NCM 112: FLUID AND ELECTROLYTES FINALS NOTES

ELECTROLYTES o SODIUM helps regulate acid-base

- Are substances that, when in a solution, balance – by combining with
separates into ELECTRICALLY CHARGED CHLORIDE and BICARBONATE.
particles called IONS (emits electrical (ACIDOSIS combines with
charges) CHLORIDE which makes it SODIUM
- Positively Charged (+) ions CATIONS CHLORIDE NaCl to lessen the
- Negatively Charged (-) ions ANIONS effects of offending acid.
- Very vital for the functions of the cells (ex. ALKALOTIC combines with
Cellular reactions or actions) BICARBONATE to lessen the toxic
- Important Rules: Conducting nerve effect of base.
pulses, contracting muscles, keeping body - NORMAL SERUM Na Level: 135 to 145
hydrated, and Regulating body pH level. mEq/L
- ANION (-) - INSIDE THE CELL: 10 mEq/L
o Bicarbonate, Chloride, and - POSSIBLE DIETARY SOURCES OF SODIUM
Phosphate (anything that is salty)
- CATIONS (+) o Canned foods
o Calcium, Magnesium, Potassium, o Cheese
Sodium o Ketchup
- Several pairs of oppositely charged ions are o Processed meat
crossly linked together (ex. Sodium o Salt
Chloride – if there’s a problem on a o Salty snack foods
particular electrolyte, the other o Sea foods
electrolytes will also be affected. If there’s - DAILY REQUIREMENT FOR SODIUM
a decreased in sodium, it affects the INTAKE: 0.5 to 2.7 grams/day. The more
amount of chloride in our body. sodium we take, the more the kidneys will
escalate. Sodium is absorbed in intestines
ELECTROLYTE IMBALANCES and excreted in kidneys. Can be also in
- Electrolytes are loss from sweating, stools, GI tract and sweat.
diarrhea etc. REGULATION OF SODIUM AND WATER
1. SODIUM IMBALANCE Serum NA Level DECREASES Serum NA Level INCREASES

- Hyponatremia (low serum sodium level) VS Serum OSMOLALITY FALLS Serum OSMOLALITY RISES
Hypernatremia (high serum sodium level)
- SODIUM accounts for 90% of ECF CATIONS Thirst Diminishes Thirst INCREASES

evidenced by normal serum sodium level ADH release is SUPPRESSED ADH release INCREASES
135-145 mEq/L and MOST ABUNDANT
solute in the ECF. Renal water excretion Renal water excretion
INCREASE DIMINISHES
- FUNCTIONS (sodium attracts water)
o SODIUM helps maintain proper ECF Serum Osmolality Normalizes Serum Osmolality Normalizes
concentration. (Helps preserve ECF
volume / osmolality and fluid
distribution in our body)
o SODIUM helps transmit impulses –
nerves and muscles fibers
QUINDIPAN, Hannah A. 1
BSN 3C
UNP-CN
 NCM 112: FLUID AND ELECTROLYTES FINALS NOTES
HYPONATREMIA
- Sodium DEFICIENCY in relation to body
water
- Serum NA Leve: Less than 135 mEq/L
- Serum sodium level decreases, the serum
osmolality decreases. Fluid will then shift
from extracellular compartment (ECF) to
intracellular compartment (ICF) cause our
blood is less concentrated. There will be
loss of water in intravascular compartment
causing Hypovolemia. Shifting of ECF and
ICF in central nervous system causing
Cerebral Edema (there will be changes in
level of consciousness of the client).
SERUM NA LEVEL DECREASES
FLUID SHIFT OCCUR FROM ECF TO ICF
HYPOVOLEMIA CEREBRAL EDEMA
CLASSIFICATIONS / CAUSES OF HYPONATREMIA
I. DEPLETIONAL HYPONATREMIA
o Depleted sodium in our blood.
Increase in blood volume decreases
in sodium level.
o Hypovolemic Hyponatremia
II. DILUTIONAL HYPONATREMIA
o Dilution of blood
o Hypervolemic Hyponatremia
o Euvolemic / Isovolemic
Hyponatremia
DEPLETIONAL HYPONATREMIA
HYPOVOLEMIC HYPONATREMIA
- DECREASE in the total body WATER with
disproportionately GREATER DECREASE in
total serum SODIUM.
- Presence of clinically evident VOLUME
DEPLETION.
QUINDIPAN, Hannah A.
BSN 3C
UNP-CN
CAUSES OF HYPOVOLEMIC HYPONATREMIA
- Nonrenal: Vomiting (depletion and less
absorption of sodium), Diarrhea, Excessive
sweating, Fistula (opening between two
organs ex. Fistula between large and small
intestine there will be less absorption of
sodium in small intestine.)
- Renal: Diuretic use (thiazide – increases
urine output as well as with different
electrolytes like the sodium), adrenal
insufficiency (hypoactive adrenal gland,
there will be an increase in Aldosterone
secretion. Aldosterone is responsible for
water and sodium retention.)
DILUTIONAL HYPONATREMIA
HYPERVOLEMIC HYPONATREMIA
- INCREASES in total body WATER with a
relatively SMALLER INCREASE in total
serum SODIUM.
- Presence of clinically evident EDEMA
(there will be shifting of fluids from the
Intravascular spaces going into the
Interstitial as well as into the intracellular
compartment)
- Heart Failure (POSSIBLE CAUSES)
o There will be a decreased in cardiac
output which can lead to decrease
of blood supply into the kidneys.
o Decrease in Glomerular filtration
rate
o Decrease in Urine output
o Water Retention
EUVOLEMIC / ISOVOLEMIC HYPONATREMIA
- MILD to MODERATE INCREASE in total
body WATER with NORMAL or NEAR
NORMAL SODIUM levels
- ABSENCE of clinically evident EDEMA
- Renal Failure / SIADH
o Decreased urine output
2
 NCM 112: FLUID AND ELECTROLYTES FINALS NOTES
HYPERNATREMIA
SERUM NA LEVEL INCREASES
- EXCESS of Na RELATIVE to body water
- Serum Na Level: >145mEq/L
FLUID SHIFT OCCUR FROM ICF TO ECF CAUSES OF HYPERNATREMIA
- EXCESSIVE sodium intake
o table salts, foods, medications,
Cellular DEHYDRATION near drowning, Cushing’s
HYPOVOLEMIA syndrome, hyperaldosteronism.
SIGNS AND SYMPTOMS OF HYPONATREMIA - WATER DEFICIT
The signs and symptoms of Hyponatremia is o Insensible water losses, extensive
primarily NEUROLOGIC. burns, severe water diarrhea,
- Headache Hyperosmolar Hyperglycemic
- Nausea Nonketotic Syndrome (HHNK),
- Abdominal cramps Diabetes Insipidus.
- Muscle twitching (involuntary movement SIGNS AND SYMPTOMS OF HYPERNATREMIA
of muscles) - NEUROLOGIC SIGNS
- Tremors o Restlessness
- Weakness o Agitation
LABORATORY FINDING OF HYPONATREMIA o Weakness
- Serum osmolality – DECREASED o Lethargy
- Serum Na level – DECREASED o Confusion
- Urine specific gravity – DECREASED o Stupor
TREATMENT OF HYPONATREMIA o Seizure
- Restrict fluid intake o Coma
- High Na diet - NEUROMUSCULAR IRRITABILITY
- IVF – NSS (if w/ hypovolemia) o Twitching
NURSING INTERVENTIONS OF HYPONATREMIA o Hyperreflexia
- MONITOR and record VS o Ataxia
- MONITOR NEUROLOGIC STATUS o Tremors
frequently - OTHER S/SX
- Accurately MEASURE and record Intake o Low grade fever, flushed skin,
and Output extreme thirst
- WEIGH patient daily o Hypervolemia increase BP,
- ASSESS skin turgor bounding pulse, dyspnea.
- Watch for EXTREME CHANGE in Lab results o Hypervolemia dry mucous
- RESTRICT FLUID as ordered membrane, oliguria, orthostatic
- INCRESE intake of DIETARY Na(sodium) hypotension.
- ADMINISTER Na (sodium) supplements as
ordered
- ADMINISTER IV as ordered
- Provide SAFE environment

QUINDIPAN, Hannah A. 3
BSN 3C
UNP-CN
 NCM 112: FLUID AND ELECTROLYTES FINALS NOTES
FUNCTION OF POTASSIUM
SIGNS AND SYMPTOMS OF HYPERNATREMIA - MAINTAIN cells electrical neutrality and
osmolality.
- Aids in neuromuscular transmission of
nerve impulses
- Assists in skeletal and cardiac muscle
contraction and electrical conductivity
- Affects acid-base balance
( ACIDOSIS HYPERKALEMIA)

POTASSIUM DIETARY SOURCES

- Chocolates
- Dried (fruits, nuts, seeds)
- Fruit (oranges, bananas)
- Meats
- Vegetables (potassium, mushrooms,
tomatoes, carrots)
BALANCING POTASSIUM (K)
LABORATORY RESULTS (HYPERNATREMIA)
- 80% of K intake is EXCRETED in the URINE,
- Serum Osmolality INCREASES
the rest is EXCRETED in FECES and SWEAT.
- Serum Na Level INCREASES
- Anabolism
- Urine Specific Gravity INCREASES
o Potassium (K) moves from ECF to
TREATMENT OF HYPERNATREMIA
ICF
- INCREASE oral fluid intake. Gradually
- Sodium Potassium Pump
- IVF salt free (D5W), followed by HALF NSS
o Moves sodium (Na) from the cell
- Diet RESTRICT Na
into the ECF and pumps K into the
- Diuretics INCREASE Na loss (Loop Diuretics
cell
-Lasix)
- Sodium (Na) and Potassium (K)
NURSING INTERVENTIONS (HYPERNATREMIA)
o Have a reciprocal relationship
- MONITOR and record VS
- pH
- INSERT IVF as needed
o Hydrogen ions and K ions freely
- MEASURE and record INTAKE and OUTPUT
exchange across plasma cells.
- Assess SKIN and MUCOUS MEMBRANE
2. POTASSIUM IMBALANCES
- Assess ORAL HYGIENE
HYPOKALEMIA
- DECREASE serum potassium level
POTASSIUM (K)
- Potassium DEFICIENCY in
- Major CATION in the ICF (intracellular
- relation to body water
fluid) - Serum potassium level of <3.5mEq/L
- 98% is in ICF
CAUSES OF HYPOKALEMIA
- 2% is in ECF
- Too much output
- Serum K Level: 3.5 – 5mEq/L - Diuretics
- Corticosteroids
- Insulin
QUINDIPAN, Hannah A. 4
BSN 3C
UNP-CN
 NCM 112: FLUID AND ELECTROLYTES FINALS NOTES
- Alkalosis o If client is on digoxin therapy, teach
- Malabsorption syndrome patient to recognize and report
S/Sx of digoxin toxicity
SIGNS AND SYMPTOMS OF HYPOKALEMIA
o Make sure the client can identify
- NEUROMUSCULAR
the signs and symptoms of
o Skeletal muscle weakness
hypokalemia
- GIT
o Constipation, Paralytic ileus HYPERKALEMIA
- CHANGES IN ECG (can cause - Potassium EXCESS in relation to body
water
ARRYTHMIAS)
- Serum potassium level of >5mEq/L
o Flattened T wave, Depressed ST - INCREASE serum potassium level
segment, characteristic U wave. CAUSES OF HYPERKALEMIA
LABORATORY FINDING OF HYPOKALEMIA - Little output
- ECG: - Beta-blockers
o Flattened T wave
- K-sparing diuretics
o Depressed ST segment
o Characteristic U wave - Chemotherapy
- Serum K level decreased - Severe infection
- ABG result elevated pH and HCO3 - Trauma/Crush injury
Elevated serum glucose - Acidosis
TREATMENT OF HYPOKALEMIA - Insulin deficiency
- High K diet - Blood transfusion
- Oral K supplements
- IV K replacement therapy
NURSING INTERVENTIONS (HYPOKALEMIA) SIGNS AND SYMPTOMS OF HYPERKALEMIA
- Monitor VS - NEUROMUSCULAR
o especially pulse and BP – weak, o Skeletal muscle weakness
irregular ; orthostatic hypotension - GIT
o HR – tachyarrhythmias
o Nausea, Diarrhea, Abdominal
o RR – WOF shallow and rapid
cramping
respiration
- Monitor serum K levels - CHANGES IN ECG (can cause
- Monitor I and O ARRYTHMIAS)
- Check for signs of alkalosis o Tall, tented T wave
o Irritability and paresthesia LABORATORY FINDINGS OF HYPERKALEMIA
- ECG:
- Insert and maintain an IV access as
o Tall, Tented T wave
ordered - Serum K level INCREASED
- Provide safe environment - ABG result DECREASED pH
- Check for signs of constipation TREATMENT OF HYPERKALEMIA
- Health teachings: - Restrict K in the diet
o Importance of taking K - Loop diuretics
supplements as prescribed - Discontinue medications associated with
high K levels
- Hemodialysis
QUINDIPAN, Hannah A. 5
BSN 3C
UNP-CN
 NCM 112: FLUID AND ELECTROLYTES FINALS NOTES
- Drugs 3.MAGNESIUM IMBALANCES
o Sodium polystyrene sulfonate MAGNESIUM
- Emergency cases (>6mEq/L) - is the 2nd most abundant cation in the ICF
o Closely monitor cardiac status (ECF – 1%, ICF – holds the rest).
o Administer 10% Calcium Gluconate - Bones – contain 60% of the body’s
o Acidosis – administer sodium magnesium
bicarbonate - Normal Serum Magnesium Level 1.6 to 2.6
mEq/L
o Administer 10 units regular insulin
- Inside the cells – about 40mEq
IV FUNCTIONS OF MAGNESIUM
o Kayexalate - Promotes enzyme reactions within the cell
NURSING INTERVENTIONS FOR HYPERKALEMIA during carbohydrates metabolism
- Assess VS - Helps the body produce and use ATP
- Monitor I and O - Takes part in protein synthesis
- Prepare patient for dialysis – acute - Influences vasodilation, helping the CV
hyperkalemia system function normally
- Implement safety measures - Helps sodium and potassium ion cross the
- Health Teachings: cell membranes
o Select foods that don’t stimulate - Magnesium also regulates muscle
peristalsis contraction
o Explain S/Sx of hyperkalemia - Magnesium influences calcium level
MAGNESIUM DIETARY SOURCES
Causes Hypokalemia Hyperkalemia
Intake Inadequate K Too much - Chocolate
- Dry beans and peas
intake intake
- Green, leafy vegetables
Output Too much Little output - Meats
output - Nuts
Drugs Diuretics, Beta Blockers, - Seafoods
Corticosteroids, K-sparing - Whole grains
insulin etc. diuretics, BALANCING MAGNESIUM (Mg)
chemotherapy - GIT - If the serum Mg level drops – GIT
absorb Mg and V.V.
Diseases Alkalosis, Sever
- Kidneys
Malabsorption infection,
Syndrome trauma/crush o Balance Mg by altering
injury, reabsorption at the
acidosis, proximal tubule and loop
insulin
of Henle
deficiency
o If serum Mg level rises –
Others Blood
transfusion the kidneys excrete
excess in the urine

QUINDIPAN, Hannah A. 6
BSN 3C
UNP-CN
 NCM 112: FLUID AND ELECTROLYTES FINALS NOTES
HYPOMAGNESEMIA - Hypocalcemia (because of the effects of
-Magnesium DEFICIENCY in relation to body water Mg to PTH)
-Serum magnesium level of <1.6mEq/L
- Decreased serum Mg

CAUSES OF HYPOMAGNESEMIA TREATMENT OF HYPOMAGNESEMIA

- Poor dietary intake of Mg
- Dietary
- Absorption problems - Magnesium Supplements
- GI Problems, Urinary Problems - Magnesium Sulfate – IV or IM
SIGNS AND SYMPTOMS OF HYPOMAGNESEMIA
- A low serum Mg level irritates the CNS NURSING INTERVENTION (HYPOMAGNESEMIA)
leading to: - Assess for mental status and report
o Altered LOC changes
o Hallucinations - Evaluate the patient’s neuromuscular
o Ataxia status regularly
o Insomnia - Check for dysphagia before food is
o Confusion given
o Psychosis - Monitor and record VS
o Delusions - Monitor respiratory status
o Seizures - If patient is receiving digoxin,
o Depression monitor for signs of digoxin
o Vertigo toxicity
- Skeletal muscle weakness - Institute seizure precautions
o Tremors - Keep emergency equipment nearby for
o Twitching airway protection
o Tetany
HYPERMAGNESEMIA
o Hyperactive DTR
- Magnesium EXCESS in relation to
o Foot or leg cramps
body water
o Paresthesia
- Serum magnesium level of >2.6mEq/L
- Breathing difficulties – laryngeal
CAUSES OF HYPERMAGNESEMIA
stridor
- Excessive Mg intake,
- Hypocalcemia
- Renal Dysfunction
- Tachycardia
SIGNS AND SYMPTOMS OF HYPERMAGNESEMIA
- Arrhythmias
- High serum Mg level depresses the
- Hypertension
neuromuscular system
- Anorexia
o Decreased muscle and nerve
- Dysphagia
activity – hypoactive DTR
- Nausea and vomiting
o Generalized weakness – starts
- Digoxin Toxicity
with weak hand grasp
- Yellow-tinged vision
(progresses to flaccid
paralysis)
LABORATORY FINDINGS OF HYPOMAGNESEMIA
o Occasional Nausea and
- ECG: vomiting - Decreased LOC –
o Prolonged PR interval drowsy – coma
o Widened QRS complex - Respiration
o Prolonged QT interval o slow, shallow, depressed
o Depressed ST segment - Weak pulse, bradycardia, arrhythmias
o Broad, flattened T wave U wave o decreased cardiac output and
QUINDIPAN, Hannah A. 7
BSN 3C
UNP-CN
 NCM 112: FLUID AND ELECTROLYTES FINALS NOTES
cardiac arrest
- Hypotension DIETARY SOURCES OF CALCIUM
o patient feel flushed and warm - Bonemeal
all over - Dairy products
LABORATORY FINDINGS OF o Milk, cheese, yogurt
HYPERMAGNESEMIA - Green leafy vegetables
- Prolonged PR interval - Legumes
- Widened QRS complex - Nuts
- Tall T wave - Whole Grains
- Increased serum Mg BALANCING CALCIUM
TREATMENT OF HYPERMAGNESEMIA - Parathyroid Hormone
- Increase fluid intake – oral or IV o Low serum Ca level –
parathyroid gland release PTH
- Loop diuretic
(which draws Ca from bones
- Ca Gluconate and promotes transfer of Ca
- Hemodialysis into the plasma) – increase Ca
o Mg-free dialysate level
NURSING INTERVENTIONS o PTH also promotes kidney
- Monitor VS reabsorption of Ca and
- Assess Neuromuscular system stimulates the intestinal
- Restrict dietary Mg intake & avoid absorption of Ca (Phosphorus
giving medications with Mg is excreted at the same time)
- Provide adequate fluids – oral / IV o Hypercalcemia – body
suppresses the release of PTH
- Calcitonin
4.CALCIUM IMBALANCES o a hormone produced in the thyroid
gland and acts as an antagonist to
CALCIUM (Ca) PTH
o Hypercalcemia – thyroid gland
- is a positively charged ion found in both the releases Calcitonin (inhibits bone
ECF and ICF resorption) – causes a decrease in
- 99% of the body’s Ca – found in the bones the serum Ca level
and teeth o Calcitonin – also decreases
absorption of Ca and enhances its
- 1% - serum and soft tissue excretion by the kidneys
FUNCTIONS OF CALCIUM - Vit. D
o is ingested with foods (dairy
-Responsible for the formation and products)
structure of bones and teeth o skin is exposed to UV light, it
- It helps maintain cell structure and synthesizes Vit. D
function o Active form of Vit. D promotes Ca
- Plays a role in cell membrane permeability absorption through intestines, Ca
resorption from the bones, which
and impulse transmission Affects raises serum Ca level
contraction of muscles (cardiac, smooth - Phosphorus
and skeletal muscle) o inhibits Ca absorption in the
- Participates in blood clotting process intestines (opposite effect of Vit D)
2 WAYS OF MEASURING CALCIUM o An inverse relationship between Ca
and P exists in the body
- Serum Ca Level (8.9 to 10.1 mg/dL) - Serum pH
- Ionized (free) Ca (4.5 to 5.1 mg/dL) o also has an inverse relationship
with ionized Ca level
o Increase pH (alkalosis) – more
Calcium binds with protein and
QUINDIPAN, Hannah A. 8
BSN 3C
UNP-CN
 NCM 112: FLUID AND ELECTROLYTES FINALS NOTES
ionized Ca level drops response to tapping over the
(hypocalcemia)
o pH drops (acidosis) – less calcium facial nerve
binds to CHON and the ionized Ca
increases - Fractures, brittle nails, dry skin and hair
HYPOCALCEMIA - Diarrhea
- Calcium DEFICIENCY in relation to body - DTR
water o hyperactive
- Below 8.9mg/dL (Total Ca) - Diminished response to Digoxin –
- Below 4.5mg/dL (Ionized Ca) digoxin toxicity
CAUSES OF HYPOCALCEMIA
- Inadequate intake of Ca LABORATORY FINDINGS OF HYPOCALCEMIA
- Malabsorption - ECG:
- Severe diarrhea o Prolonged ST segment
- Laxative abuse o Lengthened QT interval
- Lack of Vitamin D in the diet o Arrhythmias - Torsade’s De
- Renal failure - Pointes Serum Ca level
- Anticonvulsants (Phenobarbital and o DECREASED
Phenytoin ( dilantin) - Ionized Ca level
- High Phosphorous level o DECREASED
- Excessive Ca loss TREATMENT OF HYPOCALCEMIA
- Diuretics – loop (lasix) - Acute Hypocalcemia
- Edetate Disodium o IV Ca Gluconate
- (Disodium Edta) - Chronic Hypocalcemia
- Hypomagnesemia o Vit D supplements
- Drugs – cisplatin & gentamycin o Oral Ca Supplements
- Hyperphosphatemia o Increase dietary intake or Ca -
- Alkalosis Aluminum Hydroxide – in cases
- BT where the patient also has a high
SIGNS AND SYMPTOMS HYPOCALCEMIA Phosphorus level
- Neurologic Symptoms
o Anxiety, confusion, irritability NURSING INTERVENTIONS HYPOCALCEMIA
and seizure - Monitor VS
- Paresthesia o RR (WOF dyspnea, stridor)
o Toes, finger, face (especially - Keep tracheostomy tray, resuscitation bag
around the mouth – at bedside
circumoral) - Place on cardiac monitor
- Twitching, Muscle cramps, Tremors o notify physician if develops
o Laryngeal and abdominal
arrhythmias
muscles are prone to spasm.
- Tetany - Check for signs of Tetany
o Secondary to nerve excitability o Chvostek’s
- (+) Trousseau’s o Trousseau’s
o Carpopedal spasms caused by - Administer Ca replacement therapy
inflating the blood pressure carefully
cuff to a level above systolic - WOF
pressure for 3 minutes.
o arrhythmias
- (+) Chvostek’s
- Ensure patency (IV)
o twitching of facial muscles in o infiltration can cause tissue
QUINDIPAN, Hannah A. 9
BSN 3C
UNP-CN
 NCM 112: FLUID AND ELECTROLYTES FINALS NOTES
necrosis and sloughing - Anorexia, Nausea and vomiting
- Administer oral replacements as - Decreased bowel sound
ordered
o abdominal pain, paralytic ileus
- Give Ca supplements 1 to 1 ½ hours
after meals - Polyuria
- If GI upset occurs o DHN
o give with full stomach (milk) - Kidney stones
- Seizure precautions o Renal failure
o padding bedside rails
- Pathologic fracture
- Provide calm, quiet environment
o bone pain
HYPERCALCEMIA LABORATORY FINDINGS OF HYPERCALCEMIA
- Calcium EXCESS in relation to body - ECG :
water o Shortened QT interval
- Above 10.1mg/dL (Total Ca) o Shortened ST segment
- Above 5.1mg/dL (Ionized Ca) - Serum Ca level
CAUSES OF HYPERCALCEMIA o INCREASED
- Increase in the resorption of Ca from - Ionized Ca level
bone o INCREASED
- Hyperparathyroidism TREATMENT OF HYPERCALCEMIA
- Cancer - Reduction in the intake of Ca
- Hypophosphatemia o diet, medications containing
- Acidosis calcium must be stopped
- Drugs - Hydration
o overdose of Ca, Lithium (dec.
o to increase excretion of Ca
Ca excretion)
- Ingesting excessive amounts - NSS
o Vitamin D o Na increases renal excretion of
o Vitamin A overdose calcium
SIGNS AND SYMPTOMS HYPERCALCEMIA - Loop diuretics
- Hypercalcemia causes a decrease in cell o promote Ca excretion
membrane excitability especially in - Dialysis
tissues of skeletal muscle, heart and o for life-threatening hypercalcemia
- Corticosteroids
nervous system
o block bone resorption and
- Muscle weakness decrease Ca absorption from the
o hyporeflexia, decreased GIT
muscle tone - Pamidronate/Etidronate disodium
o reduces bone resorption
- Fatigue or confusion
- Mithramycin
o personality changes, o chemotherapeutic agent
lethargy, coma - Calcitonin
- Bradycardia o also inhibits bone resorption
o cardiac arrest
- Digoxin toxicity
QUINDIPAN, Hannah A. 10
BSN 3C
UNP-CN
 NCM 112: FLUID AND ELECTROLYTES FINALS NOTES
NURSING INTERVENTIONS HYPOCALCEMIA DIETARY SOURCES OF PHOSPHORUS
- Monitor VS
- Dairy products
o WOF bradycardia
- Meats and poultry
- Assess neurologic and neuromuscular
- Fish
function
- Eggs
o report any changes
- Nuts
- Insert and maintain IV access - Legumes
o NSS – 200 to 500 ml/ hour - Vegetables
- Monitor for signs of pulmonary - Grains
edema BALANCING PHOSPHORUS
o crackles and dyspnea
- Kidneys
- Encourage patient to drink 3-4 L of fluid o 90% is excreted (GIT – excretes
daily unless contraindicated the rest)
- Calcium
- Strain urine for calculi o inverse relationship with P
o check for flank pain - Insulin
o moves P into the cell
- Provide a safe environment - Alkalosis
- Keep side rails raised o also shifts P into the cell
- Bed in lowest position, wheels locked
- Handle patient gently HYPOPHOSPHATEMIA
o prone to pathologic fractures - Phosphorus DEFICIENCY in relation
5. PHOSPHORUS IMBALANCES to body water
PHOSPHORUS (P) - Serum phosphorus level of < 2.5mg/dl
(1.8mEq/L)
- Primary ANION found in ICF
- 85% exist in bones and teeth, 14% in soft CAUSES OF HYPOPHOSPHATEMIA
tissue, 1% in ECF - Alkalosis
- 1:2 ratio with Calcium (Ca) o hyperventilation, sepsis,
- Normal serum Phosphorus levels 2.5 to 4.5
mg/dL (1.8 to 2.6 mEq/L) acute salicylate poisoning,

FUNCTIONS OF PHOSPHORUS (P) Insulin, Decrease in intestinal

- It plays an important role in cell membrane absorption of Phosphorus ,

integrity Starvation, Malabsorption
- Primary ingredient in 2,3 DPG (2,3
syndrome, Diarrhea, Laxative
Diphosphoglycerate)
- Also involved in buffering of acids and abuse, Diuretics (loop,
bases thiazides, acetazolamide),
- It promotes energy transfer to cells
o through formation of ATP Hyperparathyroidism,
- It is important for WBC and platelet Hypercalcemia.
function
- Is an essential component of bones and
teeth

QUINDIPAN, Hannah A. 11
BSN 3C
UNP-CN
 NCM 112: FLUID AND ELECTROLYTES FINALS NOTES
S/SYMPTOMS OF HYPOPHOSPHATEMIA - WOF IV infiltration
o sloughing and necrosis
-Musculoskeletal Signs and
NURSING INTERVENTIONS
Symptoms
o muscle weakness HYPOPHOSPHATEMIA:
§ weakened hand grasp,
- Monitor VS
slurred speech,
o WOF – respiratory failure,
dysphagia, malaise,
anorexia decreased HR, decreased LOC
o myalgia - Report signs of hypoxia
§ muscle pain o increased RR, confusion,
o weakened respiratory muscle restlessness, cyanosis (later stage)
§ poor contractility of the - Report signs of infection
diaphragm (shallow o fever, increased WBC
respiration) - Monitor I and O
o bone pain - Employ safety precautions
§ loss of bone density -
Osteomalacia – softening HYPERPHOSPHATEMIA
of the bone - Phosphorus EXCESS in relation to body
o pathologic fracture
- CNS cell malfunction water
o Paresthesia, Irritability - Serum phosphorus level of >4.5mg/dL
o Confusion
§ seizure and coma (2.6mEq/L)
decreased cardiac CAUSES OF HYPERPHOSPHATEMIA
contractility –
- Increase intake of Phosphorus in the
hypotension, low cardiac
output Diet Over administration of phosphorus
- Chest pain supplement or laxatives or enemas that
o decreased oxygen delivery to
myocardium contain phosphorus (fleet enema)
- Anemia S/SYMPTOMS OF HYPERPHOSPHATEMIA
- Increased susceptibility to infection
- Bleeding tendencies - Paresthesia
o GI bleeding o fingertips, around the mouth and
LABORATORY FINDINGS HYPOPHOSPHATEMIA spread along the limbs and to the
- Serum Phosphorus level face
o DECREASED - Weakness
- X-ray o spasms, cramps, pain
o bone fractures - Hyperreflexia
TREATMENT OF HYPOPHOSPHATEMIA - (+) Trousseau’s and (+) Chvostek’s
- Diet sign
o high in phosphorus-rich foods - Arrhythmias
- Oral supplements - Decreased urine output
- Neutra-Phos-K - Impaired vision, corneal haziness,
o Side effects: nausea and diarrhea conjunctivitis
o Mix with juice to improve taste - Skin
- IV Phosphorus replacement o papular eruptions
- Should be administered slowly

QUINDIPAN, Hannah A. 12
BSN 3C
UNP-CN
 NCM 112: FLUID AND ELECTROLYTES FINALS NOTES
LABORATORY FINDINGS DIETARY SOURCES OF CHLORIDE
HYPERPHOSPHATEMIA:
- Serum Phosphorus level - Fruits
o INCREASED - Vegetables
- Serum calcium level - Table salt
o DECREASED - Salty foods
TREATMENT OF HYPERPHOSPHATEMIA - Processed meat
- Diet - Canned foods
o low-phosphorus diet BALANCING CHLORIDE
- Eliminate the use of phosphorus based - Excretion
laxatives and enemas o kidneys
- Phosphate-binding antacids - Cl and Na
o Aluminum, Mg, Ca gel o closely linked
- Insulin - Cl and Bicarbonate
o DM o have an inverse relationship
- NSS
NURSING INTERVENTIONS HYPOCHLOREMIA
HYPERPHOSPHATEMIA: - Chloride DEFICIENCY in relation to body
- Monitor VS water
- WOF signs and symptoms of worsening - Serum chloride level of <96 mEq/L
hypocalcemia
o paresthesia, muscle cramps, CAUSES OF HYPOCHLOREMIA
o hyperactive reflexes – notify MD - Decreased chloride intake
- Monitor I and O - Excessive chloride losses
o Output – less than 30ml/hour – - Prolonged vomiting
notify MD - Diarrhea
- Report any signs of calcification - Severe diaphoresis
- Diuretics
6. CHLORIDE IMBALANCES - Alkalosis
CHLORIDE (Cl) SIGNS AND SYMPTOMS HYPOCHLOREMIA
- Is the MOST ABUNDANT ANION in ECF - Slow and shallow respiration
- Normal Serum Chloride level 96 to 106 o respiratory arrest
- Tetany
mEq/L o hyperactive DTR
FUNCTIONS OF CHLORIDE - Muscle hypertonicity
o weakness, twitching, muscle
- Helps maintain serum osmolality and cramps
water balance - Arrythmias
- Chloride and sodium work together to - Seizures
form CSF o coma
- Chloride is secreted in gastric mucosa as
HCl LABORATORY FINDINGS HYPOCHLOREMIA
- Chloride helps maintain acid-base - Serum Chloride level
balance and assists carbon dioxide o DECREASED
transport in the RBC. - Serum Na level
o DECREASED

QUINDIPAN, Hannah A. 13
BSN 3C
UNP-CN
 NCM 112: FLUID AND ELECTROLYTES FINALS NOTES
- Serum pH - Serum pH
o greater than 7.45 o Less than 7.35
- Serum bicarbonate level - Serum bicarbonate level
o greater than 26 mEq/L o less than 22 mEq/L
TREATMENT OF HYPOCHLOREMIA TREATMENT OF HYPERCHLOREMIA
- Diet
- Oral replacement
o sodium and chloride restriction
o Salty broth
- IVF
- IVF
o PLRS
o NSS
- IV sodium bicarbonate
- Ammonium Chloride
o An acidifying agent used in alkalosis NURSING INTERVENTIONS HYPOCHLOREMIA
o Assess pain at the infusion site
- Monitor VS
o Contraindicated in patients with
severe hepatic disease. - Restrict sodium and chloride in the diet
NURSING INTERVENTIONS HYPOCHLOREMIA - Monitor I and O
- Monitor VS especially RR - Provide safe, quiet environment
- Offer foods high in chloride
- Provide safe environment

HYPERCHLOREMIA
- Chloride EXCESS in relation to body
water
- Serum chloride level of >106 mEq/L
CAUSES OF HYPERCHLOREMIA
- Increased chloride intake
- Acidosis
- Drug related (Ammonium chloride,
Kayexalate)
SIGNS AND SYMPTOMS HYPERCHLOREMIA
- Signs of ACIDOSIS
o Deep, rapid respiration
(Kussmaul’s respiration),
weakness, lethargy.
- Arrhythmias
o decreased cardiac output
- Signs of hypernatremia
o Dyspnea, tachycardia,
hypertension, edema
LABORATORY FINDINGS HYPERCHLOREMIA
- Serum Chloride level
o INCREASED

QUINDIPAN, Hannah A. 14
BSN 3C
UNP-CN
 NCM 112: FLUID AND ELECTROLYTES FINALS NOTES
ACIDS and BASES K leaves the cell
(goes to ECF causing
- To appreciate acids and bases, it is
hyperkalemia).
essential to understand the
REGULATION SYSTEM (ACIDS AND
potential of Hydrogen (pH).
BASES)
- The concentration of Hydrogen ions
CHEMICAL BUFFERS
in body fluids determines the
- Serve as the body’s most efficient pH-
degree of acidity or alkalinity and is
measured in terms of their pH. balancing weapon.
- Normal blood pH - act immediately to protect tissues and
o 7.35 to 7.45 cells.
o below 7.35 is acidotic - They Bind with offending acids or
o above 7.45 is alkalotic. bases to neutralize them until other
- Blood pH below 6.8 and above regulations take over.
7.8 is usually LETHAL. - INSTANTLY COMBINE with the
offending acid or base,
ACIDS
NEUTRALIZING harmful effects
- Consists of molecules that
until other regulators take over.
can GIVE UP or DONATE
- Chemical buffers include:
HYDROGEN IONS to other
bicarbonate buffers, phosphate
molecules. Example:
buffers, and protein buffers .
carbonic acid (H2CO3)

PHOSPHATE (PO43-) AND PROTEIN

- Carbonic acid is produced when CARBON
BUFFERS
DIOXIDE is dissolved in water.
- Proteins and Phosphate in
BASES
the
- Consists of molecules that can ACCEPT
body fluids bind reversely to H+
HYDROGEN IONS
- The binding of excess H+ to proteins and
- Bicarbonate (HC03-)
phosphate prevents a decrease in pH
- Regulation of acids and bases
- Conversely, when H+ concentration
- an IMBALANCE in pH can
decreases, proteins and phosphate release
COMPROMISE essential BODY
H+, which prevents an increase in pH.
PROCESSES such as electrolyte
BICARBONATE BUFFERS (H2CO3)
balance, activity of critical
- Unable to bind as many as can proteins and
enzymes, muscle contraction and
phosphate
basic cellular function.
- It can be regulated by the respiratory
o Acidosis
system and urinary system
§ can cause hyperkalemia
- Example: CO2 + H2O = H2CO3
o Hydrogen ions
- The reaction of carbon dioxide and water
increases in ECF
takes place in RBC, catalyzed by carbonic
which causes
anhydrase
hydrogen ions to
move into the ICF
o An equal number of
QUINDIPAN, Hannah A. 15
BSN 3C
UNP-CN
 NCM 112: FLUID AND ELECTROLYTES FINALS NOTES
RESPIRATORY SYSTEM
- the lungs regulate blood
levels of CARBON DIOXIDE,
a gas that combines water
to form CARBONIC ACID.
- Second line of defense
- Respiration:
o uses hypoventilation
and hyperventilation
as needed to regulate
excretion or retention
of acids within minutes
of a change in pH
- faster or deeper respiration eliminates
- more carbon dioxide from the lungs
- More carbon dioxide lost, less
carbonic acid produced, as a result
pH rises (alkalosis). • Slower or
shallow – reduces carbon dioxide
excretion, more carbonic acid
produced, as a result pH decreases
(acidosis).
RENAL SYSTEM
- Can REABSORB acids and bases or
EXCRETE them in the urine.
- Kidneys are responsible for long-
term adjustment of pH level.
- The kidneys kick in by excreting or
retaining acids and bases as
needed.
- Renal regulation can restore
normal hydrogen ion
concentration within hours or days.
ACID-BASE IMBALANCE
- 2 by-products produced as cells use
nutrients to produce energy they
need to function:
o CO2
o H
ARTERIAL BLOOD GAS (ABG) ANALYSIS
- The MAJOR DIAGNOSTIC TOOL for
evaluating acid-base balance.
QUINDIPAN, Hannah A.
BSN 3C
UNP-CN
TEST INCLUDE:
- pH
o measures H ion (indication of
blood’s acidity or alkalinity).
o Normal pH: 7.35 – 7.45
o Below 7.35 ACIDOSIS
o Above 7.45 ALKALOSIS
- PaCO2
o Partial pressure of arterial CO2
reflects adequacy of ventilation by
the lungs.
o Normal level: 35 – 45 mmHg
o Below 35mmHg (HYPOCAPNIA is a
state of REDUCED carbon dioxide in
the blood. Usually results from deep
or rapid breathing, known as
HYPERVENTILATION – ALKALOSIS)
o Above 45mmHg (HYPERCAPNIA
due to HYPOVENTILATION –
ACIDOSIS)
- HCO3
o Reflects the activity of the kidneys
in retaining or excreting
bicarbonate.
o Normal: 22 – 26 mEq/L
o Below 22 – ACIDOSIS
o Above 26 – ALKALOSIS
OTHER INFORMATION REPORTED WITH ABG
RESULTS:
- Partial pressure of oxygen dissolved in
arterial blood (PaO2)
- Arterial Oxygen Saturation (SaO2)
PaO2
- Measures OXYGEN in the blood
- Normal: 80 – 100mmHg
- Mild Hypoxemia: 60 – 79mmHg
- Moderate Hypoxemia: 40 – 59mmHg
- Severe Hypoxemia: less than 40 mmHg
SaO2
- Measure TISSUE PERFUSION
- 95 – 100%
16
 NCM 112: FLUID AND ELECTROLYTES FINALS NOTES
• Acute
ARTERIAL BLOOD GAS (ABG) INTERPRETATION o pH: <7.35
STEP 1: o PaCO2: > 45
- Check the pH – is it normal (7.35-7.45) or o HCO3: Normal
abnormal?
- If abnormal – is it acidosis (low) or alkalosis
(high)? • Partially Compensated
- then figure out whether the cause is o pH: <7.35
respiratory or metabolic.
o PaCO2: > 45
STEP 2:
o HCO3: > 26
- Check the PaCO2 which provides
• Compensated
information about the respiratory
o pH: Normal
component of acid-base balance – is it
o PaCO2: > 45
normal (35-45mEq/L) or abnormal
o HCO3: > 26
- If abnormal – low (alkalosis) or high
RESPIRATORY ALKALOSIS
(acidosis)?
- Determine if the abnormal result • Acute
corresponds with a change in pH, if it does, o pH: > 7.45
the problem is RESPIRATORY in origin o PaCO2: < 35
STEP 3: o HCO3: Normal
- Check the HCO3 level – normal (22-26 • Partially Compensated
mEq/L) or abnormal? o pH: > 7.45
- If abnormal – low (acidosis) or high o PaCO2: < 35
(alkalosis)? o HCO3: < 22
- Determine if the abnormal result
• Compensated
corresponds with a change in pH, if it does,
the problem is METABOLIC in origin o pH: Normal
STEP 4: o PaCO2: < 35
- Check for compensation o HCO3: < 22
- Compensation involves opposites METABOLIC ALKALOSIS
- If the results indicated primary metabolic • Acute
acidosis, compensation will come in the o pH: > 7.45
form of respiratory alkalosis. o PaCO2: Normal
STEP 5: o HCO3: > 26
- Check the PaO2: normal 80-100mmHg or • Partially Compensated
abnormal? o pH: > 7.45
- LOW represent HYPOXEMIA o PaCO2: > 45
- Mild 60-79mmHg o HCO3: > 26
- Moderate 40-59mmHg
- Severe less than 40mmHg • Compensated
- PaO2 values indicates when to make o pH: Normal
adjustments in the concentration of o PaCO2: > 45
oxygen being administered to a patient. o HCO3: > 26
RESPIRATORY ACIDOS
QUINDIPAN, Hannah A. 17
BSN 3C
UNP-CN
 NCM 112: FLUID AND ELECTROLYTES FINALS NOTES
MIXED DISORDERS
- Simultaneous occurrence of metabolic
acidosis and respiratory acidosis during
respiratory and cardiac arrest.
- pH- normal with abnormal PaCO2 and
HCO3 and move not in the same direction.
- Metabolic acidosis + respiratory acidosis in
cardiac arrest and respiratory failure.
o E.g. pH – 7.38, PaCO2 – 46, HCO3 –
21
- It is possible for a person to have more
than one acid-base disturbance at the
same time.
o Ex. Ingestion of aspirin (which can
produce both a respiratory
alkalosis and metabolic acidosis)
- And those with lung disease who are taking
diuretics (respiratory acidosis plus
metabolic alkalosis).

QUINDIPAN, Hannah A. 18
BSN 3C
UNP-CN
 NCM 112: FLUID AND ELECTROLYTES FINALS NOTES
ACID-BASE IMBALANCES SIGNS AND SYMPTOMS OF RESP. ACIDOSISS
RESPIRATORY ACIDOSIS - Headache
- COMPROMISE in BREATHING may result in - CNS depression
RESP. ACIDOSIS o Depressed reflexes
- Characterized by alveolar o Altered level of consciousness
HYPOVENTILATION § Restless
- pH drops BELOW NORMAL
§ Confusion
2 TYPES OF RESPIRATORY ACIDOSIS
§ Apprehension
ACUTE R. ACIDOSIS
§ Somnolence
- resulting from SUDDEN RESP. FAILURE
§ Coma
- pH drops BELOW NORMAL
- Fine, Flapping Tremors
CHRONIC R. ACIDOSIS
- Nausea / Vomiting, Skin may be warm and
- due to COPD
flushed
- pH stays WITHIN NORMAL limits
- Rapid, Shallow Respiration
CAUSES OF RESPIRATORY ACIDOSIS
- Diminished or Absent breath sounds
• Neuromuscular Problems
- Dyspneic, Diaphoretic
o Guillain-Barre Syndrome (GBS)
- Cyanosis – late sign
o Myasthenia Gravis (MG)
- Tachycardia, Arrythmias
o Poliomyelitis
o Hyperkalemia and Hypoxemia
o SCI – diaphragmatic paralysis
- Myocardial Depression
• Central Nervous System Trauma / Lesions
o Shock
o Tumors
o Cardiac Arrest
o Vascular Disorders
DIAGNOSTICS TEST / EXAMS
o Infection
• ABG Analysis
• Obesity
o pH – below 7.35; PaCO2 – above 45
• Drugs (these drugs causes RESPIRATORY
mmHg; HCO3 – normal (acute)
DEPRESSION)
o pH – Normal; PaCO2 & HCO3 – inc.
o Anesthetics
(chronic)
o Hypnotic-Sedatives
• Chest X-Ray
o Opioids
o Help determine the cause
• Pulmonary problems
• Serum Elect Level
o Resp. Infections
o Hyperkalemia
o COPD
TREATMENT
o Asthma
- AIM: Improve ventilation and lower PaCO2
o Pulmonary Edema
- Bronchodilator
• Chest Wall Trauma
o To open constricted airway
• Airway Obstruction
- Supplemental O2
o Retained secretions
- Sodium Polystyrene Sulfonate (Kayexalate)
o Tumors
- Antibiotic Therapy
o Anaphylaxis
o To treat infection
o Laryngeal Spasm
- Removal of foreign body
o Heimlich Maneuver

QUINDIPAN, Hannah A. 19
BSN 3C
UNP-CN
 NCM 112: FLUID AND ELECTROLYTES FINALS NOTES
NURSING INTERVENTIONS SIGNS AND SYMTOMS R. ALKALOSIS
- Monitor neuro-vital signs - Respiration
- Administer medications as ordered o Increase rate and depth (primary
- Administer O2 as ordered sign)
o COPD – lower concentrations of
- Tachycardia
oxygen are given
o Hypoxic drive – lack of O2 o Anxious and restless
stimulates patient to breathe - Muscle weakness , DOB
- Perform tracheal suctioning, - Extreme Alkalosis
incentive spirometry, o Confusion, syncope
postural drainage, DBE and o Alternating apnea and
coughing exercises hyperventilation.
- Hydrate patient – IV and oral
o Tingling
o I and O
§ Finger and toes
- Institute safety measures
- ECG
RESPIRATORY ALKALOSIS o Prolonged PR interval
- Results from HYPERVENTILATION and o Flattened T wave
HYPOCAPNIA o Prominent U wave
- Increase respiratory rate or depth causes o Depressed ST segment
lungs to blow-off CO2
- PaCO2 level DECREASES
- pH INCREASES – ALKALOSIS
CAUSES OF RESPIRATORY ALKALOSIS
- Hyperventilation
o Anxiety or panic attack
- Pain
- Salicylate Intoxication
o Early signs is HYPERVENTILATION - Hypocalcemia
- Drugs o Hyperreflexia
o Nicotine, xanthines, aminophylline o Tetany
- Hypermetabolic state o Arrythmias
o Dec LOC
o Fever, sepsis
o Seizures
- Conditions that affect the respiratory o Coma
control DIAGNOSTIC TEST R. ALKALOSIS
- Pregnancy - ABG Analysis
o High progesterone stimulates o pH above 7.45; PaCO2 below
respiratory center 35mmHg; HCO3 normal (acute)
- Acute Hypoxia o pH normal; PaCO2 and HCO3
o High altitude, pulmonary diseases, decreased (chronic)
anemia, pulmonary edema, - Serum Elect Level
hypotension . o Hypokalemia and Hypocalcemia

QUINDIPAN, Hannah A. 20
BSN 3C
UNP-CN
 NCM 112: FLUID AND ELECTROLYTES FINALS NOTES
METABOLIC ACIDOSIS
- Caused by INCREASE PRODUCTION of H
IONS
- Characterized by pH below 7.35 and
HCO3 below 22mEq/L
- CNS depression
o coma
- Arrhythmias
o cardiac arrest
CAUSES OF METABOLIC ACIDOSIS
- Loss of HCO3 in ECF
- Accumulation of Metabolic Acidosis
- Or Combination of both
ANION GAP
- This measurement is calculated by
subtracting the amount of negative ions (Cl
and HCO3) from the amount of Na
(positive ion)
- The gap represents the level of
unmeasured anions In ECF (organic acids,
-ECG lactic acids, ketone acids, sulfate,
o Arrythmias phosphates).
TREATMENT R. ALKALOSIS ANION GAP
- Correction of underlying cause - Anion gap – normal (8-14 mEq/L)
o Fever – cooling measures o cause of METABOLIC ACIDOSIS is
o ASA overdose – eliminate source loss of HCO3
(ASA) - Anion gap – higher than 14 mEq/L
o Hypoxemia – oxygen therapy o due to accumulation of metabolic
o Anxiety – sedative or hypnotics acids
- Hyperventilation - Cl
o 96 -106 mEq/L
o Have patient breathe into a paper
- HCO3
bag or cupped hands o 22 – 26 mEq/L
- Na
NURSING INTERVENTIONS R. ALKALOSIS o 135 to 146 mEq/L
- Monitor NVS - Anion Gap= Na – (Cl + HCO3)
- Allay anxiety - Example:
o 107 (Cl) + 27 (HCO3) = 134
o Promote relaxation, breathe into
o 180 (Na)
paper bag or cupped hands o 180 – 134 = 46 (higher than 14, so
o Stay with patient during periods of the cause of metabolic acidosis is
stress and anxiety accumulation of metabolic acid)
- Institute safety measures and seizure
precautions

QUINDIPAN, Hannah A. 21
BSN 3C
UNP-CN
 NCM 112: FLUID AND ELECTROLYTES FINALS NOTES
CAUSES OF METABOLIC ACIDOSIS lactate increases in the body
- KETOACIDOSIS faster than it can be
o OVERPRODUCTION of KETONE metabolized such as in hepatic.
BODIES SIGNS AND SYMPTOMS OF M.ACIDOSIS
o GLUCOSE supplies have been - Hyperventilation
UTILIZED - the body uses FAT stores o Increase depth and respiration
for ENERGY - fatty acids are (first clue)
converted to KETONE BODIES . o Kussmaul’s resp
- LACTIC ACIDOSIS § rapid and deep
o Shock, HF, pulmonary disease, o DKA
hepatic disorder, seizures, § fruity-odor breath
strenuous exercises. (excretion of acetone thru
o DECREASED excretion of acids in the lungs)
the kidneys - Skin
o warm and dry
o RF, Acute Tubular Necrosis (ATN)
o shock – cold and clammy
o Excessive GI losses - CNS depression
§ diarrhea, intestinal o confusion, stupor, coma
malabsorption o diminished muscle tone and
o Poisoning or toxic reaction to reflexes
drugs o Weakness and dull headache
§ ASA, HCl, ammonium Cl - Depressed myocardial function
o Other causes: o Dec CO and BP, arrhythmias
§ use of K-sparing diuretic (hyperkalemia)
and acetazolamide - GI effects
LACTATE o Anorexia, N/V
- Produce as result of CHO metabolism DIAGNOSTIC TESTS M. ACIDOSIS
and lactate is metabolized by the liver. - ABG analysis
o pH – below 7.35; PaCO2 – less than
- Normal: 0.93 – 1.65mEq/L
35; HCO3 – less than 22
- LACTIC ACIDOSIS happens when: - Serum K level
o Demand of oxygen is GREATER o elevated
than its availability. - Blood glucose
o Lactate increases in the body o elevated (DKA)
faster that is can be - Plasma Lactate levels
metabolized o elevated (lactic acidosis)
- Anion gap
o Shock, HF, pulmonary disease,
o increased
hepatic disorder, seizures, - ECG
strenuous exercises. o tall, t waves, prolonged PR intervals
o Tissue Hypoxia - Shock, HF, and wide QRS complexes
pulmonary disease, hepatic
disorder, seizures, strenuous
exercises are forced to
anaerobic metabolism (more
lactate is produced)
o Lactate Acidosis occurs when
QUINDIPAN, Hannah A. 22
BSN 3C
UNP-CN
 NCM 112: FLUID AND ELECTROLYTES FINALS NOTES
NURSING INTERVENTIONS M. ACIDOSIS DIAGNOSTIC TEST M. ALKALOSIS
- Monitor Neuro-Vital Signs - ABG Analysis
- Insert IV line o pH – above 7.45
- Administer NaHCO3 o HCO3 – above 26
- Semi-fowler’s position mEq/L
- Monitor I and O o PaCO2 may be above
- Orient patient as needed 45 mmHg (respiratory
compensation)
METABOLIC ALKALOSIS - Serum Elect Level
- Caused by DECREASE in HYDROGEN ION o Hypokalemia
PRODUCTION o Hypocalcemia
- Characterized by a blood pH above 7.45
o Hypochloremia
and HCO3 level above 26.
- ECG
CAUSES OF METABOLIC ALKALOSIS
o low T wave that merges with the P
- Electrolyte imbalances
wave
o Hypokalemia
o Hypochloremia
o Hypocalcemia
- Excessive acid loss – GIT
o Vomiting, NGT suctioning
- Diuretic use
o thiazide and loop diuretics
- OTHER CAUSES:
o multiple transfusion
o drugs
§ corticosteroids antacids
that contain NaHCO3. TREATMENT M. ALKALOSIS
SIGNS AND SYMPTOMS M. ALKALOSIS - IV administration of ammonium chloride
- Respiration - Discontinue Thiazide diuretics and NGT
o SLOW and SHALLOW suctioning
- Neuromuscular excitability - Antiemetic
o muscle twitching, weakness, NURSING INTERVENTIONS M. ALKALOSIS
tetany, hyperactive reflexes. - Monitor NVS
- Administer O2 as ordered
o Numbness and tingling
- Institute seizure precaution
§ Fingers, ties, mouth area - Maintain patent IV
o Apathy, confusion, seizures, stupor, - Monitor I and O
and coma - Irrigate NGT with NSS
- GIT o instead of tap water to prevent
o Nausea, vomiting, anorexia loss of gastric electrolytes
- GUT
o polyuria
- Arrhythmias
o death

QUINDIPAN, Hannah A. 23
BSN 3C
UNP-CN