Osmotic

Imbalances

SODIUM (Na)135mg 145mEq/L

most important cation in the ECF
controls S. osmolality levels and H2O

retention
maintains water balance throughout the body
Controls ECF osmolality
generates transmission of neuromuscular
impulses (muscle & cardiac contractions)
essential in the Na+, K+ pump
maintains A/B balance

Regulation of Na
lost through the skin, git, and gut.
Regulated by kidneys through
glomerular filtration and tubular
reabsorption
Regulated by aldosterone and ADH
When ECF Na is, the adrenal
glands send aldosterone to the
kidneys, where Na is reabsorbed.

HYPONATREMIA
< 135 mEq/L
cell swells as water is pulled in from ECF

Etiology:
a. Increased Na excretion
Excessive diaphoresis
Diuretics
Wound drainage (burns, GIT)
Decreased aldosterone secretion
Hyperlipidemia
Renal disease : scarred convoluted tubule
GIT: NGT suction, diarrhea, or laxative abuse

b. Inadequate Na intake
NPO
Low-salt diet

c. Relative Na Deficits / Delution of Na

Excessive ingestion of hypotonic fluids
Psychogenic polydipsia
Freshwater drowning
Renal failure (NS)
Irrigation w/ hypotonic fluids
Hyperglycemia
CHF
Adrenal Insufficiency : aldosterone levels

Na reabsoprtion Na excretion
SIADH : etio: tumor, head injuries, endocrine
& pulmonary disorders, meds

SIADH

Excessive ADH activity

water retention

dilutional hyponatremia &

inappropriate urinary
excretion of Na in the
presence of hyponatremia

Two Mechanisms involved

in
HYPONATREMIA
Hyponatremia
Na in the Blood &

ECF osmolality
ECF

into ICF
ECF & Cellular Fluid ECF moves

cell swells
Slower Membrane

impairs function
Depolarization

Cell Excitability

CLINICAL MANIFESTATIONS
Feeling of exhaustion
Poor skin turgor
Dry mucousa
Decreased saliva production
Orthostatic fall in BP
GIT : Abdominal cramping, anorexia, nausea
and vomiting, hyperactive bowel sounds=d/t
abnormal losses of Na or gains in water
RESPIRATORY
Pulmonary edema
Rapid shallow respiration
Moist crackles

NEUROLGIC & MUSCULOSKELETAL

SYMPTOM (Na <115meq/L)
Altered mental status cellular swelling &
cerebral edema
Muscle weakness, twitching,cramps
Headache
Papilledema
Dizziness
Convulsions
Coma
RENAL MANIFESTATIONS
urine output
USG

DIAGNOSTIC FINDINGS
S. Na level < 135 mEq / L
USG =1.002 to 1.004
S. osmolarity < 275 mosm/kg (except in
azotemia or ingestion of toxin
MEDICAL MANAGEMENT (Na++)
a. Drug Therapy
Osmotic diuretics excretion of fluids rather
than sodium
Replace other electrolyte losses (K, Ca, HCO3)
IV Saline for Na and fluid loss
2-3% Saline for severe hyponatremia

b. Diet therapy
Fluid restriction & Na intake

NURSING MANAGEMENT
Identify high-risk patients :
- diuretic therapy
- gastric suctioning
- renal disorders
- burn injuries
- fever
Na replacement :
- administer highly hypertonic solution w/ caution to
prevent circulatory overload & neurologic
complications
Osmotic Demyelization
- neurologic damage
- occurs when Na+ is over-corrected at 140mEq/dL

Highly Hypertonic Solutions:

- 3% NaCl 1L (513 mEq Na)
- 5% NaCl 1L (855 mEq of Na)
Administered only in ICU
Monitor for fluid overload (force water to leave ICF
to balance Na in ECF causing cellular shrinkage
excessive demands on the heart lead to CHF)
Relieve acute manifestations of cerebral edema
and prevent neurologic symptoms rather than to
correct Na+
Na & H2O restriction (800 ml/24)
Note for GIT symptoms

Cont Nsg Mgt

Be alert for CNS changes= lethargy,

confusion, muscle twitching, seizures

Be alert for circulatory overload
- patients w/ CVD disease
- dyspnea, puffy lids
- dependent edema
- wt gain in 24
Measure I & O & daily weight
Monitor V / S & S Na levels
Check USG
Encourage foods & fluids with high Na content
Be aware of Na content of common IVF

HYPERNATREMIA
Serum Na > 145 mEq/L
Na ECF osmolalityICF moves into ECFICF

dehydration
ETIOLOGY:
a. Decreased Na excretion
Hyperaldosteronism
Renal failure
Corticosteroids
Cushings syndrome or disease
DI
b. Increased Na intake
Exccessive oral Na ingestion
Excessive administration of Na-containing IV
fluids

Decreased water intake

NPO
Fluid deprivation in unconscious patients,
old and vey young patients.
Increased water loss
Increased rate of metabolism
Fever
Hyperventilation
Infection
Excessive diaphoresis
Watery diarrhea
Dehydration

CLINICAL MANIFESTATIONS
Early S/S
Renal : Polyuria followed by oliguria, USG
GIT: Anorexia, nausea and vomiting = d/t fluid
retention in gastric cells
CNS manifestations: d/t sensitivity of brain
cells to fluid shifting
Restlessness, Irritability, Muscle weakness
Decrease fluid in the interstitial
compartments
Dry, flushed skin
Dry, sticky mucous membranes
Tongue furrows
Fever = d/t amount of fluid available for
dissipating heat.
Increased thirst = primary characteristic of Na;
primary defender in healthy people

Cardiovascular manifestations Na
Tachycardia
Dysrhythmias
Hypovolemic hypernatremia:
orthostatic hypotension w/
compensatory tachycardia
Hypervolemic hypernatremia: BP, JV
distention, prolonged peripheral
emptying, generalized edema wt gain
Pulmonary Manifestations
Crackles, dyspnea d/t hydrostatic
pressure seen in BV

Na >155 mEq/L
Severe neurologic manifestations
resulting from shrinkage of brain
cells d/t ECF osmolality
Confusionseizurescoma
irreversible brain damage
Muscle twitching, tremor,
hypereflexia seizures = d/t altered
neuromuscular contractility and
irritability
Rigid paralysis= grave sign

DIAGNOSTIC FINDINGS
Na level > 145 mEq/L
S. osmolality > 295 mosm / kg kidneys
attempt to conserve water
Plasma Cl level > 106 mEq/L = Cl is the major
ECF ion that balances w/ Na
USG > 1.025 kidneys attempt to conserve
water
urine osmolality

POTENTIAL NURSING DIAGNOSIS

Fluid volume deficit
High risk for injury
Fatigue
Altered nutrition: less than body requirements
MEDICAL MANAGEMENT
Diuretics - poor renal excretion of Na
Diabetes Insipidus : Desmopressin acetatE, nasal
spray to slow the rate of diuresis
Patients w/ CV pulmonary and neurologic
manifestations
- Hospitalization
- IV hypotonic saline solution
To decrease total body water and replace fluid loss
- Hypo-osmolar/ hypotonic solution: 0.3 NaCl or 0.45%
- D5 W

Diet Therapy
Adequate water intake among older adults or those
who have no access to water
Dietary Na restriction
Fluid restriction

POTASSIUM (3.5 5.0 mEq / L)

major cation in the ICF (98%), 2% ECF

(neuromuscular function)
K+ imbalances are commonly associated
with various
diseases and:
injuries
Medications =diuretics, laxatives,
antibiotics
special treatments = e.g. TPN &
chemotherapy
Primarily regulated by the kidneys
Aldosterone increases the excretion of K+
by the kidneys

Functions
of
Potassium
electric impulses of the nerve, heart,
Plays vital role in the transmission of

intestinal and lung tissue

Assists in regulation of acid-base balance
by cellular exchange with H+
Works in reciprocal fashion with Na
(excessive intake of Na+ results to
excretion of K+ and vice versa
Regulation of protein synthesis, glucose
use & storage

Etiology

a. Excessive K loss
Inappropriate or excessive use of drugs
- Prolonged diuretic tx - K+ follows water & Na across the tubular membrane
- Digitalis
- Corticosteroids - influence Na retention & reciprocal K+ excretion
Hyperaldosteronism : Cushing;s syndrome
excessive absorption of Na in the proximal tubules, accounting for
accelerated excretion of K
Cirrhosis, nephritic syndrome, HF, malignant HPN
Diarrhea &

laxative use

H0kalemia
Wound drainage (esp gastrointestinal)
Recent Ileostomy -Intestinal fluid may contain as

much as 30 mEq / L of K+
Prolonged NGT suction, Vomiting : K+ is lost when
gastric fluid is lost bile is rich in K+
Heat-induced excessive diaphoresis
Renal disease impairing reabsorption of potassium
Excessive removal of K+ during peritoneal or
hemodialysis

Heat-induced excessive diaphoresis

Renal disease impairing reabsorption of potassium
Excessive removal of K+ during peritoneal or hemodialysis

b. Inadequate Potassium intake

NPO
Inadequate intake & absorption debilitated, elderly,
alcoholic, anorexia & bulimia nervosa
c. Alkalosis : Movement of K from ECF to ICF
= ICF&ECF shifting of ions
= lowered levels of extracellular H ion move out of the cells
in
alkalotic states to help correct high ph & K+ ions move in
to
maintain electrically neutral state
Hyperinsulinism
Hyperalimentation/TPN
Hypertonic glucose solution
d. Villous adenoma tumor of the intestinal tract
characterized
by excretion of K+-rich mucus

e. Hyperaldosteronism
f. Dilution of Serum Potassium
Water intoxication
IV therapy with potassium-poor solution
* Magnesium depletion causes renal K+ loss & must
be corrected first; otherwise loss of K+ will continue

Clinical Manifestations (K+ 3mEq/L)

a.Respiratory Manifestations
Shallow, ineffective respirations: profound

weakness
of the skeletal muscles of respiration
Diminished breath sounds
NR:
Assess for breath sounds, ease of respiratory
effort,
color of nail beds and mucous membranes, rate &
depth of respiration.
Assess respiratory status q 2 hours because
respiratory insufficiency is the major cause of
death.

b. Cardiovascular Manifestatons
Rapid , weak, thready pulse
Orthostatic hypotension
ST depression, inverted T wave. Prominent U wave,
Heart block
NR
Monitor for orthostatic hypotension w/c is present in
hypokalemia

c. Neuromuscular Manifestations
Anxiety, lethargy, confusion, coma
Loss of tactile discrimination
General skeletal muscle weakness
Deep tendon hyporeflexia
Flaccid paralysis
d. GIT Manifestations
Decreased motility
Hypoactive to active bowel sounds
Nausea, vomiting, abdominal distention
Paralytic ileus
Constipation

e. Renal Manifestations
Decreased ability to concentrate urine
Polyuria
Decreased specific gravity : inability to
concentrate urine
f. Musculoskeletal Manifestations
Severe hypokalemia : death through cardiac arrest
Clinical signs rarely develop before the K+ level
has fallen below 3 meq/L unless the rate has been
rapid
K+ depletion depresses the release of insulin &
results in glucose intolerance
- Fatigue
- Anorexia
- Nausea
- Vomiting

K+ = required for normal

musculoskeletal contraction
Muscle weakness & cramps
Cardiac dysrhythmia
Hypereflexia
Drowsiness, lethargy & coma
Paresthesias
bowel motility (which could develop to paralytic ileus)

b. DIAGNOSTIC FINDINGS (K+)

History

S. K+ level < 3.5 mEq / L

ECG flat T waves/or inverted T waves
suggesting ischemia & depressed ST segments
U wave = specific for hypokalemia
PH elevated above 7.45 = K+ ion move in to
maintain an electrically neural state
glucose level

 serum bicarbonate levels

MEDICAL MANAGEMENT
Goal:
Promotion of potassium balance
Prevention of complications
a. K+ replacement (oral/IV) 40 80 mEq /day (1
mEq/10ml, 5-10 mEq/hr)
b. K sparing diuretics : spironolactone, triamterene,
amiloride
c. Dietary intake of K+ rich foods raisins, bananas,
apricots, oranges, vegetables, legumes,whole grains,
meat, milk
* Oral K+ supplement can produce small bowel lesions,
patient must be assessed for abdominal distention,
pain or GI bleeding

NURSING MANAGEMENT
Nursing Diagnosis
Risk for Falls r/t skeletal muscle weakness
Constipation r/t smooth muscle atony
Decreased cardiac output r/t dysrhythmias
Self-Care deficit r/t skeletal muscle weakness
Expected outcomes
Absence of injury & normal serum potassium level.
Nursing Interventions
1. Identify high-risk patients
2. Teach patient receiving diuretic therapy at home about
hypokalemia & how to manage it
3. Patients receiving digitalis should be monitored for
digitalis toxicity
4. Careful I & O monitoring is necessary = 40 mEq of K is
lost for every liter of urine

5. Monitor ECG changes

6. Monitor blood gas analysis check for HCO3 & ph
level
7. Monitor IV K+ administration
Correct flow rate
Irritation on the insertion site
Mix solution thoroughly
Rapid K+ administration can cause sudden
hyperkalemia & cardiac arrest
Administered only after an adequate urine flow
For life threatening hypokalemia 10 mEq K+ + 100
cc IV solution over 1 hour via infusion pump is
administered
Never give IM or IV push
Monitor V / S ,I&O (20cc/2hrs)
Educate pt on the proper way of taking K+ supplement

HYPERKALEMIA
(> 5.5 mEq/L)
Seldom occurs in patients with normal renal function
Often due to iatrogenic causes (treatment induced)
More dangerous because cardiac arrest is more
frequently associated with K+ levels
ETIOLOGICAL FACTORS
a. Excessive K intake
Over ingestion of potassium-containing foods or
medications
Rapid infusion of potassium-containing IV solution
Bolus IV potassium injections
Transfusion of aged whole blood or packed cells.

b. Decreased K excretion
Adrenal insufficiency(Addisons disease,
adrenalectomy)
Renal failure : poor elimination
Potassium-sparing diuretics
c. Movement of K from ICF to ECF
Tissue damage
Acidosis : K+ moves out of the cell into ECF & H
ion shifts into the cell
Hyperuricimia

d. Medications
KCl, heparin, ACE inhibitor, NSAID

e. Cell lysis
- burns, trauma, Ca chemotherapy, severe infection or
any
condition
f. Addisons Dse and hypoaldosteronism
- deficient adrenal hormones leading to Na+ loss and
K+ retention
g. Psuedohyperkalemia
Prolonged tight application of tourniquet for drawing
blood
Hemolysis of blood sample
Drawing blood sample where K+ is infusing
Leukocytosis (WBC > 200,000) =
Thrombocytosis (pt ct > 1 million)

PSEUDOHYPYPERKALEMIA
Failure to be aware of these
causes can lead to aggressive
treatment of nonexistent
hyperkalemia resulting in
serious lowering of serum K+
levels

CLINICAL MANIFESTATIONS
Neuromuscular Effects
Early:
- Twitching of skeletal muscles,tingling, burning
- Numbness in the hands & feet & around mouth

- Flaccid paralysis (arms and legs)

- Flaccid paralysis of trunk, head, respiratory

muscles
(lethal levels of K)

Cardiovascular System
Slowed ventricular conduction
Bradycardia
Hypotension
Widened ORS complex
Tall, peaked T waves
Ventricular fibrillation
Cardiac arrest

GIT
Nausea
Intermittent intestinal colic
Increased motility Diarrhea
Urine= oliguria anuria

Laboratory Findings
ECG changes
ABG metabolic acidosis
S. K+ - > 5.0 mEq / L
Crea, BUN (RF)

MEDICAL MANAGEMENT (K+ )

1. Drug therapy

a. Lasix
b. Administration of cation exchange resin

(kayexalate ) orally or by retention enema in

patients with renal impairment

* Not given to patients with paralytic ileus (causes

intestinal perforation)
Binds with other cations in the GIT causing hypomagnesia &
hypocalcemia
Causes Na retention & fluid overload
c. Dextrose w/ insulin
d. Ca gluconate - antagonizes the action of K+ on the heart but
does not K+ level
d. Hemodialysis
e. NaHCO3 with caution, it can cause Ca++ levels to drop
2. Restriction of dietary K+ & K+ - containing
medications

NURSING MANAGEMENT
a. History
Ask about chronic illness ( renal disease, DM)
Ask about drug use (potassium-sparing, ACE inhibitors,)
Obtain diet history
Collect S/S r/t K
b. Identify high-risk patients (K+ sparing diuretics, K+
supplements, I.V. K+, RF, & metabolic acidosis)
Nursing Diagnosis: same w/ K
Nursing Interventions
Administer electrolyte-binding and electrolyte excreting
resins
Check urine output & K+ levels before administering any
K+ containing medications
Provide cardiac monitoring
Monitor BP to detect hypotension due to rapid
administration of the drug
Appearance of bradycardia is an indication to stop
the
infusion

Cont. Nursing Interventions

Monitor I & O
Maintain potassium restrictions.
Verify highly abnormal K+ levels maybe
erroneous
Avoid prolonged use of tourniquet & caution pt not
to exercise extremely to avoid false reports &
hyperkalemia
Deliver blood sample to laboratory hemolysis of
blood sample
Encourage patient to adhere to prescribed K+
restrictions
Provide health teachings: key to prevention of
hyperkalemia and early detection of complications

Funny Video

CALCIUM
(8.5 -10.5 mg/dl/ 2.1-2.6mmol/L)
99% in skeletal system, 1 % blood
Regulated closely w/ Mg & Phosphorus
transmits nerve impulses & help regulate muscle contraction

& relaxation
plays a role in blood coagulation
absorbed in the GIT & excreted in the urine
Filtered in the glomerulus & reabsorbed in the tubules
Needed for vitamin B12 absorption
Determines the thickness & strength of cell membrane
Sources: milk, cheese, dried beans, meats and vegetables
Calcitriol (Vit D) = promotes Ca absorption & limiting Ca
excretion when levels are inadequate
Calcitonin: moves Ca from plasma to bone when serum level
PTH = stimulates release of Ca from bone into the serum to
bring serum level to normal

Ca Regulation
Blood Ca level

Secretion of Calcitonin by the TG

Activation of vit D inhibited

Reabsorption of Ca by the kidneys

Absorption of Ca from the intestines
Breakdown of bone

Blood Ca level

Ca Regulation
blood Ca level

secretion of PTH by the PG

Inc. Activation of vit D

a. Reabsorption of Ca by the kidneys

b. Release of Ca into the blood stream d/t
Inc
breakdown of bone
c. absorption of Ca from the intestines

blood Ca level

ETIOLOGY
Actual Calcium Deficits
a. Inhibition of Calcium Absorption from the GIT
Inadequate intake of Ca++
Lactose Intolerance
Malabsorption syndromes: Celiac dse, Crohns dse
Inadequate intake of vit D
Inadequate exposure to UV w/c hindres conversion of VIT
D to its active form (dihydroxycholecalciferol)
ESRD : vitamin D not adsorbed which is necessary for the
absorption of Ca++
Patients with renal failure has S phosphates which
causes a reciprocal drop in S. Ca++ ;level because
phosphorous will bind to Ca++, lowering S levels
Alcohol abuse d/t intestinal malabsorption,
hypomagnesemia, hypoalbuminemia & pancreatitis
Massive administration of citrated blood (as in exchange
transfusions in new born)
=Citrate combines with ionized Ca++ & temporarily
remove it from circulation

b. Increased Ca excretion
RF- polyuric phase
Diarrhea
Steatorrhea
Wound drainage (esp GIT)
Large doses of diuretics Ca++ elimination
c. Conditions that decrease the Ionized Fraction OF
Calcium
Hyperproteneinemia
Alkalosis : HCO3 binds to Ca++ resulting to S. levels
Ca chelators or binders: citrate, mithramycin,
penicillamine, Na cellulose phosphate
Acute pancreatitis: inflammation of the pancreas causes
breakdown of proteins & lipids to fatty acids which
combine with Ca++ ions forming Ca++ soaps &
excreted in the GIT
Hyperphosphatemia
Immobility
d. Primary hypoparathyroidism or surgical
hypoparathynoidism low PTH Ca++ absorption

CLINICAL MANIFESTATIONS (Ca++)

a. Cardiovascular manifestations
heart rate
myocardial contractility
Diminished peripheral pulses
BP
ECG abnormalities: prolonged ST interval, prolonged
QT interval
b. Neuromuscular Manifestations
Anxiety, irritability, psychosis
Paresthesias followed by numbness
Irritable skeletal muscles : twitches, cramps, tetany,
seizures, tingling of fingertips, mouth (Ca, Mg)
Hyperactive deep tendon reflexes - Ca level makes
the nerve excitable because lack of Ca increases
renal permeability to Na
Seizures Ca++ irritability of the CNS &
peripheral nerves

Mental changes = depression, impaired memory,

confusion, delirium, hallucinations

Positive Trousseaus sign, Chovteks sign
c. GIT manifestations:
increased motilityhyperactive bowel sounds,
abdominal cramping, diarrhea.
d. Easy bruising & petechiae and excessive
bleeding when cut
- Ca++ is needed for blood clotting

PATHOPHYSIOLOGY
Ca is an excitable membrane stabilizer, regulating
depolarization and the generation of action
potentials
Ca decreases Na movement across excitable

membrane, decreasing the rate of depolarization.

Low serum Ca levels increase Na movement across

excitable membranes, allowing depolarization to

occur more easily and at inappropriate times

DIAGNOSTIC TESTS ( Ca++)

S. Ca++ level < 8.5 mg / dl
Hyperphosphatemia
Mg = Ca regulated w/Mg
Albumin - Ca is bound to it
Prolonged PT & PTT = Ca for blood clotting
XRAY= Osteoporosis
Sulkowitch test = confirms Ca++ in urine
ECG = prolonged QT interval due to prolongation of
ST segment

MEDICAL MANAGEMENT ( Ca++)

Acute symptomatic hypocalcemia is life threatening

& requires treatment with IV Ca++
1. Parenteral Ca salts: Ca gluconate, CaCl & Ca
gluceptate
Cardiac arrest too rapid admininistration
Dangerous to patients o n digitalis-may cause toxicity
Ca w/ D5W & given slowly via infusion pump
Ca can cause postural hypotension keep on bed &
monitor V/S
2. Vitamin D therapy, PTH supplement = to Ca+
+ absorption in the intestine
3. Aluminum & Ca++ containing antacids to
elevated phosphorous levels before treating
hypocalcemia for patient with CRF
4. dietary intake of Ca++ to 1,000 1,500 mg /
day
*

NURSING MANAGEMENT
Nursing Diagnosis
Risk for injury r/t bone density loss, mental
changes
Readiness for Enhanced Nutrition r/t the need to
increase Ca intake
Interventions
Identify patients at risk for hypocalcemia
- thyroid diseases, thyroidectomy. GI problems
Monitor trends in serum Ca levels
Monitor fluid status
Administer medications
Monitor for side effects of IV administration of Ca
- soft tissue damage w/ extravasation

Cont. Nursing Interventions

Encourage intake of Ca-rich foods.
Provide adequate intake of vit D.
Monitor neuromuscular, CV manifestations of
hypocalcemia.
Monitor for overcorrection of hypocalcemia.
Institute cardiac monitoring & secure
precautions if the patients Ca level is
dangerously low
Provide nutritional counseling if Ca is due to
dietary deficiency
Instruct the patient that exercise enhances Ca
mobilization from bone & will replenish plasma
Ca level

HYPERCALCEMIA (> 10.5 mg /

treated promptly
dl)
ETIOLOGY:

Severe hypercalcemia = mortality rate of 50% if not

a. Ca Absorption
Excessive oral intake of Ca, Vit D
b. Ca Excretion: RF, Thiazide diuretics
c. bone resorption
- Hyperparathyroidism
- Malignancy
- Hyperthyroidism : accelerates calcitonin secretion
- Immobility : alters bone metabolism
- Glucocorticoids
d. Hemoconcentration: dehydration, lithium, adrenal
insufficiency
Malignant tumor of parathyroid gland &
hyperparathyroidism

E. Malignant tumor of
parathyroid gland &
hyperparathyroidism
HYPERPARATHYROIDISM

PTH SECRETION

release of Ca from bone & Renal Absorption of

Ca

Ca++ & Phosphorous >70

Calcification of soft Tissues

CLINICAL MANIFESTATIONS ( Ca++)

A.Reduced neuromuscular excitability because it

suppresses activity at the myoneural junction

Muscle weakness
Incoordination
Anorexia, nausea, vomiting
Hypoactive bowel sounds, abdominal distention
Constipation ( tone in smooth and striated muscle).
Abdominal pain = peptic ulcer like symptoms; Ca
secretion of acid & pepsin by the stomach
B. Neurologic manifestations = Ca++ affects
conduction across nerve cells
Confusion
Personality changes
Altered LOC
Coma

Other complications
Dehydration
Urinary calculi = Ca precipitates in the kidney
Pathologic fractures
Soft-tissue calcification = when Ca level rise & Ca+
+ binds with phosphorous
Excessive urination = d/t disturbed renal tubular
function produced by hypercalcemia
Excessive thirst = 2 polyuria
Constipation - motility of the intestines
Cardiac standstill = Ca++ above 18mg/dl
(4.5mmol/LS)

LABORATORY & DIADNOSTIC TEST: ( Ca++)

S. Ca levels > 10.5 mg / dl
X-ray- bone changes & bone density & urinary
calculi
ECG dysrhythmias & shortening of QST+
interval
& ST segment
Double-antibody PTH test
- differentiates primary hyperparathyroidism &
malignancy as cause of Ca++
- PTH levels are in primary & secondary
hyperparathyroidism & suppressed in malignancy
Sulkowitch urine test
- analyzes the amount of Ca in urine
- dense precipitation is observed due
hypercalcemia

MEDICAL and Nursing MANAGEMENT ( Ca++)

Goal: the S Ca++ level reversing the process of
hypercalcemia treating the underlying cause is
essential
Drugs ,Dialysis, OFI, Diet
1. Institute measures to prevent hypercalcemia
identify high-risk pts & instruct them to avoid Ca rich
foods
Ambulate patient as early as possible
2. Initiate measures to eliminate excess Ca
Administer IV NSS
- dilutes Ca++ temporarily
- excretion of Ca++ by the kidneys by inhibiting
tubular
reabsorption of Ca++
- Fluids with Na++ favor Ca++ excretion
Administer loop diuretics = facilitate Ca++ removal

3. Administer Calcitonin as
ordered to S. Ca level
Calcitonin from salmon - skin test necessary
reduces bone resorption,
Ca & phosphorous deposit in the bone &

urinary excretion of Ca++ & phosphorous

Administer IM not SC = patients with Ca have
poor perfusion to SC tissue
4. Administer IV phosphate as ordered
- can cause reciprocal drop in S. Ca
- used with extreme caution with Ca because
it can cause severe calcification in various
tissues, hypotension, tetany & ARF

CONT.
5. OFI containing Na++ (if not contraindicated)
3 4 quarts daily
6. intake of fiber-rich foods to inhibit
absorption of Ca in the intestine & facilitate,
prevent constipation
7. Monitor for neuromuscular manifestations of
hypercalcemia.
8. Assess for sign of digitalis toxicity
Ca potentiates effects of digitalis
ECG changes PVCs, Paroxysmal atrial
tachycardia & heart block can occur
Monitor CR & rhythm
9. Monitor V / S & electrolyte status
10. Encourage mobilization to prevent bone
resorption.

MAGNESIUM

(1.5 2.5 mEq/L or 1.8 3.0 mg/dl)

most abundant ICF cation next to K+
found in heart, bones, nerves, muscle tissue
Only 1% of TBW is ionized
Dietary Mg is absorbed in the jejunum & ileum
Elimination: kidney; GIT
Regulated by parathyroid & steroid hormones
Sources = vegetables, nuts, fish, whole grain, peas

and beans

Functions
Exerts effects on the neuromuscular junction,
affecting neuromuscular irritability.
Skeletal & muscle contraction
Metabolism of CHO & proteins
Adenosine triphosphate (ATP) formation
B-complex vitamin activation
Facilitates Na & K transport across cell membrane
Influences ICF Ca levelsthrough its effect on
parathyroid hormone secretion
DNA synthesis
Contributes to vasodilation: BP; Cardiac output
Facilitate Na+ & K+ transport across a cell
membrane
Ca++ levels should be evaluated with albumin
levels; S albumin levels decrease total Mg

HYPOMAGNESEMIA
<1.5 2.5 mEq/L or 1.8 3.0 mg/dl)

ETIO:

1. G.I. losses
Vomiting
Diarrhea
Gastric suctioning
Intestinal fistulas
ileostomies
laxative abuse
Radiation
Enteritis

*Distal SI= major site of Mg absorption

= IBD & resection can lead to Mg

2. Inadequate intake or absorption

Malnutrition or starvation
Malabsorption syndrome: IBD, Pancreatitits, Celiac,
Critically ill: no enzymes for absorption
Excessive dietary intake of Ca or vit D
3. Alcohol: GI losses & malabsorption
4. Fluid & electrolyte shifts
Adm. of TPN that are Mg deficient
Ca
High dose steroid use
DKA- 2 to renal excretion during osmotic
diuresis & shifting of Mg into the cells with insulin
therapy
Sepsis
Pancreatitis

PIH
Refeeding after starvation

5. Renal disease: Mg depending on the

disease
: Diuretic phase
6. Medications: Gentamycin, chemo (esp cisplatin),
steroids, Loop, osmotic and thiazide diuretics
Aminoglycosides; cyclosporine, cisplatin, diuretics,
digitalis, amphoterecin
7. Rapid administration of citrated blood

8. Hypernatremia = Cushings syndrome or

hyperaldosteronism (inhibits Mg+ reabsorption)
9. Sepsis
10. Burns
11. Antacid overuse = inhibit uptake of Mg+ from
intestinal villi

CLINICAL MANIFESTATIONS (Mg)

Warm, flushed appearance
Diaphoresis
Nausea & vomiting/diarrhea
Drowsiness, lethargy
Weakness and flaccid muscles
Heart block and other dysrhythmias
Loss of deep tendon reflexes
Depressed respiratory function: slow & shallow
Hypotension
Bradycardia Generalized tonic-clonic or focal seizures
Athetoid movements
Coma

B. CARDIOVASCULAR CHANGES (Mg)

Hypertension
ECG changes: prolonged ORS complex, ST
segment
Cardiac dyrhythmias: PVCs, SVT, VF
susceptibility to digitalis toxicity

associated with Na+ levels

because patients receiving digoxin are

also likely to be receiving diuretic

therapy, predisposing them to renal
loss of Mg.

C. MOOD ALTERATION
1. apathy
2. depression
3. apprehension
4. extreme agitation
5. ataxia
6. dizziness
7. insomnia
8. confusion
9. delirium
10. auditory or visual hallucination
11. Frank psychosis may occur

DIAGNOSTIC FINDINGS (Mg)

< 1.5 mEq / L or 0.75 mmol /L
K+ Ca++, S albumin
QRS, ST segment, flatT waves & prominent U
wave reflect Mg+, Ca++, K+ deficiencies
PVCs, PAT, Heart block can occur
Torsades de Pointes (VTac) is associated with Mg
level
Urinary Mg levels are measured

NURSING DIAGNOSES
High risk for injury
Decreased cardiac output
Altered nutrition less than body requirements
Potential for fluid volume deficit
Impaired memory
NURSING INTERVENTIONS
Identify high risk patients: anorexia, nausea &
vomiting, diarrhea
Monitor patients w/ hypokalemia
Monitor patients with hypokalemia for impending
hypomagnesemia
Monitor patients receiving TPN without Mg added

Monitor a patient with Mg who is on digoxin

for signs of digitalis toxicity

Monitor cardiac status
Initiate seizure precaution
Administer Mg replacement with extreme
caution & slowly as ordered (infusion
pump)
Vasodilatory effect (c ardiac output, and O2

consumption in people w/ shock and sepsis)

Rapid administration cardiac arrest
Assess V/S frequently to detect cardiovascular &
respiratory changes ( BP, RR, dysrhythmias)
Monitor urine output before, during & after
administration (at least 100ml/4hrs)
Check deep tendon reflexes before administration
(patellar or knee jerk)
( - ) Patella reflexes dont give the drug

Ca gluconate must be ready to treat hypocalcemia

tetany or hypermagnesia
Assess for stridor - Mg may cause airway obstruction
Instruct the patient on diuretics about the danger of
Mg
Monitor for dysphagia the ability to swallow must be
tested with water before oral administration of foods
Monitor deep tendon reflexes. urine output

HYPERMAGNESEMIA
Plasma level >2.5mEq or 3mg/dl
False (+) hemolyzed blood
ETIOLOGY: ( Mg)
1. Mg gain
Mg containing antacids: Maalox, Riopan,
Mylanta, laxatives, milk of magnesia)
Hyperalimentation administration
Hemodialysis using hard water dialysate
2. Inadequate excretion = Renal failure
3. F&E shift:
ACTH insufficiency (Hypoadrenalism) =Na+
retention w/ Mg+
DKA glucose brings cation across cell
membrane

CLINICAL MANIFSTATION ( Mg)

A.

B.

Mildly elevated Mg level

BP due to peripheral dilation
Nausea & vomiting epigastric pain
Soft tissue calcification
Facial flushing & sensation of warmth
Higher Mg levels
depresses the CNS & peripheral neuromuscular junction
or blocked release of acetylcholine from myoneural
junction w/c results in muscle cell activity
Lethargy
Difficulty speaking (dysarthria)
Drowsiness
Absent deep tendon reflexes
Muscle weakness & paralysis
Depressed respiratory center (Mg > 10 mEq/L or 5
mmol/L)
Coma if Mg is not treated

DIAGNOSTIC FINDINGS ( Mg)

2.5 mEq/L or 3.0 mg/dh (1.5 mmol/L)
ECG prolonged PR interval, tall T waves, widened
QRS complex, prolonged QT interval & AV blocks
POTENTIAL NURSING DIAGNOSES
Decreased Output
Ineffective breathing pattern
COLLABORATIVE MANAGEMENT
Prevent Mg (early detection of high-risk patients)
Provide appropriate patient education.

Cont: COLLABORATIVE MANAGEMENT

Assess neuromuscular system for deficits
Monitor BP,RR, CR, dysrhthmias
Avoid administration of Mg to patient with RF
Careful monitoring of seriously ill patients
receiving Mg salts
Prompt D/C of oral & parenteral Mg salts
Hemodialysis of Mg ++ free dialysate
Loop diuretics and 0.45% NaCl (half-strength
saline) solution = enhance Mg excretion
Administer Ca gluconate to antagonize cardiac
effects of Mg in the cardiac muscle & temporarily
relieve s/s
Dietary restrictions : meat, nuts, legumes, fish,
vegetables, whole-grain serials

PHOSPHOROUS

Adults = 2.5 4.5 mg/dl or 0.8 1.5 mmol/L

6 mg/dl (1.94 mmol/L) Infants & children, d/t rate
of skeletal growth
85 % bones & teeth, 14% - soft tissue, < 1 % in the
ECF
Excitability of nerves & muscles, Ca balance, cell
energy
Critical component of the phosphate buffer system
to aid renal regulation of acids & bases
Necessary for the creation of energy (ATP)
Maintains cell membrane integrity by binding with
lipids to create the phospholipids cell membrane
layer
Critical for CHO, fats & protein metabolism

PHOSPHOROUS
Essential for the function of RBCs, MUSCLES &
CNS
Component of DNA & RNA (= important in cell
division and transmission of hereditary traits)
REGULATION
Filtered by the glomerulus, reabsorbed in the
proximal tubule along with Na+
When GFR , P reabsorption & vice versa
When PTH is present, tubular reabsorption is
inhibited, increasing P excretion
Ca helps to regulate P+, because P is found in
proportions inversely reciprocal to Ca++
SOURCES: most foods but especially in beef,
pork,
dried peas and beans

<1.2mEq/L<2.5mg/dl)

HYPOPHOSPHATEMIA

ETIO:
a. Inadequate intake or absorption
anorexia or malabsorption syndrome
GIT: vomiting
GUT: diuretic use
b. ICF shifts:
Hyperglycemia
Hyperalimentation
Respiratory alkalosis
UDM
DKA : urinary PO4 loss when glycogen, ketonuria
and polyuria are present.

c. Insufficient Phosphorous Intake

Malnutrition/Alcohol abuse
Starvation
Use of al hydroxide-based antacids
Use of magnesium-based antacids
d. Increased phosphorous Excretion
Hyperparathyroidism-K+, Mg r/t urinary
losses of P
Renal failure
Malignancy
Cushings syndrome =Glucocorticoid
production resulting to K+(w/ PO4)
Medications: loop diuretics

1. CNS SYMPTOMS OF ATP DEFICIENCY

Confusion, Seizures/coma d/t anoxia
Fatigue, Ataxia-loss of voluntary movements
2. CARDIOVASCULAR: Decreased contractility
Cardiomyopathy (reversible)
3. RESPIRATORY: Shallow Respirations d/t
muscle fatigue
4. Musculoskeletal Manifestations: Fatigue,
deep bone pain, muscle weakness / numbness /
paresthesia
5. HEMATOLOGIC SYMPTOMS
Bruising and bleeding from platelet dysfunction
Hemolytic anemia

LABORATORY TESTS
<2.5mg/Dl
Ca
X-rays show skeletal changes of osteomalacia or
rickets
ALK PO4 with osteoblastic activity
POTENTIAL NURSING DIAGNOSES
Ineffective breathing pattern
Fatigue
High risk for injury
Impaired mobility

COLLABORATIVE MANAGEMENT
Ensure early detection by identifying high-risk
patients
Assess for signs of Ca, which occurs in the
presence of P
dietary intake of P milk & milk products, organ
meats, nuts, poultry & fish, whole grains
Administer I.V. P slowly as ordered
EVALUATION
Normal P level
Free from injury
Normal breathing pattern

HYPERPHOSPHATEMIA

> 4.5 mg/Dl

ETIO
intestinal absorption of Ca d/t excessive vit D
intake.
Ingestion of excessive quantities of dairy products
P-containing medications (e. g. laxatives)
Renal failure most common where hypocalcemia
is present & dietary phosphorous is not excreted
Cellular destruction = release of P to serum
Ca, chemotherapy
Trauma, Rhabdomyolysis, BT
Hypoparathyroidism PTH levels Ca
concentration P
Osteoporosis removal of P from bone and enters
the serum.

CLINICAL MANIFESTATIONS (same w/ Ca)

Tetany tingling sensations in the fingertips &
around the mouth= P++ cause S.Ca++
Muscle spasm, pain, weakness
Anorexia, nausea, vomiting
Hypereflexia
Chevosteks/Trousseaus sign (+)
Soft tissue calcification = joinst, BV, cornea
DIAGNOSTIC FINDINGS
P > 4.5 mg/dL (> 1.5 mmol /L) adults
X-ray = skeletal changes with abnormal bone
development
PTH levels in hypoparathyroidism
BUN & Crea: assess renal function

POTENTIAL NURSING DIAGNOSES

Pain
Decreased cardiac output
Impaired mobility
High risk for injury
COLLABORATIVE MANAGEMENT
Identify high-risk patients (those with Ca++)
Administer phosphate-binding medications (al.
hydroxide)
Administer Ca supplements along with P- binders for a
patient with renal related hyperphosphatemia
Administer diuretics, vit D
Prepare for hemodialysis: remove excessive P
Instruct the patient to avoid foods & medications
containing P
Dietary restriction, OFI