TOPIC 1: FOUNDATIONAL CONCEPTS AND ASSESSMENTS

A) KEY ELEMENTS UNDERLYING FLUID AND ELECTROLYTE IMBALANCE

1) THE CELL MEMBRANE

CELL
 smallest autonomous functional unit of the body
 in its fetal form it is undifferentiated, but as growth continues the cell differentiates into
specific tissue types, forming organs and systems.

CELL WALL
 a semipermeable membrane that separates the intracellular from the extracellular
components, allowing for an exchange in an effort for the cell to obtain energy,
synthesize complex molecules, participate in electrical events, and replicate.
 Semipermeability – ability of cell to choose what comes in and out of cell; play major role
in fluid volume excess or deficit

Endoplasmic Reticulum Nuclear Membrane

- involved in lipid (fats) and protein - lining of the nucleus
synthesis - encloses the cell nucleus that
permits the passage of proteins
Ribosomes and certain materials
- contains the RNA
Golgi
Nucleus - involved in the secretion in the
- contains the DNA; maintains the intracellular transport
integrity facilitating transcription and
replication processes Cytoplasm
- where most activities of the cell
Nucleolus happen
- largest; most prominent organelle of - responsible for the shape of the
the cell cell
- facilitates signal recognition, facilitates
impulses Mitochondria
- the site of transcription and processing - stores energy; energy currency of
of the ribosomal gene the
cell

Chloroplast
- where the energy is processed
COMPOSITION

1. PHOSPHOLIPIDS
 Double phospholipid bilayer
 arranged in one end hydrophilic and the other end hydrophobic

Hydrophylic head (loving water)

 faces the outside of the membrane, retaining water and adhering to the neighboring
cell

Hydrophobic tail (hating water)

 associates with other fatty groups to exclude the hydrophilic groups

2. PROTEINS
 second major component of the cell membrane where most of the functions of the
cellular membrane occur
 They transport lipid-insoluble particles acting as carriers to pass these compounds
directly through the membrane. Some proteins form ion channels for the exchange of
electrolytes. The type of protein involved depends on the cell’s function.
 Protein channels – speciifc gates that would allow something to pass through
(solutes, fluids, nourishments, electrolytes)

3. CELL COAT
 long chains of complex carbohydrates make up glycoproteins, glycolipids and lectins
that form the outside surface of the cell. This intricate coat helps in cell-to-cell
recognition and adhesion.

FIGURE 1-1 THE CELL MEMBRANE

*aquaporins – open for water, main channel where water flow in and out of cell
HOW SOLUTES MOVE IN AND OUT OF CELL

 Solube – easily dissolved

 insoluble – bigger; need specific protein channel (carrier mediated facilitated diffusion)

B) BODY FLUID COMPOSITION

➢ Body fluid is composed of water and various dissolved substances (solutes)

1) WATER
 Water is the primary component of body fluids and functions in several ways to maintain
normal cellular function.
 Water provides a medium for the transport and exchange of nutrients and other
substances such as oxygen, carbon dioxide, and metabolic wastes to and from cells;
provides a medium for metabolic reactions within cells; and assists in regulating body
temperature through the evaporation of perspiration.
 Total body water constitutes about 60% of the total body weight, but this amount varies
with age, gender, and the amount of body fat. Total body water decreases from 45% to
50% of total body weight with obesity and with aging (Porth & Matfin, 2009).
 Fat cells contain comparatively little water. In the person who is obese, the proportion of
water to total body weight is less than in the person of average weight; in a person who
is very thin, the proportion of water to total body weight is greater than in the person of
average weight. Adult females have a greater ratio of fat to lean tissue mass than adult
males; therefore, they have a lower percentage of total body water.
 ADULT: weight of body contains 60% of water in males and 50% in female
 If younger, mas taas ang fluid composition
 As you grow older, mas liliit fluid compositon
 Urine output of pt with renal failure: decreased fluids = fluid retension = edema
o Weigh pt daily to know if management/treatment is effective – decrease in weight
 If may fluid volume overload, cold clammy skin; if dehydrated – febrile
 Fats and water can’t mix together

Functions:
1. Temperature regulation: controls temperature
2. Transport of materials to/from the cells: maintain homeostasis
3. Aqueous medium for cellular metabolism (provides a medium for metabolic reaction)
4. Assist in food digestion (hydrolysis): saliva, gastric juices, enzymes
 5. Acts as solvent in which solute are available for cell function: water is a universal solvent
i Solute + Solvent = Solution
6. Maintain blood volume: plasma (90% water), RBCs, WBCs and platelets
i low fluid = low blood volume = decrease blood pressure
ii high fluid = high BV = high BP
iii given diuretics to decrease water and BV to decrease BP_
7. Medium of waste excretion: in a form of sweat, urine, and feces
8. Cushion body parts from injury: CSF cerebrospinal fluid for the spine; synovial fluid for the
joints

Factors Affecting Body Water:

1. Age: the amount of water decreases with age

Infant 70-80%
Adult 50-60%
Elderly 45-50%

2. Sex: males have more water because of energy expenditure

Male 60%
Female 50%

3. Body Fats: more fat cells, the lesser water content

Fat cells contains little H2O
If BMI keeps increasing, lower fluid composition

NOTE: To maintain normal fluid balance, body water intake and output should be approximately
equal. The average fluid intake and output is about 2500ml over a 24-hour period.
*approximately equal if healthy; does not apply to hospitalized patients (expect lesser
output in sick person because body is trying to recover from loss of water)

INSENSIBLE WATER LOSS

 occurs through the skin (sweating), lungs (exhalation) and feces
 hard to measure
 can increase significantly during

1. Exercise;
2. High environmental temperatures;
3. During illnesses that increases respiratory rate, perspiration or GI losses

Table 1-1 Approximate Values of 24-Hour Fluid Gain and Loss of An Adult
Intake (Gain) vs Output (Loss)
H2O (Orally) 1,000 Urine 1500
Water in Food 1,300 Feces 200
Oxidation 200 Perspiration 500
Total 2,500 ml Respiration 300
Total 2,500 ml
2) ELECTROLYTES
 These are minerals in your body that have an electric charge.
 In blood, urine, tissues and other body fluids
 Help balance the amount of water in body
 Body fluids contain both water molecules and chemical compounds. These chemical
compounds can either remain intact in solution or dissociate into discrete particles.
 Electrolyte Imbalances – deficit (hypo) or excess (hyper)
 Electrolytes – sodium, potassium, calcium, magnesium, phosphate

Electrolytes are substances that dissociate in solution to form charged particle called ions.
Cations (+) are positively charged electrolytes; anions (-) are negatively charged electrolytes.
 electrically charged particles and is expressed in terms of milliequivalent per liter
(mEq/L)
*IONS – dissociated electrolyte particles which carry either (+) (-) charge
(+) charge = cations
(-) charge = anions

4 MAJOR FUNCTIONS OF ELECTROLYTES:

1) Assisting with regulation of water balance
a Where sodium goes, water follows
b Sodium and potassium
2) Regulating and maintaining acid-base balance
a If high potassium – acidosis
3) Contributing to enzyme reactions
a Sodium potassium pump
4) Essential for neuromuscular activity
a Need sodium potassium pump for muscles to move

Table 1-2 Major Electrolyte Per Body Compartment

EXTRACELLULAR FLUID
ANIONS CATIONS
Chloride (Cl-) (most abundant) Sodium (Na+) (most abundant)
Bicarbonate (HCO3 - ) Calcium (Ca++)
Magnesium (Mg++)

INTRACELLULAR FLUID
ANIONS CATIONS
Phosphorus/Phosphate (HPO4-2) (most abundant) Potassium (K+) (most abundant)
Sulfates (SO4-2) Magnesium (Mg++) Proteins (Prot-)
  4 hours duration only = BLOOD TRANSFUSION
o Ex: in transfusing RBC (if mag lysis ang RBC sa packed RBC, lalabas ang
electrolytes)
o at risk for developing hyperkalemia or hyperphosphatemia
o as blood products stay longer, increase hemolysis (blood breakdown)

Table 1-3 Electrolyte Distribution

Cations (+) Plasma Interstitial ICF
Sodium (Na+) 142 146 15
Potassium (k+) 5 5 150
Calcium (Ca++) 5 3 2
Magnesium (Mg+ 2 1 27
+)
154 mg/L

Phosphate inside chloride outside

Anions (-) Plasma Interstitial ICF

Chloride (Cl) 102 14 1
Bicarb (HCO3) 27 30 10
Phosphate (HPO4- 2 2 100
2)
Sulfate (SO4-2) 1 1 20
Organic Acid 5 8 0
Proteinate (Prot-) 16 1 73
154 mg/L
Table 1-4 Common Electrolytes

ELECTROLYTE DISTRIBUTION IN BASIC FUNCTIONS DIETARY

ION BODY FLUID SOURCES
ECF ICF (mEq/L)
(mEq/L)
Sodium (Na+) 135-154 15-20 o regulates fluid volume o table salt
within ECF o cheese
*hypernatremi compartment o milk
a or o regulates vascular o processed
hypertension osmotic pressure meat,
*RAAS o controls water o poultry
mechanism – distribution between o shellfish
increase ECF and ICF o fish
hypertension compartments o eggs
*Primary o participates in
o foods preserved
hypertension – conduction of nerve
very active with salt (eg
impulses
RAAS, ham and bacon)
o maintains
LSLF/DASH neuromuscular
diet excitability

Potassium 3.5-5 150-155 o regulates osmolality of o Fruits,

ICF especially
o participates in bananas,
transmission of nerve oranges, and
impulses dried fruits
o promotes contraction o vegetables
of skeletal and smooth o meats
muscles o nuts
o regulates acid-base o peas
balance by cellular
exchange of hydrogen
ions
Calcium 4.5-5.5 1-2 o provides strength and o dairy products
durability to bones and (milk, cheese,
teeth and yogurt)
o establishes thickness o sardines
and strength of cell o whole grains
membranes o green leafy
o promotes transmission vegetables
of nerve impulses
o maintains
neuromuscular
excitability
 o essential for
blood coagulation
o activates enzyme
reactions and
hormone secretions
Magnesium 4.5-5.5 27-29 o activates enzyme o green leafy
systems, mainly those vegetabless
associated with vit. B o whole grains,
metabolism and the o fish
use of potassium, o nuts
calcium and protein
o promotes regulation of
serum calcium,
phosphorus and
potassium levels
o promotes
neuromuscular activity

Table 1-5 Serum Component

SERUM COMPONENT VALUES
CONVENTIONAL SI
Sodium 135-145 mEq/L 135-145 mmol/L
Chloride 98-106 mEq/L 98-106 mmol/L
Bicarbonate 22-26 mEq/L 22-26 mmol/L
Calcium 8.5- 10.0 mEq/L 2.1-2.6 mmol/L
Potassium 3.5-5.0 mEq/L 3.5-5.0 mmol/L
Phosphate/inorganic 1.7-2.6 mEq/L (2.5-4.5 0.8-1.5 mmol/L
phosphorus mg/dl)
Magnesium 1.6-2.6 mg/dl (1.3-2.1 0.8-1.3 mmol/L
mEq/L)
Serum osmolality 275-295 mOsm/kg 275-295
mmol/kg

B) BODY FLUID COMPARTMENT (DISTRIBUTION)

Body Fluid is classified by its location inside or outside the cells. Capillary and cell membranes
separate total body fluids into two main compartments: the intracellular and extracellular.

*TOTAL BODY WATER*

Total body water is the equivalent of the fluids that exist in all the fluid compartments. This
approximately 60% of the body weight of an average adult. Expressed in kilograms, 1L of fluid
is equivalent of 2.2 lb (1kg).
 FIGURE 1-2 TOTAL BODY FLUID
 BLOOD
o Plasma (55%; 90% of plasma is water, albumin)
o Formed elements (45%)
 Extravascular or interstitial space
 Hypoalbuminemia – nephrotic pt (edema)
o If low albumin in intravascular, decrease
o Albumin help pulling back liquids from extravascular to intracellular space)

 Extracellular Compartment
o Found outside of cell
o Extravascular space, interstitial space, intravascular space or plasma
 Intracellular
1. INTRACELLULAR FLUID (ICF) (40%)
Intracellular fluid (ICF) is found within cells. ICF is essential for normal cell function,
providing a medium for metabolic processes.
➢ Make’s up 2/3 of the body’s water or 40% of Body weight
➢ Larger of the two compartments
➢ Rich in electrolytes, potassium, magnesium, inorganic and organic phosphates and
proteins

2. EXTRACELLULAR FLUID (ECF) (20%)

Extracellular fluid (ECF) is located outside of cells
➢ contains all the fluid outside the cells
➢ accounts for 20% of Body weight
 ➢ rich in electrolytes: sodium, chloride and bicarbonate

ECF is further classified by location:

a) Interstitial Fluid (15%)

 located in the spaces between most cells of the body ➢ accounts for approximately
15% of Body weight

b) Intravascular Fluid (5%)

 blood vessel compartments
 called “plasma”, is contained within the arteries, veins, and capillaries

c) Transcellular Fluid (1%)

- includes urine; digestive secretions; perspiration; and cerebrospinal, pleural, synovial,
intraocular, gonadal, and pericardial fluids the transcellular space contributes approximately 1%
of the body fluid, and significant gains and losses do not occur on a daily basis

FIGURE 1- 3 FLUID COMPARTMENTS OF THE BODY

C) MECHANISM OF FLUID TRANSPORT
Four chemical and physiologic processes control the movement of fluid, electrolytes, and other
molecules across membranes between the intracellular and interstitial space and the interstitial
space and plasma. These processes are osmosis, diffusion, filtration, and active transport.

1) ACTIVE TRANSPORT
 Active transport allows molecules to move across cell membranes and epithelial
membranes against a concentration gradient.
 This movement requires energy (adenosine triphosphate [ATP]) and a carrier
mechanism to maintain a higher concentration of a substance on one side of the
membrane than on the other.
 Transport substances that are unable to pass by diffusion
o They may be too large
o They may not be able to dissolve in the fat core of the membrane
o They may have to move against a concentration gradient
 Two common forms:
o Solute pumping (sodium potassium pump)
o Bulk transport (endocytosis and exocystosis)
 Movement of solutes from an area of lower concentration against higher concentration
gradient
➢ Complex sugar, ions, large cells, proteins, and other particles are transported in this
process.

Types of Active Transport:

 Primary Active Transport: uses the initial source of energy to carry the substance
 Secondary Active Transport (cotransport): harnesses the energy obtained from the primary
active transport and uses it as a cotransporter of a secondary substance
EXAMPLES OF PRIMARY ACTIVE TRANSPORT
1. Sodium-Potassium Pump
 The sodium-potassium pump moves sodium ions out of and potassium ions into the cell.
 This pump is powered by ATP. For each ATP that is broken down, 3 sodium ions move
out and 2 potassium ions move in.
 Solute pumping
o Amino acids, some sugars and ions are transported by solute pumps
o ATP energizes protein carriers, and in most cases, moves substances against
concentration gradients

FIGURE 1-4 SODIUM-POTASSIUM PUMP

2. Endocytosis (Bulk Transport)

 plasma membrane surrounds the substance being transported and transport the
substance into the cell
 extracellular substances are engulfed by being enclosed in a membranous vesicle

3 MAIN KINDS OF ENDOCYTOSIS

a) Phagocytosis or cellular eating

 Occurs when the dissolved materials enter the cell. The plasma membrane engulfs
the solid material, forming a phagocytic vesicle.
 Cell eating; dissolved materials enter the cell -> plasma membrane engulfs the solid
material -> phagocytic vesicle

b) Pinocytosis or cellular drinking

 Occurs when the plasma membrane folds inward to form a channel allowing dissolved
substances to enter the cell. When the channel is closed, the liquid is encircled within
a pinocytic vesicle.
 Cell drnking; plasma membrane folds inward to form a channel allowing dissolved
substances to enter the cell -> pinocytic vesicle

c) Receptor-Mediated Endocytosis (RME)

  Also called clathrin-mediated endocytosis, is a process by which cells absorb
metabolites, hormones, proteins – and in some cases viruses – by the inward budding
of the plasma membrane.

FIGURE 1- 6 EXOCYTOSIS

FIGURE 1- 7 EXOCYTOSIS VS ENDOCYTOSIS

3. Exocytosis (Bulk Transport)

 Moves materials out of the cell
 Material is carried in a membranous vesicle
 Vesicle migrates to plasma membrane
 Vesicle combines with plasma membrane
 Material is emptied to the outside
2) PASSIVE TRANSPORT
 In this biological process, there is no need for any energy for transporting the molecules,
as the biochemicals move from higher to the lower concentration.
 This process is carried out to maintain the balance and the equilibrium level in a cell. All
the wastes molecules including, water and carbon dioxide is separated and moved out of
the cell using passive transport.

3 TYPES OF PASSIVE TRANSPORT

1. OSMOSIS
 Osmosis is the process by which water moves across a selectively permeable
membrane from an area of lower solute concentration to an area of higher
solute concentration. A selectively permeable membrane allows water molecules to
cross but is relatively impermeable to dissolved substances (solutes). Osmosis
continues until the solute concentration on both sides of the membrane is equal.
(Lemone, 2017)
 the distribution of water from a lesser area of solute concentration to a higher area of
solute concentration
 the direction is determined by the concentration of particles on either side of the cell
membrane
 osmosis stops when the concentration of solutes on both sides of the membrane
becomes equalized
 osmosis the primary process that controls body fluid movement between the ICF and
ECF compartments

FIGURE 1-8 OSMOSIS

OSMOLALITY
 Osmolality, or concentration of a solution, refers to the number of solutes per kilogram
of water (by weight); it is reported in milliosmoles per kilogram (mOsm/kg). The
 osmolality of the ECF depends chiefly on sodium concentration. Serum osmolality
may be estimated by doubling the serum sodium concentration (approximately 142
mEq/L). Glucose and urea contribute to the osmolality of ECF, although to a lesser
extent than sodium.
 normal serum osmolality is 280-300 mOsm/kg
 Solvent and solute
 If higher solute concentartion = increase in osmolality
 If lower solute concentration = decrease in osmolality
OSMOLARITY
 the number of solutes per Liter of fluid

OSMOTIC PRESSURE
 the power of a solution to draw water across a membrane
 regulated by solutes (such as sugar and albumin)

ONCOTIC PRESSURE
 also called colloid osmotic pressure (COP)
 inversely proportional with hydrostatic pressure
 osmotic pressure exerted by plasma proteins in the vessels (e.g., albumin)
 proteins in the bloodstream exert oncotic pressure to pull fluid out of the interstitial
space into the intravascular space to maintain fluid balance and osmolality
 average COP is 28mmHg, a pressure that remains constant across the capillary
 capillary – gas exchange
 as heart pushes blood to circulation, increase hydrostatic pressure, fludis go out from
intravascular to extravascular
 increased oncotic pressure on veins
 pressure that pulls fluids from from extravascular to blood vessels

TONICITY
 refers to the effect a solution’s osmotic pressure has on water movement across the
cell membrane of cells within that solution
 solutions (solute + solvent)

1) ISOTONIC SOLUTION (Normal)

 have the same concentration of solutes as plasma
  cells placed in an isotonic solution will neither shrink nor swell because there is no
net gain or loss of water within the cell, and no change in cell volume
 solvent = solute
 volume expander
o effect: increased blood volume
o No 1 treatment
o needed by pts with:
▪ hypovolemia (caused by cellular dehydration)
o VS: low bp, low bv = hypoxia (decerased oxygen level)
= ìncrease RR and PR = if not treated will lead to ischemia
(impede distribution of oxygen) = multiple organ failure
▪ hemorrhage

2) HYPERTONIC SOLUTION (Shrink)

 have a greater concentration of solutes than plasma
 in their presence, water is drawn out of a cell, causing it to shrink
 high solute; low solvent
 no leaking of fluids from intravascular to interstitial
 goal: increase oncotic pressure in blood vessels kasi puno na ang fluids, can’t go
back to intravascular space, to pull back fluids from interstitial to intravascular
 volume expander (of blood in intravascular)
o effect: increased blood volume
o maintenance treatment for hypovolemia
o given to pt with edema
▪ give mannitol (diuretic) – cerebral edema
o not given to pt with kidney problems (cause congestion, fluid volume
excess) – given diuretics
o needed by pts with:
▪ hypovolemia (caused by hyponatremic dehydration)
o VS: low bp, low bv = hypoxia (decerased oxygen level)
= ìncrease RR and PR = if not treated will lead to ischemia
(impede distribution of oxygen) = multiple organ failure
▪ Hemorrhage
 Fluid volume excess
o Congestive heart failure
 Left side
 Diminished breath sounds
 Crackles
 Cough
 Pulmonary edema
 Right side
 Systemic circulation
 Peripheral edema
 Anasarca
 Diuretics
o Decrease potassium levels (watch out for) – given potassium sparing
(aldactone)
o Increase potassium levels
 3) HYPOTONIC SOLUTION (Swell)
 have a lower solute concentration than plasma
 when red blood cells are placed in a hypotonic solution, water moves into the
cells, causing them to swell; rupture (hemolysis) of cells may occur with extremely
hypotonic solutions
 low solute; high solvent

HYPERTONIC ISOTONIC HYPOTONIC

o D5LR, D5NSS o D5W (not yet o D5W (if inside blood
o D10 transfused to blood vessel, metabolizes
o D50W vessels) inside, interact with
o Burns (Lactated o 0.9 PNSS, PLR molecules)
Ringer’s solution, o Hypovolemia o 0.45
NSS if no LR) o Dehydration o dehydration
o CI: diabetic o Burns (Lactated
ketoacidosis, Ringer’s solution,
hyperosmolar NSS if no LR)
hyperglycemin
nonketotic acidosis
(because high
glucose content)

[PLASMOLYSIS] [NORMAL] [HEMOLYSIS]

FIGURE 1-9 EFFECTS OF TONICITY OF A SOLUTION TO CELLS

2. DIFFUSION
Diffusion is the process by which solute molecules move from an area of high solute
concentration to an area of low solute concentration to become evenly distributed.

2 TYPES OF DIFFUSION

1) SIMPLE DIFFUSION
 Simple diffusion occurs by the random movement of particles through a solution.
 Water, carbon dioxide, oxygen, and solutes move between plasma and the interstitial
space by simple diffusion through the capillary membrane.
  Water and solutes move into the cell by passing through protein channels or by
dissolving in the lipid cell membrane.
 Unassisted process
 Solutes are lipid-soluble materials or small enough to pass through membrane process

2) FACILITATED DIFFUSION
 Facilitated diffusion, also called carrier-mediated diffusion, allows large water-soluble
molecules, such as glucose and amino acids, to diffuse across cell membranes.
 Proteins embedded in the cell membrane function as carriers, helping large molecules
cross the membrane.
 The rate of diffusion is influenced by a number of factors, such as the concentration of
solute and the availability of carrier proteins in the cell membrane.
 Substances require a protein carrier for passive transport

FIGURE 1-10 SIMPLE DIFFUSION / FACILITATED DIFFUSION

3. FILTRATION
 Process by which water and dissolved substances (solutes) move from an area of high
hydrostatic pressure to an area of low hydrostatic pressure.
 Heart (mainly) and blood vessel – responsible for giving hydrostatic pressure (pressure
that pushes fluids from intravascular to extravascular/interstitial space, kidney
 Nephron – responsible for functioning of kidney; basic functional unit
 Usually occurs across capillary membranes.
 Kidney – filters plasma (protein, RBC not allowed to pass)
 Glomerulus (specialized blood vessel), filtered by Bowman’s capsule
 Edema is caused by decreased osmotic pressure or colloid oncotic pressure (fluid
retention in interstitial space)
o Low albumin – low osmotic pressure
o Given albumin to increase osmotic pressure

*HYDROSTATIC PRESSURE
 created by the pumping action of the heart and gravity against the capillary wall
 filtration occurs in the glomerulus of the kidneys, as well as at the arterial end of
capillaries
 FIGURE 1-11 HYDROSTATIC PRESSURE

FLUID REGULATION
 Homeostasis requires several regulatory mechanisms and processes to maintain the
balance between fluid intake and excretion.
 These include thirst, the kidneys, the renin–angiotensin–aldosterone mechanism,
antidiuretic hormone, and atrial natriuretic peptide.
 These mechanisms affect the volume, distribution, and composition of body fluids.
 Fluid Volume Deficit or Fluid Volume Excess = if homeostasis is tilted
FIGURE 1-12: When the water level is below the normal range resulting in high level of solute
concentration, brain triggers thirst that stimulate us to drink more water. In addition,
hypothalamus stimulates posterior pituitary gland to releases ADH (antidiuretic hormone) into
the bloodstream. This hormone travels to the kidneys in order to stimulate nephrons to reabsorb
more water. Water is reabsorbed from the kidneys back to the blood resulting in a small volume
of more concentrated urine. Also, the solute concentration in the blood is decreased and moved
to the normal range. On the other hand, if a person drinks a lot of water, ADH will not be
secreted. As a result, there will be increase in fluid loss through the urinary system and the
urine will be lighter in color.

1) THIRST
 Thirst is the primary regulator of water intake.
 Thirst plays an important role in maintaining fluid balance and preventing dehydration.
 The thirst center, located in the hypothalamus (brain), is stimulated when the blood
volume drops because of water losses or when serum osmolality increases.
o Thirst is stimulated by dehydration or low fluid content in body (Normal)
o Thirsr by increased sugar of blood (Diabetes)
 Polydipsia (excessive thirst), polyuria (frequent urination), polyphagia
(excessive hunger)
 The thirst mechanism is highly effective in regulating extracellular sodium levels.
Increased sodium in ECF increases serum osmolality, stimulating the thirst center.
o If extarcellular is high: stimulate to drink water (blood is concentrated, abundant
cation outside cell, need to drink water to normalize)
o If extracellular is low: not be stimulated to drink
 Fluid intake in turn reduces the sodium concentration of ECF and lowers serum
osmolality. Conversely, a drop-in serum sodium and low serum osmolality inhibit the
thirst center. (Lemone,2017)
o Osmolality – concentration of solute and solvent
  Increased serum osmolality = high concentration = low solvent = stimulate
thirst
 As you grow older, declined thirst regulation (older adults and altered LOC:
at risk for dehydration and water osmolality)

NOTE: The thirst mechanism declines with aging, making older adults more vulnerable to
dehydration and hyperosmolality. Patients with an altered level of consciousness or who are
unable to respond to thirst, such as intubated patients and artificially fed patients, are also at
risk.

2) KIDNEYS

 The kidneys are primarily responsible for regulating fluid volume and electrolyte balance
in the body.
o If dehydrated, increased reabsorption of water, increased sodium (fluid volume)
o Ano ang sobra, ginaexcrete kidneys, kung ano kulang, reabsorb by kidneys
specifically in renal tubules (electrolyte imbalance)
 They regulate the volume and osmolality of body fluids by controlling the excretion of
water and electrolytes.
 In adults, about 170 L of plasma are filtered through the glomeruli every day.
 By selectively reabsorbing water and electrolytes, the kidneys maintain the volume and
osmolality of body fluids.
 About 99% of the glomerular filtrate is reabsorbed, and only about 1500 mL of urine is
produced over a 24-hour period. (Lemone, 2017)
 Besides regulating fluid balance, the kidneys also contribute to regulation of electrolyte
levels. Selectively secreting or reabsorbing electrolytes achieves body balance. Two
important electrolytes regulated by the kidneys are hydrogen and bicarbonate.
Regulation of these two ions contributes significantly to the body’s overall acid-base
balance. (Daniels, 2007)
 Regulation of Acid and Base = hdyrogen and bicarbonate = acid base balance
o Respiratory Acidosis: Increase regeneration of bicarbonate
o Respiratory Alkalosis: decrease regeneration of bicarbonate + reabsorption of
hydrogen ions

Major Functions of Kidneys in maintaining normal fluid balance

1. Regulate ECF volume and osmolality by selective retention and excretion of body fluids
2. Regulation of electrolyte levels in the ECF by selective retention of needed substances and
excretion of unneeded substances
3. Regulate pH of ECF by retention of hydrogen ions
4. Excretion of metabolic wastes and toxic substances

3) RESPIRATORY SYSTEM

 Buffer system (neutralizes weak acids, if does not work to correct blood pH, lungs and
kidneys will enter)
  The lungs participate in the maintenance of fluid balance by excreting moisture during
exhalation. Under normal conditions, this contributes about 300ml per 24hours to the
fluid output of the body.
o Insensible water loss
 However, in cases of increased respiratory rate, as may occur with fever or respiratory
problems, such as pneumonia, the amount of fluid lost during respiration can increase
significantly, potentially leading to fluid deficits.
 The lungs also play a role in acid-base balance by regulating excretion of carbon dioxide
(CO2).
 Increased excretion of moisture during exercise/physical activity (due to increased
breathing)
 Lungs regulate acid base balance by:
o Metabolic Acidosis: increase excretion through exhalation of CO2
 Compensatory mechanism: hyperventilation
o Metabolic Alkalosis: decreased excretion, conservation of CO2
 Treat cause of anxiety or hyperventilation: calm pt, breathe brown bag to circulate CO2
 Kussmaul’s respiration: fast breathing to excrete CO2, hyperventilation
 Lungs can hypoventilate: to conserve CO2; treat metabolic acidosis and alkalosis
 Fluid regulation: Increase or decrease RR
o Increase RR = Increase insnsible water loss
o Decrease RR = Decrease water loss

4) RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM
 How is RAAS activated or stimulus?
o Decrease blood pressure -> decrease blood volume -> hypoxia (decreased
oxygen distribution to tissues)
 Hypoxemia (decreased O2 levels in blood; specifically RBC, Hemoglobin) will always
result to hypoxia but hypoxia is not always caused by hypoxemia
 Hypoxia can happen even though there is normal level of oxygen in blood
o Occlusions, pt with stroke or MI, there is blockage no proper tissue perfusion
o Brain problems
 Chronic hypertension leads to congestive heart failure\
 Angiotensin II targets blood vessels and adrenal glands, adrenal cortex in kidney
 BT to address hemorrhagic shock
o At risk for multiple blood transfusion
o Hyperkalemia
o Hyperphosphatemia
o *RBC

The renin–angiotensin–aldosterone system helps to maintain intravascular fluid balance and

blood pressure (because of angiotensis II and aldosterone)
A decrease in blood flow or blood pressure to the kidneys stimulates specialized receptors in the
juxtaglomerular cells of the nephrons to produce renin, an enzyme.

Renin converts angiotensinogen (a plasma protein) in the circulating blood into angiotensin I.

Angiotensin I travel through the bloodstream to the lungs where it is converted to angiotensin II
by angiotensin converting enzyme (ACE).

Angiotensin II is a potent vasoconstrictor; it raises the blood pressure. It also stimulates the thirst
mechanism to promote fluid intake and acts directly on the kidneys, causing them to retain
sodium and water.

Angiotensin II stimulates the adrenal cortex to release aldosterone. Aldosterone promotes

sodium and water retention in the distal nephron of the kidney, restoring blood volume, Act on
renal tubules = increase renal reabsorption, secrete potassium

FIGURE 1-13 RENIN-ANGIOTENSIN SYSTEM

5) ANTI DIURETIC HORMONE (VASOPRESSIN)
 Antidiuretic hormone (ADH), released by the posterior pituitary gland, regulates water
excretion from the kidneys
o Concentrated urine, conserving water
o Increase in water/fluid reabsorption
o Promotes water reabsorption
o Decreased urine output
 What is the stimulus to activate ADH? Dehydration or fluid volume deficit
 Osmoreceptors in the hypothalamus respond to increases in serum osmolality and
decreases in blood volume, stimulating ADH production and release.
 Hyposecretion of ADH
o DI (diabetes insipidus) – it mimicks the two 2Ps of DM (polydipsia and polyuria)
o 3 features:
 Hemoconcentration – low water in plasma, increase hematocrit
 Hypernatremia – water alone is being urinated, reabsorbing sodium
 Urine dilution – water composition of urine, conservation of solute levels,
decrease specific gravity
 Hypersecretion of ADH
o SIADH (syndrome of inappropriate antidiuretic hormone secretion)
o Tumor in pituitary gland
o 3 features:
 Hemodilution – increased water retention, water solves as solvent, low
hematocrit (monitor volume of RBC and plasmta)
 Hyponatremia – not due to deficit, due to hemodilution, sodium is being
dissolved
 Urine concentration – due to excretion of solutes, less water/solvent
(reabsorption of water, increase specific gravity)
 Hematocrit and specific gravity = lab tests to determine SIADH and DI
 ADH acts on the distal tubules of the kidney, making them more permeable to water and
thus increasing water reabsorption.
 With increased water reabsorption, urine output falls, blood volume is restored, and serum
osmolality drops as the water dilutes body fluids.
 Increased amounts of ADH are also released in response to stress situations such as
nausea, pain, surgery and anesthesia, narcotics, and nicotine.
  Its release is inhibited by alcohol and medications such as phenytoin, as well as by
increased blood volume and decreased serum osmolality.

 Blood Pressure
 Blood Volume
 BloodOsmolality

Osmoreceptors in hypothalamus stimulate

posterior pituitary to secrete ADH

ADH increases distal tubule

permeability
to reabsorption
of H20

 UrineOutput
 Blood Pressure
 BloodVolume
 BloodOsmolality

Figure1-14. Antidiuretic hormone (ADH) release and effect. Increased serum osmolality or a fall
in blood volume stimulates the release of ADH from the posterior pituitary. ADH increases the
permeability of distal tubules, promoting water reabsorption.

D) ATRIAL NATRIURETIC PEPTIDE

 Atrial natriuretic peptide (ANP) is a hormone released by atrial muscle cells in response
to distention from fluid overload.
 BP stimulates ANP
 ANP affects several body systems, including the cardiovascular, renal, neural, GI, and
endocrine systems, but it primarily opposes the renin–angiotensin–aldosterone system
by inhibiting renin secretion and blocking the secretion and sodium-retaining effects of
aldosterone.
 As a result, ANP promotes sodium wasting and increased urine output.
 Helps heart when RAAS kicks in to counteract RAAS
 Address fluid volume excess
 FIGURE1-15. ATRIAL NATRIURETIC PEPTIDE MECHANISM

 Vasopressin – posterior pituitary gland

 Increased GFR = high urine output
 Decrease renin secretion, renin become hesitant to go out
 Adrenal cortex – inhibits aldosterone (mineralocorticoids), secrete cortisol
(glucocorticoid)
 Medulla oblongata decrease BP

6) CORTISOL
 AKA Cortisone or glucocorticoid
 Secreted by adrenal cortex
 Anti inflammatory drugs (Steroidal)
o SAIDS
o Steroid therapy (ex: corticosteroid)
 Short term – prevent CUSHING SYNDROME
 Taper dose (ex: 2 months of steroid therapy; 60 mg for first 2 weeks, 40
mg for next 2 weeks, 20 mg next 2 weeks, 10 mg last 2 weeks)
 Immunocompromised – increased susceptibility for infection
 Functions:
o Helps body respond to stress or danger
o Increase body’s metabolism of glucose
o Controls blood pressure
o Reduce inflammation
o RESULT: Stress eating
 Cortisol increases glomerular filtration rate, and renal plasma flow from the kidneys
thus increasing phosphate excretion, as well as increasing sodium and water retention
and potassium excretion in high amounts acting as aldosterone (in high amounts
cortisol is converted to cortisone which acts on mineral corticoid receptor mimicking the
effect of aldosterone).
  What stimulates it to be released? STRESS
 Hypersecretion of cortisol: Cushing’s Syndrome
 Hyposecretion of cortisol: Addison’s Disease

 Hematoma or bruising – thin layers in skin, prone to injury

Sodium an potassium inversely proportional

7) PARATHYROID HORMONE (PTH)

 Secreted by parathyroid gland located in the thyroid gland
 Parathyroid hormone is the most important endocrine regulator of calcium and phosphorus
concentration in extracellular fluid.
  This hormone is secreted from cells of the parathyroid glands and finds its major target cells
in bone and kidney.
 During thyroidectomy, parathyroid gland is removed as well (monitor calcium levels)
 Parathyroid gland – addressed imbalance in calcium levels in blood

*extracellular matrix of bone – calcium salts

*if low level of calcium in blood, activation of osteoclast (release stored calcium in bones to
increase calcium levels)
*due to compensatory mechanism, body keeps on telling that body has low calcium
- if there is chronic kidney disease – prone to fractures
- Vitamin D regulates absorption of calcium, acts in intestine, diffuse in bones
- no activated vitamin D if kidney is destroyed (no absorption of calcium)
*CKD – at risk for fractures
*Hypercalcemia – stimulation of thyroid gland to release calcitonin -> stimulate calcium deposition
in bone which is controlled by osteoblast, increase absorption in intestine

FLUID SHIFTS
 Osmotic pressure increases if high solute concentration
 Hydrostatic pressure (heart)
 Oncotic pressure (albumin) (protein increases COP)
 Fluid shifts
o Plasma to interstitial
 Edema (decrease osmotic pressure)
 Given albumin and hypertonic solutions to pull back to BV
o Interstitial to plasma
 Congestion
 Give diuretic

OSMOTIC FORCES IN WATER DISTRIBUTION

OSMOTIC FORCES are the principal determinant of water distribution in the body. Water
accounts for the osmotic pressure in the tissues and cells of the body. Osmotic pressure is
actually determined by the movement or draw of water through a selectively permeable
membrane toward an area of greater solute concentration. To determine the osmotic pressure
of a solute, the osmolality of the solution must be determined.

Osmolality: number of osmoles (Osm) of a substance contained within a kilogram of water

Osmole: number of molecules in 1g molecular weight of undissociated solute

A solution with 1 Osm in each kg of water has an osmolality of 1 Osm/kg, and a solution with an
osmolality of 1 milliosmole (mOsm) per kilogram contains 0.001 Osm/kg solute.

Normal serum osmolality is 285-295 mOsm/kg.

MOVEMENT OF FLUIDS AT THE CAPILLARY MEMBRANE

The capillaries are formed of endothelium, which is permeable to all of the solutes and water of
the plasma. The endothelial layer is impermeable to the large molecules and cells in the
plasma. Substances move through the gaps or spaces in the endothelial cells, and some
substances, such as carbon dioxide, oxygen, and small solutes, move through the endothelial
membrane as well. The process occurs by diffusion, so that near equilibrium exists at the
capillary line: the amount of fluid leaving the capillary nearly equals the amount reabsorbed.
This dynamic equilibrium is called Starling’s law of the capillaries and it occurs mostly through a
balance achieved between the hydrostatic pressure of the blood and the colloid osmotic
pressure within the capillaries.
 Blood entering the capillary comes in at a hydrostatic pressure that is generated by the heart.
This hydrostatic pressure varies in the different systemic arterioles, but it is always higher at the
arteriolar end of the capillary than at the venous end. As fluid filters out of the capillary into the
tissue spaces, the hydrostatic pressure decreases. The high pressure exerted at the arteriolar
end of the capillary is a simple outward force, or pushing force, which moves fluid from the
vessel to the interstitial spaces. The hydrostatic pressure at the arteriolar end of the capillary
averages 30-40 mm Hg but drops to approximately 10-15 mm Hg at the venous end. This
hydrostatic pressure provides an outward force, enhanced by a negative interstitial pressure
and the interstitial fluid colloid osmotic pressure (ISCOP). The ISCOP is minimal and is
produced by a few plasma proteins that have escaped into the interstitial space.

The pressure exerted by the plasma proteins in the vessels, the colloid osmotic or oncotic
pressure (COP), is an osmotic pulling or inward force that draws water toward it. Plasma
proteins primarily exert their colloidal effect by drawing water back into the vessel. They remain
in the vessel due to their larger size, which prohibits easy movement out of the vessel. The
average COP is 28 mm Hg, a pressure that remains constant across the capillary. Although the
amount of fluid filtered out of the vessel almost equals that reabsorbed, a larger amount is
filtered into the tissue spaces than is reabsorbed. The small amounts of protein that escape into
the tissue spaces during the process of fluid movement cannot be reabsorbed by the blood
vessels. These excesses of fluid and protein are absorbed by the lymphatic system and
returned through lymphatic channels to the blood. The lymphatic system carries away proteins
and large matter from the tissue spaces directly into the blood capillaries.

The Colloid Osmotic Pressure in the capillaries is mainly generated by albumin because it is the
most abundant of the plasma proteins.
FLUID SHIFTS

A) PLASMA TO INTERSTITIAL

EDEMA
➢ palpable swelling produced by expansion of the interstitial fluid volume
➢ may be localized (IV Infusions such as infiltation) or generalized (heart problems, RHF –
edema in upper and lower extremitites, LHF – pulmonary congestion)
➢ pitting (dent, upon pressing tagal magbalik) or nonpitting (upon pressing, paspas
mubalik), depending on its cause
➢ Danger sign: edema on face
➢ The mechanism causing skin edema also can cause fluid shifts in other vulnerable areas
of the body. These fluid shifts are sometimes termed third-space shifts

*Third spacing is a shift of fluid from the vascular space into an area where it is not available to
support normal physiologic processes. Fluid may be sequestered in the abdomen or bowel, or
in other actual or potential body spaces as the pleural (lungs) or peritoneal space
(abdomen). Fluid may also become trapped within soft tissues following trauma or burns. The
trapped fluid represents a volume loss and is unavailable for normal physiologic processes. In
many cases, fluid is sequestered in interstitial tissues and is unavailable to support
cardiovascular function.

*ascites – fluid shifting in abdominal cavity (liver problem), given albumin side drip, low protein diet
because liver can’t metabolize proteins

4 Major Causes of Edematous State

1) Decreased colloid osmotic pressure in the capillary (no pulling back of fluids)
e.g. Burns (there is tissue injury; vasodilation & increase permeability in BP), Liver failure
2) Increased capillary hydrostatic pressure
e.g. Congestive Heart Failure
3) Increased capillary permeability (labas mga enzymes and chemicals that influence shifting of
fluids; ex: -kinins)
e.g. Burns (tissue injury), Allergic Reactions
4) Lymphatic obstruction or increased interstitial colloid osmotic pressure
e.g. Surgical removal of lymph structures

Management of Edema
➢ Diuretic therapy - decrease edema
▪ Given with hypertonic solutions for BV to not congest
➢ Elevating the affected extremity – decrease or relieve pressure
▪ Helps in blood circulation
➢ Elastic support stockings in the morning – decrease pressure
➢ Albumin IV - increase colloid oncotic pressure on blood vessels

B) INSTERTITIAL (extravascular) TO PLASMA (intravascular)

➢ Movement back of edema to circulatory volume
e.g. excessive administration of hypertonic solution

 Increase blood hydrostatic pressure to push fluids from intravascular to extravascular

 GFR
TOPIC 2: FLUID VOLUME IMPAIRMENT
 There are primarily two types of fluid imbalances:
(a) Fluid Volume Deficit
a Kulang sa fluid
b Dryness, weakness, hypotension
(b) Fluid Volume Excess
a Sobra ang fluid
b Hypertension, increased BV, increased BP, edema, swelling
 Both type of imbalances can be life-threatening and are often seen in acute care settings
(ER, NICU, ICU)
 Patients with many underlying pathologies develop one of these fluid imbalances and
without careful management, serious and critical conditions may develop.

A) FLUID VOLUME DEFICIT

a. Fluid volume deficit (FVD) is a decrease in intravascular, interstitial, and/or
intracellular fluid in the body

Fluid volume deficits may be the result of: (CAUSE)

1. Excessive fluid losses (ex: diarrhea, vomiting)
2. Insufficient fluid intake (ex: lack of water, keeps on drinking coffee)
3. Failure of regulatory mechanisms (ex: hyposecretion of antidiuretic hormone, thirst
regulation did not work, low cortisol)
4. Fluid shifts within the body.

FVD is a relatively common problem that may exist alone or in combination with other
electrolyte or acid–base imbalances. (Lemone,2017)

ISO-OSMOLAR FLUID VOLUME DEFICIT

➢ Occurs when sodium and water are lost in equal amounts.
➢ No change in osmolarity concentration of blood

HYPEROSMOLAR FLUID VOLUME DEFICIT

➢ Occurs when more fluid is lost than sodium, resulting in higher serum osmolality than
normal (> 295 mOsm/kg)
➢ Rise of solutes cause increased concentration

HYPOOSMOLAR FLUID VOLUME DEFICIT

➢ Occurs when electrolyte loss is greater than fluid (rare).
➢ Higher loss of sodium than water

*Doctors need to know what type of FVD to easily manage the deficit.

ETIOLOGY
The most common causes of fluid volume deficit are:
 Vomiting
 Diarrhea
  GI suctioning (nawawalan ng fluid)
 Intestinal fistulas (fistulas – create another pathway for organ, decrease water
absorption; large intestines responsible for absorption of water)

 Intestinal drainage

Other causes:
 Diuretics
 Renal disorders
 Endocrine Disorders (diabetes insipidus)
 Excessive Exercise (insensible water loss)
 Hot Environment (lead to dehydration)
 Hemorrhage
 Chronic abuse of laxatives and/or enemas
 Inadequate fluid intake include inability to access fluids, inability to request or to swallow
fluids (mgt: IV infusion), oral trauma, or altered thirst mechanisms.

Older adults are at particular risk for fluid volume deficit.

PATHOPHYSIOLOGY
Fluid volume deficit can develop slowly or rapidly, depending on the type of fluid loss. Loss of
extracellular fluid volume can lead to hypovolemia, decreased circulating blood volume.
Electrolytes often are lost along with fluid, resulting in an isotonic fluid volume deficit. When both
water and electrolytes are lost, the serum sodium level remains normal, although levels of other
electrolytes such as potassium may fall. Fluid is drawn into the vascular compartment from the
interstitial spaces as the body attempts to maintain tissue perfusion. This eventually depletes
fluid in the intracellular compartment as well. Hypovolemia stimulates regulatory mechanisms to
maintain circulation. The sympathetic nervous system is stimulated, as is the thirst mechanism.
ADH and aldosterone are released, prompting sodium and water retention by the kidneys.
Severe fluid loss, as in hemorrhage, can lead to shock and cardiovascular collapse.
(Lemone,2017)
 Table 2-1 Pathophysiology, ECF Fluid Loss

ECF FLUID LOSS

Fluids Shift from Interstitial to Intravascular to Restore Vascular Volume & Hypernatremia State

ADH – Fluids are Inc Vasoconstriction Thirst mechanism by

Aldosterone reabsorbed Heart as Dec blood volume Osmoreceptor in the
( Posterior from the sensed by Baroreceptors Hypothalamus
Pituitary Gland, colon. sending message to
Adrenal Cortex) sympathetic nervous
System. Inc hydrostatic
pressure

H 2 O, Na Retention Fluid Shift from Inc H2O intale

Dec Urine Output Periphery to
Circulation

*If fluid loss continuous and regulatory mechanism fails = DHN (Dehydration)

*tissue perfusion – oxygen being delivered to tissues

MANIFESTATIONS

With a rapid fluid loss (such as hemorrhage or uncontrolled vomiting), manifestations of

hypovolemia develop rapidly. When the loss of fluid occurs more gradually, the patient’s fluid
volume may be very low before manifestations develop.

1. Rapid weight loss is a good indicator of fluid volume deficit. Each liter of body fluid
weighs about 1 kg (2.2 lb). The severity of the fluid volume deficit can be estimated by
the percentage of rapid weight loss:
▪ A loss of 2% of body weight represents a mild FVD;
▪ 5%, moderate FVD;
▪ 8% or greater, severe FVD (Metheny, 2000).

2. Loss of interstitial fluid causes skin turgor to diminish. When pinched, the skin of a patient
with FVD remains elevated.
▪ Poor skin turgor
▪ Low water content in body

3. Postural or orthostatic hypotension is a sign of hypovolemia. A drop of more than 15

mmHg in systolic blood pressure when changing from a lying to standing position often
indicates loss of intravascular volume.

4. Venous pressure falls as well, causing flat neck veins, even when the patient is
recumbent.

5. Compensatory mechanisms to conserve water and sodium and maintain circulation

account for many of the manifestations of fluid volume deficit, such as tachycardia; pale,
cool skin (vasoconstriction) - compensatory

6. Decreased urine output. The specific gravity of urine increases as water is reabsorbed in
the tubules. - compensatory

MULTISYSTEM EFFECTS OF FLUID VOLUME DEFICIT

Mucous Membranes
➢ Dry; may be sticky
➢ Decrease tongue size, longitudinal furrows increase
➢ Chappy lips

Urinary
➢ Decrease urine output
➢ Oliguria (severe FVD)
➢ Increase in urine specific gravity (more concentrated, less water)

Neurologic
 ➢ Altered mental status (dec LOC)
➢ Anxiety, restlessness
➢ Diminished alertness/condition (lethargy)
➢ Possible coma (severe FVD)

Integumentary
➢ Diminished skin turgor
➢ Dry skin
➢ Pale, cool extremities

Cardiovascular
➢ Tachycardia
➢ Orthostatic hypotension (moderate FVD)
➢ Falling systolic/diastolic pressure (severe FVD)
➢ Flat neck veins
➢ Decrease venous filling
➢ Decrease pulse volume
➢ Decrease capillary refill (low CRT due to dehydration; low blood volume)
➢ Increase hematocrit (diagnostic examination; total blood percentage of RBC)
o high hematocrit (concentrated, less wter) = DHN, FVD
o low hematocrit = hemodilution, FVO, anemia

Potential Complication
➢ Hypovolemic shock

Musculoskeletal
➢ Fatigue

Metabolic Processes
➢ Decrease body temperature (isotonic FVD)
➢ Increase body temperature (dehydration)
➢ Thirst
➢ Weight loss
2-5% mild FVD
6-9% moderate FVD
>10% severe FVD

DIAGNOSTICS
Laboratory and diagnostic tests may be ordered when fluid volume deficit is suspected. Such
tests measure the following:

1. Serum electrolytes.
 Test measures the levels of electrolytes such as sodium, potassium and chloride
 Expected results of FVD:
o In an isotonic fluid deficit, sodium levels are within normal limits;
o When the loss is water only, sodium levels are high.
o Decreases in potassium are common.
 2. Serum osmolality.
 2 abnormal results
o High (fluids and solute partiles) = increased concentration of solutes (FVD)
o Low = dilution (FVE)
 measures the amount of particles of chemicals dissolved in the liquid part (serum
of the blood)
 chemicals that affect serum osmolality include, sodium, chloride, bicarbonate,
proteins and sugar (glucose)
 this test is done on a blood sample taken from a vein
 Measurement of serum osmolality helps to differentiate isotonic fluid loss from
water loss.
 With water loss, osmolality is high; it may be within normal limits with an isotonic
fluid loss.

3. Hemoglobin and hematocrit.

 Hemoglobin
o When the hemoglobin level is low, the patient has anemia.
o An erythrocytosis is the consequence of too many red cells; this results in
hemoglobin levels above normal.
 HCT
o measures the volume of red blood cells compared to the total blood volume
(red blood cells and plasma)
o low hematocrit = anemia
o if high HCT = high concentration = FVD
o if low HCT = FVE
 Both the hemoglobin and the hematocrit are based on whole blood and are
therefore dependent on plasma volume. If a patient is severely dehydrated, the
hemoglobin and hematocrit will appear higher than if the patient were
normovolemic; if the patient is fluid overloaded, they will be lower than their actual
level
 The hematocrit often is elevated due to loss of intravascular volume and
hemoconcentration.

4. Urine specific gravity and osmolality.

 shows the concentration of all chemical particles in the urine
 As the kidneys conserve water, both the specific gravity and osmolality of urine
increase (compensatory mechanism)
 High: FVD
 Low: FVE

5. Central venous pressure (CVP).

 The CVP measures the mean pressure in the superior vena cava or right atrium,
providing an accurate assessment of fluid volume status.
 Check fluid content of body
  If low CVP = FVD

Central Venous Pressure (CVP) (In serious cases)

- It’s the blood pressure in the venae cavae, near the right atrium of the heart. CVP reflects
the amount of blood returning to the heart and the ability of the heart to pump the blood
back into the arterial system.

- It’s acquired by threading a central venous catheter (subclavian double lumen central line
shown) into any of several large veins. It is threaded so that the tip of the catheter rests in
the lower third of the superior vena cava. The pressure monitoring assembly is attached
to the distal port of a multilumen central vein catheter.

Figure 2-1 Central Venous Pressure Line

The CVP catheter is an important tool used to assess right ventricular function and systemic
fluid status.

➢ Normal CVP is 2-6 mmHg ➢

CVP is elevated by:
• overhydration which increases venous return
• heart failure or PA stenosis which limit venous outflow and lead to venous congestion
(increased arterial pressure or blood vessels)
• positive pressure breathing, straining (Positive pressure breathing pts need masks,
ventilators (increased intrathoracic pressure = increased CVP)

CVP decreases with:

• hypovolemic shock from hemorrhage, fluid shift, dehydration
• negative pressure breathing which occurs when the patient demonstrates retractions or
mechanical negative pressure which is sometimes used for high spinal cord injuries.
*if closed 3 way stopcock – not be filled with IV solution
*CVP monitoring (depends on doctor)
*close manometer first before stopcock

MEDICAL MANAGEMENT
Correction of fluid loss depends on the acuteness and severity of the fluid deficit. Goals are to
replace F/E (Na primarily) that have been loss.

1) Fluid Restoration

a) Oral Rehydration
The safest and most effective treatment for fluid volume deficit in alert patients who are able to
take oral fluids. Adults require a minimum of 1500 mL of fluid per day or approximately 30 mL
per kg of body weight (ideal body weight is used to calculate fluid requirements for obese
patients) for maintenance. Fluids are replaced gradually, particularly in older adults, to prevent
rapid rehydration of the cells.

➢ For mild fluid deficits in which a loss of electrolytes has been minimal (e.g., moderate
exercise in warm weather), water alone may be used for fluid replacement.

➢ When the fluid deficit is more severe and when electrolytes have also been lost (e.g.,FVD
due to vomiting and/or diarrhea, strenuous exercise for longer than an hour or two), a
carbohydrate/electrolyte solution such as a sports drink, ginger ale, or a rehydrating
solution (e.g., Pedialyte or Rehydralyte) is more appropriate. These solutions provide
sodium, potassium, chloride, and calories to help meet metabolic needs.

b) IV Rehydration
When the fluid deficit is severe, or the patient is unable to ingest fluids, the IV route is used to
administer replacement fluids. (please refer to table of IV FLUIDS)
 Generally:
Isotonic ECFVD is treated with Isotonic Solutions
Hypertonic ECFVD is treated with Hypotonic Solutions
Hypotonic ECFVD is treated with Hypertonic Solutions

TYPES OF FVD:
 Isotonic: Caused by losing fluids and solutes about equally; solute concentration in the
remaining extracellular fluid then remains relatively unchanged
 Hypertonic: Caused by losing more fluids than solutes, leading to increased solute
concentration in the remaining fluid.
 Hypotonic: Caused by losing more solutes than fluid leading to decreased solute
concentration in remaining fluid. This is the rarest type.

2) Monitor for complications of fluid restoration

➢ client with severe ECFVD accompanied by severe heart, liver and kidney disease can’t
tolerate large volumes of fluid or sodium without the risk of development of heart failur
(can have congestion = blood volume in blood vessels)
➢ Unstable clients need to be monitored to detect ↑ pressure from fluids

Monitor
1) Fluid volume status by CVP insertion
2) Lab values (Na & K = serum electrolytes, BUN = kidney function test, Osmolarity)
3) Body Weight
4) Urine output (decreased urine output = decreased GFR = kidney problem)

3) Correction of Underlying Problem (check root cause)

Medication
➢ Antiemetic (hyperemesis = excessive vomiting) (don’t give antiemetics to pts with
hyperemesis gravidarum unless become hyperemesis)
➢ Antidiarrheal
➢ Antibiotics (acute gastroenteritis – irritated BM, fast) (treat infections)
➢ Antidiuretics (for conservation of water)

NURSING MANAGEMENT
Nurses are responsible for (a) identifying patients at risk for fluid volume deficit, (b) initiating and
carrying out interventions to prevent and treat fluid volume deficit, and (c) monitoring the effects
of therapy.

1. VS every 2-4 hours, report changes from baseline VS; Assess CVP every 4hrs (if
patient has CVP access)
® Hypotension, tachycardia, low CVP, and weak, easily obliterated peripheral pulses
indicate hypovolemia.

2. I & O every 8 hours or hourly (Record all output accurately). Renal client/relatives to
report urine output ‹ than 30 m/L x 2 consecutive hours or ‹ 240 ml x 8-hour period.
 ® Urine output should normally be 30 to 60 mL per hour. Urine output of less than 30 mL
per hour in adults indicates inadequate renal perfusion and an increased risk for acute
renal failure and inadequate tissue perfusion

3. Administer IV fluids as prescribed using an infusion pump. Monitor for indicators of fluid
overload if rapid fluid replacement is ordered: dyspnea, tachypnea, tachycardia,
increased CVP, jugular vein distention, and edema.
® Rapid fluid replacement may lead to hypervolemia, resulting in pulmonary edema and
cardiac failure, particularly in patients with compromised cardiac and renal function.

4. Weight patient daily and record.

In most instances (except third spacing), changes in weight accurately reflect fluid balance.

5. Peripheral vein filling (Capillary refill 3-5 sec)

6. Renal client / relatives to report urine output ‹ than 30 m/L x 2 consecutive hours or ‹ 240
ml x 80 period

7. Assess for dryness of mucous membrane and skin turgor (check should be done)

8. Oral care to ↓ discomfort related to mucous membrane dryness

9. Monitor plasma sodium, BUN, Glucose, HCT to determine osmolality.

If high osmolality during treatment = body having a hard time reacting to treatment mgt
Goal: decreased osmolality

10. Assess the client for confusion, easy indication of ICF involvement

11. Keep fluids easily accessible

12. Administer and monitor intake of oral fluids as prescribed

13. Administer IV fluids as prescribed using an infusion pump. Monitor for indicators of fluid
overload if rapid fluid replacement is ordered: dyspnea, tachypnea, tachycardia,
increased CVP, jugular vein distention, and edema

14. Monitor laboratory values: electrolytes, serum osmolality, blood urea nitrogen (BUN), and
hematocrit.
® Rehydration may lead to changes in serum electrolytes, osmolality, BUN, and
hematocrit. In some cases, electrolyte replacement may be necessary during
rehydration.

15. Monitor for changes in level of consciousness and mental status.

®Restlessness, anxiety, confusion, and agitation may indicate inadequate cerebral
blood flow and circulatory collapse. A fluid volume deficit can lead to decreased
perfusion of renal, cerebral, and peripheral tissues. Decreased cerebral perfusion leads
 to changes in mental status and cognitive function, causing restlessness, anxiety,
agitation, excitability, confusion, vertigo, fainting, and weakness.

16. Institute safety precautions, including keeping the bed in a low position, using side rails
as needed, and slowly raising the patient from supine to sitting or sitting to standing
position. ® Using safety precautions and allowing time for the blood pressure to adjust
to position changes reduce the risk of injury. The patient with fluid volume deficit is at risk
for injury because of dizziness and loss of balance resulting from decreased cerebral
perfusion secondary to hypovolemia.

17. Teach patient and family members how to reduce orthostatic hypotension through
progressive ambulation. Side-lying position then sit on the edge of the bed for a minute
then stand. ® Teaching measures to reduce orthostatic hypotension reduces the
patient’s risk for injury. Prolonged bed rest increases skeletal muscle weakness and
decreases venous tone, contributing to postural hypotension. Prolonged standing allows
blood to pool in the legs, reducing venous return and cardiac output.

NURSING DIAGNOSIS
1) Fluid Volume Deficit
Patients with a fluid volume deficit due to abnormal losses, inadequate intake, or impaired fluid
regulation require close monitoring as well as immediate and ongoing fluid replacement.

2) Ineffective Tissue Perfusion

A fluid volume deficit can lead to decreased perfusion of renal, cerebral, and peripheral tissues.
Inadequate renal perfusion can lead to acute renal failure. Decreased cerebral perfusion leads
changes in mental status and cognitive function, causing restlessness, anxiety, agitation,
excitability, confusion, vertigo, fainting, and weakness.

3) Risk for Injury

The patient with fluid volume deficit is at risk for injury because of dizziness and loss of balance
resulting from decreased cerebral perfusion secondary to hypovolemia.

IV THERAPY
Intravenous (IV) therapy is the administration of fluids or medication via a needle or catheter
(sometimes called a cannula) directly into the bloodstream.

INDICATIONS FOR INTRAVENOUS THERAPY

Patients receive a variety of substances via IV therapy, including fluids, electrolytes, nutrients,
blood products, and medications.

1. Patients can receive life-sustaining fluids, electrolytes, and nutrition when they are unable to
eat or drink adequate amounts.

2. The IV route also allows rapid delivery of medication in an emergency. Many medications are
faster acting and more effective when given via the IV route. Other medications can be
administered continuously via IV to maintain a therapeutic blood level.
3. Patients with anemia or blood loss can receive lifesaving IV transfusions.

4. Patients who are unable to eat for an extended period can have their nutritional needs met
with total parenteral nutrition (TPN).

TYPES OF INFUSIONS

1) Continuous Infusion
 In a continuous infusion, the physician orders the infusion in milliliters (mL) to be
delivered over a specific amount of time; for example, 100 mL per hour.
 The infusion is kept running constantly until discontinued by the physician. An IV
controller or roller clamp allows the solution to infuse at a constant rate.

2) Intermittent Infusion
 Intermittent IV lines are “capped off” with an injection port and used only periodically.
 Thus, intermittent IV therapy is administered at prescribed intervals. You must ensure
that an intermittent catheter is patent (not occluded with a clot) before injecting a drug or
solution.
 Draw back with a syringe to check for backflow of blood before injection.
 Use heplock

3) Bolus (IVTT drugs)

 A bolus drug (sometimes called an IV push or IVP drug) is injected slowly via a syringe
into the IV site or tubing port.
 It provides a rapid effect because it is delivered directly into the patient’s bloodstream.
 Bolus drugs can be dangerous if they are given incorrectly, and a drug reference should
always be checked to determine the safe amount of time over which the drug can be
injected.
4) Piggy Back/Secondary Infusion/Side Drip
 Some IV medications, such as antibiotics, need to be infused over a short period of time.
 For example, an antibiotic may be mixed with 50 mL of dextrose solution and infused
over 30 minutes.
 If the patient already has a primary continuous IV infusing, the antibiotic (secondary)
infusion can be “piggybacked” into the primary IV line.
 In order for the piggyback medication to infuse, it must hang higher than the primary
infusion.
 Piggyback medications can be infused using either gravity or a controller. The medication
in the piggyback must be compatible with any other solution that is in the primary IV
tubing.

METHODS OF INFUSION

1) Gravity Drip
Gravity can be used to drip a solution into a vein. The solution is positioned about 3 feet above
the infusion site. If it is positioned too high above the patient, the infusion may run too fast.
Positioned too low, it may run too slowly. Flow is controlled with a roller, screw, or slide clamp.
A mechanical flow device can be added to achieve accurate delivery of fluid with minimal
deviation.

Factors Affecting Flow Rates

a. Change in catheter position.

A change in the catheter’s position may push the bevel either against the wall of the vein, which
will decrease the flow rate, or away from the wall of the vein, which may increase the flow rate.
Careful taping and avoidance of joint flexion above the site minimizes this problem. Patients
may need to be reminded to keep flexion to a minimum when an IV is placed near a joint. Use
IV board for pedia patients.

b. Height of the solution.

Because infusions flow by gravity, a change in the height of the infusion bag or bottle or a
change in the level of the bed can increase or decrease the flow rate. The flow rate increases
as the distance between the solution and the patient increases. A patient may alter the flow rate
greatly simply by standing up. The ideal height for a solution is 3 feet above the level of the
heart.

c. Patency of the catheter.

A small clot or fibrin sheath may occlude the catheter lumen and decrease or stop the flow rate.
Clot formation can result from irritation, increased venous pressure, or backup of blood into the
line.

Avoid use of a blood pressure cuff on the affected extremity because of the resulting transient
increase in venous pressure. A regular flush schedule helps maintain patency.

Check backflow of blood to assess patency

NEVER exert pressure with a saline or heparin flush in an attempt to restore patency; doing so
may dislodge a clot into the vascular system or rupture the catheter

2) Electronic Control Devices

Electronic pumps and controllers regulate the rate of infusion. Controllers measure the amount
of solution delivered and depend on gravity to deliver the infusion.

Pumps use positive pressure to deliver the solution. Pumps are often used for central lines to
help overcome the high pressure of the central circulation.

Pumps and controllers are used for the infusion of precise volumes of solution. Institution policy
often dictates use of controllers for infusion of potent medications, such as heparin,
concentrated morphine, and chemotherapy solutions, and for very fast or slow rates. Some
electronic infusion devices are portable and are designed to be worn on the body. These are
called ambulatory infusion devices. It is important to know the type of pump being used and its
manufacturer’s guidelines.

TYPES OF IVF SOLUTIONS

There are two types of IVFs, crystalloid and colloid solutions.

1) Colloids / Plasma Expander

 Fluids that expand the circulatory volume due to particles that cannot cross a
semipermeable membrane.
 Albumin
 They pull fluid from the interstitial space into the intravascular space, increasing fluid
volume.
  This can be a great advantage in cases of large losses of fluid, such as severe trauma
and haemorrhage.
 The main disadvantage is cost and the risk of volume overload, including pulmonary
edema.

Types of colloids are dextrans (common in the Philippines) and hetastarches

2) Crystalloids
Work much like colloids but do not stay in the intravascular circulation as well as colloids do, so
more of them need to be used. They are cheaper and are more convenient to use.
➢ primary fluid for IV therapy containing electrolytes but lacks large protein molecules
(disadvantage)
➢ they provide hydration and calories to patients and include dextrose, normal saline, and
Ringer’s and lactated Ringer’s solution.
➢ can be stored in room temperature

2 IVF CLASSIFICATION
- According to tonicity and according to purpose

TONICITY

Tonicity of IV Solutions

➢ Intravenous fluids may be classified as isotonic, hypotonic, or hypertonic.

• Isotonic fluids have the same concentration of solutes to water as body fluids.
• Hypertonic solutions have more solutes (i.e., are more concentrated) than body fluids.
 • Hypotonic solutions have fewer solutes (i.e., are less concentrated) than body fluids.

Water moves from areas of lesser concentration to areas of greater concentration. Therefore,
hypotonic solutions send water into areas of greater concentration (cells), and hypertonic
solutions pull water from the more highly concentrated cells.

1) Isotonic Solutions
➢ Normal saline (0.9% sodium chloride) solution is an isotonic solution that has the same
tonicity as body fluid. When administered to a patient requiring water, it neither enters
cells nor pulls water from cells; it therefore expands the extracellular fluid volume.
➢ A solution of 5% dextrose in water (D5W) is also isotonic when infused, but the dextrose
is quickly metabolized, making the solution hypotonic.

2) Hypotonic Solutions
➢ Hypotonic fluids are used when fluid is needed to enter the cells, as in the patient with
cellular dehydration. They are also used as fluid maintenance therapy. An example of a
hypotonic solution is 0.45% sodium chloride solution.

3) Hypertonic Solutions
➢ Examples of hypertonic solutions include 5% dextrose in 0.9% sodium chloride and 5%
dextrose in lactated Ringer’s solution.
o Hypertonic solutions are used to expand the plasma volume, as in the hypovolemic
patient. They are also used to replace electrolytes.

Table 2-2 Commonly Administered Iv Fluids with Nursing Implications

1) ISOTONIC SOLUTIONS ▪ Monitor for fluid overload; discontinue fluids

• 0.9% Saline and notify the healthcare provider.
• Lactated Ringer’s solution ▪ Do not administer lactated ringer’s solution to
patients with severe liver disease as the liver
may be unable to convert the lactate to
bicarbonate and the patient may become
acidotic. Do not administer if the patient has
a blood pH of >7.50.
▪ If administering lactated ringer’s solution,
monitor potassium levels and cardiac rhythm;
if abnormals are present, notify the health
care provider.

2) HYPOTONIC SOLUTIONS ▪ Monitor for inflammation and infiltration at IV

• 0.45% Saline or 0.25% insertion site as hypotonic solutions may
Saline cause cells to swell and burst, including those
• D5W at the insertions site; this narrows the lumen
of the vein.
 ▪ Monitor blood sodium levels.
▪ Do not administer to patients at risk for
increased intracranial pressure (e.g head
trauma, stroke, neurosurgery).
▪ Do not administer to patients at risk for third-
space shifts (burns, trauma, liver disease,
malnutrition).

3) HYPERTONIC SOLUTIONS ▪ Monitor for inflammation and infiltration at IV

Hypertonic fluids have a tonicity insertion site as hypertonic solutions cause
>350 mEq/L and include the ff: cells to shrink, exposing the basement
• Fluids containing medications membrane of the vein.
• D5W sodium chloride ▪ Monitor blood sodium levels.
• D5W in lactated ringer’s ▪ Monitor for circulatory overload.
solution ▪ Do not administer to patients with diabetic
• Total parenteral solutions ketoacidosis or impaired cardiac or kidney
function.
ACCORDING TO PURPOSE
1) Hydrating
➢ Replace water loss
➢ Dilute meds
➢ Keep veins open (KVO = at least 8-10 gtts/min)

2) Nutritional
➢ Promotes faster recuperation

3) Maintenance
➢ Replace electrolyte loss at ECF level
➢ Maintenance in patients with no oral intake
➢ Replace fluid loss
➢ Treatment for dehydration
➢ For hypovolemic shock (hypertonic + diuretics + volume expander [isotonic and
hypertonic solutions])

4) Volume expander
➢ Increase osmotic pressure thus maintain circulatory volume

Table 2-3 Complications of Peripheral IV Therapy

Local Signs and Symptoms Nursing Interventions
Complications of
IV Therapy
Hematoma Ecchymoses Remove catheter
(bruises on IV site, Swelling Apply pressure with 2x2
collection of blood Inability to advance Elevate extremity
outside blood catheter
vessels) Resistance during
flushing
Thrombosis (there Slowed or stopped Discontinue catheter
is redness, infusion Apply cold compress to site
formation of blood Fever/malaise Assess for circulatory impairment
clot) Inability to flush catheter
Phlebitis Redness at site Discontinue catheter
(inflammation of Site warm to touch Apply cold compress initially; then
blood vessel Local swelling warm
wall/walls of vein) Pain Consult physician if severe
Palpable cord
Sluggish infusion rate
Infiltration Coolness of skin at site Discontinue catheter
(Extravasation) Taut skin Apply cool compress
Dependent edema Elevate extremity slightly
(the accidental Backflow of blood absent Follow extravasation guidelines
leakage of non- Infusion rate slowing Have antidote available
vesicant solutions
out of the vein into
the surrounding
tissue)

(excape of fluids
from intravascular
to interstitial)

Local Infection Redness and swelling at Discontinue catheter and culture

site site and catheter
(wag antayin na Possible exudate Apply sterile dressing over site
magkaroon ng Increase WBC count Administer antibiotics if ordered
septicemia or blood Elevated T lymphocytes
poisining, pt can die
from septic shock)
Venous Spasm Sharp pain at site Apply warm compress to site
(occurs due to Slowing of infusion Restart infusion in new site if
severe vein spasm continues
irritation,
administration of
cold fluids or blood)
**don’t try to do IV push if hard (ayaw ipugos, madislodge thrombus = become embolus) – can
lead to MI and pulmonary embolism

Table 2-4 Systemic Complication of Peripheral IV Therapy

Complication Signs and Symptoms Nursing Interventions
Septicemia Fluctuating temperature Restart new IV system
(bacteria are just Profuse sweating Obtain cultures
freely circulating) Nausea/vomiting Notify physician
Diarrhea Initiate antimicrobial therapy as
blood poisoning, Abdominal pain ordered
especially that Tachycardia Monitor patient closely
caused by Hypotension
bacteria or their Altered mental status
toxins)

Can lead to septic

shock if not
managed

Decreased BP,
hypotension,
transfuse
hypertonic/isotoni
c solutions to help
body compensate

Septicemia ->
septic shock ->
systemic
vasodilation d/t
bacteria ->
decreased blood
flow (lumalaban si
heart –
tachycardia) ->
hypoxia -> organ
failure -> multiple
organ failue ->
septic shock
Fluid Overload Weight gain Decrease IV flow rate
( a medical Puffy eyelids Place patient in high Fowler’s
condition where Edema position
there is too much Hypertension Keep patient warm
fluid in the blood) Changes in input and output Monitor vital signs
(I&O) Administer oxygen
Rise in central venous Use microdrip set or controller
pressure
(CVP)
 Shortness of breath
Crackles in lungs
Distended neck veins
Air Embolism Lightheadedness Call for help!
(also known as a Dyspnea, cyanosis, Place patient in Trendelenburg’s
gas embolism, is tachypnea, expiratory position (supine with head
a blood vessel wheezes, cough chest inclined downwards and feet
blockage caused pain, hypotension elevated)
by one or more Changes in mental status Administer oxygen
bubbles of air or Coma Monitor vital signs
other gas in the Notify physician
circulatory
system)

INTRAVENOUS ACCESS
Intravenous therapy can be administered into the systemic circulation via the (1) peripheral or
(2) central veins.

1.Peripheral veins lie beneath the epidermis, dermis, and subcutaneous tissue of the skin.
They usually provide easy access to the venous system.

2. Central veins are located close to the heart. Special catheters that end in a large vessel
near the heart are called central lines.
ADMINISTERING PERIPHERAL INTRAVENOUS THERAPY
Precatheterization (Preparation)

1) Check Physician’s Order

➢ A physician’s order is necessary to initiate IV therapy. The order should include solution,
volume, rate, and route. If medication is ordered, the order should also include the
medication, dosage, and frequency.

2) Wash Hands
➢ Before beginning the procedure, wash your hands for 15 to 20 seconds. Wear gloves
when inserting the catheter and any time you have a risk of exposure to body fluid.
3) Gather Equipment
➢ Obtain the following equipment and inspect it for integrity.

4) Assess and Prepare Patient

➢ Several factors should be considered before venipuncture. The type of solution, condition
of vein, duration of therapy, catheter size needed, patient age, patient activity, presence
of disease or previous surgery, presence of a dialysis shunt or graft, medications being
taken by the patient (such as anticoagulants), and allergies must be assessed before a
venipuncture. Provide privacy for the procedure, explain the procedure to the patient, and
evaluate the patient’s knowledge of the procedure by talking with the patient before
assessing the upper arms for suitable venipuncture sites.

5) Select Site and Dilate Vein

➢ Proper vein selection is important to accommodate the prescribed therapy and to
minimize potential complications.

Considerations for Vein Selection

➢ Age of patient
➢ Availability of sites
➢ Size of catheter to be used
➢ Purpose of infusion therapy
➢ Osmolarity of solution to be infused
➢ Volume, rate, and length of infusion
➢ Degree of mobility desired

General Considerations When Initiating Intravenous Therapy

➢ When multiple sticks are anticipated, make the first venipuncture distally and work
proximal with subsequent punctures.
➢ If therapy will be prescribed for longer than 3 weeks, a long-term access device
should be considered.
➢ Avoid using venipunctures in affected arms of patients with radical mastectomies or a
dialysis access site.
➢ If possible, avoid taking a blood pressure on the arm receiving an infusion because
the cuff interferes with blood flow and forces blood back into the catheter. This may
cause a clot or cause the vein or catheter to rupture.
 ➢ No more than two attempts should be made at venipuncture before getting help.
➢ Immobilizers should not be placed on or above an infusion site.

• Hand veins are used first if long-term intravenous therapy is expected. This allows each
successive venipuncture to be made proximal to the site of the previous one, which
eliminates the passage of irritating fluids through a previously injured vein and
discourages leakage through old puncture sites.
• Hand veins can be used successfully for most hydrating solutions, but they are best
avoided when irritating solutions of potassium or antibiotics are anticipated.
• Vein size must also be considered. Small veins do not tolerate large volumes of fluid,
high infusion rates, or irritating solutions. Large veins should be used for these purposes.

Figure 2-2 Peripheral veins used for IV Therapy

6) Select the needle (catheter)

• Needles have been largely replaced with flexible plastic catheters that are inserted over a
needle. The needle (or stylet) is removed after the catheter is in place.

• These are available in a variety of sizes (gauges) and lengths. For patient comfort,
choose the smallest gauge catheter that will work for the intended purpose. Use smaller
gauge catheters (20 to 24 gauge) for fluids and slow infusion rates. Use larger catheters
(18 gauge) for rapid fluid administration and viscous solutions such as blood. Also
consider vein size when choosing a catheter gauge.
 Figure 2-3 Gauge of Needle and its Recommended Use

7) Put on gloves
➢ Follow standard precautions whenever exposure to blood or body fluids is likely. Wearing
latex or vinyl gloves provides basic protection from blood and body fluids.

8) Prepare the site

➢ Apply the solution in a circular motion, starting at the intended site and working outward
to clean an area 2 to 3 inches in diameter. If alcohol is used, it should be applied with
friction for at least 30 seconds or until the final applicator is visually clean.

9) Insert the catheter

➢ Hold the catheter with the bevel (slanted opening) of the needle facing up.

10) Stabilize the Catheter and Dress the Site

➢ A common problem in IV therapy is dislodgement of the catheter. Secure taping keeps
the catheter in place and stable, thus preventing complications caused by damage to the
intima of the vein.

11) Label the Site

 ➢ The IV setup should be labeled in three areas: the insertion site, the tubing, and the
solution container. Once the venipuncture procedure is completed, label the setup with
the date, time, catheter type and size, and your initials.

12) Dispose of Equipment

➢ All needles, catheters, and blood-contaminated equipment should be disposed of
according to institution policy in a tamper-proof, nonpermeable container.

13) Educate the Patient

➢ Patients have the right to receive information on all aspects of their care in a manner they
can understand. They also have the right to accept or refuse treatment. Explain the
rationale for the IV therapy that has been ordered.

14) Calculate Drip Rate

➢ All IV infusions should be monitored frequently for accurate flow rates and complications
associated with infusion therapy.

15) Document
➢ Document your actions and the patient’s response in the medical record according to
institution policy. All IV solutions are also documented on the medication administration
record.

ALTERNATIVE ACCESS ROUTES

Central Venous Catheters

Central venous catheters terminate in the superior vena cava near the heart. They are used
when peripheral sites are inadequate or when large amounts of fluid or irritating medication
must be given. Central catheter devices include a percutaneous catheter, peripherally inserted
central catheter (PICC), tunneled catheter, and implanted port.

These devices can have one, two, or three lumens in the catheter or one or more port
chambers. Each lumen exits the site in a separate line, called a tail. Multilumen catheters allow
for the administration of incompatible solutions at the same time. Be careful not to confuse a
central catheter with a dialysis catheter. Dialysis catheters should be used only for dialysis and
not for IV therapy and should be accessed only by physicians or specially trained dialysis
nurses.

1. Percutaneous Central Catheter

A percutaneous central catheter is inserted by a physician into the jugular or
subclavian vein. After insertion, correct placement is determined by x-ray before the
catheter is used.

These short-term central venous catheters may remain in place up to several weeks, but
usual placement time is 7 days. These catheters are inserted at the bedside and are cost
effective for short-term central venous access in the acute care setting.

2. Peripherally Inserted Central Catheter (PICC)

 A PICC line is a long catheter that is inserted in the arm and terminates in the central
circulation. This device is used when therapy will last more than 2 weeks, or the
medication is too caustic for peripheral administration.

3. Tunneled Catheters
Central venous tunneled catheters (CVTCs) are intended for use for months to years to
provide long-term venous access. CVTCs are composed of polymeric silicone with a
Dacron polyester cuff that anchors the catheter in place subcutaneously. The catheter tip
is placed in the superior vena cava.

4. Ports
A port is a reservoir that is surgically implanted into a pocket created under the skin,
usually in the upper chest. An attached catheter is tunneled under the skin into a central
vein. An advantage of a port is that, when not in use, it can be flushed and left unused for
long periods.

Ports can be used to administer chemotherapeutic agents and antibiotics that are toxic to
tissues and are suitable for long-term therapy. Ports should be accessed only by
specially trained RNs. Most ports require the use of special noncoring needles that are
specifically designed for this purpose.
B. FLUID VOLUME EXCESS
 Fluid volume excess results when both water and sodium are retained in the body.
 Fluid volume excess may be caused by fluid overload (excess water and sodium intake)
or by impairment of the mechanisms that maintain homeostasis.
o Aldosterone - promote sodium retention
o Increased cortisol levels
o Increased ADH (SIADH)
 The excess fluid can lead to excess:
1. intravascular fluid (hypervolemia)
a. increased blood volume
b. increased blood pressure
c. congestion (build-up of fluid on intravascular)
(2) excess interstitial fluid (edema).

ETIOLOGY
 Fluid volume excess usually results from conditions that cause retention of both sodium
and water.
o Sodium – major regulatory electrolyte for water; most abundant cation in ECC
 These conditions include:
o heart failure – due to congestion
 LSHF – one responsible to overcome pressure by systemic circulation; left
entricular hypertrophy; heart is tired to contarct; backflow of blood from left
ventricle to lungs (result to leaking capilliaries);
 Pulmonary congestion: crackles, cyanosis, dyspnea
 RSHF – backflow from RV to Vena Cavas to peripherals
 Peripheral Congestion: edema, ascites
o cirrhosis of the liver – failure of liver to thrive; manifest ascites; hepatic blood
vessels have slow blood flow leading to congestion on hepatic vessels; manifest
lower extremity edema
o renal failure – no proper function on excretion of urine, decreased urinary output
o adrenal gland disorders – cortisol and aldosterone; hypersecretion of aldosterone
corticosteroid administration – if not regulated well = cushing syndrome
o stress conditions causing the release of ADH (tumor on pituitary gland, have
SIADH) and aldosterone (hyperaldosteronism)
 Other causes include an excessive intake of sodium-containing foods, drugs that cause
sodium retention, and the administration of excess amounts of sodium-containing IV
fluids (such as 0.9% NaCl or Ringer’s solution).
 This iatrogenic (induced by the effects of treatment) cause of fluid volume excess
primarily affects patients with impaired regulatory mechanisms.

PATHOPHYSIOLOGY
1. Extracellular compartment is expanded
2. Increase in volume increases the pressure in the vasculature (due to hypervolemia,
congestion in blood vessels)
3. Baroreceptors sense the increase in pressure and increase in their firing to the central
nervous system (CNS) – send impulses to brain
4. In response, the SNS is inhibited
 5. RAAS functions declines. The resulting vasodilation promotes pooling of blood and
lowering of blood pressure. Reabsorption of sodium in the renal tubules is reduced, and
more urine is excreted.

MANIFESTATIONS
 Excess extracellular fluid leads to hypervolemia and circulatory overload.
 Excess fluid in the interstitial space causes peripheral or generalized edema.
 The manifestations of fluid volume excess relate to both the excess fluid and its effects
on circulation.

➢ Peripheral edema, or if severe, anasarca (severe generalized edema)

➢ Full bounding pulse, distended (flat) neck and peripheral veins, increased central venous
pressure, cough (from pulmonary edema), dyspnea (labored or difficulty breathing),
orthopnea (difficult breathing when supine)
➢ Dyspnea at rest
➢ Tachycardia (d/t increased congestion) and hypertension
➢ Reduced oxygen saturation
➢ Moist crackles on auscultation of the lungs, pulmonary edema
➢ Increased urine output (polyuria) – compensatory mechanism to relieve congestion
➢ Ascites (excess fluid in the peritoneal cavity) – low protein diet
 By product of protein metabolism: ammonia
 Liver needs to metabolize ammonia by liver to become urea (excreted by
kidney)
 Decrease stress level of liver
 Liver responsible for metabolizing protein
➢ Decreased hematocrit and BUN
 Dec htc: dilution of solutes in blood
 Decreased BUN, kidney is still functioning but BUN is degrading
➢ Altered mental status and anxiety
➢ Pulmonary edema

COMPARTMENTS AFFECTED:

Fluid overload can occur in either the extracellular (intravascular, interstitial) or intracellular (cell
became big) compartments of the body.

1) EXTRACELLULAR FLUID OVERLOAD

 Occurs in either the intravascular compartment or in the interstitial area
 Lead to congestion (intravascular)
EDEMA
o most common term associated with fluid overload found in the interstitial or lung
tissue

HYPERVOLEMIA
o when an overabundance of fluid occurs in the intravascular compartment
 ISOTONIC FLUID VOLUME EXCESS
o type of fluid overload wherein sodium and water remain in equal
proportions with each other. Also results from a decreased elimination of
sodium and water.

ANASARCA
o generalized edema

CAUSES OF EXTRACELLULAR FLUID OVERLOAD

➢ Excessive sodium intake through diet
➢ administration of hypertonic fluids (intravascular) (volume expander)
▪ D545 normal saline solution
▪ D5.9 normal saline solution
▪ 10% Dextrose
▪ 3% normal saline solution
(interstitial)
➢ Diabetes insipidus
➢ Congestive heart failure
➢ Cirrhosis
➢ Renal failure ➢ Cushing’s syndrome
➢ Hyperaldosteronism

MANIFESTATIONS OF EXTRACELLULAR FLUID OVERLOAD

➢ Pitting peripheral edema
➢ Periorbital edema
➢ Shortness of breath (d/t pulmonary edema/congestion)
➢ Shift of interstitial fluid to plasma (congestion)
➢ Bounding pulse and jugular venous distention
➢ Anasarca: general swelling of the whole body that can occur when the tissues of the
body retain too much fluid. The condition is also known as extreme generalized edema.
➢ Rapid weight gain (weigh pt daily every morning same time and same clothes)
➢ Moist crackles
➢ Tachycardia
➢ Hypertension

1) INTRACELLULAR FLUID OVERLOAD

➢ also known as water intoxication
➢ Hypotonic fluid from the intravascular space moves by osmosis to an area of higher
solute concentration inside the cell.
➢ Cells run the risk of rupturing if they become too overloaded with fluid.

CAUSES OF INTRACELLULAR FLUID OVERLOAD

➢ Hypotonic intravenous administration
▪ 0.45% normal saline solution
▪ 5% dextrose in water
➢ Excessive nasogastric tube irrigation with free water
 Irrigation – flushing (continuous flow of NSS solution, monitor output
because at risk for intracellular fluid volume overload
 ➢ Excessive administration of free water via enteral tube feedings

Check before and after feeding: residual osteorized feedings (if below 40,
pwede pakain, if above 40, delay ang feeding)
➢ Syndrome of inappropriate antidiuretic hormone
➢ Psychogenic polydipsia (polydipsia – excessive cellular thirst)

MANIFESTATIONS OF INTRACELLULAR FLUID OVERLOAD

➢ Neurological
▪ Cerebral edema
➢ Headache
➢ Irritability
➢ Confusion
➢ Anxiety
▪ Muscle weakness (fluid volume deficit and excess)
▪ Twitching
➢ Respiratory
▪ Dyspnea on exertion
▪ Increased respirations
➢ Gastrointestinal
▪ Nausea and vomiting (compensatory mechanism) (cause if FVD)
➢ Increased thirst (pathologic)
➢ Cardiac
• Elevated blood pressure
• Decreased pulse – upon palpation (hirap hanapin ang pulse kay tambok na ang
blood vessel)

DIAGNOSTICS
1. Serum electrolytes and serum osmolality are measured, but usually remain within normal
limits. (both FVD and FVE)
a FVD – serum osmolality: increase
b FVE – serum osmolality: decrease
c If may hypernatremic dehydration: increase serum osmolarity
2. Serum hematocrit and hemoglobin often are decreased due to plasma dilution from excess
extracellular fluid.
a FVD – high hematocrit
b FVE, anemia – low hematocrit, low hemoglobin
3. Additional tests of renal (BUN and creatinine) and liver function (ALT, AST (SGPT/SCOT))
may be ordered to help determine the cause of fluid volume excess.
4. Chest radiograph- to check for presence of pulmonary congestion
5. ABG - fluid in the alveoli impairs gas exchange resulting in hypoxia as evidenced by a low
PO2
a PCO2 in ABG reading – check hypoxia

MEDICAL MANAGEMENT
Managing fluid volume excess focuses on prevention in patients at risk, treating its
manifestations, and correcting the underlying cause.
1) DIURETICS (Needs Prescription)
➢ Commonly used to treat fluid volume excess. They inhibit sodium and water
reabsorption, increasing urine output.
➢ Potassium wasting or Potassium sparing
➢ The three major classes of diuretics, each of which acts on a different part of the kidney
tubule, are as follows:

a) Loop diuretics (work on renal tubules) - Potassium wasting

➢ Inhibit sodium and chloride reabsorption in the ascending loop of Henle
➢ Furosemide
➢ Ethacrynic acid
➢ Bumetanide
➢ torsemide

b) Thiazide-type diuretics - Potassium wasting

➢ Promote the excretion of sodium, chloride, potassium and water by decreasing
absorption in the distal tubule
➢ Bendroflumethiazide
➢ Chlorothiazide
➢ Hydrochlorothiazide
➢ Metolazone
➢ Polythiazide
➢ Chlorthalidone
➢ Trichlormethiazide
➢ Indamide
➢ Xipamid

c) Potassium-sparing diuretics
➢ Promote excretion of sodium and water by inhibiting sodium-potassium exchange
in the distal tubule
➢ Aldactone
➢ Spironolactone
➢ Amioride
➢ Triamterene

2) FLUID MANAGEMENT
➢ Fluid intake may be restricted in patients who have fluid volume excess.
➢ The amount of fluid allowed per day is prescribed by the primary care provider.
➢ All fluid intake must be calculated, including meals and that used to administer
medications orally or IV.
➢ I&O monitoring for both FVD and FVE

3) DIETARY MANAGEMENT
➢ Because sodium retention is a primary cause of fluid volume excess, a sodium-restricted
diet often is prescribed.
➢ The primary dietary sources of sodium are the salt shaker, processed foods, and foods
themselves.
NURSING MANAGEMENT
Nursing care focuses on preventing fluid volume excess in patients at risk and on managing
problems resulting from its effects.

1. Closely monitor for the vital signs including heart sounds (normal: S1 and S2) every 2-4
hours or as frequent as necessary. Assess VS, heart sounds and volume of peripheral
arteries
® Hypervolemia can cause hypertension, bounding peripheral pulses, and a third heart
sound (S3) due to the volume of blood flow through the hearts.

2. Auscultate lungs for presence or worsening of crackles (inhalation) and wheezes

(exhalation); auscultate heart for extra heart sounds.
® Crackles and wheezes indicate pulmonary congestion and edema. A gallop rhythm
(S3) may indicate diastolic overloading of the ventricles secondary to fluid volume
excess. If may wheezing tas nawala, bad sign = there is total closure of airway

3. Place in Fowler’s position if dyspnea or orthopnea is present.

® Fowler’s position improves lung expansion by decreasing the pressure of abdominal
contents on the diaphragm.

4. Monitor oxygen saturation levels and arterial blood gases (ABGs) for evidence of
impaired gas exchange (SaO2 < 92% to 95%; PaO2 < 80 mmHg). Administer oxygen as
indicated. ® Edema of interstitial lung tissues can interfere with gas exchange and
delivery to body tissues. Supplemental oxygen promotes gas exchange across the
alveolar-capillary membrane, improving tissue oxygenation. FVE and FVD lead to
hypoxia

5. Assess for the presence and extent of edema, particularly in the lower extremities and
the back, sacral, and periorbital areas.
® Initially, edema affects the dependent portions of the body—the lower extremities of
ambulatory patients and the sacrum in bedridden patients. Periorbital edema indicates
more generalized edema.

6. Obtain daily weights at the same time of day, using approximately the same clothing and
a balanced scale. (Night Shift)
® Daily weights are one of the most important gauges of fluid balance. Acute weight gain
or loss represents fluid gain or loss. Weight gain of 2.2 lbs is equivalent to 1 L of fluid
gain.

7. Administer oral fluids cautiously, adhering to any prescribed fluid restriction. Discuss the
restriction with the patient and significant others, including the total volume allowed, the
rationale, and the importance of reporting all fluid taken.
® All sources of fluid intake, including ice chips, are recorded to avoid excess fluid intake

8. Provide oral hygiene at least every 2 hours. Oral hygiene contributes to patient comfort
and keeps mucous membranes intact; it also helps relieve thirst if fluids are restricted.
 ® Oral hygiene contributes to patient comfort and keeps mucous membranes intact; it
also helps relieve thirst if fluids are restricted. FVE = hypoxia = increase chance of pt to
develop ulcers, have impaired skin integrity

9. Teach patient and significant others about the sodium-restricted diet.

® Excess sodium promotes water retention; a sodium-restricted diet is ordered to reduce
water gain. Reducing sodium intake will help the body excrete excess sodium and water.
FVE – sodium decreased, osmolality decreased

10. Administer prescribed diuretics as ordered, monitoring the patient’s response to therapy.
® Loop or high-ceiling diuretics such as furosemide can lead to rapid fluid loss and
manifestations of hypovolemia and electrolyte imbalance.

NURSING DIAGNOSIS
1) Fluid Volume Excess
Nursing care for the patient with excess fluid volume includes collaborative interventions such
as administering diuretics and maintaining a fluid restriction, as well as monitoring the status
and effects of the excess fluid volume.

2) Risk for Impaired Skin Integrity

Tissue edema decreases oxygen and nutrient delivery to the skin and subcutaneous tissues,
increasing the risk of injury.

3) Impaired Gas Exchange

With fluid volume excess, gas exchange may be impaired by edema of pulmonary interstitial
tissues. Acute pulmonary edema is a serious and potentially life-threatening complication of
pulmonary congestion.

LEARNING ACTIVITIES: https://www.youtube.com/watch?

v=6ecmOuCIoNc https://www.youtube.com/watch?v=Ft2YuF8AOBQ
https://www.youtube.com/watch?v=51FkahHUBwc&feature=youtu.be
TOPIC 4: ACID-BASE IMBALANCE

 The body constantly works to maintain a balance (homeostasis) between acids and
bases. Without that balance, cells can’t function properly.
 As cells use nutrients to produce energy they need to function, two-by products are
formed—carbon dioxide (CO2) and hydrogen.
 Acid-base balance depends on the regulation of free hydrogen ions (H+) in body fluids
determines the extent of acidity and alkalinity, both of which are measured in pH.
 Remember, pH levels are inversely proportionate to H+ concentration, which means
H+ concentration increases, pH decreases (acidosis). Conversely, when H+
concentration decreases, pH increases (alkalosis).

 PH (Potential of hydrogen)
o Acid base balance depends on the regulation of H + ions.
o pH is inversely proportional to H + levels. 7.35-7.45
 Why is there acid build up in the body? Why is there base build up in the body?
o Pathophysiologic (Cellular metabolism)
 Anaerobic – no oxygen, utilizie glucose
 Aerobic – utilize oxygen and glucose = yield CO2 and ATP
 ATP produced in aerobic is big
 Muscles sore after exercise because oxygen levels are depleted, have to hypoxia,
result to anaerobic respiration to produce ATP (there will be build-up of lactic acid,
cause acidity to blood pH)
 Produce CO2, lactic acid and H20
o Problems in lung or kidney: cause acid or base imbalance

Key Elements:
a. Acids: are hydrogen ion donors
b. Bases: are hydrogen ion acceptors
c. Ph: expression of hydrogen concentration in a solution
d. pCO2: partial pressure of carbon dioxide; the measure of carbon dioxide within arterial or
venous blood.
e. HCO3: Bicarbonate is a byproduct of the body's metabolism.

Components of ABG
 PaCO2 or partial pressure of carbon dioxide
o shows the adequacy of the gas exchange between the alveoli and the external
environment (alveolar ventilation)
 PaO2 or partial pressure of oxygen
o indicates the amount of oxygen available to bind with hemoglobin
o to check for hypoxia
 SO2 or oxygen saturation
o measured in percentage
o amount of oxygen in the blood that combines with hemoglobin
o to check for hypoxia
 HCO3 or bicarbonate ion
o alkaline substance that comprises over half of the total buffer base in the blood

2 Categories of Metabolic Processes:

a. Volatile -- can be eliminated from the body as a gas,
 e.g. Carbonic acid (H2CO3) is the only volatile acid produced in the body.

b. Nonvolatile -- that must be metabolized or excreted from the body in fluid

e.g. Lactic acid, hydrochloric acid, phosphoric acid, and sulfuric acid

Regulatory Mechanisms:
A. Chemical Buffers
 are substances that prevent major changes in pH by removing present in body fluid,
buffers bind with hydrogen ions to minimize the change in pH. If body fluids become too
basic or alkaline, buffers release hydrogen ions, restoring the pH.
 Acts fast when there is slight imbalance in pH; fastest regulatory mechanism to act on
that imbalance, only takes seconds but not sustainable (it cannot control if ever acid or
base imbalance is high)
 Kicks in seconds

1. Carbonic-Bicarbonate System, Bicarbonate (HCO3–)

 a weak base; when an acid is added to the system, the hydrogen ion in the acid
combines with bicarbonate, and the pH changes only slightly. Carbonic acid (H2CO3)
is a weak acid produced when carbon dioxide dissolves in water. If a base is added to
the system, it combines with carbonic acid, and the pH remains within the normal
range. Although the amounts of bicarbonate and carbonic acid in the body vary to a
certain extent, as long as a ratio of 20 parts bicarbonate (HCO3–) to 1-part carbonic
acid (H2CO3) is maintained, the pH remains within the 7.35 to 7.45 range.
 Acts in few seconds
 Carbonic – activated if pH become base or alkaline
 Bicarbonate (HCO3) – activated if pH is acidic

2. Phosphates
 important intracellular buffers, helping to maintain a stable pH within the cells.
 Regulates pH balance inside cell (intracellular)

3. Protein Buffer
 contribute to buffering of extracellular fluids. Proteins in intracellular fluid provide
extensive buffering for organic acids produced by cellular metabolism
 Regulates pH balance outside cell (extracellular)

* Both phosphate and CHON buffer regulates pH imbalance in their respective place

B. Respiratory System
 Regulates carbonic acid in the body by eliminating or retaining carbon dioxide.
 Carbon dioxide is a potential acid; when combined with water, it forms carbonic acid,
a volatile acid. Acute increases in either carbon dioxide or hydrogen ions in the blood
stimulate the respiratory center in the brain.
 As a result, both the rate and depth of respiration increase. The increased rate and
depth of lung ventilation eliminate carbon dioxide from the body, and carbonic acid
levels fall, bringing the pH to a more normal range. Although this compensation for
increased hydrogen ion concentration occurs within minutes, it becomes less effective
over time.
  Patients with chronic lung disease may have consistently high carbon dioxide levels in
their blood. Alkalosis, by contrast, depresses the respiratory center. Both the rate and
depth of respiration decrease, and carbon dioxide is retained. The retained carbon
dioxide then combines with water to restore carbonic acid levels and bring the pH
back within the normal range.
 Starts within minutes good response by 2 hours, complete by 12-24 hours
 Kicks in minutes to hours but high sustainability
 LUNGS - RESPIRATORY
 Lungs (regulate CO2)
o Hyperventilation
 Decreased CO2
o Hypoventilation
 Increased CO2

C. Renal System
 Responsible for the long-term regulation of acid–base balance in the body.
 Excess nonvolatile acids produced during metabolism normally are eliminated by the
kidneys, the kidneys also regulate bicarbonate levels in extracellular fluid by
regenerating bicarbonate ions as well as reabsorbing them in the renal tubules.
 Although the kidneys respond more slowly to changes in pH (over hours to days),
they can generate bicarbonate and selectively excrete or retain hydrogen ions as
needed.
 In acidosis, when excess hydrogen ion is present and the pH falls, the kidneys
excrete hydrogen ions and retain bicarbonate. In alkalosis, the kidneys retain
hydrogen ions and excrete bicarbonate to restore acid– base balance.
 Starts after few hours, complete by 5 to 7 days
 Highest sustainability
 KIDNEY - METABOLIC
 ACIDOSIS
o Increased elimination of H+ (High hydrogen low pH)
o Increased regeneration of HCO3
 ALKALOSIS
o Decreased elimination of H+ and increase in reabsorption
o Decreased regenration of HCO3

** NOTE: CHECMICAL BUFFERS - do not correct pH deviations, but only serve to reduce
the extent of the change that would otherwise occur

Table 4-1 Normal Gas Values

Normal Gas Values
pH 7.35 – 7.45
PaO2 80 – 100% (hypoxia)
PaCO2 35 – 45 mmHg
HCO3 22 – 26 mEq/L

Note: Not a clinical diagnosis or disease, rather they are clinical syndromes associated with a
wide variety of diseases.
Four (4) Types of Acid – Base Imbalance:
1. Respiratory Acidosis
a Compensated – kidney is doing something/compensating, normal pH
b Partially Compensated – kidney is compensating, abnormal pH
c Uncompensated – kidney did not do anything, abnormal pH
2. Respiratory Alkalosis
3. Metabolic Acidosis
a Compensated – lungs is doing something/compensating, normal pH
b Partially Compensated – lungs is compensating, abnormal pH
c Uncompensated – lungs did not do anything, abnormal pH
4. Metabolic Alkalosis
*Combined Alkalosis or Acidosis

Acidosis: any pathologic process that cause a relative excess of acid (volatile or fixed in the
body) Alkalosis: indicates a primary condition resulting in excess in base
CAUSES OF ACIDOSIS

Respiratory Acidosis (Carbonic Acid Excess)

When patient hypoventilates, carbon dioxide builds up in the bloodstream and pH drops below
normal
– respiratory acidosis. The kidneys try to compensate for a drop in pH by conserving
bicarbonate (base) ions, or generating them in the kidneys, which in turn raises the pH.
> pH 7.35; PaCO2 > 42 mmHg; HCO3 normal

Causes:
a. Acute respiratory conditions (pulmonary edema, pneumonia, COPD)
 less surface area decreases the amount of gas exchange that can occur, thus
impending carbon dioxide exchange.
 asthma = bronchoconstriction
 have build-up of CO2
 o COPD
 obstruction or constriction in airway
 low oxygen, high carbon dioxide (for cellular metabolism to occur, have
aerobic or anaerobic respiration)
o aerobic – product is ATP, by product is H2O and CO2
o anaerobic – by product lactic acid
 build-up because cells continue to metabolize to survive (by product of
CO2 and lactic acid; have build-up kasi kulang oxygen tas body will resort
to anaerobic respiration to attain cellular metabolism and produce ATP)
o ASTHMA

b. Depression of respiratory center (Drugs eg narcotics; head injuries)

 all metabolic acids are nonvolatile excreted to the kidneys, except carbonic acid which
is excreted as gas
 pag na depress ang respiratory center – breathing pattern is not effective =
hypoventilation - < pH level of blood
 point to CO2 build-up

c. Iatrogenic cause: inadequate mechanical ventilation

 excessive oxygen administration to client with COPD which hypoventilation occurs ➢
other factors contribute
 treatment that will lead to respiratory acidosis (medical management such as drugs)

Manifestations
a. Hypercapnia, due to rapid rise of PaCO2 level (pink puffers)
b. Headache, CO2 dilates cerebral blood vessels (1-2L of O2 only – hypoxic drive – hypoxia will
tell brain to breathe, if too high oxygen, hypoxic drive will be gone)
c. Warm and flushed skin related to the peripheral vasodilation (d/t CO 2) as well as to impaired
gas exchange
d. Fine flapping tremors (extremities)
e. Decreased reflexes
f. Rapid, shallow respirations; elevated pulse rate; tachycardia
g. Decreasing level of consciousness (feel sleepy or lethargic when low O2 levels)
 Figure 4-1 Signs and Symptoms of Respiratory Acidosis

 Decrease pH, high pCO2

 Dysrhythmias d/t hyperkalemia

Medical Management
a. ABG analysis
b. Chest X-rays can help pinpoint some cause, eg COPD, pneumonia
c. Serum electrolytes level, in acidosis potassium leaves the cell, so expect serum level to be
elevated (hyperkalemia)
d. Bronchodilators, to open constricted airways (give epinephrine if status asthmaticus –
stimulates SNS to to have dilation of bronchus) (give coffee if no gamot, like theophylline =
coffeein CNS stimulant, SNS = dilation of bronchus)
e. Supplemental oxygen
f. Drug therapy to treat hyperkalemia (calcium gluconate)

Nursing Diagnoses
➢ Ineffective breathing Pattern related to hypoventilation
➢ Impaired gas exchange related to alveolar hypoventilation
➢ Anxiety related to breathlessness
➢ Risk for injury related to decreased level of consciousness

*hypoventilation = high CO2 in blood

*hyperventilation = high O2 in blood (give paper bag)

Nursing Management

1. Maintain patent airway

® For easy access in case cardiac arrest may happen.

2. Monitor vital signs

® Respiratory acidosis can cause tachycardia, alterations in cardiac rate, respiratory rate and
hypotension. For carbon dioxide exhalation

3. Monitor neurologic status and report significant changes ® As it may progress to shock and
cardiac arrest.

4. Administer oxygen as ordered (low flow 1-2L/min)

® To be given at lower doses most especially to COPD patients as it stimulates patients to
breathe.

5. Accurate intake and output records

® To evaluate renal function.

6. Report any variations in ABG level.

7. Coughing and deep breathing exercises

® Expel to clear lungs]
  If fo CPT, chekck tlerance first
o

METABOLIC ACIDOSIS (Base Bicarb Deficit)

- The underlying mechanisms in metabolic acidosis are a loss of bicarbonate from
extracellular fluid, an accumulation of metabolic acids, or a combination of the two.

> pH 7.35; pCO2 normal; HCO3 <26 mEq/L

Causes: GI & Renal Functions (Severe Diarrhea = ass = acidosis)

a. Diabetic ketoacidosis → decrease insulin prevents glucose uptake, thus, stored fats are
oxidized (acetoacetic acid) and is metabolize for energy
 DKA is complication of DM (root cause of DKA: insulin is lacking or not accepted by
tissues)
o Insulin dependent DM (type 1)
 Absence or lack of insulin
o Non insulin dependent DM (type 2)
 Tissue resistance, no deficit in insulin
o increased blood glucose level in type 1 and 2 (thick and viscous blood)
o Primary function of glucose is it acts like a key (holds 2 glucose molecules,
potassium)
o Binds receptor site of cell for glucose and potassium to go inside cell (normal) = if
kulang insulin, build-up of glucose
o Glucose is needed for cellular metabolism
o Body will find a way to counteract abnormality regarding glucose intake
o Body will find other source of energy, use FAT/LIPIDS
o Increased utilization of fat -> by product of fat metabolism: ketones -> build-up of
ketones -> acidosis
b. Renal insufficiency→ decreased ability of the kidney to excrete acids
o Kidneys responsible for regenerating bicarbonate
c. Prolonged vomiting, severe diarrhea → due to loss of alkaline substances
o Vomiting – alkalosis; diarrhea – acidosis

Manifestations
Metabolic acidosis typically produces respiratory, neurologic, and cardiac sign and symptoms.
As acid builds up in the bloodstream, the lungs compensate by blowing off carbon dioxide.

a. Weakness, fatigue, general malaise

b. Anorexia, nausea, vomiting, abdominal pain
c. Decrease level of consciousness
d. Rapid, deep, labored breathing (Kussmaul’s respirations) → the first clue to metabolic
acidosis (high RR) – compensatory; lungs try to excrete CO2
e. Decrease cardiac output and blood pressure (due to VASODILATION)
 Low BP in sepsis -> due to systemic vasodilation (there is generalzied inflammatory
response that will trigger vasodilating effect of blood vessels)
 Tachycardia – heart try to compensate for low BP
f. Skin is warm and dry, as a result of peripheral vasodilation (fast flow of blood, have friction)
g. Diminished muscle tone and reflexes

Compensation: Increase respiratory rate/ depth to blow off carbon dioxide

Note: Increased respiratory rate as means of compensatory mechanism

Figure 4-2 Signs and Symptoms of Metabolic Acidosis

Increase in bicarbonate elimination (acidosis) - diarrhea

Medical Management
a. ABG analysis
b. Serum potassium levels → usually elevated as hydrogen ions move into the cells and
potassium moves out to maintain electroneutrality
c. Rapid acting insulin to reverse diabetic ketoacidosis and drive potassium back into the cell.
 Mgt for hyperkalemia:
o D50W + insulin (IV infusion)
o There is increased level of potassium in Extracellular compartment
o Kailangan ipasok sa cell ang abnormaly high potassium
o D50W contains glucose (need partner ng potassium to equalize ratio of
abnormally high potassium with glucose)
o Potassium wasting diuretic not sparing
d. Intravenous Sodium bicarbonate → to neutralize blood acidity in patients with bicarbonate
loss
e. Fluid replacement

Nursing Diagnoses
• Decreased cardiac output secondary to dysrhythmias and / or fluid volume deficits
• Risk for sensory/ perceptual alterations related to changes in neurological functioning
secondary to acidosis
• Risk for fluid volume deficit related to excessive loss from the kidneys or gastrointestinal
system
Nursing Management
Nursing care includes immediate emergency interventions and long-term treatment of the
condition and its underlying causes. Observe the following guidelines:

1. Monitor vital signs

® Increased RR (kussmaul’s respiration) -> metabolic acidosis

2. Monitor neurologic status.

® Changes can occur rapidly that prompt doctor’s referral.

3. Maintain patent IV line.

® For emergency situations and antibiotic administration.

4. Careful administration of sodium bicarbonate

® The chemical can inactivate many drugs or cause them to precipitate.

5. Proper positioning. (semi-fowler’s position)

® To promote chest expansion and facilitate breathing.

6. Record intake and output

® To evaluate renal Function

RESPIRATORY ALKALOSIS (Carbonic Acid Deficit)

In metabolic alkalosis, the underlying mechanisms include a loss of hydrogen ions (acid), a gain
in bicarbonate or booth. Above normal PaCO2 indicates that the lungs are compensating for
alkalosis. Renal compensations more effective, but slower as well.

>> pH 7.45; PaCO2 <35 mmHg; HCO3 normal

Causes
a. Vomiting → loss of hydrochloric acid from the stomach (vomit = “alk” sound = alkalosis)
 If frequent vomit = alkalosis (hyperemesis gravidarum) nasuka na ang HCL, suka
empty stomach
 Increase hydrochloric acid if vomit after kain (few times of vomiting, first phase) -
acidosis
b. Diuretic therapy (thiazides, loop diuretics) → can lead to a loss of hydrogen, potassium from
the kidneys
 Hyperkalemia – acidosis (if hydrogen level goes up)
 Hypokalemia – alkalosis (if hydrogen level goes down)
c. Cushing’s disease → causes retention of sodium and chloride and urinary loss of potassium
and hydrogen
 Sodium and potassium is inversely proportional
 Cushing’s disease – problem with cortisol (low cortisol = addison’s) (high cortisol =
cushing)
 Water retention = edema such as buffalo hump
d. Hyperventilation → most common cause of acute respiratory alkalosis
 Imbalance in O2 and CO2 ratio (high O2, low CO2)
  Paper bag or cuffed hands
e. Severe anemia, acute hypoxia 20 high altitude → overstimulation of the respiratory system
causes to breathe faster and deeper
 As height of altitude rises, low oxygen level
o Expect high RBC levels (physiologic means to compensate decreased oxygen
levels) – PHYSIOLOGIC POLYCYTHEMIA
o Release of erythropoietin (increase erythropoiesis)
 Low altitude, rise oxygen level

Manifestations
a. Slow, shallow respirations
b. Nausea, vomiting
c. polyuria
d. Twitching, weakness and tetany
e. Hyperactive reflexes
f. Numbness and tingling sensation
g. Confusion or syncope → lack of carbon dioxide in the blood may lead to hyperventilation
h. Dysrhythmia: related to hypokalemia and hypocalcemia (given calcium gluconate)

Buffering Response: shifting of acid from intracellular fluid to blood

Movement of bicarbonate into cell in exchange of chloride

Renal Compensation: increase bicarbonate excretion; decrease hydrogen ion secretion

Figure 4-3 Signs and Symptoms of Respiratory Alkalosis

Medical Management
a. Identify and eliminate causative factor if possible
b. Sedative or Anxiolytics agents may be given → to relieve anxiety and restore a normal
breathing pattern. (ex: Valium or Diazefam)
c. Respiratory support, e.g. oxygen therapy to prevent hypoxemia; breathe into a paper bag →
this forces the patient to breathe exhaled carbon dioxide, thereby raising the carbon dioxide
d. ABG analysis → key diagnostic test in identifying respiratory alkalosis
e. ECG → may indicate arrhythmias or the changes associated with hypokalemia or
hypocalcemia

Nursing Diagnosis
• Ineffective breathing pattern related to hyperventilation
• Altered thought processes related to altered cerebral functioning

Nursing Management
1. Allay anxiety whenever possible
® To prevent hyperventilation. Instruct client to breathe and calm

2. Monitor vital signs, and report changes

3. Report variations in ABG and ECG

® Changes can help evaluate patient’s condition. Hyper and hypokalemia

4. Maintain a calm, quiet environment

®Stress and fatigue can lead the patient to hyperventilate

METABOLIC ALKALOSIS (Carbonic Acid Excess)

• A condition in which there is an increased pH and increased HCO3
➢ pH > 7.45; HCO3 above 26 mEq/L; PCo2 normal

Causes
1. diuretic therapy → cause loss of H+, A-, k+ but precipitates ↑HCO3 level (regeneration or
production or bicarbonate), low hydrogen = alkalosis
2. ingestion of NaHCO3 or excessive NaHCO3 to correct acidosis (careful administration)
3. aldosterone excess → ↑ Na retention, ↑ H+ and bicarbonate regeneration
4. prolonged steroid therapy → same with aldosterone effects (hyperaldosteronism – FVE)
5. prolonged gastric suctioning or vomiting → loss or H+ ions; sengstaken, Blakemore tube (a
thick catheter with triple lumen with 2 balloons; inflated at the orifice of the stomach and
esophagus to apply pressure thus prevent bleeding, the 3rd lumen is for suctioning gastric
contents)
- 1st balloon – anchor
- 2nd balloon – add pressure
6. Massive blood transfusion (whole blood) → (citrate anticoagulant which is use for storing
blood is metabolize to bicarbonate) - transfusion create acidosis = leaked potassium out of
cell (hyperkalemia)

Manifestations
• Increased myocardial activity, palpitations
• Increased heart rate
• Rapid, shallow breathing
• Dizziness, lightheadedness
• Hyperactive reflexes
 • Nausea, vomiting

Figure 4-4 Signs and Symptoms of Metabolic Alkalosis

*tremors – due to hypocalcemia (mgt: calcium gluconate)

Laboratory Findings
➢ ABG analysis
➢ Serum electrolyte levels → low potassium, calcium and chloride, HCO3 elevated
➢ ECG changes, low T wave

Medical Management
➢ Replacement of electrolytes
➢ Antiemetics may be administered to treat underlying nausea and vomiting (nausea
symptom; vomiting – sign)
➢ Acetazolamide (Diamox) → to increase renal excretion

Nursing Diagnoses
➢ Ineffective breathing pattern related to hypoventilation
➢ Impaired gas exchange related to alveolar hypoventilation
➢ Anxiety related to breathlessness

Nursing Management
1. Monitor vital signs

2. Assess patient’s level of consciousness

® Apathy and confusion may be evident in a patient’s conversation.

3. Administer oxygen
® Treat hypoxemia. Hypoxemia – low oxygen levels in blood -> lead to hypoxia
4. Monitor Intake and output
® To evaluate renal function.

ACID BLOOD GAS (ABG) ANALYSIS

➢ is an essential part of diagnosing and managing a patient’s oxygenation status and
acidbase balance
➢ the usefulness of this diagnostic tool is dependent on being able to correctly interpret
results.

Table 4-2 Evaluation of Abnormal Blood Gas Values

NORMAL GAS VALUES
pH 7.35 – 7.45
PaO2 80 – 100%
PaCO2 35 – 45 mmHg
HCO3 22 to 26 mEq/L
 Figure 4-5 Acid Base Mnemonic

Table 4-3 Steps to ABG Analysis

STEPS TO ABG ANALYSIS

1 Look at the pH
a. if → ACID-BASE BALANCE
b. Fully or completely compensated acid- base disorder
c. Mixed acid – base disorder

If → pH acidosis pH alkalosis
2 Look at the PCO2, if….
Alkalosis Acidosis
Evaluate the pH – PCO2 relationship for possible RESPIRATORY
3 PROBLEM
pH Respiratory
PCO2 Alkalosis
pH Respiratory Acidosis
PCO2
4 Look at the HCO3, iif…..
 Normal
Acidosis Alkalosis

Evaluate the pH, HCO3,d base or METABOLIC PROBLEM

5 an excess f
pH
HCO3 Metabolic Acidosis
Base -2
pH
HCO3 Metabolic Alkalosis
Base +2
Look for Compensation

NOTE: Renal (HCO3) compensates for respiratory

6 problem
Respiratory (PCO2) compensates for renal problem

2 Degrees of Compensation
a. Partial - compensatory component is appropriately
abnormal but pH is not yet in normal range, either acidotic or
alkalotic
ex. pH PCO2 HCO3
METABOLIC ALKALOSIS PARTIALLY COMPENSATED

b. Full - Compensatory component alters enough to return pH

to normal
ex. pH 7.45 PCO2 HCO3
METABOLIC ALKALOSIS VS RESPIRATORY ACIDOSIS FULLY
COMPENSATED

pH SHOWS THE PRIMARY PROBLEM

7.40 is absolutely normal

(7.35 – 39 = slightly acidic 7.41-45 = slightly alkaline)

Evaluate oxygenation
7
60-79 Mild Hypoxemia
40-59 Moderate
hypoxemia
< 40 Severe Hypoxemia

PO2 < 80 mmHg – hypoxemia;

hypoventilation PO2 > 100 mmHg –
hyperventilation

Learning Activities
 1. Video on ABG interpretation (https://youtu.be/EML9vE1nOgk)

2. How to perform Allen’s Test (https://youtu.be/D1tJO0RW9UM)

3. Example Case Analysis: A 69-year-old with chronic obstructive pulmonary disease

(COPD) is admitted with an acute respiratory infection. You are the nurse assigned to
care of this client. a.) What would this client’s ABGs look like?
b.) What will you do to help improve the client’s respiratory status?
c.) Why is a client with COPD given oxygen at a low flow rate?
d.) Why is this client’s PaCO2 different than a client who does not have COPD?
e.) What teaching does this client require in order to prevent development of metabolic
alkalosis?

4. Different exercises to enhance skills in ABG interpretations:

1. pH 7.26 CO2 53
HCO3 24
PO2 50

2. pH 7.52
CO2 29
HCO3 23
PO2 100

3. pH 7.18
CO2 44
HCO3 20
PO2 92

1. Respiratory Alkalosis Fully Compensated

pH = 7.26, PaCO2 = 32, HCO3 = 18

metabolic acidosis partially uncompensated

pH = 7.38, PaCO2 = 49, HCO3 = 30

respiratory acidosis fully compensated
pH = 7.10, PaCO2 = 40, HCO3 = 18
metabolic acidosis uncompensated

pH = 7.20, PaCO2 = 57, HCO3 = 26

respiratory acidosis uncompensated

pH = 7.48, PaCO2 = 30, HCO3 = 22

respiratory alkalosis uncompensated

pH = 7.41, PaCO2 = 19, HCO3 = 30

combined alkalosis

pH = 7.50, PaCO2 = 20, HCO3 = 20

respiratory alkalosis partially compensated

pH = 7.30, PaCO2 = 50, HCO3 = 20

combined acidosis

pH = 7.60, PaCO2 = 20, HCO3 = 30

combiend alkalosis

TOPIC 3: ELECTROLYTE IMBALANCE

 Electrolytes are substances that dissociate in solution to form charged particles called
ions. Cations are positively charged electrolytes; anions are negatively charged
electrolytes.
 Electrolytes have many functions, including assisting with the regulation of water
balance, regulating and maintaining acid– base balance, and contributing to enzyme
reactions. They are also essential for neuromuscular activity (Lemone, 2011).
 Electrolyte imbalances can develop by consuming too little or too much electrolyte as
well as excreting too little or too much electrolyte. Electrolyte disturbances are involved.
 2 types:
o Deficit - hypo
o Excess - hyper

Major Roles of Electrolytes

1. Maintain body fluid osmolality - regulate water distribution
2. Nervous System - Propagation of Action Potential
3. Cardiovascular System - Cardiac conduction & contraction
SODIUM (135 to 145 mEq/L)
 Sodium is one of the most important elements in the body. It accounts for 90% of
extracellular fluid cations (positively charged ions) and is the most abundant solute in
extracellular fluid.
 The normal serum sodium levels range from 135 to 145 mEq/L. Extracellular cation
 The body needs sodium to maintain proper extracellular fluid osmolality (concentration).
Sodium attracts fluids and helps preserve the extracellular fluid volume and fluid
distribution in the body. It also helps transmits impulses in nerve and muscle fibers
(Lippincott, 2016).
 Sodium imbalances affect the osmolality of ECF and water distribution between the fluid
compartments.
 When sodium levels are low (hyponatremia), water is drawn into the cells of the body,
causing them to swell. In contrast, high levels of sodium in ECF (hypernatremia) draw
water out of body cells, causing them to shrink (Lemone, 2011).
 The kidney is the primary regulator of sodium balance in the body. The kidney excretes
or conserves sodium in response to changes in vascular volume. A fall in blood volume
prompts several mechanisms that lead to sodium and water retention:

HYPONATREMIA (<135mEq/L)
Hyponatremia, a common electrolyte imbalance, refers to sodium deficiency
in relation to the amount of water in the body. It usually results from a loss of
sodium from the body, but it may also be caused by water gains that dilute
extracellular fluid (ECF).

 HYPOALDOSTERONISM
o Hyposecretion of aldosterone or mineralocorticoid
o RAAS (angiotensin II act on adrenal cortex in kidney to secrete aldosterone)
o Once aldosterone is released, there will be increased in reabsorption of sodium
(inc secretion of potassium because K and Na are inversely proportional)
o Hyposecretion of aldosterone = hyponatremia
o Diabetes – hyperglycemia = thick consistency of blood/viscous = Blood vessel
have a hard time moving blood = high arterial pressure = atrial natriuretic
hormone or peptide (ANP) = lowers blood pressure = secretion of ANP by cardia
cells, inhibits release of aldosterone)
o Kidney disease – Kidney secretes renin = if no secretion of renin, lesser chances
of stimulating aldosterone = kidney not secrete renin, low secretions; function of
kidney will be altered as well
o Primary adrenal insufficiency – adrenal glands/cortex
o
 HYPERSECRETION OF ADH (SIADH)
o 3 Common Features:
 Hemodilution (decreased HCT)
 High reabsorption of water in kidneys
 Low hematocrit levels
 Hyponatremia
 not due to deficit byt due to hemodilution
  Urine concentration (increased urine specific gravity)
 Increased reabsorption of water
 Loss of urine outpuit
 High secretion of sodium
 Urine SG and hematocrit – inversely proportional

 HYPONATREMIA

o Take not of seizurez and coma (seizure precaution)

o Caused by dilution
o Hyponatremic dehydration
o (hyposolar) – great sodium loss; Hypernatromic dehydration (greater water loss)
o Diuretics - let pt go to the ncrm

Classifications:
(1) Hypovolemic
➢ both sodium and water levels decrease in the extracellular area, but sodium loss is
greater than water loss.
Causes: vomiting, diarrhea, fistulas, gastric suctioning, excessive sweating, cystic fibrosis,
burns, wound drainage, osmotic diuresis, adrenal insufficiency, diuretic use

(2) Hypervolemic
➢ both water and sodium levels increase in the extracellular area, but the water gain is
more impressive. Serum sodium levels are diluted, and edema also occurs.
Causes: heart failure, liver failure, nephrotic syndrome, excessive administration of hypotonic IV
fluids, hyperaldosteronism
(3) Isovolemic
➢ sodium levels may appear low because too much fluid is in the body. Patients may not
exhibit signs of fluid volume excess, and total body sodium remains stable. Causes:
glucocorticoid deficiency, hypothyroidism, renal failure

Pathophysiology
Normally, the body gets rid of excess water by secreting less Antidiuretic Hormone (ADH); less
ADH causes diuresis. For that to happen, the nephrons must be functioning normally, receiving
and excreting excess water and reabsorbing sodium.
Hyponatremia develops when this regulatory function goes haywire. Serum sodium levels
decrease, and fluid shifts occur. When the blood vessels contain more water and less sodium,
fluid moves by osmosis from the extracellular area into the more concentrated intracellular area.
With more fluid in the cells and less in the blood vessels, cerebral edema and hypovolemia
(fluid volume deficit) can occur.

Manifestations
The manifestations of hyponatremia depend on the rapidity of onset, the severity, and the cause
of the imbalance. If the condition develops slowly, manifestations are usually not experienced
until the serum sodium levels reach 125 mEq/L. In addition, the manifestations of hyponatremia
vary, depending on extracellular fluid volume. a. Poor skin turgor
b. Dry mucosa
c. Decrease saliva production
d. Orthostatic hypotension
e. Nausea, abdominal cramping
f. Neurologic changes such as: lethargy, confusion, signs of increase ICP, muscle twitch,
seizure

Laboratory Findings
➢ Serum osmolality less than 280 mOsm/kg (dilute blood)
➢ Serum sodium level less than 135 mEq/L (low sodium level in blood)
➢ Urine specific gravity less than 1.010
➢ Elevated hematocrit and plasma protein levels

Medical Management
➢ Generally, treatment varies with the cause and severity of hyponatremia.

Hypervolemia/Isovolemia
a. Fluid restrictions
b. Oral sodium supplements

Hyponatremia
a. Give isotonic IV fluids (e.g. normal saline)
b. Offer High sodium foods In SEVERE cases:
a. Infusion of hypertonic saline solution (3% or 5% saline)
b. If hyponatremia is brought about by sodium deficiency, PNSS (best solution)

Nursing Management
Watch patients at risk for hyponatremia, including those with heart failure, cancer, or GI
disorders with fluid losses. Review patient’s medications, noting those that are associated with
hyponatremia. For patients who develop hyponatremia, take the following actions:

1. Monitor and record vital signs, especially blood pressure and pulse
® Hyponatremia can lead to orthostatic hypotension and tachycardia.
 2. Monitor neurologic status frequently
® This will assess any changes in the level of consciousness. Seizure precaution

3. Accurately measure and record intake and output.

® To determine adequacy of intake and output within the span of care.

4. Assess skin turgor at least every 8 hours for signs of dehydration.

® This will assess hydration level of patient. Check capillary refill time, skin turgor,
sunkeness in periorbital region. Depressed fontanelle – dehydrated; bulging fontanelles
– overhydrated for newborns.

5. Restrict fluid intake as ordered (fluid restriction is the primary treatment for dilutional
hyponatremia).
® Fluid restriction (with a goal of 500 mL/d below the 24-hour urine volume) is generally
firstline therapy

6. Administer oral sodium supplements as ordered. ® To treat low sodium levels.

7. Seizure precautions (lower side rails)

® To provide safety

HYPERNATREMIA (>145 mEq/L)

Hypernatremia, a less common problem than hyponatremia, refers to excess of sodium

relative to the amount of water in the body.

 Hyposecretion of ADH/vasopressin (diabetes insipidus)

*ADH secreted by pituitary gland
o Idiopathic
o Related to patients who had:
 Head surgery
 Head injury/trauma
 Affect head, specifically pituitary gland
o 3 common features:
 Hemoconcentration (increased HCT)
 Hypernatremia due to hemoconcentration
 Urine dilution (decreased urine specific gravity) – urine SG and hematocrit
inversely proportional
o Manifestations:
 Polyuria
  Polydipsia
 polyphagia

*thirst regualtion declines as u grow older, elderly are at risk

Pathophysiology
The cells play a role in maintaining sodium balance. When serum osmolality increases because
of hypernatremia, fluid moves by osmosis from inside the cell to outside the cell. As fluid leaves
the cells, they become dehydrated and shrink.

Manifestations
 Thirst is the first manifestation of hypernatremia.
 If thirst is not relieved, the primary manifestations relate to altered neurologic function.
Initial lethargy, weakness, and irritability can progress to seizures, coma, and death in
severe hypernatremia.
 Both the severity of the sodium excess and the rapidity of its onset affect the
manifestations of hypernatremia.
 You may also observe the following:
a. Low grade fever – hypernatremic dehydration
b. Flushed skin
c. Dry mucous membranes
d. Oliguria
e. Orthostatic hypotension

Laboratory Findings
The following laboratory and diagnostic tests may be ordered with the following findings:
➢ Serum sodium levels are greater than 145 mEq/L
➢ Serum osmolality is greater than 295 mOsm/kg
Medical Management
Treatment for hypernatremia varies with the cause. The underlying disorder must be corrected,
and serum sodium levels and related diagnostic tests must be monitored.

Note that the fluids should be given gradually over 48 hours to avoid shifting water into brain
cells. *increased intracranial pressure

 ADDISON’S DISEASE
o low cortisol and release of aldosterone, hyposecretion of aldosterone and cortisol
 o hypoaldosteronism = hyponatremia, decreased sodium
o hyperaldosteronism = RAAS activated, sodium retention, increased sodium levels
o decreased potassium level = hypertension, hypokalemia, low plasma renin
 PRIMARY HYPERALDOSTERONISM -

Nursing Management
If patient develop hypernatremia, take the following measures:

1. Monitor and maintain fluid replacement to within the prescribed limits.

® Rapid water replacement or rapid changes in serum sodium or osmolality can increase
the risk of bleeding or cerebral edema.

2. Monitor neurologic function, including mental status, level of consciousness.

® Both hypernatremia and rapid correction of hypernatremia affect cerebral function.
careful monitoring is vital to detect changes in mental status that may indicate cerebral
bleeding or edema.

3. Institute safety precautions as necessary.

® Patients with sodium disorders are at risk for injury due to seizure activity and changes
in mental status.

4. Keep clocks, calendars, and familiar objects at bedside. Orient to time, place, and
circumstances as needed.
® An unfamiliar environment and altered thought processes can further increase the
patient’s risk for injury. Significant others provide a sense of security and reduce the
patient’s anxiety.

POTASSIUM (3.5 to 5.0 mEq/L) (intarcellular cation)

 Directly proportional to impulse transmission

o High potassium = high impulse transmission
 Manifestations: diarrhea, tachycardia, intestinal colic (abdominal pain)
o Low potassium = low impulse transmission
 Manifestations: bradycardia, paralytic ileus (less to no bowel movement =
constipation), intestinal colic
 A major cation (ion with a positive charge) in intracellular fluid, potassium plays a critical
role in many metabolic cell functions. Only 2% fluid; 98% of the body’s potassium is
found in extracellular fluid. That significant difference affects nerve impulse transmission.
 The normal serum (ECF) potassium level is 3.5 to 5.0 mEq/L. To maintain balance,
potassium must be replaced daily through diet. Virtually all foods contain potassium,
although some foods and fluids are richer sources of this element than others.
 Aldosterone helps regulate potassium elimination by the kidneys. An increased
potassium concentration in ECF stimulates aldosterone production by the adrenal gland.
 The kidneys respond to aldosterone by increasing potassium excretion. Changes in
aldosterone secretion can profoundly affect the serum potassium level.

Potassium directly affects how well the body cells, nerves, and muscles function by:
 ➢ Maintaining cells’ electrical neutrality and osmolality
➢ Aiding neuromuscular transmission of nerve impulses
➢ Assisting skeletal and cardiac muscle contraction and electrical conductivity ➢ Affecting
acid-base balance in relationship to the hydrogen ion.

*highest K content: potato

*lowest K content: strawberry

HYPOKALEMIA (<3.5 mEq/L)

Hypokalemia is an abnormally low serum potassium level. It usually results from excess
potassium loss, although hospitalized patients may be at risk for hypokalemia because of
inadequate potassium intake.

Pathophysiology
Inadequate intake and excessive output of potassium can cause a moderate drop in its
level, upsetting the balance and causing a potassium deficiency. Potassium shifts from the
extracellular space to the intracellular space and hides in the cells. Because the cells contain
more potassium than usual, less can be measured in the blood.

Causes:
a. Inadequate potassium intake
b. Severe GI losses, e.g. suction, lavage, prolonged vomiting can deplete the body’s potassium
supply as a result potassium levels drop
c. Drug associated, e.g. diuretics (esp. thiazides and furosemides or loop diuretic),
corticosteroids, insulin (acts like a key)
d. Decrease bowel motility (constipation)

*if a person has diabetes, higher glucose, normal potassium = insulin always carry potassium and
glucose by pair = N glucose, high potassium or hyperkalemia (treatment: d50W + insulin
*induce hyperglycemia to pt with hyperkalemia (once insulin given, may pair glucoe and
potassioum to facilitate entry of potassium and glucose in cell)
Pasok plain NSS, drain after, empty contents of stomach

Manifestations
The signs and symptoms of a low potassium level reflect how important the electrolyte is to
normal body functions.

*high potassium = acidosis = d50W + Insulin

*low potassium = alkalosis
*PARALYTIC ILEUS

a. Skeletal muscle weakness, especially in the legs → a sign of a moderate loss of potassium.
This also includes paresthesia and leg cramps
b. Decreased bowel sounds, constipation, paralytic ileus
c. Weak and irregular pulse
d. Orthostatic hypotension and palpitations
e. ECG changes: flattened or inverted T wave, prominent U wave
 FIGURE 3-1 (LEFT) NORMAL ECG WAVE; (RIGHT) INVERTED T WAVE

Laboratory Findings
The following test results may develop to confirm the diagnosis of hypokalemia:
a. Serum potassium level less than 3.5 mEQ/L
b. Increased 24-hour urine level
c. Characteristic ECG changes (inverted T wave)

Medical Management
a. Identify and treat the cause
- treatment for hypokalemia focuses on restoring a normal potassium balance,
preventing serious complications, and removing or treating the underlying causes
b. Oral and IV replacements (40-80 mEq/day – Kalium durule or K IV), it can be safely given
at the same time
c. Give potassium supplement
i Oral – Kalium Durule = can cau8se gastric irritant (given with meals)
ii Parenteral – Potassium Chloride (KCl)
Max dose: 10-15 meq/hr
 Do not give in high concentrations = cardiac arrest
Must be incorporated with plain NSS
Nursing Management
Careful monitoring and skilled interventions can help prevent hypokalemia and spare your
patient from its associated complications. The following actions are considered.

1. Monitor serum potassium levels in patients at risk for hypokalemia

® Potassium must be replaced daily because the body is unable to conserve it. Either
lack of intake or abnormal losses of potassium in the urine or gastric fluids can lead to
hypokalemia.
2. Check heart rate and rhythm, and ECG tracings in patients with serum potassium level
less than 3 mew/L
® Hypovolemia causes tachyarrthymias

3. Assess respiratory rate, depth and pattern

® Hypokalemia may weaken or paralyze respiratory muscles. Notify doctor immediately
if respirations become shallow and rapid

4. Monitor serum potassium levels

® Changes in serum potassium level can lead to serious cardiac complications

5. Administer potassium infusions cautiously

6. Monitor vital signs, including blood pressure, orthostatic vitals and peripheral pulses.
® As cardiac output falls, the pulse becomes weak and thready. Orthostatic hypotension
may be noted with decreased cardiac output. Hypokalemia is commonly associated with
hypovolemia, which can cause orthostatic hypotension.

7. Monitor patients taking digitalis for toxicity (such as fatigue, weakness, confusion,
dizziness, hypotension, nausea).
® Hypokalemia potentiates digitalis effects

8. Dilute IV potassium as prescribed and administer using an infusion pump. Closely

monitor IV flow rate and response to potassium replacement.
® Rapid potassium administration is dangerous and can lead to hyperkalemia and
cardiac arrest.

9. Assist with self-care activities as needed.

® Increasing muscle weakness can lead to fatigue and affect the ability to meet self-care
needs.

10. Maintain accurate intake and output records.

® Gastrointestinal fluid losses can lead to significant potassium losses.

11. Monitor bowel sounds (5-30/min) and abdominal distention.

® Hypokalemia affects smooth muscle function and can lead to slowed peristalsis and
paralytic ileus.
HYPERKALEMIA (>5 mEq/L)

Hyperkalemia can result from inadequate excretion of potassium,

excessively high intake of potassium, or a shift of potassium from the ICF
to the ECF. Hyperkalemia affects neuromuscular and cardiac function.

Causes:
a. Increased dietary intake
b. Blood transfusion (stored blood) → serum potassium level increases the longer the blood is
stored. 4 hours. If exceed, hyperkalemia and hyperphosphatemia (most abundant
intracellular electrolytes). There is hemolysis. 6 hrs in SPH if lagpas, delikado na.
c. Rapid IV potassium administration (hyperkalemia)
d. Renal insufficiency (kidneys also excrete potassium, RAAS = aldosterone help potassium
release) (there is build-up of potassium, hyperkalemia, give D50W and insulin)
e. Metabolic acidosis, potassium shift to ECF in exchange of H ions (Kussmaul’s respiration or
fast breathing)

Pathophysiology
Potassium move from the extracellular to the intracellular compartment and increases cell
excitability, so that cells respond to stimuli of less intensity and may actually discharge
independently without a stimulus.

Manifestations
Signs and symptoms of hyperkalemia reflect its effects on neuromuscular and cardiac
functioning in the body.

a. Nausea, abdominal cramping and diarrhea → the early signs of hyperkalemia due to smooth-
muscle hyperactivity
b. Muscle weakness that in turn lead to flaccid paralysis
c. Decreased heart rate, irregular pulse, decreased cardiac output, hypotension
d. ECG changes, elevated T wave

Figure 3-2 Elevated T wave

Laboratory Findings
The following test results help confirm the diagnosis and determine the severity of
hyperkalemia:

a. Serum potassium level greater than 5 mEq/L

b. Decreased arterial pH, indicating acidosis
c. ECG abnormalities

Medical Management
Treatment for hyperkalemia is aimed at lowering the potassium level, treating its cause,
stabilizing the myocardium, and promoting renal and gastrointestinal excretion of potassium.
The severity of hyperkalemia dictates how it should be treated.

a. Diet restrictions
b. May administer loop diuretics for mild hyperkalemia → to increase potassium loss from the
body or to resolve any acidosis present
a Loop and thiazides (Bumex, furosemide, hydrochlorothiazide, mannitol)
c. Sodium polystyrene sulfonate (Kayexalate) → a cation-exchange resin (common treatment
for hyperkalemia)
a MoA: exchange resin
b Adminisetred via PO or ENEMA
i Assess bowel movement
ii Watch out for hypernatremia
d. Hemodialysis, if patient has renal failure
e. Insulin + D50W = to correct ratio of potassium (if pt does not have hyperglycemia only
hyperkalemia)

*avoid what type of anti-hpn drug? ACE inhibitors because angiotensin II react to kidey and
adrenal glands which stumulate aldosterone to be released, increased secretion of potaassium
kidneys reabsorb sodium

Nursing Interventions
Patients at risk for hyperkalemia require frequent monitoring of serum potassium and other
electrolyte levels. Take these actions.

1. Closely monitor the response to IV calcium gluconate, particularly in patients taking digitalis.
® Calcium increases the risk of digitalis toxicity.

2. Monitor skeletal muscle strength and tone.

® Increasing weakness, muscle paralysis, or progression of affected muscles to affect the
upper extremities or trunk can indicate increasing serum potassium levels.

3. Monitor respiratory rate and depth.

® Muscle weakness due to hyperkalemia can impair ventilation.

4. Assist with self-care activities as needed.

® Increasing muscle weakness can lead to fatigue and affect the ability to meet self-care needs.

5. Assess vital signs

6. Monitor the patient’s intake and output = report an output of less than 30 ml/hr (renal
insufficiency) (higher potassium levels if kdiney fails because RAAS is gone)
7. Prepare to administer a slow calcium chloride or gluconate IV infusion to counteract the
myocardial depressant effects of hyperkalemia (do slow IV push)
8. Keep in mind when giving Kayexalate that serum sodium levels may rise. Watch out for signs of
heart failure
9. Monitor ECG changes
CALCIUM (4.5-5.5 meq/L)
Calcium is a positively charged ion, or cation, found in both extracellular and intracellular fluid.
About 99% of the body’s calcium is found in the bones and the teeth. Only 1% is found in
serum and in soft tissue.
 Bone formation
 Clot formation (risk for bleeding) = hypocalcemia
 Important for impulse transmission
o Inversely proportional
o High Ca = Low impulse transmission
 Manifestation: hypotension, paralytic ileus, intestinal colic
o Low Ca = High impulse transmission
 Manifestation: hyperactive reflexes (CHVOSTEK and TROUSSEAU sign)
Functions:
a. Skeletal and heart muscle relaxation, activation, excitation and contraction
b. Maintains cellular permeability
c. Promotes blood coagulation
d. Nerve impulse transmission

Glands regulating Ca levels

 Thyroid Gland
o T3 – triiodothyronine
o T4 – thyroxine
o Thyrocalcitonin (calcitonin) – stimulates calcium levels-> what stimulates it to be
released? High calcium (goal is to lower calcium to achieve homeostatsis)
 Kidney – increase in calcium excretion
  Intestine – decrease calcium reabsorption
 Bone – deposition of calcium
 Parathyroid Gland
o PTH – What stimulates it to be released? Low calcium (goal is to increase calcium
for homeostasis)
 Kidney – vitamin D formation (active form: calciferol, go to intestine for
absorption), increase excretion of calcium in renal tubules
 Intestine – increase calcium reabsorption
 Bone – increase osteoclast activity (bone destroying cells)
 NOTE: osteoporosis -> expect hypercalcemia
If hypocalcemia – lead to osteoporosis
If osteoporisis – lead to hypercalcemia (nagalabas na calcium salts)

Three (3) Forms of calcium exist in the body:

1. 45% is bound to protein, mostly albumin; part of the total serum calcium concentration
2. 40% is ionized calcium, it is the calcium that is physiologically active and clinically important
for neuromuscular transmission.
3. 15% is bound to other substances such as phosphate, citrate, or carbonate

System Interactions:
a. Parathyroid Hormone (PTH), raises the plasma calcium level by promoting the transfer of
calcium from the bone to plasma
b. Calcium is dependent upon calcitriol (increases Ca absorption), the most active from of vit
D
c. Calcitonin, a calcium-lowering hormone produced by the thyroid gland, acts against PTH
by transferring calcium from the plasma to the skeletal system

HYPOCALCEMIA (<4.5 mEq/L)

Hypocalcemia can result from decreased total body calcium stores or low
levels of extracellular calcium with normal amounts of calcium stored in
bone. The systemic effects of hypocalcemia are caused by decreased
levels of ionized calcium in extracellular fluid.

Causes:
a. Inadequate intake
b. Hypoparathyroidism, resulting from surgery (parathyroidectomy, thyroidectomy, radical neck
dissection)
c. Electrolyte imbalances → Low serum albumin (most common cause)
d. Malabsorption → can result from decreased intestinal motility
e. Vitamin D deficiency → due to lack sun exposure or malabsorption
f. Massive blood transfusion, liver unable to metabolize citrate (added to prevent clotting) g.
Chronic diarrhea
h. Diuretic phase of ARF (renal insufficiency)
i. Severe burns

Pathophysiology
Extracellular calcium acts to stabilize neuromuscular cell membranes. This effect is reduced in
hypocalcemia, increasing neuromuscular irritability. Thus, electrical activity occurs
spontaneously and continuously.

Manifestations
Signs and symptoms of hypocalcemia reflect calcium’s effects on nerve transmission and
muscle and heart functions; therefore, neuromuscular and cardiovascular findings are most
evident.

a. Anxiety, confusion and irritability that can progress to seizures

b. Paresthesia, muscle twitching, cramps or tremors
c. Diarrhea
d. Hyperactive tendon reflexes
e. Fractures may occur
f. Brittle nails, dry skin and hair
g. Positive Chvostek’s (contraction of facial muscles produced by tapping the facial nerve in
front of the ear), Trousseau’s sign (carpal spasm induced by inflating a blood pressure cuff on
the upper arm to above systolic blood pressure for 2 to 5 minutes); due to increase nerve
excitability
h. Decreased cardiac output and subsequent arrhythmias
i. Prolonged QT segment on electrocardiogram (ECG)

Figure 3-3 Trousseau’s sign / Chvostek’s Sign

*stridor – adventitious breath sounds, heard during inhalation
*status asthmaticus – closure of airway, no wheezing, given epinephrine
Twitching in mouth

Laboratory Findings
These test results can help diagnose hypocalcemia and determine the severity of the
deficiency:

a. Elevated total serum calcium level

b. Low Ionized calcium level (ionized calcium measurement is the definitive method to
diagnose hypocalcemia)
c. Low albumin level
d. Characteristic ECG changes, prolonged ST segment (Pathognomonic Sign)

Figure 3-4
ECG changes in Hypercalcemia, Hypocalcemia
Medical Management
Treatment for hypocalcemia focuses on correcting the imbalance as quickly and safely as
possible. The underlying cause should be addressed to prevent recurrence.

a. Dietary supplement, e.g milk, cheese, cereal

b. Oral/IV calcium, e.g. Calcium carbonate/gluconate
c. Vitamin D supplements, facilitates GI absorption of calcium
Nursing Management
Here’s what you can do if the patient develops hypocalcemia:

1. Frequently monitor airway and respiratory status.

® These changes may indicate laryngeal spasm due to tetany.

2. Monitor cardiovascular status including heart rate and rhythm, blood pressure, and
peripheral pulses.
® Hypocalcemia decreases myocardial contractility, causing reduced cardiac output and
hypotension. It also can cause bradycardia or ventricular dysrhythmias. Cardiac arrest
may occur in severe hypocalcemia.

3. Continuously monitor ECG in patients receiving IV calcium preparations, especially if the

patient also is taking digitalis.
® Rapid administration of calcium salts can lead to hypercalcemia and cardiac
dysrhythmias. Calcium administration increases the risk of digitalis toxicity and resultant
dysrhythmias.

4. If the patient has tetany, provide a quiet environment and institute seizure precautions.
® A quiet environment reduces central nervous system stimuli and the risk of
convulsions in the patient with tetany. (let pt. lie flat on bed then side-lying position
because there will be continuous production of saliva, time the duration (onset and end),
raise side rails, padded tongue depressor or any cloth, oxygen)
 HYPERCALCEMIA (>5.5 mEq/L) (CC: Hyperparathyroidism)
Hypercalcemia is a common metabolic emergency that occurs when
serum calcium level rises, or the rate of calcium entry into
extracellular fluid exceeds the rate of calcium excretion by the
kidneys.

Causes:
a. Hyperparathyroidism (most common cause) the body excretes more PTH than normal,
which greatly strengthens the effects of the hormone
b. Metastatic malignancy → causes bone destruction as malignant cells invade the bones and
cause the release of a hormone similar to PTH
c. Thiazide diuretics → potentiates PTH and decrease excretion in kidneys
d. Increase Vitamin D (can prompt an increase in serum calcium levels) & prolong use of
alkaline antacid (calcium carbonate)
e. Prolong immobility (accumulation of calcium > calcification)

Manifestations
Signs and symptoms of hypercalcemia are intensified if the condition develops acutely.
Symptoms are also more severe if calcium levels are greater than 5.5 mEq/L

a. Muscle weakness
b. Bradycardia
c. Shortened QT interval
d. Decreased gastrointestinal motility (anorexia, n/v)
e. Stone formation

Laboratory Findings
The laboratory and diagnostic tests that may be ordered are as follows:

a. Elevated serum calcium level

b. Elevated Ionized calcium level
c. Digoxin toxicity if patient is taking digoxin)
d. Characteristic ECG changes (Shortened QT interval)

Figure 3-5 Normal QT wave; Shortened QT wave

Medical Management
The management of hypercalcemia focuses on correcting the underlying cause and reducing
the serum calcium level.

a. ECG monitoring
b. Treat with IV saline → the sodium in the solution is typically used for hydration in these cases
c. Loop diuretics (Lasix) → promotes calcium excretion
d. Administer Calcitonin (IM/SC)

*thyroid gland secrete calcitonin

Nursing Management
Be sure to monitor the calcium levels of patients who are at risk for hypercalcemia, such as
those who have cancer or parathyroid disorders, are immobile, or are receiving a calcium
supplement. For a patient who develops hypercalcemia, you can take the following actions:
1. Institute safety precautions if confusion or other changes in mental status are noted.
®Changes in mental status may impair judgment and the patient’s ability to maintain
his or her own safety.

2. Observe for manifestations of digitalis toxicity.

® Hypercalcemia increases the risk of digitalis toxicity.

3. Promote fluid intake to keep the patient well hydrated and maintain dilute urine.
®Acidic, dilute urine reduces the risk of calcium salts precipitating out to form kidney
stones.

4. If excess bone reabsorption has occurred, use caution when turning, positioning,
transferring, or ambulating.
® Bones that have lost excess calcium may fracture with minimal stress or trauma
(pathologic fractures).

5. Closely monitor intake and output.

® loop diuretic such as furosemide may be necessary if urinary output does not keep
up with fluid administration.

6. Frequently assess vital signs, respiratory status, and heart sounds.

® Increasing pulse rate, dyspnea, adventitious lung sounds, and an S3 on auscultation
of the heart may indicate excess fluid volume and potential heart failure.

7. Place in semi-Fowler’s to Fowler’s position.

® Elevating the head of the bed improves lung expansion and reduces the work of
breathing.
*calcium – important in muscle contractions
*calcium oxalate

MAGNESIUM (1.5-2.5 meq/L)

 Mg and impulse trnamissiona re inversely proportional
 Drug of choice for PIH (toxemia of pregnancy) = MgSO4 (prevent seizure/convulsion)
o DTE, patellar reflex, knee jerk reflex (use reflex hammer on patellA)
Function:
a. Promotes enzyme reactions within the cell during carbohydrate metabolism
b. Influences vasodilation and irritability and contractility of the cardiac muscles, thereby helping
the cardiovascular system function normally
c. Aids in neurotransmission and hormone-receptor binding
d. Makes production of parathyroid hormone possible

HYPOMAGNESEMIA (<1.5 mEq/L)

Hypomagnesemia is a common problem in critically ill patients. It is may be caused by

deficient magnesium intake, excessive losses, or a shift between the intracellular and
extracellular compartment, Inversely proportional to impulse transmission.

Causes:
Any condition that impairs either of the body’s magnesium regulators – the GI system or the
urinary system – can lead to a magnesium shortage. These conditions fall into four (4) main
categories:
a. Poor dietary intake of magnesium
b. Poor magnesium absorption by the GI tract
c. Excessive magnesium loss from the GI tract
d. Excessive magnesium loss from the urinary tract

Pathophysiology
Hypomagnesemia causes increased neuromuscular excitability which commonly occurs with
hypokalemia and hypocalcemia

Manifestations
Signs and symptoms of hypomagnesemia can range from mild to life-threatening.
 Seizure/convulsiona
 Ventricular dysrhythmia
o (1) V-tach – vulsalva maneuver (decreases heart rate) (check apical pulse for 1
full minute, do vulsalva maneuver exert effort)
o (2) Torsades de pointes – polymorphic type of V-dysrhythmia

Generally speaking, your patient’s signs and symptoms may resemble those you would see
with a potassium or calcium imbalance. However, you can’t always count on detecting
hypomagnesemia from clinical findings alone.
a. Altered level of consciousness, tetany, seizures
b. Emotional lability
c. Vomiting
d. Tremors, twitching, tetany, hyperactive deep tendon reflexes
e. Rapid heart rate
f. Chvostek’s and Trousseau’s sign

Laboratory Findings
Diagnostic test results that point to hypomagnesemia include:
a. Serum magnesium level below 1.5 mEq/L (possibly with a below normal serum albumin
level) b. Low potassium and calcium level
c. Characteristic ECG changes
d. Elevated serum levels of digoxin in a patient receiving the drug

Medical Management
Treatment for hypomagnesemia depends on the underlying cause of the condition and the
patient’s clinical findings:
a. Dietary management, (green leafy vegetables, nuts, legumes, seafood, wholegrain,
chocolates)
b. Intravenous infusion/ intramuscular injection, before magnesium administration, renal function
should be assessed
D – deep tendon reflex (+)
R – respiratory rate (increase)
O – polyuria (urine output) (increase)
P – blood pressure (increase)
*inversely proportional lahat
*given mgso4

Nursing Management
The best treatment for hypomagnesemia is prevention, so keep a watchful eye on patients at
risk for this imbalance such as those who can’t tolerate oral intake. For patients who have
already been diagnosed with hypomagnesemia, take the following actions:

1. Monitor serum electrolytes, including magnesium, potassium, and calcium.

® Magnesium deficiency often is accompanied by deficiencies of potassium and calcium.

2. Monitor GI function, including bowel sounds and abdominal distention.

® Hypomagnesemia reduces GI motility.

3. Initiate cardiac monitoring, reporting and treating (as prescribed) ECG changes and
dysrhythmias. ® Low magnesium levels can precipitate ventricular dysrhythmias, including
lethal dysrhythmias such as ventricular fibrillation.

4. Assess deep tendon reflexes frequently during IV magnesium infusions and prior to each IM
dose.
® Depressed tendon reflexes indicate a high serum magnesium level.

5. Maintain a quiet, darkened environment. Institute seizure precautions.

® Increased neuromuscular and CNS irritability can lead to seizures. A quiet, dark environment
reduces stimuli.

HYPERMAGNESEMIA (>2.5 mEq/L) (CC: Renal Dysfunction) magnesium toxity

Having too much magnesium in the serum can be just as bad as having too little.
Hypermagnesemia occurs when the body’s serum magnesium level rises above the normal
range. However, hypermagnesemia is uncommon; typically, the kidneys can rapidly reduce
the amount of excess magnesium in the body.
*earliest sign of magnesium toxicity: DTR

Causes:
a. Impaired magnesium excretion, e.g. renal dysfunction, most common cause of
hypermagnesemia
b. Excessive magnesium intake

Pathophysiology
Elevated serum magnesium levels suppress cellular excitability, resulting to muscular flaccidity
and suppression of electrical impulses.

Laboratory Findings
a. Serum magnesium level above 2.5 mEq/L
b. ECG changes (prolonged PR interval, widened QRS complex, tall T wave.

Medical Management
a. Correct underlying cause
b. Intravenous infusion of calcium gluconate, to antagonize magnesium effect

Nursing Management
1. Monitor vital signs
® Essential in assessing for abnormalities.

2. Check for deep tendon reflexes

® Depressed tendon reflexes indicate a high serum magnesium level.
3. Evaluate for changes in mental status
® Changes in mental status may impair judgment and the patient’s ability to maintain his or her
own safety.

PHOSPHOROUS (1.2 to 3.0 meq/L)

The primary anion, or negatively charged ion, found in the intracellular fluid. It’s contained in the
body as phosphate.

Functions:
a. Integral part of acid base buffer system (would disrupt the buffer system)
b. Regulate ATP use for muscle contraction, nerve transmission, electrolyte transport
c. Regulates 2,3 DPG (diphosphoglycerate) a compound in red blood cells that facilitates
oxygen delivery from the red blood cells to the tissues.
d. Regulates 2,3 DPG (diphosphoglycerate) a substance in RBC affecting oxygen affinity

HYPOPHOSPHATEMIA (<1.2 mEq/L) (CC: Respiratory Alkalosis)

Hypophosphatemia occurs when the serum phosphorous level falls

below 1.2 mEq/L. although this condition generally indicates a deficiency
of phosphorous, it can occur under various circumstances when total
body phosphorous stores are normal

Causes:
a. Respiratory alkalosis → one of the most common cause of hypophosphatemia, can stem
from a
number of conditions that produce hyperventilation b.
Malabsorption syndromes
c. Diuretic use, (Thiazides, Loop diuretics, Acetazolamide)

Pathophysiology
Most effects of hypophosphatemia result from depletion of ATP and impaired oxygen delivery to
the cells due to a deficiency of the red blood cell enzyme 2,3-DPG. Severe hypophosphatemia
affects virtually every major organ system:

Manifestations
a. Muscle weakness, most common symptom
b. Malaise weakened hand grasp, myalgia (pain in the muscles)
c. Rhabdomyolysis (skeletal muscle destruction), can occur with altered muscle cell activity
d. Osteomalacia/Fracture, due to loss of bone density
e. Bruising and bleeding
Laboratory Findings
Diagnostic test results may indicate hypophosphatemia or a related condition:

a. serum phosphorous level less than 1.2 mEq/L

b. elevated Creatinine Kinase level if Rhabdomyolysis is present
c. X-ray studies that reveal skeletal changes typical of osteomalacia or bone fractures
d. Abnormal electrolytes (decreased magnesium levels and increased calcium levels)

Medical Management
Treatment varies with the severity and cause of the condition:
a. Treat the underlying cause
b. Oral and intravenous supplements

Nursing Interventions
Nursing care should focus on careful monitoring, safety measures and interventions to restore
normal serum phosphorous levels.

1. Monitor vital signs.

® Essential for detecting abnormalities.

2. Assess the patient frequently for evidence of decreasing muscle strength, such as weak
hand grasps or slurred speech, and document findings regularly. ® Poor delivery of
oxygen to the red blood cells

3. Assist in ambulation and activities of daily living, if needed, and keep essential objects
near patient to prevent accidents.
® Increased neuromuscular and CNS irritability can lead to seizures. A quiet, dark
environment reduces stimuli.

HYPERPHOSPHATEMIA (>3.0 mEq/L) (usually occurs with hypocalcemia)

Hyperphosphatemia is a serum phosphate level greater than 4.5mg/dL. As with other

electrolyte imbalances, it may be the result of impaired phosphate excretion, excess intake,
or a shift of phosphate from the intracellular space into extracellular fluids.

Causes:
a. Renal Failure
b. Hypoparathyroidism → impairs less synthesis of parathyroid hormone (PTH), when less PTH
is synthesized, less phosphorous is excreted from the kidneys.
c. Respiratory acidosis
d. Increase tissue breakdown

Pathophysiology
Effects of high phosphorous level are actually due to hypocalcemia; calcium suppresses cellular
excitability.

Manifestations
a. Hyperphosphatemia causes few symptoms (tetany, tissue calcification)
b. Symptoms occurring result from decrease calcium secondary to reciprocity
Laboratory Findings:
The following diagnostic test results may indicate hyperphosphatemia or a related condition
such as hypocalcemia:

a. Serum phosphorous above normal

b. Low serum calcium level

Medical Management:
a. Treat underlying cause
b. Restrict dietary intake
c. Administer phosphate binding antacid, this may decrease absorption of phosphorous in the
gastrointestinal system

Nursing Management
1. Monitor vital signs
® Essential for detecting abnormalities.

2. Monitor intake and output (if urine output falls below 30 mL/hour, immediately notify the
doctor ®Decreased urine output can seriously affect renal clearance of excess serum
phosphorous

3. Monitor serum phosphorous and calcium levels

4. Monitorsigns of tetany, such as positive Trousseau’s and Chvostek’s sign

®hyperphosphatemia can impair renal tubules when calcification occurs.

Learning Activities

1. Assignment on Functions of Electrolytes in the body, with its Normal Values: Sodium,
Potassium, Calcium, Magnesium, Phosphorous
2. Review on Normal Sinus Rhythm, PQRST wave.
3. Differentiate Chvostek’s and Trousseau’s sign (https://youtu.be/mrsn_dL0QHI)
TOPIC 5: BURNS

Figure 5-1 Burn Injury

A burn is an injury from exposure to heat, chemicals, radiation or electric current leading
to sequence of physiologic events. For severe burn cases if untreated it can lead to
irreversible tissue damage. Injuries result from direct contact with or exposure to any of heat
source and the heat energy from the source is transferred to the tissues of the body

Many burns can be prevented, and most major burns occur in the home during cooking,
improper use of electrical appliances and work-related handling chemical, hot objects. Infants
and adults have greater risks to morbidity and mortality when they sustain burn injuries due to
several contributing factors.

4 Major Goals Relating to Burns:

➢ Prevention of Infection (e.g. topical creams)
➢ Institution of Life-Saving Measures for The Severely Burned Person
➢ Prevention of Disability and Disfigurement Through Early Specialized Individual
Treatment
o Complications such as compartment syndrome, contractures
➢ Rehabilitation Through Constructive Surgery and Rehabilitative Programs

Review of the Skin Anatomy and Physiology

• The skin is the largest organ of the body, having a surface area of 15 -20 square feet. It
provides covering for the body thereby protecting the body’s organ and tissues from the
external environment.

Figure 5-2 The Skin Structure

➢ The skin has two layers. the epidermis and the dermal layer.
➢ The epidermis is the outer of the skin and it is thin but tough, protecting the
internal structures from bacteria, viruses, fungi and trauma. It is composed of
keratinocyte and melanocyte cells. Avascular (no blood vessels).
➢ The dermis is the inner layer of the skin and is considered as “True Skin”,
compose of thick layer of fibrous and elastic tissue. It is of composed collagen fibers
consisting mast cells responsible for phagocytosis and release histamine in burn injury.
The dermal layer also serves as supporting and nutritional bed because most of the
 blood vessels (vascularized), nerves, sweat and sebaceous glands, hair follicles are
located.

Table 5-1 The Function of The Skin

Function of the Skin Mechanism

Protection of the internal It covers the internal structures of the body from
structures against infection and the external environment. Skin is first line of
trauma defense. Desiccation (no fluids can leak
through skin except sweat (insensible water
loss)
Sensation Receptor endings of nerves senses
temperature, pain, light touch, pressure
Fluid Balance Prevents H20 loss and extra H20 release
through perspiration; serves as water repellant
Temperature Regulation Body continuously produces heat as result of
food metabolism and this heat is primarily
dissipated in the skin
Vitamin D Production/Synthesis Skin expose to UV light can convert cholesterol
molecules to vit. D. Kidney metabolizes vitamin
D.

Immune Response Function Several dermal cells are important components

of the immune system e.g. langerhaus cells,
interleukin 1

*burn patients at risk for hypocalcemia

Physiologic Response to Burn Injury

*vasoactive substance – tissue injury (inflammatory response: pain, redness, heat, loss of
function)
*inc vascular permeability – leaky capillaries (fluids from intravascular to interstitial)
*tissue pressure – compartment syndrome (there is compression of blood vessels, have hypoxia,
loss of elasticity, increased tissue pressure) (needs surgical mgt: make incision para magopen
skin and relieve pressure)
*decreased intravascular volume = decreased blood flow = hypoxia in kidney (hypocalcemia and
hyperkalemia), skin (vit D synthesis), GIT
*dec CO because napagod na heart, incraesed mean arterial pressure
*hypoxia – dec O2 in brain

Burns are cause by a transfer of energy from a heat source to the body through conduction and
electromagnetic radiation leading to skin disruption causing:
o increase fluid loss,
o massive infection
o hypothermia
o scarring
o compromised immunity
o change in body function
o appearance and body image.
o In severe cases, fluid and electrolyte imbalance ensue.

If a person inhales product of combustion, respiratory function is compromised. Cardiac

dysrhythmia and circulatory failure, profound catabolic state increasing caloric expenditure and
nutritional deficiencies are also manifestations in serious burn injury. Gastrointestinal motility if
altered, leads to ulcer and paralytic ileus. If dehydration is severe, it slows down the glomerular
filtration rate, renal clearance of toxic wastes may lead to tubular necrosis and acute renal
failure.

*hemoconcentration – increased HCT (part of plasma the one who will shift causing edema, mas
marami na formed elements sa blood so tumataas ang HCT)
*hypovolemic – way of compensating
*have hyponatremia (PISO, sodium outside part of plasma, shifting)
*interstitial to vascular = inc BV
*inc UO = diuresis
*PLR (isotonic crystalloid, also contains sodium), PNSS or 0.9 sodium chloride if walang PLR
*apoptosis in cells, labas potassium (major cation inside cell)
*albumin – helps in containing osmotic pressure in intravascular, humihila fluids from interstitial to
intravascular
*malnutrition if low negative nitrogen balance
*anaerobic and aerobic – both utilizes glucose (aerobic also utilize O2)
*aerobic give large ATP, anaerobic give small ATP
*di na kaya body sustain aerobic, going to anaerobic (by-product is lactic acid)

Categories of Burn Injury

MILD
➢ Partial thickness < 15% adult
➢ Full thickness burns < 2% adult (sunog lahat)

MODERATE
➢ Partial thickness burn 15 to 25 % adult TBSA (total body surface area)
➢ Full thickness 2% to 10 % adult TBSA
➢ Plus minor category criteria

SEVERE
➢ Partial thickness > 25% adult TBSA
➢ Full thickness burns are > 10% adult TBSA
➢ Burns are accompanied by other injuries (fractures, head injury)
➢ Presence of other criteria in the previous categories

OTHER CRITERIA
➢ Does not involve eyes, ears, nose, hands, face, feet, perineum
➢ No electrical burns / inhalation injuries
➢ Adult younger than 60 yrs. Old
➢ No pre-existing disease and other injury with the burn
*partial thickness = most painful
*deep partial is also painful if nililinisan na or tanggal debris
*insensate – wala nang nasense, masakit pa rin if linisan

Factors Determining Burn Severity

1. Burning Agent/ Cause
2. Location/Body parts involve (Rule of 9)
3. Age (60% of water in adult, higher water loss in pedia compared to adults)
4. Depth of the burn (degree of burn)
5. Size of the burn (TSBA)
6. History of cardiac, pulmonary, renal, hepatic disease (more complicated mgt)
7. Injuries sustained during burn injury

Burning Agent and Location

➢ The higher the temperature of the burning agent and longer duration of contact
can cause more severe injury.
➢ Burns sustained in the head, neck and chest is associated with higher mortality
rate because of:
o bronchoconstriction secondary to histamine release (inflammatory) causing
edema, carbon monoxide poisoning secondary to smoke inhalation
o chest constriction secondary to circumferential burns. (compartment syndrome)
➢ Burns sustained in the perineum area requires special care, these said areas are
prone to infection because of stool and urine contamination. (RISK FOR INFECTION)
(1% in rule of 9)

Table 5-2. Types of Burn Injury

Injury Causative Agent Priority Treatment

Cause/Type
Thermal open flame Extinguish flame (stop, drop, and roll)
steam Flush with cool water
hot liquids (water, Consult fire department
grease, tar, metal)
Chemical Acids Neutralize or dilute chemical
Strong alkalis Remove clothing
 Organic compounds Consult poison control center
Electrical Direct current Disconnect source of current
Alternating current Initiate CPR if necessary
Lightning Move to area of safety
Consult electrical experts
Radiation Solar Shield the skin appropriately
X-rays Limit time of exposure
Radioactive agents Move the patient away from the
radiation source
Consult a radiation expert

1st: Superficial
2nd: Superficial Partial
3rd: Deep Partial

*cold water - vasoconstriction

Age, Depth and Size of the Burn

Individuals below 2 years old and above 60 years old are of higher risk to morbidity and
mortality rates when sustaining burn injury secondary to immature and poor immune system,
fluid and electrolyte status, and existence of co-morbidities.

Another factor affecting burn severity is the depth and size of the burn, the deeper and bigger
the burn injury involved, result to more serious injuries and damage and longer healing time.
For third degree burns, skin grafting is required for a definitive wound closure. Burn size more
than 20% in adult and more than 10% of the body surface area requires fluid resuscitation.
Table 5-3: Burn Depth
DEPTH CAUSE APPEARANCE SENSATION HEALING TIME
1st Degree Flame Dry, no blister Painful 2-5 days, peeling,
Epidermis UV Light Minimal of no edema no scarring
Sunburn Increased redness May discolor

(superficial
thickness)
2nd Degree Hot liquid or
Blister, moist, pink Painful 5-21 days, no
Dermal solid, flame.
(superficial) grafting
(partial Chemical Pale, cherry red (superficial)
thickness) UV Light (deep) 21-35 days (deep)
Blanches with
pressure
(both)
rd
3 Degree Hot liquid or Dry with leathery No Pain No healing
Extends to solid, flame. eschar potential
subcutaneous Chemical White, charred, dark Requires excision
possibly UV Light tan, black, dark red and grafting
muscle and Electrical
bone

History Of Cardiac, Pulmonary, Renal, Hepatic Diseases And Injuries Sustained During
Burn Injury
 Pre-existing disease conditions would reduce normal compensatory responses to minor
hypovolemia
 Optimum systemic functioning is very vital for the burned client to respond to the burn
management such as fluid resuscitation, nutritional correction and infection prevention
 Injuries sustained during burn injury like fractures requires prolong hospitalization and
additional management

Stages of Interdisciplinary Care

The clinical course of treatment for the burn patient are divided into three stages. These stages
are useful to determine the clinical needs of the patient. The assessment and management of
the burned patient involves different group of physicians, nurses and other health care
specialists collaborating with each other to manage the patient’ s recovery.

Table 5- 4. Stages of Burn (EAR)

Care Phase Duration Priorities

Emergent / onset of injury to  1st aid (ABC – airway, breathing,
immediate completion of fluid circulation), prevention of shock
Resuscitative resuscitation 48 -72 HRS hypovolemic or hemorrhagic (CAB –
post injury circulation, airway, breathing)
 Prevention of respiratory distress
 Detection and treatment of injury
 Wound assessment/initial care
Acute Beginning of diuresis to  Wound care and closure prevention or
need completion of wound treatment, of complication nutritional
closure support
Rehabilitative From major wound closure  Prevention of scars and contractures
to return of individual’s  Physical, occupational, vocational
optimal level of physical rehabilitation
and psychosocial  Functional cosmetic reconstruction,
adjustment psychosocial counseling

I. Emergent / Resuscitative Phase

Starts with the onset of injury to completion of fluid resuscitation 48 -72 HRS post injury. The
goal in this phase is to preserve vital functions and prevent hypovolemic shock.

Pre-Hospital Care
➢ Remove person from source of burn
➢ Assess ABC and trauma
➢ Cover burn with sterile or clean cloth
➢ Remove constricting clothes and jewelry
➢ Transport immediately

Emergency Care for Minor Burn

➢ Administer pain medication
➢ Administer Tetanus prophylaxis
➢ Wound care
➢ Apply topical antibiotics

Emergency Care for Major Burns

➢ Evaluate degree and extent of burn (Rule of 9)
➢ Established patent airway and administer oxygen for burn victims in enclosed area
➢ Venoclysis and assess for hypovolemia (venoclysis – start IV line either peripheral or
central)
➢ Maintain NPO and insert NGT
➢ Insert foley catheter (to accurately monitor urine output)0
➢ Tetanus prophylaxis and give pain medication

Emergent or Resuscitive Phase

 Fluid management is one approach to treat burn patients.
 Within minutes of burn injury, a massive amount of fliud shifts from the intracellular and
intravascular compartments into the interstitium (thirdspacing). This kind of shift is called
burn shock and it continues until capillary integrity is restored within 24-36 hours of the
injury.
 Fluid resuscitation is indicated for burns greater than 20% TBSA in adults, greater than
10% BSA in children, patients older than 65 or younger than 2 years of age and patient
with preexisting disease that would reduce normal compensatory responses to minor
hypovolemia (Cardiac, pulmonary, renal, hepatic, diabetes).

Computation of Body Surface Area Burn (BSA)

The extent of the burn injury size is expressed as percentage of the total body surface area
(TBSA). Several methods are used to determine the extent of the injury. The “Rule of Nines” is
a rapid method of estimation of the burn size. This method divides the body into 5 surface areas
1. head,
2. trunk,
3. arms,
4. legs and
5. perineum and percentage that equal or total to the sum of nines are assigned
except the perineum which is only one percent.

Figure 5-5: Rule of Nines

Common Formula for Fluid Resuscitation
 Fluid resuscitation is the administration of the intravenous fluids to restore the circulating
blood volume during the acute period of capillary permeability in order to prevent burn
shock.
 #1: PLR #2: PNSS (both are isotonic, volume expanders)
 Crystalloids are administered during the first 24 hours after burn injury.
 Two commonly used formulas are the Parkland and Modified Brooke formula. These
formulas specify to infuse the 50% volume of fluid during the first 8 hours and the
remaining 50% to be infused over the next 16 hours.
o In Parkland formula, lactated Ringer solution is administered 4 ml X kg X % TBSA
burn.
o Modified Brooke lactated Ringer solution is administered 2ml X kg X % TBSA
burn.
o TBSA – use rule of 9
 Hourly urine output is measured to determine if fluid resuscitation is effective.
 Cardiac and respiratory status are also monitored.
Other Interventions During Resuscitative Phase
➢ Elevate the head of the bed to 30 degrees for facial and head burns (minimize blood flow
to burned areas to prevent further shifting of fluids)
➢ Elevate circumferential burns of the extremities with a pillow above the level of the heart
➢ Assess for infection, tracheal or laryngeal edema
➢ Protective isolation techniques shave hair around wound margins
➢ Monitor gastric output and Ph for stress ulcer (Curling’s Ulcer)
➢ Administer anti-ulcer drugs
➢ Avoid IM and SQ administration (if affected, will not function well)
➢ NPO (pt. is on IV TT) until with bowel sound
➢ Monitor daily weights (good indicator of amount of fluid resuscitation)

2. Acute Phase
- Begins with hemodynamic stability, capillary permeability restored, and diuresis begun
- Primary concern: restorative therapy to wound closure and infection control
▪ Aseptic technique and adequate debridement of wound, tetanus immunization,
IV antibiotics, topical anti-bacteria therapy, wound care are the basic
management.

SURGICAL MANAGEMENT:

Escharotomy is one approach in wound care wherein dead tissues and eschar are remove by
making a surgical incision through the eschar into the subcutaneous tissues to allow the
extremity to continue to swell without compressing the underlying blood vessels. To relieve
pressure secondary to compartment syndrome.

Management post escharotomy include:

• assessment of pulses, color, movement, and sensation of affected extremity,
• if bleeding is present control it with pressure and pack incision gently with fine mesh
gauze for 24 hours after.
Fasciotomy is another approach in wound care where the fascia is cut to relieve pressure so
as to reduce tissue death. Surgical procedure where the fascia is cut to relieve tension or
pressure commonly to treat the resulting loss of circulation to an area of tissue or muscle.
Fasciotomy is a limb-saving procedure when used to treat acute compartment syndrome. To
relieve pressure secondary to compartment syndrome.

Management:
• Hydrotherapy can also be utilized, through shower, bed bath and total immersion. To
clean wound. If total immersion is used, the tank is lined with plastic liners and
decontamination every after use is done to prevent cross infection, the temperature of
 the water to be use is 37 degrees Celsius and the immersion process should not exceed
more than 30 minutes to prevent chilling.

For wound dressing, it may be open or close dressing depending on the burn area involve in
order to maintain circulation and allows motion.

• For joints, light dressing is required to allow movement,

• Face dressings should be open type of dressing,
• Finger and toes, it should be wrapped individually.

Wound closure as a part of wound care is important.

Biologic Dressing (SIS: Sterile Intestinal Submucosa)
Synthetic and biosynthetic dressings (Biobrane & Transcyte) is applied, or skin grafting is
performed.
For graft care:
• elevate and immobilized graft site,
• keep site free from pressure,
• monitor for infection and • protect area from sunlight.

Table 5-5 Common Antimicrobial Agent

Antimicrobial Advantage Side Effects
Agent
Silver Sulfadiazine Effective against most May cause hypersensitivity
cream grampositive and gram- reaction in 5%-7% of all
negative organism patients;
Soothing on application Associated with an initial
Softens the eschar and decrease in WBC’s
increases joint mobility
Absorbed slowly reducing the
chance of nephrotoxicity
Mafenide acetate Effective against most Painful on application; May
cream grampositive and gram- cause hypersensitivity
negative organism reaction in 5%-7% of all
Rapidly diffuses through patients; Associated with
eschar (improved acid-base derangements
effectiveness in established
infections) Permits open
treatment of wounds; thus,
increasing mobility
Silver nitrate Effective against most Hyponatremia, hypokalemia,
solution grampositive and gram- and hypochoridemia
negative organism Decreased penetration of
eschar
Requires large bulky
dressings

3. Rehabilitative Phase
Starts from acute care to hospital discharge, the goals are directed for the burned patient to:
 • gain independence
• achieve maximal use of the affected part (if not 100%, dapat maximizing what is left of
the patient’s capability)
• promote wound healing
• minimize deformities (contractures)
• increase strength and function
• provide emotional support.

Nursing Management
1. Remove person from source of burn
®To remove the patient from the heat source and prevent further injury

2. Assess ABC and trauma

®To assess the extent of the injury so as to initiate and prioritize appropriate interventions

3. Cover burn with sterile or clean cloth

®Keeps air off the area, reduces pain and protects blistered skin.

4. Remove constricting clothes and jewelry

® Burn areas swells quickly, constrictive clothing can compromise circulation

5. Transport immediately
® for prompt medical intervention for severely burn patients,

Emergency Care for Minor Burn

1. Administer pain medication
® to ease pain and promote comfort

2. Administer Tetanus prophylaxis

®Tetanus is a possible complication of any burn because the damaged tissue is easily infected.
The person needs tetanus or booster shot, depending on date of last injection. Tetanus booster
should be given every 10 years.

3. Wound care
® Promotes speedy healing and prevent infection

4. Apply topical antibiotics

® Promotes speedy healing and prevent infection

Emergency Care for Major Burns

1. Evaluate degree and extent of burn
®To determine the appropriate fluid replacement and prevent shock

2. Established patent airway and administer oxygen for burn victims in enclosed area
®Systemic oxygenation is impaired by toxic gases released in most fires Inhaled smoke
contains carbon monoxide and cyanide and can travel to the alveoli and trigger inflammatory
reactions that lead to bronchospasm and impaired gas exchange.

3. Venoclysis and assess for hypovolemia

® To maintain the tissue perfusion. Burn injuries greater than 10% TBSA and including the
dermis result in circulatory compromise secondary to fluid loss via damaged tissue, widespread
vasodilation as well as increase capillary permeability and fluid shifts (third spacing). This can
result in hypovolemia leading to burns shock.

4. Maintain NPO and insert NGT

®Gastric stasis or ileus can result from potassium shifting secondary to massive burn, Insertion
of a nasogastric tube and commencement of enteral feeds should be considered for those who
sustain significant burn injuries and/or facial burns and are unable to tolerate adequate oral
intake.

5. Insert foley catheter

® Insert a Foley catheter so that urine output can be monitored as a guide for volume status.
Insert a Foley catheter in patients with burns >15% TBSA. Adequate urine output is 0.5 mL/kg/h
in adults and 1.5 mL/kg/h in children.

6. Tetanus prophylaxis and give pain medication

®Tetanus is a possible complication of any burn because the damaged tissue is easily infected,
and pain relievers promote comfort.

Other interventions during Resuscitative Phase

1. Elevate the head of the bed to 30 degrees for facial and head burns
®To minimize facial edema

2. Elevate circumferential burns of the extremities with a pillow above the level of the heart ®To
prevent or reduce swelling and pain
3. Assess for infection, tracheal or laryngeal edema
®For prompt medical intervention

4. Protective isolation techniques Shave hair around wound margins

®Hair and hair follicles harbor bacteria that increase the bacterial load, delaying wound healing
and increasing the risk of infection.

5. Monitor gastric output and Ph for stress ulcer

®To early detect development of Curling’s ulcer

6. Administer anti- ulcer drugs

®to prevent or correct Curling’s ulcer

7. Avoid IM and SQ administration

®Poor absorption of medications following burn injury due to fluid shifts

8. NPO until with bowel sound

®To prevent abdominal distention secondary to paralytic ileus, a complication of burns

9. Monitor daily weights

®For proper nutritional management. Severe burn is associated with significant changes in
body weight due to resuscitation volumes, fluid shifts, a hypermetabolic state, prolonged bed
rest, and caloric intake.

Nursing Diagnoses and Management

1. Impaired gas exchange related to carbon monoxide poisoning, smoke inhalation upper
airway loss
- Maintain adequate perfusion (outcome)
® To ensure adequate oxygenation and maintain vital organs function

2. Ineffective airway clearance related to edema and effects of smoke inhalation

- Maintain patent airway. (outcome)
® To prevent respiratory distress

3. FVD related to ↑ capillary permeability and evaporative losses from burn

wound - Restore optimal fluid balance and perfusion of vital organs (outcome)
® To promote healing and prevent further complications related to burn injury

4. Pain related to tissue/nerve/emotional impact injury

 Assess level of discomfort (interventions)
® To determine the appropriate pain intervention

 Administer pain relievers and antibiotics (interventions)

® Pain relievers promote comfort and damaged tissue is easily infected

 Provide emotional support to allay fear and anxiety (interventions)

® To allay fear and anxiety

Learning Activities
1. Assignment on the layers of epidermis layers: https://www.youtube.com/watch?
v=0X46aImj6nw

2. Compare Lund and Browder, Berkow’s Formula for computing fluid resuscitation
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC449823/
https://books.google.com.ph/books?
id=6DHMDwAAQBAJ&pg=PA8&lpg=PA8&dq=lund+and+browd
er+vs+berkow+formula&source=bl&ots=igUYn-
TNil&sig=ACfU3U2J4uw3hvcgPlaSJDYSmes9vg5jEg&hl=en&sa=X&ved=2ahUKEwih9bCGx7L
qAh WQA4gKHTMbB_EQ6AEwF3oECAkQAQ#v=onepage&q=lund%20and%20browder%20vs
%20berk ow%20formula&f=false

3. Using the Rule of Nines, assign the percentage distribution to the given body areas involved,
if the TBSA is 28 %
Head
Chest and abdomen
Perineum

4. Work example for fluid resuscitation

a) A 25-year-old man weighing 70 kg with a 30% flame burn was admitted at 4 pm. Computation
for his Total fluid requirement for first 24 hours using Parkland Formula 4 ml × (30% total burn
surface area) × (70 kg) = 8400 ml in 24 hours

b) Half to be given in first 8 hours, half over the next 16 hours

Will receive 4200 ml for 0-8 hours and 4200 ml during the next 16 hours
TOPIC 6 – URINARY ELIMINATION DISORDERS

Review of Anatomy and Physiology of the Renal System

Figure 6-1 Urinary System

The renal system is responsible for maintaining homeostasis in the body by carefully regulating
fluid and electrolytes, acid – base balance, removing wastes, and providing hormones
responsible for red blood cell production, hypertension and bone metabolism. The renal system
is composed of the upper and lower urinary tract.

Lower Urinary System

A. Bladder
The bladder is an extra peritoneal organ that lies behind the symphysis pubis. Its main function
is for storage of urine. As volume of urine increases, starting from 300-500 ml, awareness of
the need to void develops. Voluntary voiding is accomplished by stimulation of the
parasympathetic nerve fibers causing coordinated contraction of the detrusor muscle and the
bladder body.

Detrusor Muscle: a muscle which forms a layer of the wall of the bladder.

B. Urethra
The urethra drains urine from the bladder to an exterior opening of the body, the external
urethral orifice. In females, the urethra is about 3 to 4 cm. (1.5 in.). In males, the urethra is
about 15 to 20 cm (6 to 8 in.) Micturition, or urination, is the process of releasing urine from the
bladder into the urethra.

Upper Urinary System

 Figure 6-2 Structure of the Kidneys

Kidneys
The two kidneys lie on the posterior wall of the abdomen outside the peritoneal cavity. Each
kidney of the adult human that weighs about 150g is about the size of an indented region called
the hilum through which passes the renal artery and vein, lymphatic, nerve supply. The outer
part is the cortex and inner region called medulla. The medulla is divided into multiple cone
shaped masses called renal pyramids. The base of each pyramid terminates in the papilla,
which projects into the space of renal pelvis, a funnel shaped continuation of the upper end of
the ureter. The outer border of the pelvic is divided into minor calyces, the walls up the calyces,
pelvis that contain contractile elements that propel the urine toward the bladder, where urine is
stored until it is emptied by micturition.

• The right kidney is usually lower than the left kidney because of the location of the liver.

The functional unit of the kidney is the nephron. Millions of nephrons are present in each
human kidney which aid in the urine production and process of removing metabolic waste
products from the blood. These significant structures extend between the cortex and the
medulla. At one end of the nephron is closed, expanded and folded into a double-walled cuplike
structure called the Bowman’s capsule. This capsule encloses glomerulus, the nephron’s
primary structure in filtering function.

Functions of Kidney
Kidney performs different functions in order to maintain homeostasis in the body by excreting
metabolic waste products and reabsorbing necessary elements for the body. The following are
the functions of the kidney:

1. Formation of urine
➢ The formation of urine happens in three phases which are filtration, reabsorption and
secretion. Each of these processes happens in the body in order to create homeostasis
by removing those metabolic waste products and reabsorbing helpful substances.

a. Filtration
➢ The filtration process is nonselective, passive process which forms essential blood
plasma without blood protein but both of it is normally too large to pass through the
filtration membrane. If any of the two appeared in the urine, it would mean that there is a
 problem in the glomerular filters. The water and solute are smaller than proteins that are
forced through the capillary walls and pores of Bowman’s capsule into the renal tubule.

b. Tubular Reabsorption
➢ Tubular reabsorption is achieved by active and passive transfer mechanism Sodium,
potassium, calcium, phosphate, and uric acid are actively reabsorbed. Urea, water,
chloride, some bicarbonates and some phosphate are passively reabsorbed. Most
reabsorption occurs in the proximal tubule which conserves needed substances but does
not reabsorb metabolic waste products.

c. Tubular Secretion
➢ Some of substances such as hydrogen and potassium ion, creatinine, and ammonia,
move from the peritubular capillary blood and secreted by the tubule cells into the
filtration. Excreting nitrogenous waste products, unnecessary and excess substances.

2. Body’s Water Volume Regulator

➢ Regulation of water in the body contained in the blood is greatly influenced by antidiuretic
hormone (ADH), also called vasopressin. Vasopressin is produced in the hypothalamus
and stored in nearby pituitary gland. Receptors in the brain monitor the blood’s water
concentration causing the release of ADH in the bloodstream if the amount of salt and
other substances is too high. ADH in the bloodstream causes more water to be
reabsorbed into the bloodstream. In the absence of ADH, the collecting ducts become
impermeable to solute and water, making it less concentrated than plasma and the urine
is diluted.

3. Excretion of Metabolic Waste Products

➢ The kidney functions as the body’s main excretory organ, eliminating the body’s
metabolic waste products and serves as the primary mechanism for excreting drug
metabolites. 25g to 30g of urea is produced as the end product of protein breakdown and
excreted daily making it the major waste product of protein metabolism. Other waste
products are creatinine, phosphates and sulfates. Uric acid, formed as a waste product of
purine metabolism, is also eliminated in the urine.

4. Blood Pressure Regulator

➢ Regulating blood pressure is linked to the kidneys' ability to excrete enough sodium
chloride (salt) to preserve normal sodium balance, extracellular fluid volume and blood
volume.

5. Regulation of Acid-Base Balance

➢ The kidney also adjusts the body’s acid-base balance to prevent such blood disorders
such as acidosis and alkalosis. It helps maintain normal pH by retaining or excreting
hydrogen ions and regenerating lost buffer. The kidneys excrete acids that the lungs
cannot excrete and they can excrete hydrogen ions or reabsorb bicarbonate to correct
acidosis. They can reverse this process to correct alkalosis. Only renal mechanisms can
remove metabolic acids and excess bases from the body.

6. Regulation of Red Blood Cell Production

 ➢ Decreasing amount of oxygen in the renal blood flow activates the release of
erythropoietin. Erythropoietin stimulates the bone marrow to produce red blood cells,
thereby increasing the amount of hemoglobin available to carry oxygen.

7. Vitamin D Synthesis
➢ The kidneys are also responsible for the final conversion of inactive vitamin D to its active
form, 1.25-dihydroxychole-calciferol. Vitamin D is necessary for maintaining normal
calcium balance in the body.
➢ One of the most important roles of vitamin D is to maintain skeletal calcium balance by
promoting calcium absorption in the intestines.

8. Secretion of Prostaglandins
➢ The kidneys also produce prostaglandin E and prostacyclin, which have a vasodilatory
effect and are important in maintaining renal blood flow.

Renal Excretory Study

➢ URINALYSIS - assessed the nature of the urine produce and evaluates the color, ph and
specific gravity, determines the presence of glucose (glycosuria, protein,
blood(hematuria), ketones (ketonuria) and analyzes sediment for cells (WBC, called
pyuria, casts bacteria, crystals)
➢ Glycosuria: glucose in the urine
➢ Proteinuria: protein in the urine

Nursing Responsibilities:

Cleanse perineal area:

• For females: spread labia and cleanse meatus from front to back using antiseptic
sponge.
• For males: retract foreskin for uncircumcised penis and cleanse glans antiseptic sponge.
• It should be mid-stream clean catch!

!!! Must be analyzed 1 hour after of collection.

For 24 Hour urine collection (creatinine clearance):

• discard the first voided urine,
• collect all subsequent urine in a sterile container for 24 hours.

➢ Kidney, ureter, bladder X-ray (KUB) - plain film abdominal flat plate x-ray identifying the
number and size of kidneys with tumors, malformations and calculi; no special
preparations needed

➢ IVP (Intravenous pyelogram) – fluoroscopic visualization of the urinary tract after injection
with a radiopaque dye; is an x-ray exam that uses an injection of contrast material to
evaluate your kidneys, ureters and bladder and help diagnose blood in the urine or pain
in your side or lower back. An IVP may provide enough information to allow your doctor
to treat you with medication and avoid surgery.
Nursing Responsibilities
• Test for iodine sensitivity
• Enema before the procedure,
• 8 hours NPO,
• Push fluids after – to facilitate the flow of the dye; flush out the dye

➢ ULTRASOUND – non- invasive visualization of the kidney, ureter, bladder through the
use of sound waves

Nursing Responsibilities
• Supine position,
• NPO not required,
• Cleanse conducting gel from skin after the procedure

➢ CYSTOSCOPY – use of lighted scope to inspect the bladder (CYSTOSCOPE); maybe

use to remove tumors, stones, or other foreign materials or use to implant radium, place
catheters in the ureters.

Nursing Responsibilities Before the Procedure

• Explain the procedure will be done under local or general anesthesia,
• Secure consent,
• Administer sedative as ordered,
• NPO for general anesthesia, or NPO after light breakfast for local anesthesia,
• Enema as ordered,
• Let client assume a lithotomy position

Post Procedure
• Mild analgesic or warm sitz bath to relieve pain,
• I &O and temperature monitoring,
• Explain that hematuria expected post 24-48 hours,
• Assess for clots,
• Burning sensation upon urination maybe felt, and
• Force fluids.

➢ RENAL BIOPSY – removal of kidney tissue for microscopic study

Open method promotes better visualization but high risk for infection, close method none by
aspiration with a fine needle and has less risk for infection.

Nursing Responsibilities Before and During the Procedure

• Secure consent,
• NPO after midnight,
• Assess hemoglobin and coagulation studies, (patient is prone to bleeding)
• Assist client to assume prone position with a pillow below the abdomen,
• Apply pressure for 20 minutes on the aspirated area after the procedure

Post Procedure
 • Flat bedrest for 24 hours, (limit any activity coming from the patient)
• Monitor for hemorrhage, hypotension, dizziness, tachycardia, pallor, back, flank and
shoulder pain, (hypotension, monitor BP)
• Avoid strenuous activities, coughing, sneezing and straining, (movement can add
pressure and cause pain)
• Encourage fluid to avoid urinary retention and clots,
• Monitor hemoglobin,
• Assess for hematuria and if present should cease 24 hours after the procedure.
• Administer analgesics

➢ Blood chemistry and Hemoglobin tests - these tests or panels are groups of tests that
measure many chemical substances in the blood that are released from body tissues or
are produced. For kidney function, creatinine and blood urea nitrogen.

Nursing Responsibilities
• NPO is not required for BUN, hemoglobin and creatinine,
• Instruct the client not to eat red meat a day prior to creatinine test, intake of red meat can
affect the result.

A. INFECTIOUS DISORDERS

Figure 6-3 Urinary Tract Infection

UTI – ascending infection

An infection (UTI) cause by bacteria, virus, fungus, that occurs in the urinary tract. Risk for UTI
increases when a patient has:
• indwelling catheter,
• urinary retention,
• urinary and fecal incontinence
• poor perineal hygiene practices.

Urinary incontinence – no control of urine

Other risk factors are:

• renal scarring from previous infection (cause hardening)
• decrease ureteral peristalsis (stasis)
• urinary retention (anatomical or abnormal function such as neurogenic bladder)
• instrumentation of urinary tract (indwelling catheter [invasive], cystoscopy [invasive])
 • presence of urinary tract obstruction (calculi, tumor)
• being a female (shorter urethra)
• veicoureteral influx (backflow of urine from bladder into the ureters and structural
anomaly)
• sexual activity (abuse, masturbation SI)
• use of spermicidal compounds (condom, diaphragm)
• voluntary urinary retention

TYPES OF UTI
• UPPER – KIDNEY
• LOWER – BLADDER, URETHRA

CLASSIFICATION OF RECURRENT UTI:

RELAPSE
REINFECTION

The common causative microorganisms are:

• escherichia coli,
• staphylococcus,
• streptococcus,
• enterobacter,
• klebsiella and
• aerobacter,
• pseudo aeriginosa.

Pathophysiology
The epithelilium of the kidneys, ureter and bladder are sterile in healthy individuals, infection
begins when bacteria enter, usually starting at the opening of the urethra travelling up to the
bladder. If the flushing or urinating cannot stop the bacteria it can move up further to the ureters
and kidney. Lower urinary tract infection (UTI) rarely cause complications but upper UTI if
untreated can spread into the blood stream potential for chronic illness and death (septicemia
lead to septic shock – generalized vasodilation, decrease BP).

*female – shorter urethra (increased risk of developing UTI

 lower uti:
o cystitis (bladder infection)
o prostatitis (prostate infection)
o urethritis (urethra infection)
o can progress and cause upper UTI
 upper uti:
o pyelonephritis (kidney infection)
 How does UTI occur?
o Bacteria contaminates lower UTI
o Colonization in urethra, bladder
o Inflammatory response
o Neutrophil infiltration
o Bacteria multiply *immune system evasion (virulence)
o Ascension to kidneys
o Colonization if kidney (upper UTI)
o Bacteremia (infection goes to circulation = cause septic shock)
 Urinary catheterization may cause UTI
 Pregnancy UTI is common (progesteron relaxes smooth muscle causing stasis)
 TRIAD: vomiting, flank pein, fever
MEDICAL/PHARMACOLOGICAL/NURSING MANAGEMENT
 Increase OFI 3l/day
o Drinking water = increased UO = gerater stream to flush
 Administer analgesics, antiseptics,antibiotics
 Acid ash diet for calcium and phosphate stone formers (staph & proteus cause ammonia
breakdown leading to urine alkaline ph) Stones can cause UTI
o Cranberry, citrus fruits
o Stone – renal calculi/nephrolithiasis
o Urine is acidic in nature talaga
 Strict aseptic technique when inserting a catheter (3-7 days)
 Meticulous perineal care
 Provision of adequate rest
 Back massage
o Loin pain or renal colic (lower back pain)
 I/O monitoring
 Avoid sexual intercourse until symptoms subside or treatment is completed and avoid use
of sanitary pads ( for urethritis )
 High calories, low protein diet, cranberry juice
 Monitor signs of renal failure
o Urine Output – oliguria (magkaroon edema kay di malabas water)

NURSING DIAGNOSES
 Acute pain related to inflamammation of urinary mucosa as evidence by suprapubic
discomfort, and dysuria
 Impaired urinary elimination related to UTI
 Infection related to urinary frequency burning urination, fever , elevated wbc, foul-smelling
urine and suprapubic tenderness
 Knowledge deficit related to: Disease process, Health behaviors, Treatment regimen
COMMON MEDICATIONS USED FOR UTI
 ANTIFOLATES – first choice in uncomplicated UTI, inexpensive but not effective for
pseudomonas infection
 o trimethoprim-sulfamethoxazole (Bactrim)
o Trimethoprim (primsol,proloprim,trimpex)
 FLUOROQUINOLONES – indicated for pseudo and multiple drug resistant gram negative
infections, expensive and indicated for patients with sulfa allergy
o Eg ciprofloxacin (cipro, cyloxan) should not be administered within 2 hours after
taking antacid
 CEPHALOSPORIN: first generation
o Cephalexin (biocef, Keflex, keftab) less effective than other alternatives for short
course treatment
 PENICILLIN
o amoxicillin and clavulanic acid (augmentin)
o nitrofurantoin (macrobid,furalan, macrodantin)

1. URETHRITIS – is inflammation of the urethra. Ascending infection.

Causes: C/C STI: Sexually Transmitted Infection

Microorganisms (Escherichia coli, Chlamydia Trichomonas, Neisseria gonorrhoeae, and herpes
simplex virus type 2), trauma, or hyper-sensitivity to chemicals in products such as vaginal
deodorants, spermicidal jellies, or bubble bath detergents.
 Bacterial invasion, bubble bath, perfumed soaps, feminine hygiene sprays

Signs and Symptoms

➢ dysuria (painful urination), frequency, nocturia, burnign sensation on urination, urgency,
and bladder spasms. A urethral discharge may be noticed.

Medical Diagnosis
Based on patient signs and symptoms, urinalysis, and urethral smear

Medical Treatment
Antimicrobials when it is caused by microorganisms. If the patient is sexually active, the patient
and the sexual partner may be treated with antimicrobials to prevent reinfection.

Nursing Intervention
1. Sitz baths are soothing
® Reduce the pain.

2. Instruct female patients to wipe from front to back after toileting

® To deter transmission of microorganism from anus to the urethra

3. Discourage bubble baths and vaginal deodorant sprays.

® It has chemicals that can alter natural pH, leaving you more vulnerable to vaginal and urinary
tract infection.

4. Instruct uncircumcised male patients to clean the penis under the foreskin regularly.
® The foreskin is the sheath of skin that covers the head (glans) of the penis. Without regular
cleaning, a build-up of a whitish-yellow substance known as ‘smegma’ can occur which may
cause infection.
5. Advise patients to void after swimming.
® To flush bacteria present in pool or sea water

2. CYSTITIS - is inflammation of the urinary bladder wa;; frequently caused by ascending

infection. The most common.

*cholecystitis

INCIDENCE HIGHER IN WOMEN:

 Coitus – may manipulate urethra to allow bacteria to enter
 Shorter urethra
 Pregnancy & childbirth
 Damage to pelvic floor muscles
 Men- not susceptible due to bactericidal properties of prostatic secretions

Causes
Bacterial contamination, prolonged immobility, renal calculi, urinary diversion, indwelling
catheters, radiation therapy, and treatment with some types of chemotherapy.

Signs and Symptoms

➢ urgency, frequency, dysuria, hematuria, nocturia, bladder spasms, incontinence, and
lowgrade fever. Urine may be dark, tea colored, or cloudy. Fever, fatigue, and pelvic or
abdominal discomfort and bladder spasms experienced as pain behind the symphysis
pubis.
 Burning sensation upon urination
 Frequency/urgency ( sudden, compelling need to urinate)
 Cloudy urine
 Hematuria
 Low back pain
 Chills/fever
  nausea, vomiting
*RBC and protein can’t pass Bowman’s capsule (they are too big)

Medical Diagnosis
Urinalysis, culture, and sensitivity. The presence of bacteria does not mean that the patient has an
infection unless the patient also has white blood cells (WBCs) in the urine.

Medical Treatment
Antibiotic, mild analgesic such as acetaminophen is useful for relieving discomfort.
Phenazopyridine (pyridium) and Oxybutynin chloride (Ditropan may be ordered for 2 to 3 days
to decrease discomfort and bladder spasms.

Nursing Care
1. Advise patient to complete the entire course of antibiotics and take analgesics as ordered.
® To stop the infection from returning, as well as reduce the risk of the bacteria becoming
resistant to the antibiotics. Analgesics promote comfort and alleviate pain.

2. If phenozopyradine is given, advise patient that the drug causes red-orange urine.
® Change in color of the urine may cause the patient to be alarm

3. Warm sitz bath.

® To promote comfort

4. Oral fluid intake - 30m/kg of fluid per day. (facilitate flushing of bacteria)
® To increase urine formation and flush the urinary tract

5. To reduce risk of future infection, teach patient to, wear cotton undergarments, avoid tight-
fitting clothing in the perineal area.
® Wearing looser, cotton clothing will allow air to keep the area around the urethra dry. Tight-
fitting jeans can trap moisture and help bacteria grow.

6. Take shower instead of tub bath, avoid caffeine drinks, apple, grapefruit, orange these
irritates the bladder, maintain high fluid intake and void often, wiping from front to back after
voiding for female and drink a glass of water after swimming, before and after intercourse to
flush the bacteria.
® Soaking in the bathtub makes the bacteria and harsh chemicals from your bubble bath to
get inside and irritate the urethra

7. Avoid caffeine drinks, apple, grapefruit, orange

® Acidic food sources irritate the bladder, maintain high fluid intake and void often R. To
increase urine formation and flush the urinary tract

8. Wiping from front to back after voiding for female

® To deter transmission of microorganism from anus to the urethra

9. Drink a glass of water after swimming, before and after intercourse.

® To flush the bacteria.
3. PYELONEPHRITIS – inflammation of the renal pelvis. It may affect one or both kidneys.
URETERITIS IS ASSOCIATED WITH PYELONEPHRITIS
PYELONEPHRITIS - is the Bacterial invasion of the renal,calyces, parenchyma, & renal pelvis

2 TYPES / FORMS
• Acute
o temporary, minimal symptoms even asymptomatic but recurrence is frequent
o Sudden
o Within 6 months
o S/S
o Lower UTI S/S
o Chills, fever, malaise, flank pains, leukocytosis (increased WBC)
• Chronic
o permanent tissue damage through repeated inflammation/ scarring.
 Reflux nephropathy – problems in nephrons (functional units in kidney)
o About 6 months already
o S/S Hypertension, increase BUN, creatinine (due to inflamamtion
o 5 cardinal signs of inflammation: redness, swelling, pain, heat, loss of function
o Renal insufficiency if there is loss of function (kidney not capable of excretion)

DIAGNOSTIC TESTS
 Urinalysis,RBC, PUS,CASTS,NITRITES, LEUKOCYTE ESTERASE
 Urine GSCS (Gram staining – identify if posi or nega) (CS – culture sensitivity = grow
bacteria, check if bacteria is sensitive to antibitoics)
 CBC - ↑ WBC
 IVP(excretory urography) for chronic cases
o Intravenous pyelogram (contrast medium – ask pt if allergy to seafoods or iodine)
 Voiding cystourethrography
 Cystoscopy

Cause
Acute pyelonephritis is most often caused by an ascending bacterial infection, but it may be
bloodborne. Chronic pyelonephritis most often is the result of reflux of urine from inadequate
closure of the ureterovesical junction during voiding. It is also usually caused by long standing
UTIs with relapses and reinfections, may even lead to chronic renal failure. (Urinary stasis – not
totally emptied)

Signs and Symptoms

High fever, chills, nausea, vomiting, and dysuria. Severe pain or a constant dull ache in the
flank area.

The patient with chronic pyelonephritis experience fatigue, hypertension, increase BUN and
creatinine and a slight aching over one or both kidneys.

Medical Diagnosis
Urinalysis, urine culture and sensitivity, CBC, IVP, cystoscopy
Medical Treatment
• Antibiotics, urinary tract antiseptics, analgesics, and antispasmodics (for bladder
spasms).
• Additional medications may be needed to treat hypertension. Adults are advised to drink
at least eight 8-oz glasses of fluids daily.
• Intravenous fluids may be ordered if the patient has nausea and vomiting.
• Dietary salt and protein restriction may be imposed on the patient with chronic disease.
• Follow-up cultures to determine whether the infection has been resolved.

Nursing Interventions
1. Record the presence of signs and symptoms.
® To assess the presence and severity of the UTI

2. Record history of previous urinary disorders.

® To determine if the UTI is recurring or a reinfection

3. Fluid intake at least 8 oz of glasses a day.

® To promote urine formation and to flush the bacteria.

4. Advise patient to complete the entire course of antibiotics and take analgesics as ordered. ®
To stop the infection from returning, as well as reduce the risk of the bacteria becoming
resistant to the antibiotics. Analgesics promote comfort and alleviate pain.

5. Limit physical activity and exercise

® To conserve energy

6. Protein and salt dietary restrictions if advised by the physician.

® Protein increases metabolic waste product build up and salt cause water retention of which
the failing kidneys might not able to filter and excrete those.
 Glomerolus – part of nephron, filtered by bowman’s capsule
 Once immunoglobulins are deposited on gloemrualr membrane (start attack)
 Self antigen will be treated as foreign body
 Glomerulonephritis
o GFR is affected (glomerular filtration rate) = directly proportional to UO
 Low GFR = low UO
 High GFR = high UO
o BUN materials will just circulate
o Irritable patients
o Edema (decreased GFR)
o Oliguria – low frequency urine; dysuria – painful urination
 Nephrotic syndrome
o Nephritic syndrome is different (inflammation, low protein lumalabas)
o Leaky glomerulus lets protein out
o Pts have edema (hypobilirubinemia – less albumin less pressure to pull fluid from
interstitial to intravascular)
  Can migrate to heart or kidney via bloostream
 Check history of RHD
 Decreased viscosity of blood

Two types of Glomerulonephritis:

Acute – usually by beta-hemolytic strep infection
Chronic - may follow acute disease but is usually insidious (hidden), patient is asymptomatic
S/S of acute glomerulonephritis:
 Proteinuria
 Hematuria
 Mild to generalize edema
 hypertension
 decrease urine output
 increase serum creatinine, BUN (renal insufficiency)
 SOB, weakness, anorexia, flank pain
o Chronic inflammation – anorexia of inflammation

Chronic S/S:
 Gross hematuria
 Dark smoky, cola colored or red brown urine
 Proteinuria
 Hypoalbuminemia
 Edema
 Increase antistreptolysin o titer (200 IU)
 Hypertension (increased blood volume because decreased GFR)
 Metabolic acidosis (hyperkalemia – can’t be xcreted, RAAS not functioning anymore)

DIAGNOSTIC TESTS
• CBC
• urinalysis (UA) and culture (GSCS)
• electrolytes
• BUN, creatinine levels (check if progressed to renal failure)
• skin and throat culture

Medical management
 VS, I&O, weight monitoring
 Restrict fluid intake (bcoz FVE)
 Administer diuretics and anti – hypertensives, antibiotics
 Monitor for signs of renal failure
 Bed rest
 Diet modification (high calories, low protein [kidney & liver], low sodium)
o Low protein only not totally exclude in diet – trying to alleviate workload of liver and
kidney; livers neets to metabolize ammonia (by-product of amino acids, protein) to
urea for excretion
 albumin transfusion (to increased colloid oncotic pressure), dialysis & kidney transplant

Nursing care for Glomerulonephritis:

1. Prevention:
a. Prompt treatment of strep infection
b. Vitamin c rich diet
2. Symptomatic relief:
a. Fever: tsb, increase ofi (if no signs of FE, not low UE below 20 cc/hr)
b. Oliguria & hematuria: i & o monitoring
c. If with ↓albumin and edema: ↑ chon diet (egg white), limit ofi skin care
3. Monitoring / preventing possible complications:
a. Prevent recurrence: compliance esp to meds
b. ARF: monitor crea, BUN, UO.
c. Fluid retention: monitor edema, crackles, cardiac status
d. GBM status: monitor urine for chon, rbc, wbc and serum albumin

Nephrotic Syndrome
 is an alteration of kidney function caused by increased glomerular basement membrane
permeability to plasma protein (albumin)
 results from injury of the glomerulus

*puffy face, ascites

Altered glomerular permeability result in characteristic symptoms of:
 • gross proteinuria,
• generalized edema (anasarca),
• hypoalbuminemia,
• oliguria, and
• increased serum lipid level (hyperlipidemia).

It maybe primary or secondary:

 Primary = wherein the pathology is the kidney itself
 Secondary = renal manifestation of a systemic disease.

Nephrotic syndrome usually occurs in children between ages 2-6 but may affect adults, both
sexes and any race.

Pathophysiology
Normally large protein cannot pass through the glomerulus. Proteinuria occurs because of
changes to capillary endothelial cells of the glomerulus. The mechanism of damage to these
structures is unknown in primary and secondary glomerular diseases, but evidence suggests
that T cells may upregulate a circulating permeability factor or downregulate an inhibitor of
permeability factor in response to unidentified immunogens and cytokines. Other possible
factors include hereditary defects in proteins that are integral to the slit diaphragms of the
glomeruli, activation of complement leading to damage of the glomerular epithelial cells and
loss of the negatively charged groups attached to proteins of the Glomerular Basement
Membrane.
 Figure 6-5 Pathophysiology of Nephrotic Syndrome
Oncotic pressure – helps retain fluids; prevents fluid shifting

Signs and Symptoms

Triad:
• Massive proteinuria
• Hypoalbuminemia,
• Generalized edema/anascara,
• Hyperlipidemia (cholesterol levels of more than 300 mg/dl)
• Lipiduria
• Hypercoagulability
• Hypertension

Dx Exams And Findings

• History
• Kidney Biopsy (check if there is tumor) / USD: Slerosed Glomerulos (capillaries)
• Decreased Serum Albumin, Proteinuria, ↓ B Lymphocytes
• RBCs, “ Tea – Colored / Smoky Urine”
• ↑ Serum Cholesterol, LDL, TGL, Clotting Factors
o LDL – bad cholesterol (low density, magpilit BV, contribute formation of
atherosclerosis)
o HDL – good cholesterol (bring bad choles to liver)

Medical Diagnosis
• Urinalysis,
• Serum albumin,
 • Renal ultrasound and
• Biopsy.
• Serologic studies for infection and immune abnormalities e.g. antinuclear antibody.

Medical/Pharmacologic Management
➢ Blood-pressure medications, ACE inhibitors and ARBs, which curb the pressure in the
glomeruli and lower the amount of protein in the urine
➢ Diuretics to reduce swelling
➢ Cholesterol-lowering drugs
➢ Blood thinners, or anticoagulants
➢ Corticosteroids
➢ Limit salt to reduce swelling and low in saturated fats and cholesterol diet. ➢ Dialysis if
conservative management is not effective.

Medical mgt:
• infection: antibiotics
• inflammation: corticosteroids (WOF: cushing’s)
• chon loss: albumin transfusion (diet, egg white)
plus if with the ff:
• edema: diuretics
• HPN: anti-hpns
• ↑cholesterol: lipid lowering drugs (“statins”) eg * atorvastatin, simvastatin
• clotting: anti-coagulants (warfarin/heparin) = check clotting time

*hypoxia = ischemia = tissue necrosis = gangrene (nabulok na tissue, foul order)

Nursing care:
1. Prevention: prompt treatment of strep infection
2. Correct the etiology: manage DM & SLE
3. Symptomatic care:
a. Edema: limit ofi, low na diet, i & o, skin care
b. Hypoalbuminemia: low chon = .5-.6 gms/kg high chon diet (1-1.5 g/kg day)if dialyze
c. Prone to infection: reverse isolation, vit C rich diet, monitor lymphocytes & wbc
4. Monitor complications
a. pulmo edema/chf: ausculate (rales and crackles), check cardiac status
b. report hpn
 c. report fever, malaise & adverse effects of meds
d. observe for s/s of CVA, CAD, MI, embolism, ARF (AKI now)
e. monitor proteinuria

Nursing Management
1. Limit oral fluid intake, low sodium, protein and saturated food sources diet
® Too much water and sodium can contribute to high blood pressure and edema. Moderate to
low protein will reduce the amount of protein lost in the urine and preserve kidney function.
Patients with nephrotic syndrome have high levels of cholesterol and triglycerides, saturated fat
food sources like butter, lard, full fat dairy, sour cream, pastry and biscuits, coconut milk,
chicken skin and visible fat on meat increase the risk of heart disease.

2. Intake and Output

® Accurate measurement of intake and output determines fluid balance

3. Skin care
® Skin irritation and breakdown are likely related to edema

4. Protection against infection

® Reverse isolation, vitamin C rich diet

5. Monitor lymphocytes & WBC

® To determine immunocompression and presence of infection

6. Monitor complications (pulmonary edema, hypertension, CHF, renal failure, stroke)

® For prompt medical intervention and prevent further complications

7. Report fever, malaise & adverse effects of medications.

® For prompt medical interventions

Nursing Diagnoses a.
Fluid Volume
b. Imbalanced Nutrition: Less Than Body Requirements
c. Fatigue
d. Deficient Knowledge
e. Risk for Infection

DIET
ACID ASH DIET
• A diet consisting largely of meat or fish, eggs, and cereals with a minimal quantity of milk,
fruit, and vegetables, that when catabolized leaves an acid residue to be excreted in the
urine. Helps in flushing of bacteria

ALKALINE ASH DIET

• A diet consisting mainly of fruits, vegetables, and milk with little meat, fish, eggs, cheese,
and cereals, that when catabolized leaves an alkaline residue to be excreted in the urine.
 DASH DIET (LSLF)
• The DASH diet emphasizes vegetables, fruits and low-fat dairy foods — and moderate
amounts of whole grains, fish, poultry and nuts. In addition to the standard DASH diet, there
is also a lower sodium version of the diet

B. OBSTRUCTIVE DISORDERS

Figure 6- 4 Renal Calculi (Urolithiasis)

Renal calculi are the formation of stones in the urinary tract. These are crystalline structures
that form from the components of urine.

Pathophysiology
Most calculi are precipitations of calcium salts (phosphate and oxalate), uric acid, magnesium
ammonium phosphate (struvite) or cystine. These substances are normally found in the urine.

Factors Fostering Calculi Formation

➢ Concentrated urine
➢ Excessive intake of vitamin D, animal protein, oxalates, sodium, sucrose, vitamin C,
calciumbased antacids
➢ Familial history
➢ Immobility, urine stasis, sedentary lifestyle
➢ Altered urine pH
➢ Lack of kidney substance that inhibits calculi formation

Signs and Symptoms

• Pain depends on the location of the stone.
• Nausea, vomiting, hematuria and signs and symptoms of UTI

Medical Diagnosis
 ➢ Urinalysis, urine culture and sensitivity, IVP, ultrasound
➢ Computed tomography (CT) scan

Medical, Surgical and Pharmacologic Management

Phases of Stone Management

1. Acute phase
➢ narcotics, antispasmodic, anti -emetic, warm bath to relieve flank pain

2. Elimination of stone
➢ Waiting to be passed out
➢ Mechanical intervention
➢ Surgical intervention

3. Long term prevention of recurrence

➢ OFI (3-4l/day), diet, medication

1. Potassium citrate therapy - It attaches to calcium in the urine, preventing the formation of
mineral crystals; prevents the urine from becoming too acidic.
2. Thiazides (diuretics) – increases urinary Ca excretion
3. Allopurinol – prevents formation of uric acid nidus

FOR SMALL STONES

4. Alpha blockers or α-adrenergic-antagonist - It relax muscle tension in the ureter and

facilitate passage (E.g. tamsulosin)
5. Sodium bicarbonate
6. Pain relievers

Surgical and Non-surgical Management of Stone

Often calculi pass spontaneously, if it does not pass and symptoms continues, other options
may be used to destroy or remove the calculus.

Surgical management are indicated if there is progressive renal damage, obstruction of urine
flow, presence of infection and severe pain. The surgical procedures are:

• Nephrolithotomy (removal of kidney stones) and

• Ureterolithotomy (removal of stones in the ureters)

For non-surgical approach, options include:

• Ureteral Stent Placement: is a surgery to place a soft plastic tube in the ureter.

• Lithotripsy – is a medical procedure that uses shock waves or a laser to break down
stones in the kidney, gallbladder, or ureter. The remaining particles of small stone will exit
the body when a person urinates.
 • Cystoscopic stone removal or Ureteroscopy: is a procedure to address kidney stones,
and involves the passage of a small telescope, called a ureteroscope, through the
urethra and bladder and up the ureter to the point where the stone is located.

• Percutaneous Nephrolithotomy: is a procedure used to remove kidney stones from the

body when they can't pass on their own. A scope is inserted through a small incision in
your back to remove the kidney stones.

Ureteral Stent- are small tubes inserted into the ureter to treat or prevent a blockage that
prevents the flow of urine from the kidney to the bladder.

Lithotripsy is a process of eliminating a calculus in the renal pelvis, ureter, bladder by crushing
the stone. It can be accomplished by Extracorporeal shock wave lithotripsy (ESWL) which
utilizing sound, laser, or shockwave energy with a use of a lithotripter. It is guided by an
ultrasound probe, the energy is directed to the stone through a water-filled cushion.

Table 6-1 Complications of ESWL

Related to Shock Fragments Related to Shock Waves

Colic Bruising /hematoma
Incomplete fragment urosepsis
Blocking of ureters by the multiple stone
fragments

Cystoscopy/Ureteroscopy - use of lighted scope or a tube inserted into the urethra into the
bladder and ureters to remove stone and uses a laser fiber to crush the stone in the case of
ureteroscopy.

Percutaneous nephrolithotomy – The surgeon creates a tunnel directly through the skin into
the kidney and uses ultrasound or electrohydrolysis to break the stone into pieces. this
approach is usually used when stones are large and cannot be broken with lithotripsy.

Dietary Management
Prevention of stone recurrence is important. Apart from high fluid intake to keep urine diluted
dietary restrictions are also important and the dietary restrictions depend on the type of stone.

Table 6- 2 Recommended Diet for Stone Management

Acid Ash Diet (To acidify the Alkaline Ash Diet (To alkalinize the urine)
urine)
Calcium Stones Oxalate Stones
▪ cranberry, prune juice, meat, ▪ milk, vegetables, fruits except prunes,
egg, poultry, fish, grapes, cranberry, plums
whole grains ▪ Avoid tea, chocolate, rhubarb, spinach
▪ limit milk and other dairy
products Uric Acid Stones -
▪ Reduce foods high in purine like liver,
brain, kidneys, venison, shellfish, meat
soup, gravies, legumes
Nursing Management
1. Administer prescribed analgesics
2. Reassure client that most stones smaller than 4mm can pass out spontaneously
3. Provide education to prevent future and recurrence of stone
4. Encourage OFI
5. Instruct client to avoid foods that contribute to the diagnosed type of stone

Nursing Diagnoses
1. Acute pain related to renal calculi
2. Ineffective coping related to anxiety, low activity level and inability to perform ADL
3. Impaired urinary elimination related to renal calculi
4. Risk for infection
5. Nutrition imbalance, less than body requirements related to nausea
D. NEUROGENIC BLADDER
➢ urinary bladder malfunction due to neurologic dysfunction emanating from internal or
external trauma, disease or injury.
➢ Interference of the bladder normal mechanism cause by the disruption of the central and
peripheral nervous system

Review of The Neuro Anatomy

The normal function of the urinary bladder is to store and expel urine in a coordinated,
controlled fashion. This coordinated activity is regulated by the central and peripheral nervous
systems. Normal voiding is essentially a spinal
reflex, modulated by the central nervous system
(brain and spinal cord), which coordinates function of
the bladder and urethra.
The brain receives input via afferent
pathways that ascend from the bladder and
provide feedback on how full the bladder is.
Higher brain centers then determine whether it is
socially acceptable to void and trigger
downstream structures to permit or suppress the
voiding reflex. The pons is a major relay
center between the brain and the bladder. The
mechanical process of urination is coordinated by the pons in the area known as the
pontine micturition center (PMC).
The Pontine Micturition Center coordinates the urethral sphincter relaxation and detrusor
contraction to facilitate urination. Emotions, experienced in higher brain centers, may exert
downstream effects on the PMC, which is why some people can experience incontinence with
excitement or fear. The spinal cord functions as a long communication pathway between the
brainstem and the sacral spinal cord (terminal portion of the spinal cord, situated at the lower
back in the lumbar area responsible for bladder contractions) When the sacral cord receives the
sensory information from the bladder, this signal travels up the spinal cord to the pons and then
ultimately to higher brain centers. a spinal cord injury can lead to urinary frequency, urgency,
and urge incontinence, which may be complicated by difficulty emptying the bladder. This
occurs because the urinary bladder and the sphincter are no longer coordinated.
Pathophysiology Normal bladder function relies on information travelling through neural
pathways from the cerebral cortex, through the spinal cord, and on to the bladder to coordinate
normal micturition and urinary continence. When this pathway is damaged, it can result in loss
of bladder sensation and also the loss of the coordination between urethral sphincter and its
muscles, these muscles may not contract even when the bladder fills, or the person has the
urge to void, leading to bladder dysfunction such as urinary incontinence and retention (Mauk,
2012).

TYPES OF NEUROGENIC BLADDER

A. Spastic
- Sensory and voluntary control of
urination is disrupted partially or
totally. The stimuli generated by
bladder filling cause
frequent spontaneous
detrusor muscle
contraction and
involuntary emptying
caused by disruption of CNS
transmission above the sacral spinal
cord segment.
Causes:
1. Spinal cord injury- most
common cause
2. Stroke
3. MS - immune mediated inflammatory disease attacking the myelin and
axons
4. CNS lesions

B. Flaccid
- Damage to the sacral spinal cord at the level of the reflex arc, cauda equina, sacral nerve
roots leading to loss of detrusor muscle tone resulting to overdistention, weak and
ineffective detrusor muscle contraction.
Causes:
1. Spinal shock phase (6-12 weeks) in SCI
2. Myelomeningocele or meningocele — type of neural tube birth defect wherein the
backbone and spinal canal don't close before the baby is born; a type of spinal bifida
3. Peripheral neuropathies - DM most common cause, metabolic derangement of the
Schwann cell results in segmental demyelination and impaired nerve conduction.
4. Multiple Sclerosis
5. Chronic alcoholism
6. Prolonged overdistention of the bladder

Symptoms of Neurogenic Bladder

Overactive bladder, frequent urination, stress incontinence, urge incontinence, urinary
retention, underactive bladder (bladder cannot send signal when full)

Diagnostic Tests
Table 6- 3 Neurogenic Bladder Diagnostics
MEDICAL MANAGEMENT OF NEUROGENIC BLADDER
GOAL: Maintain continence and avoid complication associated with overfilling or incomplete
emptying of bladder through self-care. Thus, teaching is the primary intervention.
I. MEDICATIONS

GOAL:
• increase or decrease contractility of detrusor muscle.
• increase/decrease internal sphincter tone.
• relax external urethral sphincter.
Table 6-4 Medications for Neurogenic Bladder

ANTICHOLINERGIC DRUG TO PREVENT CHOLINERGIC DRUGS TO

SPASTIC BLADDER STIMULATE MICTURITION
1. Bethanechol chloride
(Urecholine)
1. Oxybutynin (Ditropan) stimulates parasympathetic NS
2. Solifenacin succinate (vesicare) detrusor muscle tone producing
4. Trospium (santural) enough to produce micturition
5. Tolterodine (destrol)
6. Propantheline bromide (pro-bannthine)
7. Flavoxate hcl (urispas)
 Inhibits response to acetylcholine relaxing the
*acetylcholine is a neurotransmitter causing
muscle to contract, activate pain responses,
regulates endocrine and REM sleep functions
II. NUTRITION

• Moderate to increase OH to decrease UTI and stone formation

• Diet to acidify urine (cranberry)

III. BLADDER RETRAINING

• Measures to stimulate reflex voiding for patients with spastic neurogenic bladder
• Stroke or pinch abdomen, inner thigh, glans penis (trigger points to stimulate urination)
• Pulling pubic hair
• Tapping suprapubic region
• Inserting gloved finger to rectum and gently stretch anal sphincter
• Crede's method - applying suprapubic pressure with finger of one or both hands

ALERT: may stimulate sympathetic nervous system causing sudden increase of blood pressure
for patients with SCI (autonomic dysreflexia -medical emergency)

Valsalva maneuver- bearing down while holding one's breath

CATHETERIZATION- intermittent for patients with SCI

Nursing Management
1. Promote urinary drainage and continence
® To ensure adequate micturition and prevents infection and stone formation

2. Prevent complication
® To prevent progressive renal damage

3. Teach patient and family self-care techniques

® To enhance patient's self-confidence and independence. The patient needs to be
involved in their own bladder management program to ensure it works for them and fits in
with their lifestyle. Family support is essential for the patient to adhere to the treatment
regimen.

Nursing Diagnoses
1. Impaired urinary elimination related to impaired bladder innervation
2. Toileting self-care deficit related to neurologic injury
3. Risk for impaired skin integrity related to urinary incontinence
4. Risk for infection related to impaired urinary reflex.
E. RENAL FAILURE
- A condition wherein the kidneys cannot remove the body's metabolic waste
products or when it cannot perform its regulatory functions. Different causes may
lead to renal failure.
- There are two types of renal failure, acute renal failure (ARF) or acute kidney injury
(AKI) and chronic renal failure (CRF).
- if kidney failure, urine will circulate in parts of body (uremia or urine in blood)
- ammonia = by product of amino acids (if may failure, di maconvert to urea)
- nephron – functional unit of kidneys
- glomerulus – specialized vessel, filtration
- bowman’s capsule – where filtration happen
- hydrostatic pressure produced by heart
- components of blood: plasma (90% water) and formed elements
o only water pass through glomerulus
o formed elements can’t pass through they are too big
- nincturition – formation of urine
- if may RF, nephrons ang matamaan (irreversible if madamage na nephron)
- Decrease GFR, decrease UO

FUNCTIONS OF KIDNEY:
 Excretory function
o Inc BV, Inc BP
o Edema (third shift)
 RAAS
 Vit D synthesis
o Calcitriol active form
 Act on small intestines to increase absorption of calcium
 Hypocalcemia if no absorption of calcium
 Release of erythropoietin
o Stimualtion of RBC
o Inc RBC formation (erythropoiesis)
o Formation of blood (hematopoiesis)
o Decrease RBC or anemia if renal failure
 Regulates hydrogen and bicarbonate
o metabolic acidosis if RF:
 increase calcium levels - hypercalcemia

Acute Renal Failure

- Acute Renal Failure occurs with reversible clinical syndrome wherein there is a sudden
and almost complete loss of kidney function. (nephrons are still damaged)
- This type of Renal Failure may last for days, weeks or even months.
- Some of the patients with ARF may die and for some may progress to chronic renal
failure. (heart problems, arrythmia)
Categories of AKI

• Prerenal
o occurs in 60% to 70% of cases which result from impaired blood flow due to
occlusion -> hypoxia
o if the kidneys do not receive sufficient blood that leads to hypoperfusion of
the kidney and decreases GFR. (decreased UO)
o Atherosclerosis – occlusion
o Arteriosclerosis (hardening of BV, can’t proceed to peristaltic movement)
HPN
o Hypoxia = ischemia = tissue necrosis (irreversible) = organ failure
• Intrarenal
o This result from parenchymal damage to the glomeruli or kidney tubules,
resulting from prolonged renal ischemia resulting from myoglobinuria
▪ Myoglobin (muscle protein that is a product of breakdown of muscle
cells), can pass through glomerulus
▪ Build-up of myoglobin in kidney = toxic (cause damage to nephrons)

• Postrenal
o ARF is usually the result of an obstruction somewhere distal to the kidney.
o Pressure increases in the kidney tubules and eventually the glomerular
filtration rate decreases. (due to backflow of urine)
o Blockage causes urine to back up and harm the kidneys.
o Common causes are urinary tract obstruction like calculi, tumors, benign
prostatic hyperplasia or an enlarged prostate, kinked ureter, and blood clots.
o Increase in blood urea nitrogen and creatinine are noted in postrenal acute
renal failure.
o Benign Prostatic Hyperplasia (for men) – dribbling of urine, feel mo full ka
palagi, no complete emptying of bladder
Table 6-5 Causes of AKI
PRERENAL INTRINSIC INTRARENAL POSTRENAL
Hypotension Acute Tubular Necrosis (ATN) Calculi
Cardiogenic Shock Diabetes Mellitus Tumors
Acute Malignant Hypertension Blood Clots
Vasoconstriction
Hemorrhage Acute Glomerulonephritis BPH
Burns Tumors Strictures
Septicemia Blood Transfusion Reactions Anatomic
Malformation
CHF Nephrotoxins
Trauma

Stages of Acute Renal Failure

1. Initiation Period
 At this phase the kidney begins with the initial injury and ends when oliguria develops.
 Its manifestation is the reduced blood flow to the nephrons.
 This causes decreased reabsorption of water, electrolytes, and excretion of protein
wastes and excess metabolic substances.
 This phase can last from hours to days and is characterized by urine output at 30 cc per
hour or less.
 Decreased GFR

2. Oliguria Period
 At this period, this is caused by reduction in the glomerular filtration rate.
 There is an increase in the serum concentration of creatinine, urea, uric acid, and the
intracellular cations like potassium and magnesium. (BUN and serum creatinine test =
kidney tests) (hyperkalemia, hypermagnesemia)
 In this phase the uremic symptoms first appear and may develop life-threatening
condition.
  Other manifestations would include hyperkalemia, hypernatremia, hyperphosphatemia,
hypocalcemia, hypermagnesemia and metabolic acidosis. (hyper- kasi decreased
excretory function)
 Decreasing renal function happens with increasing nitrogen retention with urine output of
less than 400 ml /24 hours and may last for 1 to 2 weeks.

3. Diuresis Period
 At this period, there is a gradual increase in urine output, which signals that glomerulus
filtration has started to recover. (functionality of nephrons is coming back)
 The laboratory results show an increased BUN and creatinine result.
 The urine output ranges from 3 to 5 liters per day due to partial regenerated tubule's
inability to concentrate urine which lasts for 2 to 3 weeks.

4. Recovery Period
 This period signals the improvement of renal function and may take 3 to 12 months.
 Laboratory values return to the patient's normal value.

Figure 6-6 Pathophysiology of AKI

*inc retention of waste: edema, crackles

Signs and Symptoms

- The symptomatology of acute kidney injury depends on the cause.

Figure 6-7 Common Symptoms of AKI

  Loss of appetite - chronic inflammation = satiety centerv = anorexia
 SOB – dec GFR = dec excretion = fluid/water retention = inc BV
(FVE, crackles/congestion in pulmonary, cause SOB) = inc BP
 Irregular heartbeat – electrolyte imbalance (high potassium,
hyperkalemia leads to dysrhythmias)
 Chest pain – congestion
 Dec UO – dec GFR
 Edema – excess fluid

Diagnostic Management
1. History taking , physical exam (etiology
2. Identify precipitating cause
3. Creatinine, BUN, Serum electrolytes
4. Urinalysis

Medical Management
1. Treatment of precipitating cause
2. Fluid restriction
3. Dietary management (LSLF if hypertensive, CHON diet) limit fluid intake
4. Dialysis
5. Total Parenteral Nutrition (TPN) if indicated
6. Measures to decrease potassiumK (most life-threatening disturbance) (hyperkalemia)
a. administer cation — exchange resin
1. sodium polysterene sulfonate (kayexalate) given PO or enema
*exchange resin = exchange sodium and potassium para ma excrete potassium
through BM to lower potassium levels in blood
*monitor sodium level of pt
 *hypo/hypernatremia can cause seizure
2. Calcium Polysterene Sulfonate (Kalimate) Major site of potassium exchange is the
colon if enema is administered and Intestinal tract for oral administration . Sorbitrol is
often administered with kayexalate to induce diarrhea type effect.

b. IV glucose and insulin — This will cause the potassium to move into the cell,
decreasing the serum potassium serum level
i Insulin + glucose = D50W (prevent hypoglycemia)
ii Insulin acts like a key: pasok potassium
iii Give glucoe to normalize levels since insulin carry one protein and one glucose

c. Ca gluconate - Protects the heart from the effects of hyperkalemia

d. Bicarb IV - Corrects metabolic acidosis

e. Dialysis - A procedure to remove waste products and excess fluid from the blood when
the kidneys stop functioning properly.

f. Dietary restriction — restrict fruits high in potassium like citrus fruits, banana, grapes,
watermelon, for protein intake 1 gm /kg during oliguric phase and sodium 2 g / day.

Nursing Management
Nursing goal of treating patients with acute renal failure is to correct or eliminate any
reversible causes of kidney failure. Provide support by taking accurate measurements of
intake and output, including all body fluids, monitor vital signs and maintain proper
electrolyte balance.
1. Precise intake and output monitoring
® Accurate monitoring of l&O is necessary for determining renal function and fluid
replacement needs and reducing risk of fluid overload.

2. Vital signs
® To assess the intravascular volume, especially in patients with poor cardiac function.
Check apical pulse at risk for dysrhytmias

3. Dietary management
® Help promote kidney function and slow the progression of complete kidney failure.

4. Fluid management base on the clinical manifestation (FVE is present)

5. Daily weight (to check if body is responding to teratment, inc weight if not respond
to tx)
6. Assess signs and symptoms of electrolyte imbalance such as mental status,
neuromuscular status and cardiac rate and rhythm.

Nursing Diagnoses
1. Fluid volume excess related to impaired kidney function
2. Decrease cardiac output related to high output renal failure (diuretic phase)
3. Fluid volume deficit related to high output renal failure (diuretic phase)
4. Potential for complications of immobility related to therapeutic restrictions
5. Deficient Knowledge related to condition and treatment
6. Risk for Imbalanced Nutrition: Less Than Body Requirements

Chronic Renal Failure

Chronic renal failure (CRF), or End Stage Renal Disease (ESRD), is a progressive, irreversible
deterioration in renal function in which the body's ability to maintain metabolic and fluid and
electrolyte balance fails, resulting in uremia or azotemia (dirty blood). The development of
uremia happens and adversely affects every system in the body. The greater the buildup, the
greater are the symptoms and are considered fatal.

The pathology of chronic renal failure occurs in 4 stages and the conditions that may contribute
to end stage renal disease include systemic diseases such as diabetes mellitus (no insulin,
buildup of glucose, thick blood, circulation problem, slow daloy ng dugo, dec oxygen levels,
have hypoxia in kidneys, cause RF, chronic kasi need maintenance DM), hypertension
(arteriosclerosis, atherosclerosis), chronic glomerulonephritis (inflammed glomerulus),
pyelonephritis (inflammed kidney and ureter), obstruction of the urinary tract. Hereditary lesions
include polycystic kidney disease, vascular disorders, autoimmune disorders, infections,
medications which are nephrotoxic (NSAIDS)

Stage 1. Decreased Renal Reserve

In this stage, the residual renal function is 40-75% than the normal and patient is asymptomatic
with normal BUN and plasma creatinine. Excretory and regulatory renal functions are
undamaged.
Stage 2. Renal Insufficiency
The renal function is 20-40% marked decrease in glomerular filtration rate, solute clearances,
ability to concentrate urine and hormone secretion. The signs and symptoms include rising
BUN, plasma creatinine, mild azotemia, polyuria, nocturia and anemia.
Stage 3. Renal Failure
Renal function is approximately 5% of normal. Serum urea & creatinine levels rise rapidly and
urine output is less than 500ml/day. Symptoms of uremia develop.
Stage 4 End Stage Renal Disease
End Stage Renal Disease (ESRD) with residual renal function less than 15% or normal. Its
excretory, regulatory and hormonal renal functions are severely impaired.
Unable to maintain homeostasis like fluids and electrolytes imbalance may occur as well as pH
imbalances. Noticeable are elevated BUN and plasma creatinine, anemia, hyperphosphatemia,
hypocalcemia (decreased calcium levels,) hyperkalemia, fluid overload, usually oliguria . Uremic
syndrome may occur and all body.
*hypocalcemia
- Parathyroid gland = parathyroid hormone = bones (osteoclast destroy bone) =
demineralization = released to blood stream (calcium salts) = high calcium levels
- hyperparathyroidism = bone will be chipped = brittle bone = inc chances of fracture

*as stage progresses, nagababa renal function and functionig of residual renal function

*urea is just circulating in body kasi di maexcrete, body compensate through integumentary
system (sweat is composed of urea and salts), urea being excreted in skin to help decrease levels
of urea
Table 6- 6 Clinical Manifestations of CRF

Medical Management
1. Serum studies (nitrogenous wastes, electrolytes) BUN, Crea
2. Complete blood count - check infections
3. Urinalysis / Culture
4. 24 hour creatinine clearance (to determine GFR) (if low GFR, kidney damage)

Medical Treatment Goals:

• To prevent further damage to the kidneys
• To promote recovery of renal function
• To prevent complications

1. Pharmacologic (anti-hypertensive(anemia), erythropoletin(anemia), iron

supplement(anemia), phosphate binding(acidosis), calcium supplement (protect heart),
anti seizure(inc or dec sodiumlvl), ketoanalogues (for ketoacidosis), Sodium Bicarbonate,
Potassium resin exchange (Kayexalate)

*DM = DKA = inc ketones (by-product of fat metabolism) = inc fat metabolism = ketones
build-up = comatose (EMERGENCY SITUATION)
No glucose DM, resort to fat metabolism

2. Nutritional - reduce protein potassium food sources, fluids

3. Blood transfusion to correct anemia

4. Correction of fluid and electrolyte imbalance

5. Dialysis

6. Kidney transplant
DIALYSIS
A technique in which a substance move from the blood through a semi permeable membrane
into a dialysis solution.
3 PHYSICAL PRINCIPLES
1. Osmosis
2. Diffusion
3. Ultrafiltration

Indications of Dialysis
1. GFR less than 5 to 10 ml/min
2. Manifestations of uremic syndrome

TWO TYPES
1. Hemodialysis removal of waste and water by circulating the blood into a dialyzer through
a dialysis machine.
2. Peritoneal dialysis — repeated cycles of instilling dialysate into the peritoneal cavity.

4 BASIC GOALS OF DIALYSIS

1. Remove waste products from protein metabolism.
2. Maintain safe concentration of serum electrolytes
3. Correction of acidosis and replenish blood's bicarbonate system.
4. Removal of excess water
 ➢ silastic cannula in the forearm or leg inserted into the artery and the vein to form an
external blood path.
Arteriovenous Fistula (AVF)
➢ anastomosis of the artery and the vein Arteriovenous graft
➢ artificial graft made of gore-tex or a bovine carotid artery is used
Internal Jugular Catheter — A dialysis catheter containing arterial and venous lumens inserted
in the jugular vein

Complications in Hemodialysis
➢ Hypotension — Decrease blood pressure as a consequence of reduce cardiac output
secondary to excessive water and sodium removal

➢ Blood loss from technical problem — Blood loss related to blood clotting in the circuit or
blood loss due to loose connections.

➢ Muscle cramps — Involuntary muscle contraction due to excessive water and sodium
removal

➢ Disequilibrium syndrome — A neurologic deterioration during dialysis manifested as

headache,nausea,vomiting due to marked decrease of blood urea nitrogen in the
cerebrospinal fluid and brain tissue.

➢ Air embolism — Obstruction of the circulation by air related to air entry in the blood circuit

➢ Hypoglycemia — Low blood sugar concentration related to glucose diffusing out of the
blood

➢ Cardiac arrythmia- Disturbance in the electrical impulse formation or conduction related

to electrolyte and ph changes during dialysis or underlying heart disease

Nursing Care Before and During Dialysis

➢ Check the dialysis order { BFR, duration, bath, UFR, heparin, K+ } * SLED
➢ Chart client's weight { DRY WEIGHT}
➢ Assess vital signs
➢ Check patency of vascular access
➢ Withhold antihypertensives
 ➢ Ensure bed rest with frequent position change
➢ Monitor closely for complications
➢ Monitor blood line connections, arterial and venous and transmembrane pressure in the
dialysis machine

Nursing Care Post Hemodialysis

➢ Check VS Nursing
➢ Record post dialysis weight
➢ Resume all medications
➢ Apply pressure dressing on decannulated sites
➢ Protect IJ/subclavian catheter with sterile dressing

NURSING CARE FOR AVF/GRAFT

➢ Assess for bruit or thrill
➢ Assess for bleeding, pain
➢ May squeeze rubber ball to help in the development of the vessel
➢ Avoid venipuncture, blood pressure taking on the arm with the vascular access
➢ Avoid sleeping and wearing of tight fitting clothing on access extremity Instruct client not
to lift heavy objects using the extremity with the vascular access.
➢ Keep dressing dry
➢ Keep catheter taped to the skin and prevent pulling of the catheter to prevent accidental
removal
➢ The patient to clamp remaining tail of the catheter and apply direct pressure at insertion
site with occlusive dressing if accidental removal of catheter happen

PERITONEAL DIALYSIS
➢ repeated cycles of instilling dialysate into the peritoneal cavity and the peritoneum is the
dialyzing membrane.

CYCLES OF PD
1. Inflow ( infusion)
➢ the solution is introduced into the peritoneum through a catheter by gravity tenckhoff
catheter, a siliconized rubber catheter, inserted 3-5 cm below umbilicus, stabilized by
dacron cuffs where fibroblast and blood vessel grow, fixing the catheter in place,
occurring 1-2 weeks after insertion

2. Dwell (equilibrium)
➢ solution is retained in the peritoneal cavity for a prescribed period to allow better
exchange and clearance.

3. Drain ( outflow)
➢ process of removing the previously retained solution in the peritoneal cavity by gravity.

Peritoneal Dialysis Complications

➢ drainage obstruction — Presence of fibrin or clots in the tubings
➢ Difficulty of breathing — Dialysis solution in the peritoneum during dwell time may push
the diaphragm
 ➢ Bleeding — Bloody dialysate or in the PD catheter insertion site related to the procedure,
manipulation or trauma
➢ Peritonitis — Microorganism gaining entry into the peritoneum related to poor aseptic
technique during the dialysis procedure

Nursing Responsibilities
1. Vital signs and complication monitoring
2. Pre warm the solution
3. Documentation of the three phases of Peritoneal Dialysis (Solution use, time infused,
retain, drain including the amount, color, appearance)

Table 6-7 Sample Documentation OF Peritoneal Dialysis

KIDNEY TRANSPLANT
➢ Is the surgical implantation of a human kidney from a compatible donor to a recipient.

DONOR: LIVING
1. ABO Screening
2. Tissue specific antigen & human leukocyte antigen histocompatibility
3. Excellent health
4. Full functioning kidneys
5. Emotionally ready
6. Full understanding of the process

CADAVER
1. Below 60 yrs of age
2. Brain death
3. Normal renal function
4. No metastatic disease, HIV, Hepatitis B

Signs and Symptoms OF REJECTION

• oliguria fever pain
• tenderness over transplant site
• hypertension
• creatinine increase

COMPLICATION POST TRANSPLANT

 ➢ rejection infection
➢ malignancy (basal and squamous cell carcinoma.-skin,lips, vulva, lungs) ➢
cardiovascular — hypertension

IMMUNOSUPPRESSIVE DRUGS
• Cyclosporine (Neoral) — blocks interleukin
• Azathioprine (imuran) — blocks DNA preventing lymphocyte proliferation
• Corticosteroids (prednisone) — block cytokines
• Cyclophosphamide (cytoxan)
• Tacrolimus (prograft) — blocks calcineurin and T cell
• Mycophenolate (cellcept) — inhibit B & T lymphocyte
• OKT 3 — antilymphocyte globulin

NURSING DIAGNOSES POST KIDNEY TRANSPLANT

➢ Altered nutrition: more than body requirements related to side effects of
immunosuppressant agents o Less than body requirement: related to increased caloric
needs after transplant

➢ Altered protection and risk for infection related to immunosuppression required after
transplantation

➢ Effective management of Therapeutic Regimen related to post-transplantation regimen

➢ Pain related to transplantation surgery

➢ Risk for Ineffective Individual Coping after transplantation related to increased stress,
anxiety, fear, and lifestyle changes

Learning Activities
1. Video presentation on the following: a. Urinary system
(https://www.youtube.com/watch?v=H2VkW9L5OSU)
b. Kidney Stone Treatments (https://www.youtube.com/watch?v=kca0Mr0iyJs)
(https://www.webmd.comia-to-z-quides/what-is-nephrotic-svndrome#2-5)
c. Neurogenic Bladder (https://www.ausmed.com/cpci/articles/neurooenic-bladder-dysfunction)
d. Renal Replacement Therapy; Hemodialysis VS. Peritoneal Dialysis Animation
(https://www.voutube.com/watch?v=SuBMoCArNak) e. Activity on documentation on
peritoneal dialysis.
PAINSTAKINGLY COMPILED BY: CHERRY ROSE C. QUIÑONES 😊