MSN I: BT21 NOTES PRESENTS

MSN LEC 4.1: FLUID AND ELECTROLYTES CONT.

CALCIUM IN F&E BALANCE ● Controlled by PTH and Calcitonin

CALCIUM: ○ ↓ Ca level → PTH secreted by parathyroid glands → ↑ Ca
● Majority within bone matrix. absorption from GI tract and reabsorption from renal tubule →
● <1% ECF is absorbed in the GIT (+ acid, vit D, and PTH for Ca to be If Ca is still not enough, bone will release Ca → Resultant ↑
reabsorbed) serum Ca → suppresses PTH secretion
● Excreted in the feces (majority) and some in the urine ○ Excessive Ca → Calcitonin is secreted by thyroid gland →
● Controlled by PTH and calcitonin Inhibits Ca reabsorption from bone and ↓ serum Ca
○ Decreased Ca → PTH produce Ca concentration
○ Increased Ca → normal, suppressed the fxn of PTH
● Excessive Ca 1. HYPOCALCEMIA (<8.8 mg/dL)
○ Inhibit the reabsorption ○ occurs in a variety of clinical situations
● Serum Calcium exists in plasma in 3 forms:
1. Protein bound (40%), CAUSES:
2. Complexed to PO4 & other anions (10%; phosphate, citrate, ● Large transfusion with citrated blood
and carbonate) ○ may cause transient hypocalcemia since it can
3. Ionized (50%; can be measured directly and it determines combine with ionized Ca and temporarily remove it
clotting factors and neuromuscular fxn) from circulation.
■ If ionized Ca is <50% → Problem in clotting factors ○ (Also, promoting alkalosis and K is not abundant in
■ Protein bound medication blood)
● Should be given once a day (Protein bound ● Excess Ca loses, Inadequate intake of Ca (↓ GIT and bone
medications) absorption of Ca)
● Omeprazole ○ Draining fistula (leaking of fluid)
○ Ex. given 6:am → sumakit tiyan ng pt ● ↓ absorption in GIT
● Digoxin ○ With the influence of Vit D deficiency (↓ absorption of
○ Given 8am Ca)
● Now ang dami na ng concentration ng drug ○ ↓ PTH , increased Mg and Calcition
and leads to toxicity ● Severe burn
○ Ca is present in blisters for renovation
INSTRUMENTAL IN: ■ Blisters should not be remove because it
1. Transmission of nerve impulses serves for barrier for bacterial infection
2. Helps regulate muscle contraction/relaxation (esp. cardiac muscles) ○ Surgery (e.g. thyroidectomy and parathyroidectomy
3. Activates enzymes that stimulates chemical rxns (accidentally remove along with thyroid))
4. Blood coagulation NOTE: We do not need Ca supplements because as long as the body is
5. Bone and teeth function normal, our body will produce Ca
○ Pregnant woman without proper interval are prone to dental ● Pancreatitis
problems since developing fetus is taking the Ca deposit of the ○ causes breakdown of proteins and lipids and the fatty
mother) acids (Released by lipolysis) may combine with Ca
ions, leading to hypocalcemia.
CALCIUM BALANCE

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 MSN I: BT21 NOTES PRESENTS

MSN LEC 4.1: FLUID AND ELECTROLYTES CONT.

○ Also, it may be related to excessive secretion of

numbness and tingling, Chvostek sign and (+)
glucagon that ↑ Calcitonin secretion
Trousseau sign (tetany induced by neural
● Alkalosis
excitability), ↑ nerve irritability and convulsion or
○ BT (unionized)
seizure may follow, spasm (Carpopedal spasms),
○ Monitor infants since they may become alkalotic
parestesia, ↑ DTR, anxiety, delirium, hallucinations
NOTE:
CARDIOVASCULAR ↓ BP, dysrhythmia followed by cardiac arrest, HF;
● Older adults or those with disability have ↑ risk due to immobility, lack
Bronchospasm, impaired clotting time, ↓
of weight-bearing activity, and ↑ bone resorption
Prothrombin
● Pt with CKD or kidney diseases → they frequently have ↑ Phosphorus
→ causes reciprocal drop in Ca
RESPIRATORY Dyspnea and laryngospasm
S/Sx: LABS INDICATE & ECG ↓ Mg++; Prolonged QT due to prolongation of ST, T
● Bone wave inversion, Heart blocks, Ventricular
○ osteoporosis fibrillation
● GIT
○ increased n/v diarrhea
● Cardio (tingnan sa video) MANAGEMENT FOR HYPOCALCEMIA
● CNS ➔ Monitor breathing pattern
○ increase irritability communication pathways lead to seizure or ◆ Laryngeal stridor ( esp. post thyroid surgery)
convulsions ● Napapaos or robotic voice → pt is suffering from
● Muscle hypocalcemia
○ muscle spasm, tetany trousseau (paggalaw ng hands yung ◆ Talk to the pt every hr and assess breathing status since post
display na pusa na gumagalaw) and chvostek (spasm) sign thyroidectomy pt may experience removal of one or more
● Bleeding parathyroid.
◆ To know of affectation of parathyroid gland
MEDICATIONS: ➔ Give calcium gluconate and dilute with D5W (this is because sodium
Medications predisposing to hypocalcemia: chloride will promote calcium loss)
● Aluminum-containing antacids, aminoglycosides, caffeine, cisplatin, ◆ Cannot be given in hypercalcemia
corticosteroids, mithramycin, phosphates, isoniazid, loop diuretics, and ◆ 0.9 NaCl promotes loss of Ca
PPI ◆ D5W can be given to pt with diabetes with insulin
➔ SOLUTIONS CONTAINING PHOSPHATES OR BICARBONATE SHOULD
NOT BE USED WITH CALCIUM SINCE IT PRECIPITATE CA LOSSES
SYSTEMS SYSTEMS ➔ Advise client to consume Ca in diet
◆ 1,000 - 1,500 mg/day through supplements
GI ↑ Peristalsis; Hyperactive bowel sounds, dry brittle
◆ Seafoods, leafy greens and sea foods
hair (chronic)
➔ Administer Aluminum Oxide
◆ If pt have increase P, give that to excrete P in the urine
NEUROMUSCULAR Osteoporosis, fracture, weakness, coma, bone pain,
➔ Give Vit. D supplements

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 MSN I: BT21 NOTES PRESENTS

MSN LEC 4.1: FLUID AND ELECTROLYTES CONT.

➔ ○ Potentiate the effect of PTH in kidneys

➔ Give high Ca diet (1000-1500 mg/day) — broccoli, nuts, seafoods, green ● Reduce neuromuscular irritability
leafy vegs, carrots; Calcium supplements no higher than 500 mg in ● CNS
divided doses ○ Decreased DTR
➔ Aluminum-based antacid or Calcium-based to decrease the phosphorus ○ Lethargy and coma
level (but they cannot increase Ca); Additional meds to lower ● Cardiovascular
phosphorus are aluminum hydroxide, ○ Depressed activity of cardiac muscles
➔ Vit D to increase Ca absorption from GI tract or PTH supplement ○ Dysrhythmic episodes leading to cardiac muscle
● Muscles
NURSING CONSIDERATION ○ Fatigue, hypotonia, paralytic ileus (lumaki ang tiyan)
1. Administer Ca gluconate ● Bone
○ NOTE: Do not infuse any electrolytes (esp. K, Ca) without using ○ Pain and fracture due to osteoporosis
an infusion pump since it may lead to cardiac arrest. Hence, ● Kidney
infuse slowly to prevent CA and the pt must be hooked in a ○ Prone to develop stone formation → kidney damaged
cardiac monitor. ○ Increased urine output
2. Prevent suctioning (causes laryngospasm) ○ polyurea leading to dehydration
3. Increase dietary consumption of Ca ○ 1M unit of nephrons → nawawala due to kidney stones
4. Weight bearing exercises for pt ■ Pwede naman operahan through shockwaves
○ To promote release of calcium in the bloodstream → madudurog ang stones → can be excreted
5. Health teaching about osteoporosis in the urine
○ Weakened bone can lead to increased occurrence of bone
fracture
SYSTEMS HYPERCALCEMIA
6. Inform that alcohol and caffeine in ↑ doses inhibit Ca absorption and
moderate cigarette smoking ↑ urinary Ca excretion
Decrease GIT movements and
constipation; Ca stone formation,
2. HYPERCALCEMIA (<10 mg/dl):
GI & RENAL damaged kidneys, polyuris,
● very dangerous when severe due to the possibility of CA and it can
polydipsia, DHN, increased anorexia,
affect many organ systems
n/v, flank or abdominal pain
CAUSES:
Reduce neuromuscular irritability
● loss of calcium from the bone (coma patients due to prolonged
(suppressed activity into the
immobilization
myoneural junctions into the brain),
○ Do ROM to not lose of Ca deposit in bones
↓ DTR, lethargy leading to coma,
● excess Ca intake (e.g. milk and calcium based antacid daily) NEUROMUSCULAR
muscular weakness, deep bone pain,
● Ca based antacid
pathologic fractures, fatigue and
● pt with ↑ PTH
hypotonia
○ Increased Ca released from bones → dadaan sa GIT
and Genitorenal → increased din and reabsorption
● Thiazide diuretics use

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 MSN I: BT21 NOTES PRESENTS

MSN LEC 4.1: FLUID AND ELECTROLYTES CONT.

○ for pt with malignant type of hypercalcemia;

Depressed heart activity,
○ 25ug/kg with D5W 500cc TO RUN FOR 4-6 HRS
CARDIOVASCULAR dysrhythmia, cardiac arrest will
■ Get the pt weight
follow, HPN
4. IV Phosphate:
○ Causes reciprocal drop to Ca since they are inversely
shortened ST segment and QT
proportional.
interval, bradycardia, heart blocks;
○ This may cause severe calcification of kidneys, hpn, and Acute
ECG prolonged PR and QRS, Increased
Renal Failure (ARF)
QRS voltage, T wave flattening, AV
5. CALCITONIN
block
○ 4-8ug/kg IM/SQ q 6-12 H (↓s Ca by 1-3 mg/100 ml)
○ To ↓ bone resorption, ↑ Ca and Phosphorus deposition in bone,
and to ↑ urinary excretion of phosphorus and Ca
MANAGEMENT FOR HYPERCALCEMIA ○ This is useful for pt with heart diseases or AKI who cannot
➔ ↑ Fluid intake to dilute serum calcium and promote excretion tolerate large sodium loads
(3-4L/day). 6. Bisphosphonates:
◆ reduces risk of stone formation and relieves thirst. ○ inhibit osteoclast activity, resulting in reabsorption of Ca into
➔ Diet → Acid-ash fruit juices, contains Vit. C can acidify in urine the bone (e.g. Pamidronate disodium; Aredia, 0.9NaCl/ D5W +
◆ Specific for hypercalcemia only 60-90 mg x 24H).
◆ Stone formation can be caused by other like acids and such 7. INORGANIC PO4 Salts:
● If meron, should be analyze for the origin ○ oral or NGT (in the form of Neutra-phos, phospho-soda), rectal
● If confirmed that stones in formed by hypercalcemia (as fleet enema – rectal administration), and IV. This is to
then this diet can be prescribed eliminate excess Ca thru defecation but used with extreme
➔ Protect from injury by having safety precautions (esp. confused caution since it can lead to severe calcification.
patients) 8. Corticosteroids:
◆ Hypercalcemia can cause confusions ○ use to ↓ bone turnover and tubular reabsorption for pt with
➔ Mobilizing the pt and frequent ambulation for outpatients sarcoidosis, myelomas, lymphomas, and leukemias
➔ Fluids containing Na should be given unless contraindicated since Na
assists with Ca excretion HYPERCALCEMIC CRISIS
➔ Serum Ca >16mg/dL
PHARMACOLOGY ➔ Severe thirst, polyuria, DHN leading to Cardiac Arrest
1. IVF containing Na:
○ IV containing 0.9% NaCl sol. temporarily dilutes the serum Ca
ECG CHANGES
level and ↑ urinary Ca excretion by inhibiting tubular
reabsorption of Ca
HYPERCALCEMIA ● Shortened QT
2. Diuretics (Furosemide, loop type):
● Prolonged PR, QRS
○ often used in conjunction with saline sol. to also ↑ Ca excretion
● Increased QRS voltage
3. Mithramycin (Mithracin):
● T wave flattening
○ lower cytotoxic antibiotic, which inhibits bone resorption of Ca
● AV block
and thus ↓ Ca levels

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 MSN I: BT21 NOTES PRESENTS

MSN LEC 4.1: FLUID AND ELECTROLYTES CONT.

HYPOCALCEMIA ● Prolonged QT
● SODIUM BALANCE
● T wave inversion
○ Mg is similar to Ca in two aspects:
● Heart blocks
■ Ionized fraction of Mg is primarily involved in NM
● Ventricular fibrillation
activity and other physiologic processes
■ Mg levels should be evaluated in combination with
Albumin levels (30% of Mg is protein bound; a
decreased serum albumin lvl can reduce total Mg
CORRECTION MEDICATION
concentration but it does not reduces ionized plasma
Mg concentration)
Calcium gluconate 10%= 100 mg/ml
PARENTERAL (9 mg elemental) & Calcium Chloride
1. HYPOMAGNESEMIA:
10% (27mg elemental)
● below-normal Mg concentration and frequently associated with
hypokalemia and hypocalcemia
Calcium Carbonate (Tums) 40%
ORAL elemental Ca carbonate→ ALSO
CAUSES:
USED FOR HYPERACIDITY
● Alcohol
● malabsorptive disorders
○ Prolonged TPN can repel Mg
MAGNESIUM IN F&E BALANCE ● GI loss
MAGNESIUM: ○ Fistula, IBD, colon receptions(?)
● Acts as an activator in many intracellular enzyme systems (abundant ● Hyperparathyroidism and polyuria
intracellular cation). ○ Excessive excretion of Mg in the body
● 1/3 is bound to protein (e.g. albumin), the remaining 2/3 exist as free
cations (the active component, Mg++). ASSESSMENT (S/SX):
○ CHO and CHON Metabolism ● Neuromuscular irritability/excitability
○ Important in fxn of Na/K pump → low Mg have effects on ● CNS
intracellular influxes of K and myocardial ions fluxes ○ Tremors
○ Acts together with K+ ○ Ataxia
○ Mg balance is important in neuromuscular function ○ Convulsion
■ Acts directly on Myoneural junction → variations in ● Mental Changes
Mg levels affect neuromuscular irritability and ○ Agitation
contractility ○ Depression
■ ↑ Mg → diminished excitability of muscle cells ○ Insomnia
■ ↓ Mg → increased NM irritability and contractility ● Cardio
○ Inhibits the release of AcH (acetylcholine) → thus, Mg ○ Increased HR
produces sedative effect on neuromuscular junction ○ Tachycardia
○ Mg also affects CV system → producing peripheral vasodilator ○ Dysrhythmic episodes
→ ↓ peripheral vascular resistance → hpn ● Muscles

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 MSN I: BT21 NOTES PRESENTS

MSN LEC 4.1: FLUID AND ELECTROLYTES CONT.

○ spacity ● Renal problem

○ (+) Trousseau sign and Chvostek sign (due to accompanying ● excessive IV Mg administration
hypocalcemia) ● Addison's Disease
○ Tetany ● Antacid Mg
○ Only given at a specific condition
NOTE: SYMPTOMS DO NOT USUALLY OCCUR UNTIL MG LEVEL HAS DROPPED
TO <1.8 MEQ/L
a. Conditions → adrenocortical insufficiency, Addison disease, or
ECG: hypothermia
● PVCs, flat or inverted T waves, depressed ST segment, prolonged PR b. Medications → excessive use of Mg-based antacids or laxatives
interval, and widened QRS; predisposing to arrhythmias and medications that decrease GI motility (opioids and
anticholinergic); Lithium intoxication
MANAGEMENT FOR HYPOMAGNESEMIA
● Mild Mg deficiency can be corrected by diet alone (Sources of Mg → ASSESSMENTS (S/SX):
green leafy vegetables, beans, lentils, white potatoes, wheat bran, ●
roasted almonds, milk, banana, oranges and peanut butter) ● Hpn
● Mg Supplement → IV/Oral; Mg salts can be given orally in an oxide or ● n/v
gluconate form to replace continuous losses but can produce diarrhea ● Facial flushing
● Monitoring urine output is essential before, during, and after Mg ● Warm sensations of the pt
administration as this is how Mg++ is excreted. ● Decreased DTR
○ Notifying the physician is urine vol. decreases to less than 100 ○ Muscle weakness, paralysis, lethargic, dysarthria, false
mL over 4 hrs stroke
● Pt receiving parenteral nutrition require Mg in the IV sol. to prevent ● Decreased RR → dysrhythmic episodes → cardiac arrest
hypomagnesemia
● Monitor pt receiving digitalis since a deficit in Mg predisposes them to ECG:
digitalis toxicity. ● tachycardia → bradycardia, prolonged PR interval and widened
○ Pt receiving digoxin are likely to be receiving diuretic therapy QRS, peaked T waves, prolonged QT intervals, and AV block
(predisposing them to renal loss of Mg)
● Safety precautions for seizures; Promotion of safety — Protect from MANAGEMENT FOR HYPERMAGNESEMIA
injury and WOF digitalis toxicity ● Discontinue all IV the contains Mg salts
● Monitor for laryngeal stridor → laryngospasm ○ Increased Mg level in the body
○ Intubation set readily available at the bedside ● Put pt in the ventilator
○ Ambu Bag should be available at the bedside
2. HYPERMAGNESEMIA ● Administer Ca glucunate to protect the heat and repel too much Mg
● a rare electrolyte abnormality since the kidneys efficiently excrete Mg. ● Administer 0.45 Nacl + loop diuretics (Furosemide)
● Serum Mg level can appear falsely elevated if blood specimens are ● Hemodialysis with a Mg-free dialysate (for severe hypermagnesemia or
allowed to hemolyze. pt with kidney injury)

CAUSES

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 MSN I: BT21 NOTES PRESENTS

MSN LEC 4.1: FLUID AND ELECTROLYTES CONT.

SYSTEMS DECREASED INCREASED CORRECTION

GI Dysphagia (difficulty in ORAL ● Protein-magnesium Tablets

swallowing) (133 mg elemental)
● DOSE: 6-15 mg elemental
NEUROMUSCULAR Apathy, depressed decreased DTR, muscle mg/kg/24h QID
mood, apprehension, weakness, chesng in
extreme agitation, LOC, Coma PARENTERAL ● MgSO4 50% (48mg
ataxia, dizziness, elemental)
insomnia, and ● 25-50 mg/kg/dose QID prn
confusion; delirium, ● hpn, respiratory depression
hallucinations possible

CARDIOVASCULAR hpn and shallow ANTIDOTE: Calcium gluconate

respirations,
arrhythmias,
PHOSPHORUS IN F&E BALANCE
bradycardia, heart
PHOSPHORUS:
block, platelet
● critical constituent of all body tissues (primary intracellular anion)
clumping, delayed
● 85% bones/ teeth, 14% soft tissues, 1% ICF (Higher in children)
thrombin formation; AV
● Responsible for maintaining energy production in the form of glycolysis
herat block, and CA
or high energy phosphate products such as ATP
(greatly elevated and
● Essential to the fxn of RBC’s and muscles, critical to nerve and muscle
untreated)
fx., and provides structural support to bones and teeth
○ Formation of ATP and 2,3-diphosphoglycerate, which facilitates
the release of O2 from hgb
ECG CHANGES
● Higher P requirement in children and decrease in age
● Controlled by renal excretion
HYPERMAGNESEMIA ● Increased PR interval
● Maintenance of acid-base balance, as well as NS and the intermediary
● Widened QRS
metabolism of CHO, CHON, and fat
● Elevated T waves
● Major component of the cell structure, phospholipids, nucleotides, and
HYPOMAGNESEMIA ● Prolonged QT, PR nucleic acids
● ST depression
● Flattening/inversion of P PHOSPHORUS BALANCE
waves ● Controlled by renal excretion
● Torsades de pointes ● It requires active transport mechanisms to maintain its presence inside
● Arrhythmias cells
● Most IC PO4 is bound to proteins and lipids

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 MSN I: BT21 NOTES PRESENTS

MSN LEC 4.1: FLUID AND ELECTROLYTES CONT.

● PO4 homeostasis is maintained thru absorption and secretion in the GI MANAGEMENT FOR HYPOPHOSPHATEMIA
tract, filtration, and absorption in kidneys and shifts into and out of ● Increase consumption in diet
bone ○ Or IV 1mg P
● PTH and it D assist in PO4 homeostasis by varying PO4 reabsorption in ● Oral phosphate supplements are usually adequate for mild
the kidneys hypophosphatemia. Sources of phosphorus → dairy foods, meats,
○ PTH allows shift of PO4 from bone to plasma beans, organ meats, nuts, fish, poultry, and whole grains
● Glucose and insulin administration can decrease in the serum
1. HYPOPHOSPHATEMIA: phosphorus level
○ this may occur under a variety of circumstances in which ○ PREVENTIVE MEASURES: gradually introducing the solution to
total-body phosphorus stores are normal; Rarely ocurs due to avoid rapid shifts
inadequate intake ● Vit D may also be necessary to increase absorption of PO4 and Ca
Moderate hypophosphatemia → supplements such as Neutra-phos
CAUSES: capsules, K-phos, and fleet Phospho-soda may be prescribed
● Prolong malnutrition lead to hypophosphatemia ● Aggressive IV phosphorus correction only limited to serum levels
● Administration of calories through TPN can lead to <1md/dl. Possible effects → tetany from hypocalcemia and calcification
hypophosphatemia in tissues from hyperphosphatemia
● Prolonged in ventilation ● IV preparations of phosphorus → Na or K+ Phosphate (must not exceed
○ Too much O2 in the body → body become alkalotic → to 3 mmol/h); The site must be also checked because of tissue
body repels P sloughing and necrosis
○ Pt will lead into alkalosis ● Serum Ca and PO4 blood levels must be monitored q 4hrs
● Burns → bagsak ang P → increased renal excretion
● Prolonged diuretics Hyperlipoproteinemia
● Hyperparathyroidism
● Pt drinking antacid → repels P → because it binds to P Causes:
● Decreased Vit. D → osteomalacia (brittleness of the bone) → ● Renal failure
excretion of P in the urine → losses both deposit of P ● Chemotherapy
● Decreased PTH
ASSESSMENT (S/SX): ● Coca-cola colored skin
● Deficient ATP production → leads to acidosis ○ Kulay kahoy
○ Impairment of cellular resources ○ P is deposited in the skin
● Paresthesias, muscle weakness, bone pain and tenderness
● Pt can die due to respiratory failure S/sx:
● Cardiomyopathy → chest pain due to tissue hypoxia ● Related to hypocalcemia
○ Due to decrease ATP, heart will double pump to
compensate Management:
● Increased susceptibility to infection ● Directed to the underlying disorder
○ Ipasama ang check for P if pt have infections kapag ○ If may RF or decreased GIT absorption
may order for laboratory ● Vit. D should be supported by other measures
● Ca binding antacid to decrease P

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 MSN I: BT21 NOTES PRESENTS

MSN LEC 4.1: FLUID AND ELECTROLYTES CONT.

● Phosphate binding antacid (aluminum based)

● Decreased P in the diet
● Dialysis

PHOSPHORUS ABNORMALITIES

HYPOPHOSPHATEMIA HYPERPHOSPHATEMIA

● Impaired renal function ● Decreased intake

● Hypoparathyroidisms or (malnutrition)
hyperthyroidism ● Symptoms are usually
● Cell destruction related to a decrease in high
● Most are asymptomatic energy phosphates and
○ Metastatic soft manifested ast cardiac
tissue calcium dysfunction or muscle
phosphorus weakness
complexes