Module 2 - Alterations in Fluids and Electrolytes Flashcards
Every disease process involves some alteration in ..
fluids and electrolytes
Molecule
When two or more atoms combine to form a substance
Ion
an atom carries an electrical charge because it has either gained or lost electrons
some ions have a negative charge and some positive charge
Cation
Ion that carries a positive charge and it has given away or lost electrons
Positive charge
fewer electrons than protons
Anion
an ion that has gained electrons and therefore carries a negative charge
negative charge
gained or taken on electrons (more electrons than protons)
In health there is ___ amounts of cations and anions in the body
equal
Electrolytes
substance dissolved in solution and some of its molecules split or dissociate into electrically charged atoms or ions
critical for life and muscle function
What is the unit of measurement for volume of fluids ?
metric - L or mL
In the body, non-dry areas are in ___
solution
The unit of measure that expresses the combining activity of an electrolyte is …
the milliequivalent (mEq)
One mEq of any cation will …
always react chemically with one mEq of an anion
What information does mEq’s provide?
information about the number of cations or anions available to combine with other cations or anions
The fluid in each of the body compartments contains …
a particular composition of electrolytes which differ from that of other compartments
To function normally, body cells must have …
the right amount of fluids and electrolytes (and being in the right compartments)
Whenever an electrolytes moves out of a cell..
another electrolyte moves in to take its place
Homeostasis
a state that requires the number of cations and anions to be the same in order to exist
Body compartments are separated by..
semi permeable membranes
Intracellular Compartments
Fluids inside the cells
Most of the body fluid (2/3) is inside the cells
Extracellular Compartments
Refers to all fluid outside the cells (plasma, blood, interstitial fluids)
Intravascular Compartment
Fluids in the blood vessels (ECF subtype)
Interstitial Fluids
fluid between the cells and blood vessels
What compartment is the most important to view electrolyte levels from?
The intracellular compartments (ex: potassium is highest in the cell, not blood or ECF; almost no calcium in cells; small traces of Na, etc)
Most sodium is in …
the blood
this is also the most sensitive electrolyte to the blood
What does body fluid do for us?
Transports nutrients to the cells and carried waste products from the cells
How much of the body weight is body fluids?
60%
What losses of body fluid are serious or fatal?
Serious - 10%
Fatal 20%
ex: 70 kg person has about (152 lbs) 42 L of body fluids (60%). 4.2 L 10%, and 20% is 8.4 L
How might body fluid amounts be different?
Older people usually have less fluid; Muscular people often have more
So factors other than just loss is important like age and situation
Body fluid consists of what?
Water and dissolved substances
The largest single fluid constituent of the body is ..
water
Why is it important whether a substance dissolves or not in solution?
Some do not dissolve, glucose, urea, and creatinine, and therefore cannot be moved as simple substances
Some larger ones do (ex: NaCl) and then their constituents can be moved easily
What is the ratio of ECF to ICF in the body
2/3 ICF to 1/3 ECF
Of extracellular fluid, what makes it up?
80% Interstitial Fluid
20% Plasma
How does body fluid differ between genders?
Males are 40% solid and 60% fluid, and Females are 45% solid and 55% fluids
Women naturally have more body fat so they have less fluid, and fat does not hold water like muscle does
How does body fluid correlate to muscle and fat?
Increased fat = decreased total body water
Increased muscles = increased total body water
So, even if a person is heavier, they are at risk for dehydration
Diffusion
the movement of particles in all directions through a solution
the process by which a solute may spread through a solution or solvent
Goes from high to low concentration with little/no energy used
Solute
the substance that is dissolved
Solvent
the solution in which the solute is dissolved
When a solute diffuses how does it spread the molecules?
It spreads the molecules from an area of high concentration to an area of lower concentration (not a lot of energy to do this)
Permeable Membrane
a membrane allowing substances to pass through/diffuse without restriction
we do not want these, we want some control
Selectively Permeable Membrane
membrane allowing some solutes to pass through without restriction but will prevent others from passing freely
Osmosis
Like a PULL of water or solvent across a membrane
occurs when there is a more concentrated solution on one side of a selectively permeable membrane and a less concentrated solution on the other side - so osmotic pressure draws water through the membrane to the more concentrated side or the side with more solute
Water Osmosis occurs from ___ concentrated to ___ concentrated
low concentration to more concentration (in order to have equal concentrations on each side)
Osmotic Pressure
force that draws the water (pull) from less concentrated solution through a selectively permeable membrane into a more concentrated solution
the difference determines strength
Hydrostatic Pressure
the force for filtration (PUSH pressure) - like water pushing against a water balloon
the force exerted by the weight of a solution
it moves from an area of greater pressure to an area of lesser pressure
Filtration
movement of solutes and solvents by hydrostatic pressure
it moves from an area of greater pressure to an area of lesser pressure
Osmolality
refers to the number of osmotically active particles per kilogram of water
What unit is osmotic pressure measured in
Milliosmols
Normal osmolality of plasma is …
280-294 mOsm/kg
just a little less than 300
When there is a difference in hydrostatic pressure on two sides of a membrane, ___ and ___ ____ move out of the solution that has the ___ hydrostatic pressure by process of ____
When there is a difference in hydrostatic pressure on two sides of a membrane, water and diffusible solutes move out of solution that has the higher hydrostatic pressure by process of filtration
How does pressure differ at the arterial end of the capillary?
At the arterial end, hydrostatic pressure or push is greater than osmotic pressure - so more fluids and diffusible solutes move out of the capillary (via filtration)
How does pressure differ at the venous end of the capillary?
At the venous end, osmotic pressure or pull is greater than hydrostatic pressure - so fluids and some solutes move into the capillary (via osmosis)
What occurs to excess fluid and solutes remaining in interstitial spaces after osmosis and diffusion?
The excess fluid and solutes are returned to intravascular compartment by lymph channels
What separates interstitial fluid from intravascular fluid?
cell membranes (selectively permeable - may need energy like ATP with the NaK Pump)
The greater the number of particles in a concentrated fluid, the more ___ there will be to move ___ through the memvbrane
pull; water
Isotonic Solution
“Same”
Solutions on both sides of the membrane have established equilibrium or are equal in concentration
Equal tonicity - no shift in fluid
Isotonic solutions have the same tonicity as body fluids
Tonicity
refers to concentration of dissolved molecules held in solutions
isotonic solutions have same tonicity as body fluids and it occurs between the membranes
this refers to being hypotonic, isotonic, and hypertonic
Examples of Isotonic Solutions
0.9% Sodium Chloride(Isotonic Saline / Normal Saline) - good for replacing fluid volumes
5% Dextrose
5% Dextrose in 0.225% Saline
Lactated Ringer’s Solution (for emergencies)
There is ___ to ___ mOs/kg in Normal Saline
280 to 294
same osmolality as plasma
What occurs for movement when an isotonic fluid is given?
little fluid movement / osmosis occurs
Hypotonic Solutions
When a solution has a lower concentration of salt than other solutions - it is hypotonic
It has less salt OR more water than isotonic
Fluid ends up moving into the cells
Restores cells from dehydration
Examples of Hypotonic Solutions
0.45% Saline (dilutes blood by moving fluid into the cells - moves from a less concentrated to more concentrated)
Distilled Water (no solutes)
What is the highest electrolyte in the blood
Salt
Hypertonic Solutions
A solution that has a higher concentration of solutes than another solution is a hypertonic solution
Examples of Hypertonic Solutions
10% dextrose in water
5% dextrose in 0.9% saline
5% dextrose in 0.45% saline
5% dextrose in lactated Ringer’s Solution
What is the difference in hypotonic and hypertonic concentrations for blood and cells?
Hypotonic - fewer particles in blood, but more in the cell, so the cell gets water moving in and causes swelling (a problem)
Hypertonic - more particles in the blood and fewer in the cells, so water moves out of cells to the blood - this dehydrates the cells
If the selectively permeable membrane will allow the solvent to pass through but will not allow the solute through freely…
the solvent will move to the side of greater solute concentration
If the extracellular fluid is 300 mOsm/kg in 17 L and inside the cell is 280 mOsm/kg in 25 L, what is the tonicity and changes after osmosis?
The ECF is hyperosmotic with ICF being Isotonic
It will go from 300 in 17L in the ECF to 290 in 18 L; It will go from 280 in 25 L in the ICF to 290 in 24 L - this occurs because the water moves from inside the cell moves out to the higher concentration
If the ECF is 260 mOsm/kg in 19 L and ICF is 280 mOsm/kg in 25 L, what is the tonicity and changes after osmosis?
ECF is hypotonic with the inside of the cell being isotonic
ECF goes 260 in 19 to 270 in 18 while ICF goes 280 in 25 to 270 in 26
Hypertonic solutions cause ___ while Hypotonic solutions cause ___
shrinkage ; swelling
Active Transport
moving an ion from low concentration to high concentration requires energy and active transport
Active transport moves molecules or ions ___ concentration and osmotic pressure
against
Energy for active transport is supplies by ___ ___ in the cell
metabolic processes (ex: ATP)
What are some substances that require active transport to move through the cell membranes
Na Ions, K ions, Ca, Iron, Hydrogen, some sugars, amino acids
What ways do fluids leave the body
Skin
Lungs
GI Tract
Kidneys
The ___ excrete the largest quantity of fluid
kidneys
__ of urine can tell a lot about extra fluid amounts in the body
color
How much water is lost by the skin via diffusion per day?
300-400 mL per day
Water loss from perspiration depends on what?
depends on the temperature of the environment and of the body
Average amount of water lost via perspiration is ___ mL per day
100
How is water lost by the lungs and how can the amounts change?
lost via expired air which is saturated with water vapor
amount varies with the rate and depth of respiration
Average amount of water lost from the lungs is …
300-400 mL per day
Insensible Loss
water lost from lungs and skin that is lost without the person being aware of the loss
You are unaware and cannot be measured
How does body fluid excretion relate to the GI tract
very large amounts of electrolyte containing liquids are secreted into the GI tract but almost all of this fluid is reabsorbed - and returns again to the ECF
A LOT of it is reabsorbed
The average amount of water lost in the feces is ___ mL/day which is equal to ….
200 mL/day which is equal to the amount of water gained through oxidation of foods
How does severe diarrhea influence electrolyte and fluid balance?
loss of large quantities of fluids and electrolytes occurs
What organ plays a major role in regulating fluid and electrolyte balance?
Kidneys - they can adjust the amount of water and electrolytes leaving the body
What determines the quantity of fluid excreted by the kidneys?
determined by the amount of water ingested and the amount of waste and solutes excreted
Usual quantity of urine output is approximately ____; but this can vary greatly depending on ….
1500 mL per day
Fluid Intake
Amount of Perspiration
Other Factors
Daily Body Fluid Excretion? Skin by Diffusion = \_\_ Skin by Perspiration = \_\_ Lungs = \_\_ Feces = \_\_ Kidneys = \_\_ Total = \_\_
Diffusion (Skin) - 350 mL Perspiration (Skin) - 100 mL Lungs - 350 mL Feces - 100 mL Kidneys - 1500 mL Total - 2400 mL / day
What are the three sources for water entering the body?
Oral Liquids
Water in Foods
Water formed formed by oxidation of foods
(this includes tubes when doing I&O)
Average total amount of water taken into the body by the 3 sources of water is ___ mL per day
2400 mL/day
About how much water is released by metabolism of each 100 calories of fat, carbs, and proteins
10 mL
How are electrolytes replaced?
Electrolytes are present in foods and liquid and in a normal diet an excess of essential electrolytes is taken and the unused electrolytes are excreted via urine
Homeostasis
Balance
a term which indicates the relative stability of the internal environment
It is needed because concentration and composition of body fluids must be nearly constant
How is homeostasis directed in the deficiency and excess of electrolytes?
Deficiency - must replace fluids and electrolytes via either intake of food and water or by therapy like IV or meds
Excessive - excess fluid or electrolytes needs therapy or diuretics directed toward assisting the body to eliminate the excess
Kidney role in maintaining fluid and electrolyte balance
play a major role in controlling all types of balance in fluid and electrolytes
Adrenal Glands role in maintaining fluid and electrolyte balance
it secretes aldosterone (direct sodium -retention- which water follows)
it ends up aiding in controlling ECF volume by regulating the amount of sodium reabsorbed by the kidneys
ADH role in maintaining fluid and electrolyte balance
Antidiuretic hormone from pituitary gland regulates osmotic pressure of ECF by regulating amount of water reabsorbed by the kidneys
ADH and Aldosterone lead to ..
increased fluid volume (low flow states to the kidneys)
Factors that influence fluid intake
Climate
activity level (like breathing faster using more fluid)
social events
emotions (binge or anorexia)
LOC - confused/coma
age-elderly (decreased sense of thirst, loss of taste buds, immobility, purposeful restriction, confusion and depression)
What are the total gains and loss of fluid in a day?
Gain = liquids 1100-1400 + solid foods 800-1000 + oxidation of CHO, proteins, fats 200-350 = 2500 mL/day
Loss = respiration 300-400 + skin 300-400 + sweat 100 (1-2 L with exercise) + feces 100 + urine 1500 = 2500 mL/day
A lot of things are reabsorbed by the kidneys, but one thing that does not get reabsorbed is a good indicator of kidney function?
Creatinine (1.4 g)
_____ is a potent vasoconstrictor
Angiotensin II
What does aldosterone control?
salt which water then follows –> increased circulating volume
Pathway of the RAA system?
Renin release stimulated by low flow states to the kidneys and angiotensinogen works with it –> angiotensin I –> converted via enzyme to Angiotensin II –> Renal autoregulation, increased blood pressure, increased circulating volume
What gland releases Renin/RAA?
adrenal medulla
What gland releases ADH
posterior pituitary
What does ADH control?
governs water to increase fluid volume
does this by telling kidneys to hold water and decrease osmolarity of plasma until it is right and gets negative feedback
ADH pathway?
increased plasma osmolarity or decreased circulating blood volume –> thirst –> increased fluid intake –> increased water retention
increased plasma osmolarity or decreased circulating blood volume –> ADH secretion –> decreased water excretion –> increased water retention
Increased water retention –> increased circulating fluid volume -> decreased plasma osmolarity –> decreased ADH and thirst
What things does decreased blood volume, increased serum osmolarity, and increased thirst and water intake lead to? (RAA and ADH)
stimulates ADH production in hypothalamus
stimulate increased ADH release into the blood stream from posterior pituitary
decreased arterial BP
What does a drop in arterial blood pressure lead to? (RAA and ADH)
increased sympathetic discharge –> decreased renal perfusion –> increased renin release –> angiotensin I and II –> increased aldosterone by the adrenal cortex –> drop in salt and H2O excretion and an increase in blood pressure
increased sympathetic discharge –> decreased renal perfusion –> drop in water and salt filtered by the kidneys –> drop in salt and H2O excretion and an increase in blood pressure
What does a drop in salt and H2O secretion and an increase in blood pressure lead to? (RAA and ADH)
increased circulating volume of water and H2O with a loss of potassium –> increased blood volume and decreased serum osmolarity –> increased ADH production in hypothalamus
What does Increased ADH release into the blood stream from the posterior pituitary lead to? (RAA and ADH)
increased reabsorption of H2O by the kidneys –> decreased urine secretion –>increased circulating volume of water and H2O with a loss of potassium –> increased blood volume and decreased serum osmolarity –> increased ADH production in hypothalamus
The best way to measure daily fluid volume is …
Daily Weight
Why can I&O be inaccurate?
it can be hard to get every bit of intake and output
but it is a way to measure fluid weight / balance
Fluid Volume Deficit
dehydration in which water and electrolytes are lost in the same proportion
Goal of Fluid Volume Deficit treatment is to …
goal of treatment is to restore fluid volume, replace electrolytes as needed, and eliminate the cause of the fluid volume deficit
Causes of Fluid Volume Deficit
vomiting
diarrhea
increased respiration
use of diuretics and increased urine output
insufficient IV fluid replacement
GI suctioning
draining fistulas
ileostomy or colostomy drainage
How/things to/that assess fluid volume deficit?
increased respiration
increased heart rate
decreased central venous pressure (CVP)
weight loss
poor skin turgor
dry mucous membranes
decrease in urine volume
urine is dark in color and odorous
increased specific gravity of the urine
increased hematocrit
altered level of consciousness
confusion
Things to Implement for Fluid Volume Deficit
Assess vital signs
assess neck and hand vein turgor
assess mucous membranes and skin turgor
monitor hematocrit and electrolyte values
replace fluids by PO or IV (lactated ringers solution, 0.9% normal saline) as prescribed
administer medications as prescribed
monitor weight daily
monitor I&Os
test urine for specific gravity
monitor bowel sounds
Hypovolemia
Greater fluid loss than fluid intake
Isotonic Hypovolemia
this is Total Fluid Volume deficit
water and lytes (Na+) lost in equal proportions
ECF is iso-osmolar –> no change in ICF
Hypotonic Hypovolemia
decrease in solutes but not the water
so, ECF is hypo-osmolar –> fluid shifts from ECF to ICF (in cell causes swelling)
Hypertonic Hypovolemia
decrease in water but not solutes
ECF is hyper osmolar –> fluid shifts from ICF to ECF (shrinkage & dilute blood)
When talking about Hyper, Hypo, and Isotonic issues we are talking about …
the BLOOD
Etiologies of Hypovolemia
GI Fluid Loss Kidneys Hyperosmolar Tube Feedings Fever Decreased Fluid Intake Skin Hemorrhage Third Spacing
What tonicity fluid hypovolemia does GI fluid loss get and examples of this loss?
Isotonic, Hypotonic
Prolonged vomiting
gastric suction
excessive diarrhea
What tonicity fluid hypovolemia does Kidney loss get and examples of this loss?
Isotonic, Hypotonic
Polyuria d/t DKA
Renal Disease
Diuresis
What tonicity fluid does hypovolemia due to fever loss get?
Hypertonic
What tonicity fluid does hypovolemia from decreased fluid intake get and examples of this loss?
Isotonic and Hypertonic
Decreased LOC, sedation, NPO status
Anorexia, N/V, Dysphagia
Decreased Access, Depression
Examples of hypovolemic fluid loss from skin?
Excessive sweating
burns
Why would we give isotonic and then hypotonic fluids to hypovolemics?
If there was loss from the GI or kidneys the isotonic can replace fluid volume and then the hypotonic solution moves fluid into the cells
Why would we give hypertonic solution to someone with a fever (hypovolemia)
Cells are getting more fluid than blood because of increased metabolic demand so this will bring fluid back into the blood
Why would we give isotonic and then hypertonic fluids ?
if they have decreased fluid intake the isotonic will correct circulating volume and then the hypertonic fluids prevent cell and brain swelling
Third Spacing
there is an appropriate amount of fluid in the body but it is stuck in the interstitial space between cells and the blood
this can lead to hypovolemia
Why do we give isotonic fluids to third spacing?
it reestablishes circulating volume
What are some manifestations of Hypovolemia?
Rapid weight loss (1 L = 1 kg = 2 lbs; 1 lbs = 500 mL)
Decreased skin turgor
oral changes (dry membranes; longitudinal furrows on tongue)
Decreased urinary output (oliguria <30 mL/hr or <400mL/24 hrs; increased urine specific gravity > 1.030)
increased BUN (>10:1 BUN:Creat ratio)
VS changes (decreased T, increased RR, orthostatic hypotension, increased FVD –> decreased BP in all positions)
Decreased CVP (JVD)
Decreased peripheral blood flow (>3 cap refill; cold extremities)
increased thirst, HCT, confusion, weakness
BUN
nitrogen in the blood (urea)
increase BUN indicates decreased renal function or dehydration (increased ratio is concerning)
How should solutions be taken in mild hypovolemia and severe hypovolemia?
Mild - Oral Intake
Severe - IV Fluids
How should treatment go for Hypovolemia?
- Isotonic Solutions (NS or LR) to re-expand plasma volume, increase BP, and possibly administer blood if d/t hemorrhage
- Once normotensive, give a hypotonic solution (ex: 1/2 saline) to provide lytes and free water to make urine (ECF –> ICF)
Fluid Challenge
Something we do if we are unsure if the hypovolemia is due to a kidney problem or volume problem
We give a bolus of water and if they do not increase urination then it may be a kidney problem, but good urinary output indicates dehydration.
Nursing Interventions for Hypovolemia
Measure I and O
Daily Weight
VS
Skin
BUN:Creat Ratio
CVP
PO Intake - oral care (consider tube feedings if cannot PO)
Turn and Position - Moisturize Skin
Evaluation of Adequate Fluid Replacement
What should be some signs of adequate fluid replacement from Hypovolemia?
increased urinary output (40-60 mL/hr)
decreased urine specific gravity
increased body weight
T, BP, HR, RR normal
skin turgor, oral moisture
increased CVP
increased sensorium and strength
Fluid Volume Excess
actual excess of total body fluid or a relative fluid excess in one or more fluid compartments
also called Overhydration or Fluid Overload
Hypervolemia
What is the goal of fluid volume excess treatment?
restore fluid balance, correct electrolyte balances, and eliminate or control the underlying cause of the overload
Difference between Peripheral Edema and Cellular Edema?
Peripheral Edema is ECF fluid excess leading to fluid between the cells
Cellular Edema is ICF fluid excess leading to fluid in the cells
Hypervolumia
Fluid intake > Fluid loss
Isotonic Hypervolemia
water and lytes (Na+) gained in equal proportions
ECF is iso-osmolar –> no change in ICF
Hypotonic Hypervolemia
Water intoxication
increase in water but not solutes
ECF is hypo-osmolar –> fluids shift ECF to ICF
Hypertonic Hypervolemia
Increase in solutes but not water
ECF is hyper-osmolar –> fluid shifts ICF to ECF
Etiologies of Hypervolemia
Excessive intake of sodium and water either PO or IV
Fluid retention d/t renal failure, SIADH (brain lesions can do this), cardiac disease (does not move water well), corticosteroid use (puffiness), cirrhosis of the liver, analgesic/anesthetic/psychotropic use
The Major cause of Hypervolemia is …
Heart Disease
Manifestations of Hypervolemia
Rapid Weight Gain (5-7 pounds is severe)
Circulatory Overload (Heart Failure)
Interstitial Edema (peripheral edema (dependent) when legs are down; pulmonary edema (inspiratory fine crackles = minimum of 1500 cc) which can be life threatening
JVD - distended neck veins
Bounding pulse
Treatment for Hypervolemia
sodium restricted diet
diuretics
fluid restriction
Why would a sodium restricted diet be used for Hypervolemia?
if the hypervolemia is d/t HF, RF, liver disease, HTN (cautiously)
Loop Diuretic
lasix, bumex
works on the loop of henle
stronger diuretic
Thiazide Diuretic
HCTZ (not for HF or RF)
not as strong as loop so its not for HF or RF
K Sparing Diuretic
Aldactone
not as strong as loop or thiazide so not for HF or RF use either
Can diuretics fix everything for Hypervolemia?
no
it could even reverse the problem to hypovolemia
What things can Diuretics cause?
FVD
Hyponatremia
Potassium Imbalances
Loss of Mg
Changes in Ca Excretion
Acid Base Problems (Metabolic Acidosis)
Nursing interventions for Hypervolemia
I and O
weight
breath sounds
edema in the feet, ankles, and sacrum
lab value check (BUN and HCT)
Rest (favors diuresis)
response to diuretics
IV fluids
education on low sodium diet and self monitoring weight
upright position for dyspnea
turn and position
Hyponatremia
Serum sodium level <135-145 mEq/L
d/t excessive sodium loss (without water) or excessive water gain (without sodium)
The most common electrolyte imbalance in a hospital setting is ..
hyponatremia with a 3% prevalence
Decreased Serum Osmolality in Hyponatremia leads to …
First fluid moves from the ECF to ICF to cause swelling, and the second shift then cocurs where sodium shifts from ICF to ECF
Examples of electrolytes traveling together?
sodium and chloride
potassium, calcium, magnesium
Most abundant lyte in the blood
Na+
Most abundant lyte in the cell
K+
Etiologies of Hyponatremia
Excessive Sodium Loss
Insufficient Sodium Intake or Absorption
Excessive Water Gain
Adrenal Insufficiency
SIADH
Excessive Sodium Loss examples that cause Hyponatremia
prolonged diuretic therapy
burns
excessive diaphoresis
GI fluid loss: prolonged vomiting, NG suction, diarrhea, laxative abuse, repeated TWEs
renal disease
Examples of things that lead to insufficient sodium intake or absorption leading to hyponatremia
anorexia
acute alcoholism
Examples of things that lead to excessive water gain leading to hyponatremia
excessive administration of water PO or IV (D5W)
psychiatric disorders with compulsive water drinking
How does adrenal insufficiency lead to hyponatremia?
low aldosterone compromises sodium reabsorption (and kidneys hold K instead)
How does SIADH lead to hyponatremia?
dilutional hyponatremia d/t water retention
Manifestations of Hyponatremia
Decreased Na+
I > O , decreased UO
decreased urine specific gravity (<1.010)
decreased Cl- (<100 mEq/L)
decreased serum osmolality (<285)
Weight gain - no significant edema
Fingerprinting over sternum
What manifestations does decreased Na+ levels >125 lead to?
asymptomatic
What manifestations does decreased Na+ levels 120-125
nausea
malaise
abd cramps
What manifestations does decreased Na+ levels 115-120
headache
lethargy
obtunded
What manifestations does decreased Na+ levels <110-115
seizures
coma
personality changes
What is the hallmark of Hyponatremia?
Fingerprinting over the sternum
ONLY hyponatremia causes this
actual swelling of the cells, not in tissues or spaces, lead to this
Cause and Effect of Hyponatremia
Causes: Excessive sodium loss or Sodium dilution with excess water
Effects: Increased water in the brain, headache, weakness, lethargy, confusion, GI issues like not wanting to eat and diarrhea, plasma sodium low and urine gravity is low
A lot of issues occur ____ for hyponatremia
neurologically (d/t cell swelling)
How to treat Hyponatremia
If its sodium loss: replace sodium PO or IV - NS for mild to moderate or 3% saline pump for severe (it is hypertonic so we dont wanna shift too fast from cells to circulatory system) (Na<120)
For excessive water gain - restrict fluid intake
Nursing Interventions of Hyponatremia
Restrict Fluids (teach family, fluid restriction, post sign)
Accurate I and O (via IV pump)
Daily Weight
VS - BP and HR
Neurologic Assessment (LOC, pupillary responses, muscle strength)
Safety Precautions (side rails, seizures, precautions)
Monitor lab values
Turn and position
The most important assessment for a hyponatremia patient is?
the Neurologic Assessment
Hyponatremia has less salt in the blood, so where does fluid shift?
it will move into the cell which has higher salt concentration
Hypernatremia
serum sodium level >145 mEq/L
d/t excessive sodium gain (without water) or excessive water loss (without sodium)
What does the increased serum osmolality do for fluid shifting in hypernatremia?
fluid shifts from ICF to ECF (cellular shrinking)
There is a higher concentration in the blood so it must be diluted
Hypernatremia is most often a ___ problem
water problem
never occurs in alert patients with normal thirst and access to water because of their thirst mechanism
Etiologies for Hypernatremia
Water deprivation (i.e unconscious, debilitated, infants)
Hypertonic Tube Feedings (without water supplements)
Inadequately diluted baby formula
High protein diets (without adequate fluids)
Insensible water loss (i.e. burns hyperventilation or heat stroke)
Watery Diarrhea
Excessive administration of 3% saline (hypertonic) or sodium bicarb
Diabetes insipidus (lack ADH - water loss without salt loss)
Near drowning in sea water
Manifestations of Hypernatremia
Dry Stick Mucous Membranes
Neurologic (CNS) issues like hyperactive DTRs, disorientation, agitation with stimulation, hallucinations, lethargy –> Coma
Neuromuscular issues like muscle twitching and convulsions
Extreme thirst
VS (increase T and HR, decreased BP)
Oliguria and Anuria
Lab values (increase Cl-, serum osmolality >295, urine specific gravity > 1.015)
What are the hallmark symptoms of Hypernatremia?
Extreme Thirst
Dry Sticky Mucous Membranes
Cause and effects of Hypernatremia
Causes: Excess salt intake, Decreased salt loss, lack off sufficient water intake
Effects: mucous membranes dry and sticky, intense thirst, tachycardia, agitation, restless - overall feelings hyper rather than lethargic
Treatments for Hypernatremia
Slow correction
-with 1/2 NS or 1/4 NS (hypotonic solution) to get water into cells (but not too fast like with D5W so there is no fluid overload or brain swelling)
Drug Intervention
- ADH, DDAVP, Thiazide Diuretics
What is the paradoxical effect of thiazide diuretics for hypernatremia and diabetes insipidus?
it causes keeping water but getting rid of sodium
Hypernatremia Nursing Interventions
Identify Pts at Risk (i.e. hypertonic tube feeding or hypertonic TPN)
Monitor I&O, VS, Mental Status, Daily Weight, Assess mucous membranes, monitor lab values, ensure adequate fluid intake
teach about food salt contents, how to minimize salt intake, and salt restricted diets
No less than how much salt should be given a day for renal patients and non-renal patients?
Renal - 1.5 g
Non-renal - 2000g
Hypokalemia
Serum potassium levels (low) < 3.5 mEq/L
D/t excessive potassium excretion or inadequate potassium intake
Normal K+ levels in a person?
3.5 to 5.5
K is greatest in what area? And by how much?
It is the major cation in ICF inside cells, and is 28x greater in the cell than outside it
Do we store excess K+?
no we get rid of excess with urine
Etiologies for Hypokalemia
GI Losses (vomiting, diarrhea, suction, ileostomy, villous adenoma, alcoholism)
Intracellular shifts (metabolic alkalosis, DKA)
Anorexia Nervosa
Dialysis treatment (excess removal)
Excessive Insulin
Renal losses (d/t hyperaldosteronism, nephrotic syndrome, diuretics, drugs, excess steroid release [Cushing’s syndrome, excessive stress, tumors of adrenal cortex])
K+ is essential for …
the heart and GI system function
What typically regulates potassium?
The kidneys
Why does Metabolic Alkalosis lead to Hypokalemia?
It is a decreased H+ concentration - to correct this H+ moves from the cell to the blood and K+ moves into the cell to correct alkalosis to maintain neutrality
If pH is above 7.45 this is metabolic alkalosis - low K+ in blood by correcting for H+ and moving into cells
Manifestations of Hypokalemia
Decreased Serum Potassium
Cardiac issues (Dysrhythmias, digitalis toxicity)
Lab values (increased pH and bicarb, urine sg < 1.010, slight increase in serum glucose)
Muscular weakness
GI issues (anorexia, prolonged gastric emptying, gaseous distension, paralytic ileus)
Renal Issues (inability to concentrate urine - dilute urine, polyuria - nocturia, polydipsia)
Digitalis Toxicity
it is a medicine and if there is not enough K+ it can be toxic for the heart
How does muscular weakness progress in Hypokalemia?
it progresses from the extremities inward
Cause and Effects of Hypokalemia
Causes: Decreased K intake, Increased Loss of K, Shift of K into cells
Effects: cardiovascular effects, kidney effects, muscle weakness
Treatment for Hypokalemia
IV replacement (never give K in any form if there is no kidney function - there needs to be urine output before giving K) (never IV push K as it can lead to cardiac arrest) (mix thoroughly and it is an irritant)
Dietary (foods and salt substitutes)
Oral Supplements (administer w/ meals to decrease GI irritation, give with full glass of water, contraindicated if on K sparing diuretic)
When is potassium oral supplements contraindicated?
When on a K Sparing Diuretic
Or with bad kidney function
Why must you never pump more than 10 mEq/hr or in 100 mL over 1 hour with a pump for potassium?
It is IV pushing and can lead to arrythmias and potential cardiac arrest
Hypokalemia Nursing Interventions
Prevention for Pts at risk
Monitor I and O
Cardiac Monitoring
Adminsiter Potassium Supplements
VS (HR, BP)
Monitor Lab Values (for alkalosis)
Teaching on dietary intake, salt supplements, and supplements to take with food
What are some foods high in potassium
apricots
bananas
oranges
carrots
baked potatoes with skin
How do you know kidney function is good enough for K treatment?
they have good urine output
Hyperkalemia
Serum Potassium levels > 5.0 mEq/L
d/t excessive potassium intake or impaired potassium excretion
Hyperkalemia seldom occurs in what situations?
In patients with normal kidney function
What is the most common reason for Hyperkalemia?
Often due to iatrogenic causes and more common in hospitalized older adults
SO, its more common WHEN WE CAUSE IT
What is more dangerous, hyperkalemia or hypokalemia
Hyperkalemia due to a higher risk for lethal arrhythmia (more likely to get dysrhythmia in hypokalemia)
Etiologies for Hyperkalemia
Decreased Renal Excretion
Hypoaldosteronism (not holding enough Na and its leaving in urine and you have more K)
K Sparing Diuretics (block hypoaldosteronism)
Drugs (trimethoprim, NSAIDS, ACE inhibitors, B adrenergic drugs, cyclosporine)
Metabolic Acidosis
Tissue injury and lysis of cells (28x more in cells so release is bad)
Excessive oral or IV intake (use of potassium containing salt substitutes in RF)
Bowel obstruction
Manifestations of Hyperkalemia
Cardiac Issues (high lethal arrhythmia issues; cardiac arrest; bradycardia)
CNS - confusion
Neuromuscular (muscle weakness, flaccidity, paresthesia, numbness, ascending paralysis from LEs)
GI (Nausea, intermittent colic, diarrhea)
Oliguria
What EKG changes occur from Hyperkalemia?
Depressed ST Segment
Peaked T Waves
Widened QRS Complex
Prolonged PR Interval
Loss of P Waves
What does ST Segment depression mean
ST segment does not return to isoelectric line - so ischemia occurs (hyperkalemia)
What does Peaked T Waves mean
K sets the resting membrane potential so we get peaked T waves - which is abnormal (hyperkalemia)
What does Widened QRS complex mean
signals have trouble going through the ventricle (hyperkalemia)
What are the major manifestations of Hyperkalemia?
Cardiac Arrhythmias leading to cardiac arrest and bradycardia and CNS confusion
How does metabolic acidosis lead to Hyperkalemia?
The body corrects acidosis (<7.35) by moving H+ into cells which moves K+ out into the blood
all comes from buffer system for pH
What symptoms are in both hypo and hyperkalemia and therefore cannot tell you which it is alone?
Neuromuscular manifestations
How does activity differ between Hyper and Hypokalemia?
Hyperactive - Hyperkalemia
Hypoactive - Hypokalemia
Cause and Effect of Hyperkalemia
Cause: Excess intake, decreased loss, shift of K out of cells
Effects: Cardiac issues, muscle problems, GI vomiting/nausea, renal oliguria –> anuria, confusion
Treatment for Hyperkalemia
Kayexalata PO or PR (Cation Exchange Resin)
IV Diuretics (if renal functioning properly)
Dialysis
Kayexalate
cation exchange resin
must be used cautiously when person has HF must either take by mouth and excrete it in 24 hours with diarrheal stool or take a retention enema for 30-60 minutes with an indwelling cath
Emergency Treatments for Hyperkalemia
Calcium Gluconate
Sodium Bicarbonate
GIK Mechanism (Insulin)
Calcium Gluconate
slow IV infusion
protective mechanism for the heart - it increases the threshold to make sure the heart does not fire as quickly, but it does not get rid of potassium
What is the mechanism of action for Calcium Gluconate
decreased K lowers resting membrane potential and increased K raises it
Ca++ raises the threshold to correct the difference from potassium
the difference is what usually causes arrhythmia
How does sodium bicarbonate help treat Hyperkalemia?
it moves K into cells temporarily - could be life saving
How does GIK treat Hyperkalemia?
Insulin moves BOTH K and Glc into cells - temporarily but a quick fix
Normal glc levels means give both insulin and glucose to remove K
Nursing Interventions for Hyperkalemia?
Prevention for pts at risk
Monitor I and O
Cardiac Monitoring
Administer K depleting meds
VS watching (HR and BP)
Monitor lab values (acidosis)
Assess bowel function
Teach about renal failure and insufficiency, foods high in potassium, salt substitutes, and not using K sparing diuretics
Proper venipuncture technique (false potassium increases occur d/t cell lysis)
Pseudohyperkalemia
false potassium increase from cell lysis from improper venipuncture technique
EKG differences between Hypokalemia and Hyperkalemia
Hypo - flat T wave; Hyper - peak T wave
Both have depressed ST Segment
Hyper has prolonged PR interval potentially
What is the EKG changes that signifies Hyperkalemia more so than others?
A peak T Wave
What charge is Calcium ions
2+
Hypocalcemia
Serum Calcium Level <8.5 mg/dL
d/t inadequate calcium intake or absorption, or excessive calcium excretion or elimination
99% of Ca2_ is stored in ..
bones and teeth as calcium phosphate (so when it is released both phosphate and calcium release)
Narrow calcium range in the blood ?
8.5 to 10.5 (since most is in bones or teeth)
What happens with PTH when Ca2+ levels drop
PTH pulls from bones: so decreased Ca2+ causes increased PTH
You can end up with weak brittle bones if there’s PTH too much because Parathyroid ___
pulls!
What is needed to absorb calcium?
Vitamin D
Why can loss of renal function lead to Hypocalcemia
we need the kidney to activate Vitamin D in order to absorb calcium
How does Celiac disease influence Hypocalcemia?
it is a malabsorption problem that impacts the serum calcium levels
How does calcium travel in the blood?
Calcium travels the blood freely in a metabolically active form that is ionized
50% of this is unbound calcium
50% is a form of calcium bound the plasma proteins
___ calcium + ___ calcium = Total Serum Calcium Levels
Bound + Unbound = Total
How does Total Calcium change and symptoms occur depending on how bound and unbound levels of calcium change?
If both levels lower, total calcium lowers
If plasma proteins are loss and there’s less bound calcium, but there is still unbound calcium present you also get lower total levels, BUT you will not get s/s if you have normal unbound ranges (ionized)
However, if things move from unbound to bound to correct imbalance, that wont be reflected in total Ca, so we do need to look at more to know Serum Calcium Levels
What things may decreased bound calcium levels?
some with decreased protein intakes, nursing home residents, or liver disease get hypoalbuminemia and decreased plasma proteins –> decreased bound calcium with normal unbound still the same –> total calcium decrease but not S/S
The body regulates via __ calcium
unbound calcium
bound is not metabolically active since its on proteins, only when unbound is high or low does hyper or hypocalcemia occur
If protein or albumin levels are low you can infer what?
That bound calcium levels are low, especially is there is no s/s
What form of calcium is more informative ?
Unbound/Ionized calcium
S/S of Hypocalcemia and Hypercalcemia only occur when …
unbound calcium is low and total calcium lowers as a result
A balance between what things allows for calcium homeostasis?
absorption from the gut, excretion from the kidney, and reabsorption or deposition from bone
What cascade of actions fix low calcium levels?
Hypocalcemia –> PTH pulls calcium from bones, tells kidney to increase calcium reabsorption/activate Vitamin/excrete more PO4 3+, increases calcium uptake in GI tract
What is the most important step of the bodies natural attempt to fix hypocalcemia?
Activation of Vitamin D, after the Kidneys get PTH, which leads to increased calcium uptake by GI
Etiologies of Hypocalcemia
Post Op (Parathyroidectomy, thyroidectomy, radial neck dissection)
Renal Failure (d/t hyperphosphatemia)
Alkalosis (citrated blood)
Acute Pancreatitis
Drugs
Inadequate intake or absorption (anorexia, chrons, vit D deficiency, lack of sun exposure, etc)
Excessive elimination (low PTH levels d/t hypomagnesemia s/t alcoholism or diuretics)
Hypoalbuminemia
Manifestations of Hypocalcemia
Neuromuscular (Calcium sets resting membrane potential so low amounts lead to firing sooners) - so muscular irritability, tingling, parathesias, cramps, spasms, tetany, seizure, positive chvostek and trousseau sign, hyperactive DTR.
CNS - confusion, anxiety, depression, psychosis, loss of sensorium
Cardiovascular - decreased Myocardial contractility, hypotension, dysrhythmia, EKG prolonged QT and ST
Hematologic - prolonged PT, PTT, bleeding and bruising (no calcium for the clotting cascade)
Overall irritability, hyperactivity, no clotting, low heart power, depressed CNS
Trousseau’s Sign
Sign for Latent Tetany (spasm)
You pump 20 mmGHg above normal systolic, and if there is hypocalcemia leave it a minute and the patient will end up having a carpopedal spasm (arm twitch down)
It is a sign of neuromuscular irritability along with Chvostek’s sign
Chvostek’s Sign
Sign for latent tetany (spasm)
Tap facial nerve, and the lip on that side of the face will twitch
It is a sign of neuromuscular irritability along with Trousseau’s Sign
Cause and Effect of Hypocalcemia
Cause Decreased unbound calcium, inadequate intake, excess loss, decrease in GI tract and bone absorption
Effect: CNS issues, Cardiovascular system dysrhythmia (weak heart ability), increase GI tract irritability, abnormal calcium deposits, muscle tetany!
Acute Hypocalcemia Treatment
Calcium gluconate via slow IV infusion
Need to monitor as calcium in the tissue can cause necrosis!
Do not give with Digoxin
The CaGlc cn prevent laryngospasm and protect the heart and life threatening spasm
Chronic Hypocalcemia Treatment
Oral Calcium Supplements w/ Vit D an Mg
HRT - estrogen replacement, soy
Calcitonin (prevention in osteoporosis)
Fosamax (inhibits bone resorption)
Whys is Fosamax a nasty drug?
must take upright
take firs tin the morning
must be taken on an empty stomach with water only
very nasty drug
Nursing Interventions for Hypocalcemia
Prevention for pt at risk
Administer calcium supplements
calcium gluconate at bedside for thyroid/neck surgery
Cardiac monitoring
Maintain airway patency
Monitor lab values
Seizure/Safety Precautions (if severe)
teach about alcohol and cig influence, dietary sources, exercise (weight bearing exercise), estrogen
Dietary Sources of Calcium
Dairy Products
Green Leafy Vegetables
Hypercalcemia
Serum calcium levels > 10.5 mg dL
Acute > 13 mg/dL
Severe >16 mg/dL
d/t excessive calcium intake or absorption; or; increased release of calcium from bone
Occurs when the rate of calcium entry into the ECF . rate of renal calcium excretion
Etiologies of Hypercalcemia
Excessive Intake of calcium supplements
Excessive use of calcium containing antacids
Excessive vitamin D intake (stims absorption)
Use of thiazide diuretics
Hyperparathyroidism (or tumor makes too much PTH pulling lots of calcium from bones)
Prolonged immobility
malignancies
drug
thyrotoxicosis
hypophosphatemia (means less exchange of calcium at kidney level)
milk alkali syndrome
Milk alkali Syndrome
ingest sodium bicarbonate and get calcium from milk, they then combine to form extra calcium in the bloodstream
Manifestations of Hypercalcemia
Neuromuscular (sedate effect, weakness, decreased DTRs)
GI (decreased motility, constipation(ca is chalky), anorexia, N/V)
CNS (confusion, memory impairment, bizarre behavior, decrease in LOC–> Coma) - decreased innervation leads to decreased nerve speed
Renal (polyuria, polydipsia, renal colic, renal failure from urinary calculi)
Cardiac (dysrhythmia, EKG shortened QT, increased BP)
Bone (soft tissue calcification, pathologic fractures)
Why does polyuria and polydipsia occur with Hypercalcemia?
Glucose AND calcium increases tonicity of urine - so filtrate absorbs more fluid and polyuria occurs, with polydipsia since there is less fluid and you want to replace it
Cause and Effect of Hypercalcemia
cause: loss from bones, excess intake, increase from factors increasing mobilization from bones
effect: cardiovascular system, bradycardia, dysrhythmia, kidney issues GI issues, muscle issues (EVERYTHING SLOWS DOWN MORE)
Treatment for Hypercalcemia
High Fluid intake (3-4 L / day)
Eliminating contributing drugs (thiazides, vitamin D, calcium antacids)
Increase mobility
IV NS 200-500 mL/Hr to dilute calcium and increase GFR and loop diuretic prevents overload and increases excretion
Hourly I and O and breath sounds
Etidronate, Plicamycin, Calcitonin
When is Etidronate (Didronel) used for Hypercalcemia
tx for malignancies that are NOT hyperparathyroidism
When is Plicamycin (Mithracin) used for Hypercalcemia
tx for breath cancer
How is Calcitonin used to treat Hypercalcitonin
skin test first
it decreases bone resorption by stopping PTH to protect bones and ionized calcium levels
temp effect of 6-10 days so you need to target the root cause still
Nursing Interventions for Hypercalcemia
Prevention for Pts at risk
Increased mobility
Monitor I and O
3-4 L of fluid per day
Bulk fiber in diet to decrease constipation
Safety Precautions
Check for pathological fractures and digoxin toxicity
Encourage cranberry juice to increase calcium solubility in urine
Calcitonin
Monitor lab values
Teach about s/s to watch for and avoid dairy products and calcium containing antacids
How is calcium balance regulated when calcium levels get high
Decreased PTH and Increased Calcitonin –> (d/t PTH) decreased renal activation of Vit D) –> DECREASED intestinal absorption of calcium, renal reabsorption of calcium and decreased excretion of phosphate, and calcium resorption from bone
How is calcium balance regulated when calcium levels get lower
Increased PTH and Decreased Calcitonin –> (d/t PTH) Increased renal activation of Vit D –> INCREASED intestinal absorption of calcium, renal reabsorption of calcium and decreased excretion of phosphate, and calcium resorption from bone
EKG differences between Hypocalcemia and Hypercalcemia ?
Hypo - prolonged ST segment and QT interval
Hyper - shortened ST segment and QT interval
Second most abundant cation in the cell behind potassium?
Magnesium
Percentages of Magnesium Cation distribution?
60% in bones
2% in ECF
38% in interstitial spaces
Normal Magnesium levels
MG 1.5-2.3 mEq/L or 1.8 - 2.6 mg/dL
Sources of magnesium
unprocessed cereal grains
nuts
chocolate
legumes
green leafy vegetables
dairy products
dried fruit
meat
fish
water not processed through a water softener
Hypomagnesemia
A decreased serum Mg level of less than 1.5 mEq/L or 1.8 mg/dL
Serum does not reflect ___!
Stores!
Causes for hypomagnesemia
decreased Mg intake
excessive loss of calcium and potassium
vomiting
diarrhea
NG suction
GI losses
Intestinal malabsorption
Intestinal Fistulas
increased renal excretion
prolonged diuretic therapy
excessive aminoglycoside use
rapid administration of citrated blood
renal disease
chronic alcoholism
diabetic ketoacidosis
burns
pancreatitis
Why does calcium and potassium loss lead to hypomagnesemia?
Magnesium moves with Potassium and Calcium together so loss of one leads to loss of the others
Why does GI loss lead to hypomagnesemia so easily
There is a lot of Mg in the lower GI tract and intestinal absorption determines this so malabsorption here can lead to hypomagnesemia
The biggest causes of hypomagnesemia are…
malabsorption
intestinal fistula
(things that impact GI tract (lower))
Why does rapid citrated blood administration lead to hypomagnesemia
the preservative turns your blood alkalotic so buffer systems move things causing this
What can be sued to treated hypomagnesemia from alcoholism
folate and multivitamins
S/S of Hypomagnesemia
CNS - convulsions, paresthesia’s, tremor, ataxia
Mental changes - agitation, depression, confusion
Cardiovascular System- tachycardia, dysrhythmia
Muscle - cramps, spasticity, tetany, athetoid movement, BABINSKI REFLEX, CHVOSTEK SIGN
Neurologic irritability- tetany, weakness
EKG - broad T wae, ST shortened, Prolonged QT interval, and wide QRS complex - severe can invert T waves and prominent U waves
Laryngeal Stridor, coma, or sudden death if severe
Why is babinski reflex abnormal in hypomagnsemia?
it usually is gone by an early age
Implementation to care for Hypomagnesemia
Monitor VS, neuromuscular changes, I and Os
Initiate seizure precaution
Administer oral or IV magnesium
Monitor Ca2+ and K+ levels and administer both if levels are low as prescribed
Monitor for DTR suggesting hypermag when administering
Monitor serum Mg levels every 12-24 hours when client is receiving Mg by IV
Instruct client to eat food high in Mg Ca2+ and K+
Hypermagnesemia
increased magnesium serum levels of 2.3 mEq/L or 2.6 mg/dL
Causes of Hypermagnesemia
Advanced renal failure
excessive laxative use that contains magnesium
overuse of antacids (that have Mg)
ECF fluid deficit (concentrated with Mg)
Administration of Mg in toxemia of pregnancy
Untreated acute diabetic ketoacidosis
Hemodialysis w/ hard water or dialysate too high in Mg
Adrenal insufficiency
Pheochromocytoma (rare)
Most common cause of Hypermagnesemia
Advanced Renal Failure
S/S of Hypermagnesemia
Neurologic Depression - Slowing Down
Drowsiness
Lethargy
Bradycardia
Dysrhythmias
ECG shows peak T wave, prolonged PR and QT intervals, wide QRS
Respiratory Depression
Paralysis of resp center and voluntary muscles
severe hypotension along w/ nausea and vomiting
muscle weakness
areflexia
loss of DTR
coma
Hypermagnesemia looks like ___ and ___
death and hypercalcemia
Areflexia
no reflexes at all - dangerous
Implementations for Hypermagnesemia Patients?
Monitor VS, Resp. Depression, hypotension, bradycardia, and dysrhythmias, neuro and muscular activity, LOC
remove source of excess Mg
increase renal excretion by forcing fluids or administering diuretics
administer 10% calcium gluconate as prescribed
mechanical ventilation in severe Mg excess
pacemaker for bradycardia
dialysis if renal function is impaired with Mg free dialysate
instruct clients regarding avoiding the use of laxatives and antacids containing Mg
Calcium Glouconate protects the ___ and ___s Mg
protects the heart and antagonizes Mg
EKG differences between Hypomagnesemia and Hypermagnesemia?
Hyper - wide QRS, prolonged PR, Tall T wave
Hypo - Prolonged QT, slightly longer PR, widened QRS, Flat T waves / broad flat T wave, prominent U wave
What is in Hypomagnesemia’s unique EKG finding
Prominent U Wave
Phosphorus Normal Values
3-4.5 mg/dL or 1.8-2.6 mEq/L
What is a major anion in cells (negative charge)?
Phosphorus
How is phosphorus distributed in the body?
85% of phosphorus in bones and teeth
less than 1% in blood
rest in soft tissue
What is phosphorus responsible for
proper mineralization of bone and for energy metabolism - and is a part of ADP and ATP
Sources of Phosphorus
Almonds Dried Beans Barley Bran Pumpkin Squash Cheese Cocoa Chocolate Eggs Lentils Meats Poultry Pork Beef Legumes Fish Sardines Liver Milk Oatmeal Peanuts Dried Peas Walnuts Wheat and Rye Soft Drinks
What kind of soft drink has more phosphorus?
darker color soft drinks - so renal patients that hold Phosphorus should not drink these
Hypophosphatemia
serum phosphorus level below 3 mg/dL or below 1.8 mEq/L
below normal serum level
Most phosphorus is absorbed in the ___ and excreted via the ___
phosphorus; kidneys
Causes of Hypophosphatemia
Decreased Nutritional Intake
Poor Absorption from the bowel due to a lack of Vitamin D
Intake of carbonate antacids (may hinder absorption)
Malabsorption Syndrome
Increased renal excretion due to hyperparathyroidism or renal insufficiency
Diabetic Ketoacidosis
Steatorrhea
A poor nutritional state as in alcoholism
Fever
Long term TPN
Burns Hepatic Disease
What is Phosphorus relationship to Calcium
they are inverse
so if you get rid of Calcium you keep Phosphorus and vice versa via level of kidneys
Steatorrhea
fat in stools
floats
very smelly
S/S in assessment of Hypophosphatemia
Anorexia Dysphagia Weakness Malaise, Lethargy Skeletal Pain and Aches Bone Pain Pathologic Fractures Pulmonary Fractures Tachypnea Shallow Respiration Confusion, Stupor, Delirium Seizures Hematologic Changes
Need Phosphorus for ATP so you have less energy!!!!
(A LOT OF THESE ARE SIMILAR TO HYPERCALCEMIA)
If hypophosphatemia is occurring, what else is happening?
Hypercalcemia (so many s/s are similar)
Implementations for Hypophosphatemia
Monitor respiratory status
Move client carefully
Administer potassium phosphate
Assess renal system before administering phosphorus
Monitor calcium, phosphorus, sodium, and chloride levels - renal failure DOES hold Phosphorus
Administer vitamin D
Monitor for decreased neuromuscular activity
Monitor for calcium excess and kidney stones
Monitor for hematologic changes
Monitor clients receiving TPN for electrolyte imbalances
Instruct client regarding the use of antacids
When do kidney stones occur?
when calcium is exchanges and phosphorus leaves - so damage can occur
Hyperphosphatemia
A serum phosphate level greater than 4.5 mg/dL or 2.6 mEq/L
Seen more clinically then hypophosphatemia
Causes of Hyperphosphatemia
Excessive dietary intake of phosphorus
Overuse of phosphate containing laxatives or enemas
Hypoparathyroidism
Vitamin D intoxication (more vit D - more absorption)
Renal failure
Adrenal insufficiency
Excessive bone growth in infants and children (cows milk has more phosphorus than breast milk)
Metabolic and hormonal imbalances
Tissue damage
Parathyroid Surgery or Hypoparathyroidism
S/S seen in Assessment for Hyperphosphatemia
Neurological Excitability
Hyperreflexia, tetany
Positive Chvostek’s or Trousseau’s Sign
Seizures
Conjunctivitis
Pruritis
Renal Deposits leading to renal failure
Opp of hypophosphatemia - looks like hypocalcemia
Hyperphosphatemia goes alongside ___
hypocalcemia (since they exchange)
What is seen more clinically, hyperphosphatemia and hypophosphatemia?
Hyperphosphatemia
Pruritis
itching
How does hyperphosphatemia instigate further renal failure?
Renal deposits occur from increased phosphorus that leads to deposits in renal tissue binding with calcium thus stimulating further renal failure
Implementation of Nursing Interventions for Hyperphosphatemia
Increase fecal excretion of phosphorus by binding phosphorus from food in the GI tract (aluminum hydroxide gel)
Prepare for dialysis if prescribed
Administering calcium if hypocalcemia exists
Monitor neuromuscular irritability
Monitor for hyperreflexia, tetany, and seizures
Monitor for signs of hypocalcemia
Monitor for Trousseau’s and Chvostek’s signs
Instruct clients to avoid phosphate-containing
medications including laxatives and enemas
Instruct clients to decrease their intake of foods high in phosphorus
Instruct clients how to take phosphate-binding drugs emphasizing that they should be taken with meals or immediately after meals
