcium is released into the bloodstream
Renal disease – inability to excrete
What gland abnormality causes the following?
Kidney stones, painful bones, moans
from constipation, nausea & vomiting
Parathyroid
S/S of Hypercalcemia
- Neuromuscular
muscle weakness
diminished or absent DTRs - GI
hypoactive bowel sounds (constipation) - Renal
kidney stones
-Stones, bones, abdominal moans
Hypercalcemia Interventions
Administer IV fluids = 0.9% saline to get the kidneys to excrete calcium
D/C calcium
discontinue oral meds with calcium & vitamin
Loop diuretics
furosemide
Medications
phosphorous
inverse relationship with calcium
calcitonin
bisphosphonates
Dialysis if medications fail
Educate on avoiding calcium-rich foods
Less severe hypercalcemia interventions
IV NS
and loop diuretics
Magnesium normal levels
1.5-2.5
Magnesium functions
Support muscle and nerve function & energy production
- Direct relationship with calcium
- Inverse relationship with phosphorous
Helps to maintain
- blood glucose control
- blood pressure
- skeletal muscle contraction
- neurologic function
- ATP formation
- Immune system – fights inflammation
Causes of hypomagnesemia
Chronic alcohol use - #1 cause
- poor diet/malnutrition; starvation
- malabsorption due to the effects of alcohol on the GI tract
Renal loss – overuse of alcohol increases excretion of Mg
GI loss – NG, diarrhea, vomiting
Diuretics
If the patient is unable to maintain order; everything goes crazy.
What condition is this?
Hint: Magnum PI
hypomagnesemia
S/S Hypomagnesemia
Neuromuscular
tetany, twitches, paresthesias
positive Trousseau’s & Chvostek’s signs
- due to direct relationship with Ca+
Increased DTRs
Laryngeal stridor: can’t breath
Tachycardia
What electrolytes are best friends
Calcium and Magnesium
Hypomagnesemia Interventions
replace Mg+ and Ca+ (IV or PO)
when replacing Mg+ IV give slowly (can slow HR)
seizure precautions
monitor DTRs – if diminished or absent = hypermagnesemia
discontinue medications that cause Mg+ loss
Monitor K+ if magnesium is low
Secondary K+ depletion
Hypocalcemia accompanies ________________; interventions
aim to restore ________ levels
hypomagnesemia; calcium
Treat _____________ prior to ____________;
when the body is in a state of low Mg+, it is unable to process & absorb K+
hypomagnesemia; hypokalemia
Causes of Hypermagnesemia
Increased Mg+ intake (OTC and meds contraindicated - laxatives)
Decreased renal excretion of Mg+
Calm and Slow
Hypermagnesemia S/S
- Heart – calm & quiet
respirations low and shallow
bradycardia
hypotension - Lung
respirations low and shallow - GI
hypoactive bowel sounds
Neurological
drowsiness, lethargy - MS
Diminished or absent DTR’s
What is the antidote of a magnesium overdose?
Calcium Gluconate
Hypermagnesemia Interventions
Calcium Gluconate for magnesium overdose
Diuretics for Mg+ excretion
Phosphorus normal levels
2.4-4.5
Phosphorus Main functions
Regulated by parathyroid and calcitriol
Helps regulate calcium
inverse relationship with calcium and magnesium
Cellular metabolism and energy production through ATP (Adenosine Triphosphate)
Essential for bone and teeth
Hypophosphatemia Causes
- Insufficient phosphorous intake
malnutrition
starvation
‘Refeeding Syndrome’ – fatal shift of fluids &
electrolytes that may occur in malnourished patients - Increased phosphorous excretion
hyperparathyroidism – calcium rises; phosphorous drops
malignancy
diuretics and diarrhea
use of magnesium-based or aluminum-based antacids
increased Ca+ depletes phosphorous
S/S of Hypophophatemia
Cardiovascular
decreased BP, HR
GI – hypoactive bowel sounds
GU – kidney stones
Neurological–altered LOC decreased DTR
Musculoskeletal – severe muscle weakness
Bone pain & fractures
MOANS GROANS AND STONES
Hypophosphatemia Interventions
Replace phosphorous IV or PO slow
phosphorous slow if severely low
administer oral phosphorous with Vitamin D
Fracture precautions
Hyperphosphatemia Causes
Increased phosphorous intake
Overuse of laxative and enemas with phosphorous
Decreased excretion of P- due to renal insufficiency
Hyperparathyroidism
Hypocalcemia
hyperphosphatemia S/S
*Neuromuscular
irritable skeletal muscles – twitching, cramps, tetany, seizures, paresthesias
painful muscle spasms in calf or foot
positive Trousseau’s and Chvostek’s signs
hyperactive deep tendon reflexes (DTRs)
osteoporosis – body trying to get more calcium
-GI
hyperactive bowel sounds
diarrhea
Hyperphosphatemia Interventions
Same interventions as hypocalcemia
Replace Calcium (IV or PO)
IV calcium gluconate 10%
monitor BP, HR & place patient on heart
Vitamin D if giving PO
Aluminum hydroxide (Tums) calcium supplements
Initiate seizure precautions & bleeding precautions
Move patient carefully
Educate on calcium rich foods
dairy, cheese, milk, yogurt
collard greens, broccoli
Chloride functions
Major anion of ECF
Sodium is major cation of ECF
Moves in and out of the cell with sodium
Involved in regulating acid base balance
chloride likes sodium; if Na+ loss = Cl- loss
What is the major anion of the ECF?
Chloride
Chloride normal levels
95-105
Corticosteroids
bone loss; increased blood glucose; Na+ retention
- low potassium
Ace Inhibitors, Spironolactone (Aldactone), ARBs
hold on to K+
- low sodium
Insulin
move K+ into the cell
Furosemide
potent diuretic; should monitor all electrolytes
Laxatives (Mg)
NSAIDs (Ibuprofen)
decrease renal perfusion
Potassium normally lives in what fluid
Intracelular
Potassium is responsible for
Nerve impulse induction and muscle contraction
Medications to avoid renal failure
Ace inhibitors
steroids (hold)
furosemide (hold)
give this instead = spironolactone (Aldactone)
ARBs
NSAIDs
If a patient with renal failure needs NSAIDs, what is a safer alternative?
Tylenol
What is the best/accurate way to monitor fluid changes?
Daily weight
ARBs
Angiotensin Resistant Blockers
What do you hold when the patient is in renal failure or high potassium?
ACEs and ARBs
Laxatives contain what if in renal failure?
Mg
Lisionopril is a
ACE inhibitor
Spirinolactone is a
potassium sparing diuretic
ARBs end in
sartans (valsartan)
If the patient is in post-cardiac arrest, what is the organ that was affected besides the heart?
kidney acute failure
If there is a sudden change in LOC, then what do you think might be the cause?
Hypoxia (low O2)
With Lasix, what do you monitor? How slow do you give it?
BP; 2-4 mins
If you don’t v-fib, hearing loss, hypotension, lethal dysrhythmia
If you do not give Lasix at 2-4 mins, then what can occur
v-fib, hearing loss, hypotension, lethal dysrhythmia
What patient might have Furosemide?
heart failure
, liver, renal
calcium is high, phosphorous
low
If you have lupus and have a high-dose steroid, what ELECTROLYTE IMBALANCES might occur?
osteoporosis
- hypocalcemia
hypernatremia
hypokalemia
increases blood glucose
suppresses immune system
If magnesium is out of order, then
chaos and not order of electrolytes
Why is magnesium needed?
help nerve function
controls glucose
immune system stronger
helps calcium
sleep and focused
If you have heart failure and have high doses of furosemide, then what lab would you need to know?
Potassium (worry about hypokalemia)
Magnesium (if not normal take care of first)
If you have a low potassium level, then check
magnesium level
Why should you never give potassium on an empty stomach?
GI upset
What should also be given if you send home a patient on a diuretic?
What should you stop if you run out of diuretics?
Potassium, yes
What is given if the patient has hypokalemia
Kayexssolate Insulin
If I over-treat a diabetes inspidus patient, what will happen?
water intoxication (HA, altered LOC)
When monitoring a client for hyponatremia, which assessment findings would the nurse consider significant? Select all that apply.
- Thirst
- Seizures
- Erythema
- Confusion
- Constipation
Seizures
Confusion
