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1. FLUIDS AND ELECTROLYTES
AMOUNT OF FLUID IN THE BODY:
 Fetus – 100%
 Baby – 80-85% (no muscles yet)
 Adult – 70%
 Elderly – 50%
> amount of water taken must be equal to the amount of
water lost
WATER INTAKE
 Food and drink – 2300 mL
 Cell Metabolism – 200 mL
 Total: 2500 mL
OUTPUT
 Kidneys – 1800 mL
 Skin (sweat) – 300 mL
 Lungs (expiration) – 300 mL (ᛏ RR, more fluid lost)
 GI Tract (feces) – 100 mL
 TOTAL: 2500 mL
FLUID COMPARTMENT
Intracellular – 40% (cytoplasm/protoplasm)
Extracellular – 20%
 Intravascular – 5%
o Plasma (light yellow)
o Cellular components (darkish red)
 Interstitial - 15% (third space)
MECHANISMS OF FLUID BALANCE
1. ANTI-DIURETIC HORMONE (ADH)
- Stored in the posterior pituitary gland
- Causes renal tubules to reabsorb water so
that kidneys will not form too much urine
- Released when dehydrated
dehydrated > hypothalamus will feel that
there is ᛎ in circulating blood volume >
stimulate post. pituitary gland to release
ADH > ADH will have an effect on the renal
tubules to reabsorb water >> ᛎ urine output
no reabsorption of NA
>> output is less because body is compensating after surgery
2. THIRST MECHANISM
- Compensatory mechanism
perspire > excrete lots of body fluids > thirst
center in the brain (hypothalamus) will be
stimulated > tells us to drink water
ᛎ blood volume (d/t vomiting, diarrhea, etc)
will cause ᛎ BP > ᛎ BP = less blood going to
the kidneys > kidneys will compensate by
releasing renin > RAAS mechanism >
angiotensin 2 > angiotensin 2 stimulates
thirst center
- thirst mechanism MAY NOT work (ex. Patient is
unconscious)
- unconscious patient should receive IV fluids (N/I: do not
slow down)
FLUID INGESTION
 Stretch receptors (stomach & intestine) will
send inhibitory signals to the thirst center
 Thirst mechanism will stop if stomach and
intestines are stretched (by eating)
3. ALDOSTERONE
- From the adrenal cortex
- Causes reabsorption of NA > water follows
- Hypovolemia > RAAM
 hypovolemia (d/t bleeding/vomiting) >
there will be ᛎ in circulating blood volume =
priority is primary organs = less blood to
secondary organs > kidney will compensate
by releasing renin > renin goes to liver and
converts a precursor protein
(angiotensinogen) to angiotensin 1 (mild
vasoconstrictor) > angiotensin 1 goes to
lungs and converts ACE to angiotensin 2
(potent vasoconstrictor) > angiotensin 2 >
produce aldosterone > reabsorb NA >>
water retention > ᛏ BP
4. SYMPATHETIC STIMULATION (SNS)
- ᛎ in blood volume > ᛎ BP > SNS is stimulated
> trigger adrenal glands > adrenal medulla >
epinephrine and norepinephrine will be
released
 Epinephrine – causes ᛏ in cardiac rate > more blood
will be pumped by the heart > more blood will go to
the different organs of the body
 Norepinephrine – will cause vasoconstriction, ∴ ᛏ
BP → more blood will go to the priority organ (brain)
** if less blood is going to the kidneys > less oxygen and
nutrients > less urine
 If there is vasoconstriction, assess:
 Pale and cold skin – because blood is being
directed to the brain
 ATRIAL NATRIURETIC PEPTIDE
- cardiac hormone stored in the cells of the atria
- released when atrial pressure is increased

2. - opposed the RAAM by ᛎ BP and reducing intravascular
blood volume
ACTION:
1. Suppresses serum renin levels
2. ᛎ aldosterone release from A.G.
3. ᛏ glomerular filtration w/c ᛏ urine excretion of Na & h2o
(when water is reabsorbed, there will be increase
pressure in the heart)
4. ᛎ ADH release from PPG
5. Reduced vascular resistance by causing vasodilation
>> released whenever there is ᛏ pressure in the atrium,
plenty of blood in the atrium > ANP will oppose RAAM
When is atrial pressure increased? > heart failure, COPD
FLUID & ELECTROLYTE IMBALANCES
Extracellular Fluid Volume Deficit
- loss of body fluid from the intravascular and/or interstitial
(3rd
space) compartment
> Intravascular – ((bleeding))
> Interstitial – ((diarrhea, vomiting))
ISO-OSMOLAR FLUID VOLUME DEFICIT
 When both fluid and Na are lost in equal amounts
Example:
1. Vomiting & diarrhea
2. GI fistula & GI suctioning
3. Fever (sweat = ᛏ RR = more fluid loss)
4. Hemorrhage
5. Burns
6. Ascites (fluid accumulation in peritoneal cavity
HYPEROSMOLAR FLUID VOLUME DEFICIT
 If the amount of water is in excess of the amount of
sodium loss, the serum sodium level is increased
 Only water is lost
Example:
1. Inadequate fluid intake
o Unconscious
o Bed Ridden
o Giving excess OF
2. Severe vomiting & diarrhea
3. Diabetic ketoacidosis
o Excess glucose from the blood will go to the kidneys
and it will cause osmotic diuresis (glucose that goes to
the kidneys attract water to go to the kidneys). And this
will cause frequent urination
o Complication of Type 1 diabetes
4. Sweating
o More fluid is lost than sodium
o ᛏ solute intake (salt & sugar) = attract water
 Possible CELLULAR DEHYDRATION
- bec. there are plenty of solutes outside, it will
attract water from the cells going outside >> will
cause shrinkage of cells
 Early manifestations of cellular shrinkage:
o Restlessness, Apprehension
o These neurological manifestations are
serious because patient can go into
coma and even death
ASSESSMENT
Signs and symptoms of dehydration
 Poor skin turgor
 Dry mucous membrane
 Slow filling of hand veins
 ᛎ urine output
o dehydration > hypothalamus will sense it >
stimulate PPG to release ADH > ADH
prevents kidney from releasing urine by
stimulating renal tubules to reabsorb water
 Tachycardia - ♡ is compensating to give more blood
to the organs of the body
NURSING INTERVENTIONS for FLUID VOLUME DEFICIT
1. Monitor VS every 4 hours. ((If there is volume deficit, BP
and CR are decreased))
2. Promote adequate fluid replacement. ((IV fluids; oral))
3. Report if urine output is below 250cc/8hrs. ((normal: 30 to
50 cc per hour // 240 to 250 cc per 8 hours))
4. Monitor lab results such as:
 Blood Urea Nitrogen (BUN) - is a parameter that
will measure the kidney function (if kidneys are
still working)
o Urea - waste product of protein
metabolism that should be removed by
the kidneys
o If BUN is high, it means that the kidneys
are not working efficiently. (kidneys
probably not receiving sufficient
amount of blood due to fluid volume
deficit to work efficiently)
 Hematocrit blood test – determines the
percentage of RBCs in the blood
o Hematocrit - proportion, by volume, of
the blood that consists of red blood
cells
o Our blood is composed of RBC, WBC,
plasma
o If there is fluid (plasma) loss, there will
be ᛏ hematocrit level
5. Provide oral hygiene several times per day
 Dry mouth causes bad breath (halitosis)
 Oral hygiene ᛏ amount of saliva (saliva has plenty of
lysosomes w/c can kill bacteria in the mouth)

3. 6. Routinely check body weight
 To monitor if there’s overload or deficit in the
amount of water in the body
 2.2 lbs = 1 kg = 1L fluid loss
ELECTROLYTES
SODIUM (Na)
- main electrolyte outside the cell
- transmission and conduction of the nerve impulse
- attracts fluid and helps preserve the extracellular fluid
volume and fluid volume distribution on the body
- combines w/ chloride and bicarbonate in order to
regulate acid-base balance
- main acid-base balance of the fluid (7.35 – 7.45 pH)
- maintains extracellular fluid (main cation)
SODIUM-POTASSIUM PUMP
- prevent accumulation of Na inside the cell
>> Na inside the cell will attract h2o, ∴ cell will rupture
- prevents osmotically active sodium particles from
accumulating inside the cells, which would cause them
to swell from the influx of water following sodium.
- When there is excess sodium inside the cell, the ATP
(Adenosine Triphosphate) will drive it out so that the
sodium will accumulate outside and not inside. And
when (3) sodium goes out, (2) potassium goes in
- Na concentration: 14x bigger than inside the cell
- K inside cells: 35x greater than the outside of the cell
NORMAL VALUE OF NA – 135-145 mEq/L
HYPONATREMIA
- lots of Na inside the cells (attract water from outside)
- the extracellular fluid moves by osmosis to the
intracellular compartment (lesser to greater
concentration)
- cause cerebral edema - ᛏ ICP
CAUSES OF HYPONATREMIA:
 GIT losses
- V & D
- GI suction
- GI surgery
- repeated tap water enema (water only; no
sodium)
 RENAL losses
- prolonged diuretic therapy (urinate often)
 Hormonal influences
- SIADH → excess ADH (fluids will be
reabsorbed) = plenty of water, ∴ hyponatremia
 Altered cellular function
- HF, cirrhosis
- Burns
- Excessive diaphoresis
- Fever (sweat a lot, ᛏ RR = hyponatremia)
 Patient with sodium levels above 125 mEq/L may
not show signs of hyponatremia
 If Na level drops to 110 mEq/L, the patient’s
neurologic status will deteriorate further leading to
stupor and even coma
ASSESSMENT:
 Dry skin, pale, dry mucous membrane
 Neuromuscular: muscle twitching, muscle
cramps
 GIT: n&v, diarrhea, abdominal cramps
 Cardiac: tachycardia (BP goes down) = low Na in
the extracellular, Na inside the cell = low BP
 CNS: headache, confusion & seizures
o For hyponatremia associated with hypervolemia
 Restrict fluid intake
 Oral Na supplement
(sodium became low because of many fluids in the
body)
o Hypovolemia r/t hyponatremia
 IV fluids
 High Na diet (bec. of hyponatremia)
MANAGEMENT:
 If serum Na level is below 110 mEq/L, give 3% -
5% of saline solution
> hypertonic S.S. causes fluid to shift
out of cells
HYPERNATREMIA
- increased sodium, less water
- excess Na r/t ᛎ body water
- thirst (mechanism) is the body’s main defense against
hypernatremia

4. >> plenty of sodium outside > it will attract
water > cells will shrink. To prevent this, the body will
compensate. The hypothalamus, where the thirst center
is, will be stimulated and you are going to drink a lot of
water
- people who can’t drink voluntarily (unconscious) >>
SEVERE HYPERNATREMIA
o Infants
o Confused elderly people
o Unconscious patients
 The movement of fluids is from the
INTRACELLULAR COMPARTMENT to EXTRACELLULAR
COMPARTMENT >> cells will shrink
CAUSES OF HYPERNATREMIA:
 Hypercortisolism (or Cushing’s Syndrome – over
cortisol = Hypernatremia, Hyperglycemia, Hypokalemia),
Hyperventilation (you lose fluids)
** occurs when the pituitary gland makes too much
of the hormone ACTH. ACTH then signals the adrenal glands
to produce too much cortisol
 Increased intake of sodium (Oral / IV)
 GI feeding without adequate water supplement
 Hypertonic Solution – particles is higher than water
** example: osteorized feeding (TPN) – plenty
of salt will attract water
 Sodium Excretion decreased (you cannot bring out
the sodium, ∴ body keeping too much sodium);
corticosteroids (when you’re taking steroids, s/e is
sodium retention)
 Aldosterone Insufficiency (Hyperaldosteronism)
 Loss of body fluids (∴ sodium is retained)
(dehydrated), infection (Fever), sweating, diarrhea, and
diabetes insipidus (deficient; renal tubules will not
reabsorb water and this will go to the urine; frequently
voiding; Losing plenty of fluids)
 Thirst Impairment
ASSESSMENT:
 GIT → nausea, vomiting, anorexia
 Cardiac → ᛏ BP (flow of blood is sluggish, slow
perfusion of blood, heart will compensate to
give more blood to give to the organs of the
body)
 CNS → restlessness, agitation, stupor
 Neuromuscular → muscular twitching, tremor,
hyperreflexion
 Skin → dry
SIGNS AND SYMPTOMS
 Skin Flushed
 Agitation – The water in the cells are being
sent out
 Low-Grade Fever
 Thirst
 Can be as a result of dehydration with no or
minimal Na ((accompanied by hemoconcentration
in hypernatremia))
Na outside = water will go out = cells will shrink
 Moderate to severe hypernatremia can stimulate
seizure (WHY? Pulling the water out of the cells in
the brain = shrink = seizure)
 Correcting hypernatremia too quickly could cause
water to shift rapidly into the cells and may cause
the brain cells to swell ((treatment = infusion
pump))
o Use infusion pump to control delivery of IV
to prevent cerebral edema
 Correcting water deficit orally should take about 3
days (48-72 hours is safest)
o 0.45% NaCl solution allows a more gradual
reduction of serum Na, reducing the risk of
cerebral edema
POTASSIUM
(( if many sodium, potassium has to go (hypokalemia) ))
- promotes transmission and conduction of nerve
impulses and the contraction of skeletal, cardiac, and
smooth muscles
- assists in the regulation of intracellular osmolality
- 98% of body’s K is seen in the intracellular
compartment; plenty in the GI tract
- assists in the maintenance of acid-base balance
 Metabolic acidosis – plenty of acid in the
body (ex. Having hypovolemic shock
(bleeding) > less circulating blood > if there
is less circulating blood, plus bleeding,
metabolism continues with less o2 > if
metabolism goes on with less o2, the body
is going to produce lactic acid > anaerobic
metabolism
 Plenty of hydrogen ions outside so
hydrogen ions will go inside the cells > in
exchange of the entrance of the hydrogen
ions inside the cell, K goes out >>
hyperkalemia = cardiac dysrhythmia /
cardiac arrest

5.  K in acid-base balance: K let acid in
 Kidneys are damaged that’s why metabolic
acidosis > plenty of acid > ᛏ RR > hyperventilate
bec. you are removing some of the acid in the
form of carbon dioxide
 Kidneys also maintain acid-base balance
- poorly stored in the body; daily intake is important
- 80%-90% of K is removed by the kidneys; if kidneys are
damaged = hyperkalemia
- 10% is excreted in the feces
- foods rich in potassium
 Cantaloupe
 Honeydew
 Orange juice
 Medium sized potato
 Banana
 Dried fruits
 Raisin
 Peaches
NORMAL VALUE OF K: 3.5 – 5.3 mEq/L
- a serum K level less than 2.5 mEq/L or greater than 7.0
mEq/L can cause cardiac arrest
 Nursing intervention: Serum K values need to
be closely monitored
HYPOKALEMIA
- plenty of K is excreted
CAUSES:
 Medications (diuretics - ᛏ urine output)
 Dialysis (cleans blood – potassium will be
removed in the blood) (protein is also removed)
 GI suctioning / Vomiting
 NPO / Diarrhea
 Cushing’s disease
 Hyperventilation
 Insulin – bring the glucose with potassium
inside the cells, ∴ hypokalemia
 Malnutrition
 Steroids (cause sodium retention) – Na is
retained, K has to go out
o “opposing effect”
o Stress ᛏ the production of steroids in
the body
 Cellular damage (surgery, burns) – trauma >
bleeding > metabolic acidosis
 Laxative abuse (10% of K is excreted through
feces)
 Ketoacidosis – osmotic diuresis
 Trauma – when there is breaking down, K will
leave the cells > when tissues are destroyed
(trauma), you’re starving it > large quantities of
K will leave the cells
 “opposing effect” – when one is
retained, the other is excreted
HYPOKALEMIA affects cardiac conduction inducing
a:
o Depressed ST segment
o Flat or inverted T waves
o Increased U waves
P – (ATRIAL DEPOLARIZATION)
- Impulse is in the atrium (SA node)
- Atria are contracting (filling the ventricles with
blood)
- Atrioventricular (AV) valves are open
- Semilunar valves are close
(impulse will travel to AV node)
PR INTERVAL
- Impulse is at the AV node
- Trying to open the atrioventricular valves so
more blood can fill the ventricles
(impulse will now be received by the Bundle of His and
the Purkinje fibers)

6. ** once impulse is received by left and right BOH and
PF, the atrioventricular valves close **
QRS – VENTRICULAR DEPOLARIZATION
- Atrioventricular valves are closed
- Semilunar valves are open
- Ventricles are contracting
ST – EARLY VENTRICULAR REPOLARIZATION
- Ventricles are starting to rest
T – VENTRICULAR REPOLARIZATION
- Ventricles are now relaxed
- Atrium starts contracting again (depolarization
of atrium)
 Most PROMINENT CHARACTERISTIC of
HYPOKALEMIA is the PRESENCE OF U WAVE.
EFFECTS OF HYPOLKALEMIA
ᛎ cerebral function (bec. cardiac dysrhythmia =
heart is beating irregularly = cardiac output is less)
>> less blood is going to the brain
Manifested if patient has cardiac dysrhythmia:
 Restlessness
 Apprehension
 Lethargy
 Confusion
 Inability to perform problem-solving tasks
 Disorientation
 Coma
ᛎ the excitability of all excitable tissues and causes
skeletal muscle weakness = ᛏ risk for fall
Leads to orthostatic hypotension – also increasing
the patient’s risk for fall and injury
Cardiac dysrhythmia causes ᛏ cardiac rate, ∴ less cardiac
output = less blood to brain
Nursing diagnosis: RISK FOR FALL
Depress all excitable tissues, including GI smooth
muscles
o Patient who has ᛎK have reduced or absent
bowel sounds and constipated
 MOST LIFE THREATENING COMPLICATION is
RESPIRATORY INSUFFICIENCY
(potassium is needed for muscle contraction and
diaphragm is a muscle if there is less potassium the
muscle will have a hard time to contract)
ASSESSMENT FINDINGS:
 Skeletal Muscle Weakness
 U wave (ECG Changes)
 Constipation, anorexia, vomiting
 Toxic effects of digoxin (inotropic)
o ᛏ contraction of the heart
o Usually given with furosemide
 To prevent this, give with K-
sparing diuretics
o Given if you have heart failure
 H.F > edema (fluid volume
excess) > diuretics (furosemide)
> pee a lot > K goes with pee
 Irregular Weak Pulse
 Orthostatic Hypotension (decreased systolic
(20mmHg) decreased diastolic (10 mmHg))
(sudden change of position; from flat to upright
position), vertigo
 Numbness
In case of mild hypokalemia:
 KCl supplement
 Take liquid or K supplement with glass or
more of water or juice or with food to
prevent GI irritation (w/ water to neutralize
acid)
 IV Potassium
 Normal dose for IV K is 20-40 mEq in a liter
of IV fluids to run for 8 hours
 Dilute/Mix in IV fluids
 IV K cannot be given via IV push because it
can cause cardiac arrest (IV push is direct to
the vein)

7.  Cardiac monitor must be used to ensure
safety
For severe K deficit:
 10-20 mEq of KCl can be given every hour
 Dilute in IV fluids
NURSING INTERVENTIONS:
 K products should be mixed well to prevent
unintended bolus administration
 IV K should be diluted with N.S.
 Site should be changed every 72 hours or
sooner if tenderness occurs
 Potassium-rich foods:
- Cantaloupe - Fish
- Avocado - Spinach
- Beans - Banana
- Orange Juice
- Med. sized potato
Hypokalemia/Hyperkalemia
 CARDIAC DYSRHYTHMIA – irregular
heartbeat
o Causes ᛎ in cardiac output
If cardiac dysrhythmia isn’t corrected immediately, it
can cause cardiac arrest
 Cardiac arrest - when the heart suddenly stops
pumping blood round the body, commonly
because of a problem with electrical signals in
the heart
 When the heart stops pumping blood,
the brain is starved of oxygen. This
causes unconsciousness and to stop
breathing
Heart attack - happens when blood supplying the heart
muscle is cut off due to a clot in one of the coronary
arteries
INSERT CARDIAC CYLE
HYPERKALEMIA
- causes ᛏ cardiac rate
 Respiratory/Metabolic Acidosis
o hyperkalemia > cardiac dysrhythmia > ᛏ
cardiac rate > ᛎ cardiac output > less
oxygen & nutrients going to the body >
hypoxemia > px will become weak
because there is less oxygen >
anaerobic metabolism > lactic acid is
produced > metabolic acidosis
o Anaerobic metabolism - creation of
energy through the combustion of
carbohydrates in the absence of oxygen
> lactic acid is produced
 patient will be given o2
 HOW METABOLIC ACIDOSIS LEADS TO
HYPERKALEMIA?
- Anaerobic metabolism > lactic
acid is produced > metabolic
acidosis > plenty of H+
ions
(acid) > plenty H+
ions will be
filling the blood > H+
will go into
the cells > entrance of H+
will
push K outside > hyperkalemia
 Medication (to correct acidosis)
- Na HCO3 (ᛏ base)
- since the acid-base balance is
corrected, the K that went out
goes back in
 CAUSES OF METABOLIC ACIDOSIS
o If kidneys are damaged. 1)
kidneys
function in maintaining acid-base
balance by excreting waste products
like uric acid & urea (these are going to
flood blood) || 2)
Kidneys produce
bicarbonates (base)
o Lungs. Lungs control acid in the form of
CO2.
o Bleeding
o Diarrhea (removes bicarbonates)
CAUSES OF HYPERKALEMIA:
 IV K infusion
 ᛎ renal function

8.  Metabolic acidosis
 Severe traumatic injury (bleeding)
o Ex. Burns – cells are destroyed > K
goes out > hyperkalemia
o Bleeding - (less blood circulating >
anaerobic metabolism > lactic acid
<metabolic acidosis)
 Blood for transfusion that is 1-3 weeks old
o Old RBC > K goes out of blood cells
ASSESSMENT FINDINGS:
 GIT – ab cramps, chronic diarrhea (lose HCO3),
nausea
 Cardiac – tachycardia later bradycardia (heart
weakens = ᛎ BP) & finally cardiac arrest
o Medications: (beta-blockers –olol)
 (-) inotropic: ᛎ contractility of heart
 (-) chronotropic: ᛎ CR
 Renal – oliguria (ᛎ urine output *600cc and
below in 24hrs); anuria (absence of urine *50cc
in 24hrs)
o There’s oliguria because of the
tachycardia effect of hyperkalemia.
Increase cardiac rate closes the AV
valves immediately so less blood is
filling the ventricles from the atrium >
less blood output > less blood going to
the kidney (secondary organ) > kidney
will not function well
 Neuromuscular – weakness, numbness, muscle
cramps
ECG manifestations:
5.5 – 6.0 mEq/L
o Tall, peaked T waves
6.0 – 7.0 mEq/L
o Prolonged PR interval
o Widened QRS interval
ᛏ 8.0 mEq/L
o Complete heart block & cardiac arrest
MANAGEMENT:
(MILD) 5.5 – 6.5 mEq/L
- Restrict K intake
(MOD) 6.5 – 7.5 mEq/L
- Give Kayexalate or Kalimate (1 sachet in
100cc of water)
o Kayexalate lowers the K in the body
by binding K in the intestine
o Kalimate
- Give diuretics: furosemide
- Give beta-2 agonist (salbutamol, albuterol)
through nebulization
o Causes K to move from ECF to ICF
(SEVERE) ᛏ 7.5 mEq/L
- Calcium gluconate (10mL/ampule in 10%
solution)
o Given because effect of
hyperkalemia is cardiac dysrrythmia;
o Slow IV push
 Rapid administration may
cause hypotension
o ᛎ the antagonistic effect of K excess
on the myocardium when the
cardiac disturbance is due to ᛏK
o Ca ᛎ the irritability of the
myocardium resulting from ᛏK
o Not promote K loss
- Glucose insulin (50mL)
o Insulin is given as a treatment for
the hyperkalemia
o Insulin will carry the K to enter the
cell (one way of decreasing the K in
the blood)
o Since insulin is also a carrier of
glucose, the glucose in the blood is

9. also being sent inside the cells, so
possible for the px to become
hypoglycemic > not good because
normal serum glucose is 80-100
mg/dL, glucose is needed by the
cells for energy > if you bring it all
inside the cell, there will be less
sugar > brain will immediately suffer
o Brain cells – do not store glucose;
depend on the blood circulating in
the brain per minute
- NaHCo3 1 ampule dilute in 100cc D5 water;
slow IV push
o to correct the acid-base balance
o if already corrected, K that went out
goes back in
o K shift occurs in less than 15 mins.
o fastest way to decrease K
MILD HYPERKALEMIA
Loss of P wave; tall, peaked T
NURSING INTERVENTIONS
 Monitor VS and ECG strips. Report
abnormal reults
o Peaked T wave
o Wide QRS complex
o Prolonged PR interval
 Monitor K serum levels. Report values more
than 5.3 mEq/L
 Recognize that ACE inhibitors (-pril), beta-
blockers, K-sparing diuretics increase serum
levels and should be monitored in older
adults and those with renal insufficiency
 Advice patients who use Na substitute to
use them cautiously, as each tsp may
contain up to 60 mEq of K
 Eggs has the lowest K content
 Low K foods:
o Cucumber
o Apples
o Cherries
o Coffee
o Eggplant
o Onion
o Peas
o Grapes
o Rice
o Coleslaw
o Watermelon
CALCIUM
- 99% is stored in bones and teeth
- function: muscle contraction; blood clotting
process; transmission of nerve impulses;
formation of bones
- exists in plasma in 3 forms: ionized, bound, and
complexed
CALCIUM METABOLISM
- Vitamin D is needed for the absorption of
calcium (in the small intestine)
- Vitamin D – from exposure to sunlight; egg
yolks;
- Vitamin D that we get from the environment is
still inactive and therefore cannot be used yet
by the body
- Kidney activates the vitamin D
- Once activated, vit. D will be absorbing the
calcium we ate (milk, cheese)
- If with renal failure, calcium will not be
absorbed because vitamin D is not activated =
hypocalcemia
- Hypocalcemia > decrease in calcium will be felt
by the parathyroid gland at the back of thyroid
gland > parathyroid gland will release
parathormone > parathormone will order the
bones to release calcium because there is less
Ca in the blood (bone resorption) > bones will
become brittle & soft
- parathormone will also increase Ca absorption
from the GIT (small intestine)
(N/I: gentle handling of the px; avoid
falls – side rails up)
- if there’s excess Ca in the blood, the thyroid
gland will secrete calcitonin

10. - calcitonin inhibits the reabsorption of Ca from
bones and decrease serum Ca level > Ca will go
to kidneys, therefore prone to develop renal
calculi
PTH:
- ᛏ calcium absorption from the GIT
- ᛏ calcium reabsorption from the renal tubules
- releases calcium from the bone
 NORMAL CALCIUM LEVEL: 8.5 to 10.5 mg/dL
low Ca – parathyroid is stimulated > bone resorption
high Ca – thyroid is stimulated > secrete calcitonin
 Calcium and phosphates have an opposing
effect
o Phosphates are being removed by the
kidneys
o Foods rich in protein = rich in
phosphates
o If kidneys are damaged, phosphates
level will be high > calcium will become
low
o Kidneys damaged > for calcium to be
absorbed, doctors will give an active
vitamin D (calcitriol) and they will
remove phosphates (calcium carbonate)
and this will lower the phosphates >
once phosphates are lowered, calcium
will be absorbed
HYPOCALCEMIA
CAUSES:
 Chronic diarrhea
 Hypoalbuminemia (main prob: edema)
 Renal failure (kidneys are resp. for activation of
vitamin D w/c is needed for Ca reabsorption)
 Citrated blood transfusion
- Citrate is added to stored blood to prevent
clotting, binds with Ca and renders it
unavailable for use
- Combine with ionized calcium and
temporarily remove it from circulation
- 1 or 2 bags of blood transfusion in a day
won’t have an effect in decreasing the
serum Ca level
- 3 or more bags in one day > citrate is
increased in level > possible hypocalcemia
(because there’s so much citrate and this
will bind with the calcium)
1. Alkalosis
2. Hypoparathyroidism
 Patient receiving massive blood trnsfusion are
at risk for hypocalcemia
 Calcium gluconate (med given)
o Additional calcium given bec of the
binding factor of the citrate to Ca may
cause hypocalcemia
MANIFESTATIONS of hypocalcemia:
LATE SIGNS
 Chvostek’s sign
o Tap the px
 Trosseau’s sign
o Apply BP cuff > increase systolic
pressure 20mmHg to normal > leave for
3-5 minutes > indicate there is TETANY
ASSESSMENT FINDINGS:
 Anxiety, irritability
 Tetany (EARLY SIGNS)
o twitching around the mouth
o tingling & numbness of fingers
 Laryngeal spasm (brief spasm in the vocal
chords (larynx/voice box) – there will be DOF,
px can die), spasmodic contraction
 Abdominal cramps
 Muscle cramps
ECG READING
HYPOCALCEMIA
o < 8.5 mg/dL
- lengthening ST
- lengthening QT
HYPERCALCEMIA
o > 10.5 mg/dL
- shortened ST
- shortened QT
HYPOCALCEMIA TREATMENT
o CHRONIC TREATMENT
 Ca carbonate – given because there’s
low Ca; Calci-Aid & Calsan (antacid)
 Active vitamin D3 – Calcitriol

11. o I.V. Ca Chloride
 Given very slowly because it may cause
extravasation
 In general, Ca gluconate is preferred then Ca
chloride because it is less likely to cause tissue
necrosis
MANAGEMENT
I.V. CALCIUM SUPPLEMENT
 Ca solution are highly irritating to vein.
Administer the solution SLOWLY.
 Frequently assess IV site.
 Close monitor the patient because too rapid
infusion can cause cardiac arrest
 Ca SHOULD NOT BE GIVEN with saline solution
because S.S. increase Ca loss
 Ca SHOULD BE GIVEN in big vein. (phlebitis)
ORAL CALCIUM SUPPLEMENT
 Administer at least 30 minutes prior to a meal
to enhance intestinal absorption
 Teach patient to eat foods rich in Ca, vit. D and
protein
 Check for prolonged bleeding or reduced clot
formation. (Ca can cause clotting of the blood)
CALCIUM-RICH FOODS
- Okra
- Broccoli
- Cabbage
- Coconut meat
- Almonds
- Pumpkin seeds
- Avocado
- Celery
- Onions
- Spinach
NURSING INTERVENTION
 Limit alcohol and caffeine intake. (Limit calcium
absorption)
 Limit cigarette smoking w/c increases urinary
excretion of Ca
 Avoid laxatives and antacids that contain
phosphorus because they decrease Ca
absorption.
o Antacids – should never be given with
other drugs because antacids decreases
the absorption of other drugs
 Give 1 hour before or 2 hours
after all drugs
 Handle the patient gently. (severe bone calcium
loss makes the bone soft and brittle)
 Use bed sheet to lift patient.
HYPERCALCEMIA
CAUSES:
 Excess use of Ca supplement
 Use of thiazide (mild diuretic used for HTN
patient to remove excess fluids) – decreases the
excretion of Ca
 Prolonged immobilization – lose calcium in the
bone because bone is not being used, Ca goes
out)
 Hyperparathyroidism - increasing the workload
of parathyroid > always giving out
parathormone > parathormone will remove Ca
from the bone > Ca will be in the blood
 Steroid therapy – mobilize Ca absorption from
the bone
o Taking steroids for more than 3 months
will cause osteoporosis
ASSESSMENT FINDINGS
 Abdominal cramps and constipation.
(Hypercalcemia can decrease the peristalsis)
 Anorexia, nausea & vomiting
 Confusion, lethargy
 Bone pain (bec the bone loses Ca)
 Extreme thirst
 Muscle weakness (because muscles are
connected to the bones through ligaments and
tendons)
 Increase BP – Ca is + inotropic
DANGER SIGNS
 Arrythmia – bradycardia
 Cardiac arrest
 Coma
 Paralytic ileus
MANAGEMENT
 0.9 NaCl solution
o 200 – 300 cc/hr
o Na in the solution inhibits the renal tubular
reabsorption of Ca
o To achieve urine output of 200 cc/hr
o To dilute the serum Ca concentration (Ca
may crystallize)
 Furosemide
o 20 – 40 mg, 8-16hrs after volume re

12. o Do not give thiazide because it causes
increase Ca
o Monitor urine over 200 – 500 cc/hr
 Steroids
o Inhibit calcium absorption
o Do not abruptly stop taking steroids
because it can cause Addysonian crisis
 BiPhosphates
o Alendronate – Fosamax
o Pamidronate –
o Taking fosamax:
 Drink with glass of water so it can
immediately go down the stomach
 Never take with food because it will
not absorb the drug. (Take it 30
minutes before breakfast)
 Never take with coffee, OJ because
these decrease the absorption of
the drug by 60%
NURSING INTERVENTIONS
 Active and passive exercise for bedridden
patients.
 Encourage patient to drink 3 – 4 liters of fluid
daily. (To remove Ca from kidneys – urine)
 Avoid food rich in Ca.
o Cheese
o Avocado
o Milk
o Yogurt
o Almonds
 Encourage food that increases urine acidity.
(WHY?
o Acid-ash diet
 Meat
 Cheese
 Eggs
 Prune juice
 Whole grains
 Cranberry juice
 Provide safe environment,
o Side rails up
o Position bed in lowest position
MAGNESIUM
- Abundant intracellular cation
- Acts as an activator for many intracellular
enzyme systems and plays a role in both carbohydrates
and protein metabolism
- Acts directly on the myoneural junction
- ᛏ Mg diminishes the excitability of the muscle
cells; ᛎ Mg increases neuromuscular irritability
and contractility
- Produces its sedative effect at the
neuromuscular junction, probably by inhibiting
the release of the neurotransmitter
acetylcholine
- Increases the stimulus threshold in nerve fibers
- (effect in CV) acts peripherally to produce
vasodilation and decreased peripheral
resistance
- After potassium, magnesium is the next
abundant cation in the ICF
- Bone contains about 60% of the body’s
magnesium
- 60% is excreted in the feces and 40% via urine.
- Promotes carbohydrates metabolism
- Produce and use ATP for energy
- Takes part in protein synthesis
- Helps in the contractility of cardiac and skeletal
muscles
- Vasodilation – helps the SVV function normally
for it decrease the afterload but not for patient
with renal failure
 NORMAL Mg LEVEL: 1.3 – 2.3 mg/dL
(1/3 of serum Mg is bound to protein; 2/3 exists
as free cations)
HYPOMAGNESEMIA
- Can cause hypokalemia and hypocalcemia
o The hypomagenesemic state inhibits K+
absorption
- Laxative abuse
- Diverticulosis
o Plenty of balloons in the colon > patient
always constipated > Valsalva maneuver
> increase pressure in the large
intestine > smooth muscle weakens.
The balloons pop (peritonitis) and you
will undergo surgery
Mg levels should be evaluated in combination
w/ albumin levels (WHY? 30% of Mg is protein
bound, principally to albumin)
CAUSES:
1. Important route of Mg loss is the GI tract:
o Nasogastric suction

13. o Diarrhea
o Fistula
 Fluid from the lower GI tract
has a higher concentration of
Mg (10-14 mEq/L) than the
upper tract, so loss from
diarrhea and intestinal fistulas
are likely to induce ᛎ Mg
2. Disruption in small bowel function
 Major site of Mg absorption – distal small
bowel
o Intestinal resection
o Inflammatory bowel disease
3. Withdrawal from alcohol
 chronic alcohol abuse – major cause of
symptomatic ᛎ Mg
o N/I: serum Mg level should be
measured at least every 2 or 3
hours (may be normal on admission
but may ᛎ as a result of metabolic
changes, such as the intracellular
shift of Mg associated with IV
glucose administration)
4. Nutritional replacement
 The major cellular electrolytes move from
the serum to newly synthesized cells
o Administration of tube feedings or
parenteral nutrition (
o TPN
o Prolonged IV fluid therapy
5. DM (d/t osmotic diuresis)
o Increase urination > Mg is lost in urine
40% > Decrease Na+, K+, Mg+ =
electrolyte imbalance
6. Inadequate intake of Mg
MAGNESIUM-RICH FOODS
- Almonds
- Spinach
- Soybeans
- Cashews
- Avocados
- Potatoes
- Brown rice
ASSESSMENT FINDINGS
 3T’s and hyperactive DTR’s
o Tremors
o Twitching
o Tetany
o Hyperactive deep tendon reflexes
Tonicity refers to what the cell does in a certain
environment. If the environment is hypertonic, the
cell will shrink due to water leaving the cell.
Hypotonic means water enters the cell and caused
it to expand and possibly explode.
Osmolarity refers to the relative concentration of
two solutions. If the outer environment is
hyperosmotic, the concentration of solutes outside
the cell is greater than the concentration inside the
cell.
Tonicity and osmolarity generally will have the
same prefix. However, there are some solutes that
will act oddly and can create a situation where the
system is hypertonic and isoosmotic. Just look at
what the cell does and relative concentration of
each solution, and you can figure it out.