LECTURE-ON-F-E.pptx

Topic: Fluids , F & E; Acid-
Base Imbalances

I. Review of common terms related to fluids,
electrolytes , & acid-base
• 1. body water – the aqueous medium of the body minus the
electrolytes, the major component in the body.
• 2. body fluid – body fluid in which electrolytes are dissolved.
ex. ECF, ICF, Interstitial fluid.
3. Intracellular fluid – body fluid located within the cells. 70% of total
body weight is normally within the cells.
4. Extracellular fluid – body fluid located outside the cells ; 30 % of
the total body weight.

4. Interstitial fluid – fluid found in between the cells ; 25% of total body
water is in the interstitial space.
5. Plasma – ECF fluid that contains colloids, proteins, & is the liquid part
of the blood, along with the RBC.
- It maintains the blood volume, which makes 5% of the body water.
• Terms R/T Electrolytes
1. Electrolyte – a substance when placed in solvent like water breaks up
into separately charged particles called ions.

2. Ion – atom having positive or negative electrical charge.
3. Cation - is positively charged ion like; sodium, potassium,
magnesium, calcium, hydrogen
4. Anion – is negatively charged particles like chloride, phosphate,
bicarbonate
5. Colloids – macronutrients of protein, that are located within the
plasma.
* Milliequivalent ( mEq ) the measure of the combining power of an ion

* Terms Related to F & E Movement
1. Osmolality – the total number of dissolved particles/liter of solvent.
2. Hyperosmolality – decrease in water in relative to solvent
3. Hypo-osmolar – increase in water relative to solute concentration
4. Active transport – an energy requiring process that transport ions
across cell membrane.
5. Blood Hydrostatic pressure – pressure of the blood within the
capillaries: it depends on the: 1. level of the arterial BP; 2. rate of
blood flow through the capillaries; 3. venous pressure

5. Colloid Osmotic Pressure – called oncotic pressure; pressure exerted
by the plasma proteins w/c holds water w/in the vessels & draws back
water that escapes from the vessels.
6. Filtration pressure – the net pressure that forces fluid out of vessels.
• Hormones that Regulate Fluid & Elect Balance
1. Antidiuretic Hormone ( ADH ) – hormone released from the
posterior pituitary gland which controls water reabsorption by the
kidneys & regulates fluid osmolality.

• Factors that stimulate ADH release : hyperosmolality of body fluid, reduced
circulating blood volume.
2. Aldosterone – hormone secreted by the adrenal cortex.
- It increases renal reabsorption of sodium & water, thus regulates fluid
volume in the ECF.
*Other hormones that regulate electrolytes:
* PTH – secreted by the parathyroid gland to maintain serum calcium level.
Thyroid Hormone – thyroxine ( T4 & triiodothyronine ( T3 ).
* Calcitonin is secreted by the thyroid gland enhance calcium shift to the
bones.

Terms Related to Hydrogen Ions
1. Acid – a hydrogen ion donor. An acid gives ions to a base, thereby
neutralizing the base
2. Base – hydrogen ion acceptor. A base accepts hydrogen ion from an
acid, thereby neutralizing the acid.
3. pH – signifies the chemical concentration of hydrogen ion,
describes the alkalinity or acidity of a solution.
- Its normal value is 7.35 – 7.45. below 7.35 is acidic; above 7.45 is
alkali
4. Buffers – pair of chemicals that donate or accept hydrogen ions.

I. Body Water: Basic Concepts
• A. Volume of body water
- The normal human body consists of 47 -80% water, varies with age,
sex, & individual body physical characteristics
- Body water as a percentage of body weight declines with age
- Infants body is 77-80% water
- Elderly adults body is 47 % water
- Based on sex, male has greater percentage of water( 60-70% of their
BW) compared to females which has 50-54% of their BW is water.

B. Distribution of Body Water
- 70% of total body water is located in the intracellular compartment
- 30 % is distributed in the extracellular compartment
24% is in the interstitial space
6% is in the intravascular space, as plasma
C. Functions of Water
1. Provides aqueous medium for cellular metabolism
2. Acts as solvent for solutes for cell function
3. Transports substances to & from cells
4. Aids in regulation of body temperature, and digestion.

C. Fluid Transport/Movement
1. By Osmosis – the movement of fluid from lower to a higher
concentration ex. administration of hypotonic solutions
2. Diffusion – movement of solute particles from a higher
concentration to a lower concentration.
3. Hydrostatic Pressure – there is pressure that is exerted to move
fluid pushing outward against the boundaries.
4. Filtration pressure – fluid achieve its equilibrium by moving from
the space w/ higher pressure across a semi-permeable membrane.
smaller electrolytes move along w/ H20, larger solutes remain on
the other side of the membrane.

D. Balance & Imbalance of Water:
- Balance of water depends on balance between I & O.
- Normally, a person must have balance of intake & output of 2600 ml/day.
- Average sources of water intake * Average water losses
1200 ml water in beverages 1500 ml losses from urine output
1100 ml hidden water in foods 1000 ml from skin & lungs
300 ml water form oxidation 100 ml/day from GIT (FECES )
2600 ml – /day (total ) 2600 ml/day total

E. Normal Body Requirement for Water
- normally, an adult person needs 2600 ml of fluid/day to meet body’s
fluid requirements
- Adults can live 10 days without water, while children 5 days, provided
weather conditions are moderate.
F. Homeostatic Regulation of Water
1. ADH – increase water reabsorption
2. Kidneys – maintain concentration & volume of urine
3. Thirst Mechanism – the hypothalamus is activated by an increased
in body fluid osmolality results to increase water intake

II. F & E Imbalances: Basic Concepts
A.
a. Disorders that can be caused by a deficit or excess of essential body
substances
b. Disorders caused by protein deficiency
c. Fluid shifts to the interstitial and/or fluid shifts into the plasma
B. Causes of F & E Imbalances
a. Deficiency of F & E due to insufficient dietary intake
b. Increased excretion or loss
c. Compartmental shifts of fluids or electrolytes

2. Excess of fluids & Electrolytes
a. Intake is greater than excretion
b. Decreased excretion due to kidney disease or impaired homeostatic
regulation.
c. Sequestration of fluid and/or electrolytes in one compartment.
Ex. ascites, anasarca

B. Persons susceptible to F & E Imbalances
1. Conditions contributing to imbalances:
- Vomiting - patients who will undergo surgery
- Diarrhea, Renal or Cardiac disease – patients who needs blood
- Burns transfusion
- Hormonal disorders like in DM
- Cirrhosis of the Liver
- Severe insensible fluid losses
& hyperventilation

2. Interventions Contributing to Imbalances
• 1. IVF therapy
2. Diuretics
3. Dietary management
4. Surgical procedures
5. Medications to treat the main cause of imbalances.
6. Administration of blood transfusion, if condition is due to blood
loss.

III. Alterations in fluid Balance
• A. Fluid Volume Deficit
- Is called hypovolemia is decreased in fluid volume or blood volume
- Maybe isotonic, hypotonic, hypertonic
B. Fluid Volume Excess – commonly called hypervolemia, fluid intake
excess loss, or excess adm of hypotonic solutions, inc ADH released
- Its danger is it may result to CHF
- Maybe isotonic, hypotonic, hypertonic

Isotonic Volume Deficit
• Causative Factors:
a. Due to excessive loss of isotonic body fluids from vomiting,
diarrhea, NGT suctioning
b. Losses from the kidneys through diuresis in renal disease
c. Fluid loss through excessive diaphoresis
d. Hemorrhage
e. Lack of intake of fluids & electrolytes due to inability to ingest orally
f. Shift of fluids into body spaces like in ascites, edema, fluid is not
readily available for exchange ( third space fluid shift )

Assessment Findings:
• Acute weight loss (esp.if greater than 5% of total body weight
• Changes in cardiac function ( increased HR, dec.BP, signs of postural
hypotension, increased RR.
• Decreased hydration of the skin & mucous membrane, dry oral cavity.
• Decreased & concentrated urine output
• Increased Hematocrit
• Sunken eyeballs
• If dehydration is severe, patient may be irritable

Potential Nursing Diagnosis
1. Fluid Volume Deficit
2. Altered tissue perfusion
3. High Risk for Injury
4. Ineffective Breathing Pattern
5. Decreased Cardiac Output
6. Altered Nutrition, less than Body Requirements
7. Altered Oral Mucous Membrane
8. Fatigue
9. . Risk for activity intolerance

Interventions
A. Medical Interventions
1. IVF replacement with isotonic solutions
2. Adm.of BT if deficit is due to blood loss
3. Treatment for contributory underlying cause. (vomiting, diarrhea,
blood loss ).
4. Removal of third space fluid shift ( paracentesis in ascites, insertion
of peri-cardiac tube if pericardial effusion, thoracostomy tube ).
5. Mobilization of interstitial fluids into the vascular system with
caution.

Nursing Interventions
1. Assess cardiovascular, respiratory, & neurologic status.
2. Assess skin turgor & condition of oral mucous membrane.
3. Monitor laboratory values.
4. Measure & monitor I&O, minimum 30 ml/hr of urine output
5. Monitor body weight daily, weight loss of more than 0.5 lb/d is
considered fluid loss.
6. Provide teaching about medication regimen, prescribed diet, &
foods to avoid.
7. Monitor signs of cardiac overloading during IVF replacement.

Evaluation:
1. Patient’s v/s are within normal.
2. Characteristics of urine output are normal; urine output is 30 ml/hr
3. Breaths sounds clear.
4. With good skin turgor.
5. Patient is free from injury
6. With I& O balance.

Hypotonic Volume Deficit
• - there is the loss/decrease solute concentration with water volume
remaining normal.
- Due to loss of solutes in the ECF, fluid shifts into the cell by osmosis.
a. Causes:
- GI fluid losses through diarrhea, vomiting
- Renal loss of electrolytes like in Na wasting
- Iatrogenic fluid replacements with hypotonic solutions

b. Clinical symptoms:
- Same with isotonic fluid volume deficit
Add.symptoms:
- Fatigue
- Weakness
- Muscle cramps
- Postural hypotension
- Confusion if deficit is severe

c. Medical Interventions
1. Same interventions with Isotonic Volume Deficit
2. Additional: replacement of electrolyte losses like Na, potassium, if
below normal.
3. Nursing interventions are the same as in isotonic volume deficit.
4. Same evaluation with isotonic volume deficit.

Fluid Volume Excess
- Fluid volume excess is an increase in water volume & solute
concentration in the ECF.
a. Causes:
- Excessive intake of sodium & water, or through IVF replacement.
- Iso-osmolar fluid retention due to compromised regulatory
mechanisms
- Use of corticosteroids.
- chronic Liver Disease

b. Signs and Symptoms
1. Increased BP, HR. RR – due to circulatory overload
2. Interstitial edema
3. Rapid weight gain esp.if more than 5% of total body weight
4. In severe cases, condition not resolve, patient’s condition may
progress into CHF, and pulmonary edema which makes the
condition life threatening.
5. Excretion of diluted urine
6. Low serum sodium level

1. Fluid Volume Excess
2. Decreased Cardiac Output If heart fails to function
4. Anxiety
5. If fluid will shift into the cells, it will result to swelling of the brain
cells, wherein patient manifests neurologic symptoms like lethargy,
headache, seizures, irritability, nausea.

Medical Interventions
1. Restriction of water intake to a volume less than urine output
2. Increase salt in the diet
3. Administration of IVF with sodium. Observe for rebound effect of
sodium administration.
*Nursing interventions are the same with isotonic fluid volume excess.

Hypertonic Volume Excess
- An increase in sodium concentration with water volume remaining
normal.
- ICF shifts into ECF
• Causes:
- Excess intake of hypertonic fluids or adm.of hypertonic solutions
through IV.
- It is manifested by neurologic symptoms such as muscle twitching,
possible seizure, with subsequent dehydration of cerebral cells.
- Hypernatremia, where Na is retained or in excess from abnormal
sources, increase aldosteronism.

Nursing Diagnosis
1. Fluid Volume Excess
2. Impaired neurologic function, lethargy
3. Risk for injury
*INTERVENTIONS
1. Treat underlying cause of the disease.
2. Adm of potassium sparing diuretics
3. Monitor I & O, v/s, body weight
4. Provision of safety

II. Electrolytes
1.These are solutes found in body fluids
2.They developed an electrical charges once dissolved in water.
3. Major Body Electrolytes:
a. Sodium f. chloride
b. Potassium g. Phosphorous
c. Magnesium h. Bicarbonate
d. Calcium
e. H+

A. Sources of electrolytes
1. Normal sources are intake from foods and fluids.
2. Abnormal sources:
- Medications
- IVF solutions
- Hyperalimentation
*Functions of Electrolytes:
1. Maintain osmolality of body fluids; & cellular osmolality
2. Regulate acids & bases
3. Aid in neurologic & neuromuscular conduction

Electrolyte Distribution & Excretion
1. ICF ELECTROLYTES
a. Potassium – major intracellular electrolyte
b. Phosphorous – the chief or major anion
c. Large amount of CHON
d. Small amount of magnesium, calcium, S04, & HCO3
e. Extremely small amount of sodium & chloride

ECF Electrolytes
1.Sodium – the chief/major cation
2. Chloride – the chief anion
3. HCO3
4. Small amounts of potassium, calcium, Mg, SO4, PO4
5. The intravascular has the same amount of electrolytes with that of
the interstitial, but the intravascular fluids is the only measurable fluid
to determine the serum sodium level of the body fluid.

Excretion of Electrolytes
1. They are lost during excretion of body fluids.
2. Renal excretion of electrolytes are abnormal with the use of
diuretics.
3. GIT excretion of electrolytes occur during vomiting, & diarrhea.
( during vomiting potassium & HCL acid is excreted )
4. In lower GI elimination, hydrogen & potassium are lost.
5. Excessive diaphoresis contributes to Na & Cl losses.
6. Surgical drains also contribute to electrolyte loss.

Electrolyte Renal Regulation
1. Renal Regulation
a. Renal Regulation – in the kidneys, electrolytes are balanced by
glomerular filtration, tubular reabsorption, and secretion.
- In the distal & collecting tubules, water is reabsorbed only in the
presence of ADH.
- Electrolyte secretion occurs when an electrolyte moves from the
blood into the tubule.

1. Sodium: Normal & Altered Balance
A. 1.Normal balance
- It is the major cation in the ECF
- Normal serum Na – 135-145 mEq/L
- Most Na is found in the ECF where it can be measured by serum tests
- It can be taken from the foods we eat, & beverages we drink
- The normal requirement for an adult individual is 2 gms daily

b. Endocrine regulation
- The pituitary adrenocorticotropic hormone stimulation enhances
adrenal release of aldosterone.
- It enhances sodium reabsorption , another positively charged
electrolyte- K+ is secreted into the tubules for excretion
c. GI Regulation
- Electrolytes are secreted, absorbed across the small intestines same
way in the kidneys

2. Function:
a. Facilitate transmission of impulse in nerves & muscle fibers
b. Assist in acid-base balance by combining with HCO3 & Cl
c. It determines the volume & osmolality of the ECF, thereby regulates
body water
3. Regulation of sodium to maintain balance
a. The kidneys through filtration, reabsorption in the presence of ADH
b. Through endocrine regulation, secretes aldosterone & ADH

Sodium Imbalance
• A. Hyponatremia – serum sodium level below 135 mEq/L
1. Causes:
- Prolonged use of diuretic therapy ( impairs Na reabsorption in the
loop of Henle)
- Excessive burns in which it results to loss of Na in the ECF, Na leak into
the burned areas of the body.
- Excessive diaphoresis
- Prolonged vomiting, diarrhea, NGT suction
- Renal disease result to Na wasting

5. Excessive administration of water through IV route
6. SIADH where water is retained results to hyponatremia
b. Clinical symptoms:
1. vomiting, diarrhea, which maybe the cause of hyponatremia
2. Neurologic & musculoskeletal symptoms like muscle cramps,
muscle twitching, headache, confusion, convulsion coma
(due to shifting of fluid into the cells resulting to swelling of brain cells)
c. Potential nursing diagnosis: Potential for fluid volume excess; High
risk for injury; anxiety; impaired physical mobility)

d. Interventions
1. Early detection of signs & symptoms of hyponatremia by identifying
risk patients for hyponatremia.
2. Restrict fluid intake to allow Na & water to balance naturally.
3. Replace sodium through administration of IVF solutions with Na.
4. Monitor I & O
5. Monitor v/s, & serum sodium levels.

B. Hypernatremia: Serum level above 145
mEq/L
1. Causes:
a. Sodium gain in excess of water from adm of excessive IVF solutions
containing sodium or tube feedings
b. Excessive intake of sodium in the diet.
c. Water loss in excess like severe diarrhea, burns, osmotic diuresis
d. Fluid shifts out of the ICF into ECF to balance the excess ECF Na.
2. S& S: commonly associated with dehydration
a. Thirst c. dry mucous membrane e. seizures
b. Tachycardia d. hyperactive reflexes

3. Potential Nursing Diagnosis
a. Fluid volume deficit
b. High risk for injury
c. Altered nutrition: Less than body requirements
4. Interventions for Hypernatremia
a. Identify risk individuals; those receiving hypertonic solutions, TPN
b. Monitor I & O, monitor body weight
c. Monitor v/s
d. Provide safety
e. Administer hypotonic solution with caution; hypotonic Na solutions

Potassium: Normal &Altered Balance
A. Normal – Serum level k +- 3.5.- 5 mEq/L
- Major cation in the ICF
- Sources: fruits, vegetables, chocolates
- Nutritional supplements of k+
- IV infusion of K+
1. Functions of potassium
a. Regulates ECF osmolality by exchanging with Na.
b. Maintain normal neuromuscular contraction by participation in Na-
K+ pump.

c. Maintain muscular activity – with particular sensitivity to cardiac
muscle
d. Regulate acid-base balance in exchange with hydrogen ion.
e. It is needed for all metabolic processes ( CHO, Glycogen, CHON )
3. Regulation of potassium in the body
1. Renal System
2. Renin-aldosterone Mechanism
3. Regulated by plasma CHON

Potassium Imbalances
• 1. Hypokalemia – serum K+ below 3.5 mEq/L
a. Causes:
1. Prolonged used of osmotic diuretic like furosemide
2. Prolonged vomiting, diarrhea, laxative abuse, NGT suctioning
3. Renal disease where potassium is not secreted by the kidney tubules for
absorption
4. Excessive removal during dialysis.
5. Inadequate intake during anorexia & alcoholism
6. Adm of hypertonic glucose, shift of k+ from ECF to ICF
7. During administration of insulin, where k+ moves into cell w/glucose

8. During metabolic alkalosis where potassium moves into the cell in
exchange of hydrogen ion.
9. During hyperaldosteronism, increased Na enhances K+ excretion.
2. S&S of hypokalemia
a. Vomiting or diarrhea which may be the actual cause of the imbalance.
b. Muscle weakness & cramps, hyporeflexia, paresthesia, hypotension,
cardiac dysrhythmia due to decrease muscular contraction
c. Serum level below 3.5 mEq/L, increased bld pH, elevated blood glucose
d. ECG tracing appear inverted flat Twave.

c. Potential Nursing Diagnosis
1. Decreased cardiac output 5. Risk for cardiac dysrhythmia
2. High risk for injury
3. Impaired physical mobility
4. Activity intolerance
d. Interventions:
1. Identify high risk patients to prevent hypokalemia.
2. Teach patients receiving diuretics to increase intake of potassium
rich-foods.
3. Monitor I & O, keeping in mind diuresis increase k+ loss.

4. Caution patients receiving digitalis, digitalis toxicity may occur along
with the use of diuretic furosemide.
5. Replace potassium losses through dietary interventions.
6. Administer oral potassium supplements, note these drugs are GI
irritants, give with water.
7. Administer IV solutions with potassium, note kCl should not be given
by IVP or in concentrated forms. It can result to dysrhythmia
8. Monitor v/s,
9. Monitor serum potassium level, after IV K+ replacement.

Nursing Considerations in IV infusion of K+
1. Concentrated use of potassium should not be given by direct IVP,
make sure to have adequate solvent to administer by drip.
- Commonly potassium is ordered to dilute 20 mEq dissolved in 90-100
cc of solvent given in 1 hour drip for 3 doses depends on the ordered
medication to correct hypokalemia.
2. It is recommended that IV cannula should be inserted in a central
vein, because drug is irritating to the veins.
3. Monitor urinary output while patient is given potassium supplement
to ensure excretion of potassium.

e. Evaluation:
1. Serum potassium level is within normal range.
2. Patient’s cardiac output is normal.
3. Patient is free from injury.
4. With balance intake & output.
5. Vital signs within normal.
6. Patient’s mobility improved, able to ambulate without assistance.

Hyperkalemia – serum K+ above 5.0mEq/L
a. Causes/ etiology
1. IV replacement of potassium 7. Adm of WB nearly of its expiry
2. Potassium rich hyperalimentation date
3. Excessive use of salt substitutes
4. Poor elimination of potassium due to kidney failure.
5. In metabolic acidosis where hydrogen ion enters the cell in
exchange of potassium.
6. In cases of great cell damage like in burns, chemotherapy to treat
Cancer, potassium is released into the serum.

• S & S:
1. Confusion, paresthesia, abdominal cramps, muscle paralysis –
hyperkalemia affects the musculoskeletal system, smooth muscle
function, & nerve cell function.
2. ECG changes which appears prolonged P-R intervals, wide QRS &
tented T-wave, which may result to cardiac arrest.
*Potential Nursing Diagnosis:
1. Decreased Cardiac Output 3. Impaired Physical Mobility
2. Risk for Injury 4. Anxiety

Interventions:
1. Identify risk individuals those receiving IV potassium replacement,
patients with severe burns, cellular damage, those with renal
failure.
2. Check patient’s urine output, and serum potassium levels.
3. Attach patient to cardiac monitor if they have signs of hyperkalemia
4. Administer sodium bicarbonate as ordered with caution
5. To patient with CKD, they may undergo dialysis
6. Monitor I & O, report if urine output is below 30 ml/hour

Calcium: Normal & Imbalance
• A. Normal Calcium in the blood – 8.5 mg/dl-10.5 mg/dl
- It is regulated with Mg & PO4
- Its sources: 99% found in the bones & teeth
- Calcium not bound to bone is either bound to plasma proteins or
ionized ( calcium that is not attached to proteins)
- It is taken through the diet

1. Functions of calcium:
a. Calcium that are bound to bones & teeth maintains their strength &
rigidity.
b. Calcium is needed for nerve, muscle, and cardiac conduction
c. It is required for hormonal secretion
*2. Regulation of calcium levels:
a. It is absorbed in the small intestine & excreted in the urine.
b. Vit D in its active form 1,25- dihydroxycholecalciferol is required in the
absorption of calcium in the S.I. Conversion occurs in the kidneys

• Renal Regulation of Calcium:
a. Calcium is filtered in the glomerulus and absorbed in the tubules.
b. If excessive calcium is present, it can precipitate into stone.
*Endocrine Regulation:
a. The parathyroid gland responses to low calcium level by releasing
PTH, stimulates the release of calcium from the bones until it
becomes normal.
b. If serum phosphorous level is higher than normal, calcium binds
with phosphorous.

Calcium Imbalance
A, Hypocalcemia – serum calcium level below 8.5 mg/dl
1. Causes:
a. Inadequate intake of calcium in the diet due to anorexia, dieting.
b. In CKD, vit D is not activated or dihydroxycalceferol is not activated.
c. Vit D deficiency
d. Inadequate exposure to sunlight, w/c hinders activation of vit D
e. Malabsorption of calcium due to GI disease, or alcohol abuse.
f. Acute pancreatitis which results to hypocalcemia
g. Low PTH level, reduce calcium absorption.

Signs & Symptoms
a. Tetany & seizures
b. ECG result prolonged Q-T intervals
c. Appearance of petechiae and easy bruising observed on the skin.
d. Hyperphosphatemia is noted
e. Prolonged prothrombin time
*Potential Nursing Diagnosis:
a. Decreased cardiac output d. risk for bleeding
b. Risk for injury e. Ineffective breathing pattern
c. Impaired physical mobility f. Activity Intolerance

• Because calcium is a critical part in neuromuscular contraction, low
calcium levels affect the contraction of the smooth, skeletal, & cardiac
muscles which include:
- Muscle cramps in arms & legs
- Muscle spasms ( spasms in bronchial & laryngeal muscles which are
dangerous signs of hypocalcemia)
- Cardiac dysrhythmias ( prolonged Q-T interval)
*it is also a critical part of nerve cell conduction, w/c makes nerve cells
more excitable results to hyperactive deep tendon reflexes,
paresthesia, +Chvostek’s sign, +trousseaus sign.

4. Interventions:
a. Identify patients at risk for hypocalcemia; those with thyroid
disease or have undergone thyroidectomy, or patients with GI
disorders.
b. Assist patient to restore serum calcium level to normal
c. Patient maybe prescribed of calcium supplements, vit D, provide
calcium rich foods.
d. Provide safety always.
e. Monitor v/s

f. Administer calcium gluconate with caution & to patients receiving digitalis,
it may result to digitalis toxicity.
g. Ca gluconate is also use to antagonize magnesium toxicity.
h. Encourage patient to ambulate & do some exercises as tolerated
*B. Hypercalcemia – serum calcium level above 10.5 mg/dl
1. Causes:
a. Over administration of calcium supplements.
b. Increased vit D intake
c. Hyperparathyroidism which accelerates PTH effects on bones

d. Increased in renal disease which decrease renal regulation of
electrolytes.
e. Hypophosphatemia due to inverse relationship of calcium with
phosphorous
f. Thyrotoxicosis accelerates release of calcitonin.
g. Immobility, if bones are not used, calcium moves out from the bones
h. In cases of bone cancer, calcium moves out from the bones.

2. S & S:
a. Assess level of serum calcium level especially to patients who are at
risk for hypercalcemia.
b. Hypercalcemia affects the skeletal, cardiac & smooth muscles which
are manifested by dec intestinal peristalsis, muscle weakness,
cardiac dysrhythmia manifested by shortened Q-T interval.
c. Excess calcium may result to formation of urinary calculi manifested
by hematuria, dysuria, presence of calcium oxalate in the urinalysis.
d. Patient is risk for pathologic fracture.

*3. Potential Nursing Diagnosis
a. Decreased cardiac output
b. High risk for injury
c. Altered nutrition: less than body requirements
d. Risk for constipation R/T decreased GI function from immobility.
e. Impaired memory, confusion R/T altered neurologic function.

4. Interventions:
a. Institute measures to prevent hypercalcemia to high risk patients.
b. Encourage patient to ambulate and do exercise as tolerated.
c. Institute measures to eliminate excess calcium from the blood by
administration of loop diuretics as ordered
d. Administer calcitonin as ordered enhance movement of calcium
into the bones.
e. Monitor v/s, and electrolytes

Magnesium: normal & imbalance
A. Description:
- The second most abundant cation in the ICF
- Normal serum Mg level – 1.5-2.5 mEq/L
1. Causes:
a. Increased intake of Mg rich-foods, or administration of magnesium
through IV route in the treatment of eclampsia, IV supplements,
Hyperalimentation.

2. Functions of Mg
a. Assists in the contraction of cardiac, & skeletal muscles
b. Has an effect of vasodilation, results to decreased BP & cardiac
output.
c. Facilitates sodium & potassium transport across cell membrane.
*3. Regulation:
1. Mg is filtered along with other electrolytes in the tubules
2. Mg is reabsorbed in the renal tubules as the body needs Mg. If
serum Mg level is low, Mg is re-absorbed, if high excreted.
3. Osmotic diuretics can excrete excess Mg.

4. Hypomagnesemia – Mg level below 1.5
mEq/L
1. Causes:
a. Can be loss from vomiting, diarrhea, NGT suction ( more Mg is lost
from the bowel compared to vomiting)
b. Administration of loop diuretics.
c. Inadequate intake or absorption due to malnutrition, starvation,
excess dietary intake of calcium or vit D
d. Hypercalcemia
e. Hypoparathyroidism

2. Signs & Symptoms
1. Patient may be manifesting vomiting & diarrhea which may be the
cause of the Mg deficit.
2. Hypotension, because Mg is required for neuromuscular & cardiac
muscle function
3. Patient may manifest same manifestation with that of a patient
with hypocalcemia: tetany, seizure, tremors, confusion, hyperactive
deep tendon reflex, positive Chvostek’s & trousseau’s signs.
4. Memory loss
5. Lab results: Mg below normal, hypocalcemia, hypokalemia
6. ECG results; prolonged P-R interval, inverted T-wave.

2. Potential Nursing Diagnosis
a. Risk for injury
b. Decreased cardiac output
c. Altered nutrition: less than body requirement
d. Altered memory
*Interventions:
1. Prevent hypomagnesemia to high risk patients; early detection of
hypomagnesemia to high risk patients.
2. Monitor patients with hypokalemia for impending
hypomagnesemia

3. Monitor patients with hypomagnesemia who are receiving digoxin
for signs of digitalis toxicity.
4. Assess for deep tendon reflex, refer to physician if noted.
5. Monitor v/s, intake & output.
6. Institute seizure precaution.
7. Infuse MgSO4 with caution, can be given by IM, IVP, IV infusion with
caution. Assess patient’s status:
- v/s, deep tendon reflex, RR, urine output of patient.

Magnesium Excess: above 2.5 mEq/L
1. Causes:
a. Mg gain from medication & hyperalimentation
b. Inadequate excretion due to renal disease.
2. Signs and Symptoms:
a. Decreased cardiac output manifested by hypotension.
b. Since magnesium causes warm systemic sensation, patient may
appear flush, may verbalized feeling of warmth.
c. Hypoactive deep tendon reflexes or decreased motor function of
extremities; decreased neuro-muscular activity

1. decreased cardiac output
2. risk for injury
3. Ineffective breathing pattern
*Interventions:
a. Prevent hypermagnesemia to high risk patients by identifying early
signs of the deficit.
b. Monitor v/s, urine output
c. Administer calcium gluconate as ordered to countereffect
magnesium toxicity

III. Acid-base Normal & Imbalance
A. Hydrogen ion Balance: Basic Concepts
a. Hydrogen ion is present in body fluids, both in the ECF & ICF
b. It determines the acidity or alkalinity of a solution or body fluids.
c. The greater the number of hydrogen ion the more acid the solution
is; the smaller the hydrogen ion the more alkaline the solution.
d. the acidity or alkalinity of body fluids or blood is measured in terms
of pH – normal blood pH – 7.35-7.45
e. If blood pH drops to below 7.35, it is acidosis; if blood pH is above
7.45 it is alkalosis.

f,. Hydrogen circulates within the body in 2 forms:
1. Volatile hydrogen, when CO2 is dissolved in water, it forms carbonic
acid, excreted in gaseous form by the lungs.
2. Non-volatile hydrogen ion ( metabolic ) – produced as a result of
metabolic processes.
- Some are formed from organic acids like uric acid; some are found in
the form of sulfuric acid , phosphoric acids, some are formed from
catabolic processes from fats forming ketone acids when glucose is
elevated & not used by the cells as source of energy.

- Excess metabolic acids formed as a result of anaerobic metabolism
like in severe tissue damaged forming lactic acids in burns, or tissue
injury or trauma.
g. Excretion of hydrogen ion:
1.The lungs primarily eliminate volatile hydrogen ion of carbonic acid as
CO2 & water.
2.The kidneys eliminate volatile acids in the form of:
- 60% is excreted in the urine as NH4 chloride.
- 40 % is excreted as weak acids

B. Hydrogen Ions Concentration Regulation
1. Dilution of EXCESS hydrogen ion in the ECF, first line of defense
2. Buffer by the following systems ; H2CO3- HCO3 buffer system;
Protein Buffer System ; Phosphorous Buffer System.
3. Respiratory Buffer System
4. Kidney Buffer System

1. Local Dilution of the Hydrogen Ion
• Example: if you do exercise, hydrogen is build up in the circulation, then
automatically distributed within the body with out any symptoms of
increased hydrogen ion, later it will have normal distribution.
2. Buffer system
a. The buffer system of the body is composed of weak acid that coexists
with a salt: ex. HCl ( strong acid) + NaHCO3 > H2CO3 ( WEAK ACID ) +
NaCl ( salt ). Results to normal blood pH.
- It can buffer 90% of the hydrogen ion in the ECF.
- It is the most important buffer system in the ECF; Lungs excrete H2C03
while the kidneys excrete HCO3 ( alkali )
- There should be 1 part of H2CO3 & 20 parts of HCO3 ( 1:20 ) ratio.

3. The Respiratory System
1. The lungs removed CO2 from the body in response to increase
hydrogen ion concentration in the blood.
- Arterial blood gases is measured by partial CO2 pressure ( PaCO2 )
Normal is 35-45 mmHg.
- The partial pressure of oxygen ( PO2 ) is called oxygen tension.
Normal is 75-100 mmHg.

2. Feedback Mechanism in the Regulation of
CO2.
- The respiratory center in the medulla controls the carbonic acid in the
bicarbonate-carbonic acid buffer system by means of a feedback
mechanism between the respiratory center & the lungs.
- When H2CO3 decreases in the blood, blood pH increased, the PCO2 is
decreased which maybe due to hyperventilation, the respiratory
center will decreased its function resulting to hypoventilation.
- Hypoventilation results to retention of CO2, combines with water to
form carbonic acid until blood pH returns to normal

- But if blood pH is decreased, H2CO3 is increased, CO2 is retained
maybe due to hypoventilation from sedation, obstruction of air
passages, CO2 is not given off, reaction of the medulla is to stimulate
respiration through hyperventilation to excrete the excess CO2 that
are retained until the H2CO3 & blood pH back to normal level.
- Lungs limitation to correct acid-base imbalance is they are only
capable of excreting volatile acids.

4. The Renal System
- The kidneys regulate bicarbonate in the HCO3-H2CO3 in the buffer
system & eliminate non-volatile hydrogen ions.
- It works slowly, takes several days to correct imbalance.
- The kidneys work to correct acid-base imbalances by:
1. Reabsorption of filtered bicarbonate
2. Hydrogen ion secretion in the kidney tubules
3. Production of NH3.

*Reabsorbing filtered bicarbonate- blood entering the glomeruli
contains bicarbonate ions, passes through the tubules & reabsorbed if
needed & excreted if the body’s blood pH is normal.
*Net secretion of H+ - cellular metabolism produces hydrogen ions that
must be excreted in the urine to keep the blood from too acidic.
H+ entering the renal tubular fluids combines with ammonia rather
than with HCO3.
*NH3 Mechanism – when certain amino acids break down, NH3 is
formed w/in the distal tubular cells. When NH3 diffuses from the cells
into the renal tubules, it reacts w/ H+ to form NH4,excreted in the
urine, this will increase the bicarbonate level.

Hydrogen Ion Imbalances
- Hydrogen ion balance depends on the normal function of the buffer
system, lungs & kidneys.
A. Types of hydrogen imbalances:
1. Acidosis – a condition where the hydrogen ion concentration in the
blood is elevated, normal bicarbonate is elevated, blood pH is
decreased.
2. Alkalosis – a condition where hydrogen ion concentration in the
blood is decreased, bicarbonate is elevated, blood pH is increased.

Defense Mechanism against Imbalances
1. Correction of the buffer system
- The first line of defense against hydrogen imbalance is through buffer
system
2. The second line of defense is the respiratory system
3. The third line of defense is the renal system
2. Assessment: all major manifestations are caused by the CNS.
- In respiratory or metabolic acidosis, the major problem is CNS
depression resulting in decreased respiratory & renal function
- In respiratory or metabolic alkalosis, the problem is CNS stimulation

Diagnosis of Hydrogen Ion Imbalances
1. Blood pH – determines the acidity or alkalinity of the blood; it does
not indicate if imbalance is respiratory or metabolic in nature.
- Normal – 7.35-7.45
- Below 7.35 – acidosis ; above 7.45 is alkalosis
2. PaCo2 determination – measures the amount of CO2 pressure of
arterial blood which its normal value is 35-45 mmHg
3. HCO3 – measures the bicarbonate level of the arterial blood; normal
level is 22-26 mEq/L.
*the above diagnostic exam is known as the ABG exams.

Interventions to Correct Acid-Base
Imbalances
1. Identify & treat cause of imbalance
2. Assist the respiratory &/ or the renal system through supportive
interventions to correct & compensate for the imbalance.
3. Monitor the renal & respiratory functions.
4. Asses for patient’s condition, ensure physiologic & psychologic
safety.
5. Administer medications that neutralize excess acids or base with
caution; commonly bicarbonate is given to correct acidosis, &
ammonium chloride to correct excess base or alkali.

The Four Major Acid-Base Imbalances
1. Respiratory Acidosis
2. Respiratory Alkalosis
3. Metabolic Acidosis
4. Metabolic Alkalosis

Respiratory Acidosis
1. Causes:
- Conditions that results to retention of CO2 results to increased CO2
level of the blood, decreased serum pH level.
a. Any condition that obstruct the excretion of CO2
b. Impaired neuromuscular function e.g. GBS, chest trauma
c. Depressed respiratory function
2. Assessment: dyspnea upon exertion, DOB, tachycardia, restlessness,
irritability, in severe cases patient may become disoriented, confused,
then coma

Interventions for Respiratory Acidosis
Goal: improve respiratory function, Provide patient’s comfort and
safety.
1. Plan activities that patient able to have rest periods in between
activities
2. Encourage deep breathing, coughing exercises to improve exchange
of CO2 & oxygen in the respiratory system.
3. Place patient in semi-fowler’s position. Encourage change of
position q 2 hrs.
4. Institute chest physiotherapy

5. Suction secretions if needed.
6. Provide emotional support & reassure to allay anxiety
7. Monitor respiratory rate, depth, & rhythm. Monitor O2 saturation,
indicate if room air, w/ O2 via nasal cannula,/ face mask
8. Administer low flow of oxygen as ordered.
9. Monitor ABG levels
10. Force fluids as tolerated and if not contraindicated.
11. Administer nebulization, antibiotics as ordered
12. Attach to mechanical ventilator if indicated

Respiratory Alkalosis
1. Causes: excessive CO2 excretion which results to decreased in
PaCO2, increased in H2CO3, increased in blood pH.
- This may be the result of hyperventilation & overstimulation of the
respiratory center.
- Anxiety may result to hyperventilation
- After a series of exercises, a person hyperventilates
- Hypoxia in high altitudes
- Defect in the adjustment of ventilators

Conditions that causes overstimulation of the
respiratory center of the brain:
1. Fever
2. CNS infection like meningitis
3. Intracranial surgery
4. ASA toxicity
* The increased blood pH of the blood increased neuromuscular
irritability manifested by hyperreflexia, positive Chvostek’s sign, &
muscular twitching, seizures sometimes occur.

Interventions for Respiratory Alkalosis
1. Identify patients at risk for respiratory alkalosis. Identify early
symptoms of the disease.
2. Assist the patient to breath slowly or normally.
3. Listen with sympathy to a patient with anxiety having
hyperventilation.
4. Ask the person to re-breath his/her own exhaled CO2 in a paper bag
thus increasing the H2CO3 in the blood.
5. Take precautions to prevent injury.
6. Monitor v/s, I& O, record. 7. check adjustment of ventilators.

Metabolic Acidosis- increased in H2CO3 &
Blood pH.
• A. Causes:
1. Overproduction of metabolic acids produced from metabolism,
such as DM, high fat, low CHO diet, prolonged fasting.
2. Excessive ingestion of acids like ASA, ferrous SO4, ammonium
chloride.
3. Renal Disease – in renal disease, the kidneys are unable to excrete
the excess acids from the blood, and decrease retention/
reabsorption of HCO3.
4. Abnormal losses of Alkali – losses from pancreatic, biliary, & lower
GI secretions through diarrhea results to retention of acids.

5. Severe tissue anoxia results to anaerobic metabolism like in cases of
burns, anemia, cardiac disorders.
*Interventions:
Goals: restore normal blood volume & osmolality; Correct HCO3 deficit;
Prevent electrolyte imbalances; Maintain safety of patient.
1. Restore normal blood volume & osmolality.
- Commonly patients with acidosis are dehydrated, monitor body
weight, I & O, administer isotonic solutions as ordered.
2. Correct HCO3 deficit. Na HCO3 may be given cautiously as ordered.

- It maybe add to IV solutions or given by IVP slowly or IV drip through
volumetric set.
3. Prevent electrolyte imbalances.
- Patients w/ metabolic acidosis may develop hyperkalemia as k+ shifts
from ICF to ECF in exchange of H+.
- Observe for signs of hypocalcemia, because as metabolic acidosis is
corrected, calcium bind to plasma protein, citrate, which contribute to
hypocalcemia. Observe for signs of tetany, because calcium regulates
neuromuscular irritability.

4. Protect patient from potential injury.
- Patients w/ metabolic acidosis may have altered level of
consciousness like seizure, irritability.
- Always put side rails up, don’t leave patient unattended.

Metabolic Alkalosis – bld pH above 7.45,
HCO3 ABOVE 26 mEq/L
1. Causes: it results to excessive loss of hydrogen ion or excessive
ingestion of alkali.
a. Excessive use of hydrogen ion
- From severe vomiting where Hcl acid stomach content is lost.
- Patients w/ GI suction where there is no electrolyte replacement.
- Loss of chloride which causes the kidneys to retain bicarbonate.
b. Excessive ingestion of alkali – patients with peptic ulcer & given
antacids

Interventions:
1. Identify cause of imbalance, & correct the imbalance.
2. Patients treated with peptic ulcer disease should be careful not to
overdose the intake of antacid.
3. Commonly patient is given PLR to replace fluid losses like in
vomiting, it contains 10 mEq of chloride, an alkali.
4. Correct water, cl-, Na, & potassium deficits, important when
correcting alkalosis.
5. Monitor v/s, I & O, record.
6. Observed signs of rebound effect of metabolic alkalosis.

• Evaluation:
1. Patient has normal breathing pattern.
2. Vomiting is controlled, able to tolerate oral feeding.
3. Intake & output are within normal balance.
4. Patient is free from injury.

Nursing Experiencing Burns
• A. Burns as defined caused by flames, chemicals, radiation, or
electrical current.
- Thermal burns is the most common, caused by fires in home,
vehicular accident, playing with matches in children, poorly stored
gasoline.
B. Functions of the skin 4. produce vit D
1. Protection against infection.
2. Prevent loss of body fluids.
3. For excretion, use for sensation

Pathophysiology of Burns
• Following burns, increased capillary permeability results, plasma
seeps into surrounding tissues, causing edema.
- This leads to body fluid loss w/c is greatest within 18-36 hrs.
- In mild cases of burns, fluid leak into the burned areas; while in
severe cases, it leads to systemic fluid loss.
*Factors determining burn severity:
A. Burn depth
1. First degree – affects superficial part of the skin or the epidermis
- Skin appears pink & red, w/ small thin blisters

2. Second degree burn or partial thickness, where only part of the skin
is damaged
- Both dermis & epidermis are affected.
- Large thick-walled blisters develop, commonly covering the burned
area.
3. Third degree burn or full thickness burn – all the skin, dermis,
epidermis are destroyed including the subcutaneous, muscle & bone,
- The color may be deep red, white or black, or brown.

4. full-thickness burn – structures beneath the skin are severely
affected.
• Determining Burn Size: determine BSA affected
- It is determined by the “Rule of Nine” or the “ Lund and Browder”
method. But commonly the rule of nine is used in the hospital.
- According to the rule of nine, the body is divided into 9% of the total
body areas affected.
- Head & neck – 9% ; right upper ext. 9%; left upper ext. 9%; anterior
trunk – 18%; posterior trunk – 18%; right lower ext. 18%; left lower
ext. 18%; perineum 1%

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