Fluids and Electrolytes
 Feces- 150
 The two body fluid compartments are as
follows:
1. Intracellular Fluid Compartment (ICF)
 Fluid found inside the cells
 It comprises 2/3 (70%) of the body fluid
2. Extracellular Fluid Compartment (ECF)
 Fluid found outside the cells
 It comprises 1/3 (30%) of the body fluid
 The ECF may be interstitial fluid (between
the cells); intravascular fluid (plasma);
transcellular fluid (digestive juices, water in
the renal tubules, pleural fluid, CSF)
 The 2 factors that influence body water
distribution are: age and gender
Water has the following functions in the body:
1. Maintains blood volume (plasma)
2. Transport gases, nutrients and other
substances to the cells
3. Promotes cellular chemical function
4. Maintains normal body temperature
5. Eliminates waste products from the cells
FUNCTIONS OF ELECTROLYTES IN THE
BODY
1. Promotes neuromuscular irritability
2. Maintain blood fluid volume and osmolality
3. Distribute body water between fluid
compartments
4. Regulate acid- base balance
SOURCES OF FLUID INTAKE
 Water in food- 1,000ml
 Water from oxidation- 300ml
 Water as taken as liquid- 1, 200ml TOTAL
2,500ml/ day
SOURCES OF FLUID OUTPUT
 Skin – 500ml
 Lungs- 300ml
 Kidneys- 1,500ml TOTAL 2,500ml/ day
SODIUM AND WATER REGULATION
 Thirst is the major control of actual fluid
intake
 Kidneys the major organ controlling output
 ADH- retains water in the renal tubules
 RAAS- aldosterone retains in sodium and
water
 Sodium primarily determines osmolality
(concentration) of body fluids
POTASSIUM REGULATION
 Aldosterone and hydrogen ions regulate
potassium levels
 Aldosterone retains sodium and excretes
potassium
 Potassium is the major cation in the ICF
 Potassium is necessary in the conduction of
nerve impulses and promotion of skeletal
and cardiac muscle activity
CALCIUM REGULATION
 Parathormone, thyrocalcitonin and Vitamin
D regulate calcium levels
 Parathormone elevates serum calcium levels
through withdrawal of calcium from the
bones or bone resorption
 Thyrocalcitonin lowers serum calcium levels
by depositing calcium into the bones
 Vitamin D promotes calcium absorption
 Calcium promotes neuromuscular
irritability, bone and teeth development and
blood clotting
ARTERIAL BLOOD GAS
 provides information about the effectiveness
of both oxygenation and ventilation
 A blood sample for ABG analysis may be
drawn by percutaneous arterial puncture or
from an arterial line.
PURPOSE
  To evaluate the efficiency of pulmonary gas
exchange
 To assess the integrity of the ventilatory
control system
 To determine the acid-base level of the
blood
 To monitor respiratory therapy
Collection of an arterial blood gas specimen
 Obtain vital signs
 Determine whether the client has an arterial
line in place
 Perform the Allen’s test to determine the
presence of collateral circulation
 Assess factors that may affect the accuracy
of the results, such as changes in the O2
settings, suctioning within 20 minutes, and
client’s activities
 Provide emotional support to the clien
REFERENCE VALUE
 PaO2: 80 to 100 mmHg (SI, 10.6 to 13.3
kPa)
 PaCO2: 35 to 45 mmHg (SI, 4.7 to 5.3 kPa)
 pH: 7.35 to 7.45 (SI, 7.35 to 7.45)
 O2CT: 15% to 23% (SI, 0.15 to 0.23)
 SaO2: 94% to 100% (SI, 0.94 to 1)
 HCO3: 22 to 26 mEq/L (SI, 22 to 25
mmol/L).
CRITICAL FACTS ABOUT ABG
 Remember the Normal Values
 Look at the pH. Does it indicate presence of
acidemia or alkalemia or normal ph?
 (pH low)= ACIDOSIS= below 7.35
 (pH high) = ALKALOSIS = above 7.45
3. Look at the PaCO2
 PaCO2 is the RESPIRATORY
INDICATOR
 CO2 acts as an ACID when CO2 combines
with plasma, CARBONIC ACID is formed
(CO2 + H2O = H2CO3)
 (PaCO2 low) = RESPIRATORY
ALKALOSIS = below 35mmHg
 (PaCO2 high) = RESPIRATORY
ACIDOSIS = high 45 mmHg
4. Look at the HCO3 (Bicarbonate)
 (HCO3 high) = METABOLIC ALKALOSIS
= above 26mEq/L
 (HCO3 low) = METABOLIC ACIDOSIS =
below 22mEq/L
5. Determine the PRIMARY ACID- BASE
disturbances
 The changes that matches the pH is the
primary acid- base disturbance
 pH and PaCO2- match: Respiratory Acid-
Base Imbalance
 pH (low)
 PaCO2 (high) = RESPIRATORY
ACIDOSIS
 b. pH and HCO3- match: Metabolic Acid-
Base Imbalance
 pH (low)
 PaCO2 (low) = METABOLIC ACIDOSIS
 Therefore, pH and PaCO2 are opposite, pH
and HCO3 are equal.
6. Look at the degree of compensation
 Check the relationship between PaCO2 and
HCO3
 Remember: the lungs and kidneys normally,
attempt to help each other to maintain acid-
base balance
 If the lungs unable to maintain acid- base
balance, the kidneys will attempt to adjust
levels of HCO3
 If the kidneys are unable to maintain acid
base balance, the lungs will attempt to adjust
levels of CO2
 If CO2 and HCO3 levels move towards the
same direction, (both are high or low), then
the acid base imbalance is compensated
When is the acid- base imbalance considered as
partial or complete compensation?
 When the acid- base balance is
compensated, but the pH is still
 ABNORMAL; PARTIAL
COMPENSATION
 When the acid- base balance is
compensated, and the pH is NORMAL;
COMPLETE COMPENSATION
When is the acid- base imbalance considered
uncompensated?
 When the CO2 and HCO3 levels move
toward opposite direction (The problem is
worsened)
 Or when PaCO2 is abnormal and HCO3
remains normal and vice versa, the acid-
base imbalance is also uncompensated
EDEMA
 Edema is an excess accumulation of fluid in
the interstitial space
 Localized edema occurs as a result of
traumatic injury from accidents or surgery,
local, inflammatory process, or burns
 Generalized edema, also called anasarca,
is an excessive accumulation of fluid in the
interstitial space throughout the body and
occurs as a result of conditions such as
cardiac, renal, or liver failure
PITTING EDEMA
 A grading system is often used to determine
the severity of the edema on a scale from +1
to +4. It is assessed by applying pressure on
the affected area and then measuring the
depth of the pit (depression) and how long it
lasts (rebound time).
 Grade +1: up to 2mm of depression,
rebounding immediately.
 Grade +2: 3–4mm of depression,
rebounding in 15 seconds or less.
 Grade +3: 5–6mm of depression,
rebounding in 60 seconds.
 Grade +4: 8mm of depression, rebounding
in 2–3 minutes
BODY FLUID TRANSPORT
DIFFUSION
 Diffusion is a process whereby a solute
(substance that is dissolved) may spread
throughout a solution or solvent (solution in
which the solute is dissolved)
 Diffusion of a solute spreads the molecules
from an area of higher concentration to
an area of lower concentration
 A permeable membrane allows substance to
pass through without restriction
 A selectively permeable membrane allows
substances to pass through without
restriction
 Diffusion occurs within fluid compartments
and from one compartment to another if the
barrier between the compartment is
permeable to the diffusing substances
OSMOSIS
 Osmotic pressure is the force that draws the
solvent from a less concentrated solute
through a selectively permeable membrane
into a more concentrated solute, thus tending
to equalize the concentration of the solvent
 If a membrane is permeable to water but not
to all the solutes present, the membrane is a
selective or semi permeable membrane
 Osmosis is a movement of solvent
molecules across in a membrane in response
to a concentration gradient, usually from a
solution of lower to one of higher solute
concentration
 When a more concentrated solution is on
one side of selectively permeable membrane
and a less concentrated solution is on the
other side, a pull called osmotic pressure
draws water through the membrane to the
more concentrated side, or the side with
more solute
FILTRATION
 Is the movement of solutes and solvents by
hydrostatic pressure
 The movement is from an area of high
pressure to an area of lower pressure
HYDROSTATIC PRESSURE
 Is the force exerted by the weight of
solution.
 When a difference exists in hydrostatic
pressure on two sides of membrane, water
and diffusible solutes move out of the
 solution that has the higher hydrostatic
pressure by the process of filtration
 At the arterial end of the capillary, the
hydrostatic pressure is higher than the
osmotic pressure therefore fluids and
diffusible solutes move out of the capillary
 At the venous end, the osmotic pressure, or
pull is higher than the hydrostatic pressure,
and fluids and some solutes move into the
capillary
 The excess fluid and solutes remaining in
the interstitial spaces are returned to the
intravascular component by the lymph
channels
OSMOLALITY
 Refers to the number of osmotically active
particles per kilogram of water, it is
concentration of a solution
 In the body, osmotic pressure is measured in
milliosmoles (mOsm)
 The normal osmolality of plasma is 270 to
300 mOsm/kg water
ARTERIAL BLOOD GAS
 provides information about the effectiveness
of both oxygenation and ventilation
 A blood sample for ABG analysis may be
drawn by percutaneous arterial puncture or
from an arterial line.
PURPOSE
 To evaluate the efficiency of pulmonary gas
exchange
 To assess the integrity of the ventilatory
control system
 To determine the acid-base level of the
blood
 To monitor respiratory therapy
Collection of an arterial blood gas specimen
 Obtain vital signs
 Determine whether the client has an arterial
line in place
 Perform the Allen’s test to determine the
presence of collateral circulation
 Assess factors that may affect the accuracy
of the results, such as changes in the O2
settings, suctioning within 20 minutes, and
client’s activities
 Provide emotional support to the client
 Assist with the specimen draw by preparing
a heparinized syringe
 Apply pressure immediately to the puncture
site following the blood draw; maintain
pressure for 5 minutes or for 10 minutes if
the client is taking anticoagulants
 Appropriate label the specimen and transport
it on ice to the laboratory
 On the laboratory form, record the client’s
temperature and the type of supplemental
oxygen that the client is receiving
REFERENCE VALUE
 PaO2: 80 to 100 mmHg (SI, 10.6 to 13.3
kPa)
 PaCO2: 35 to 45 mmHg (SI, 4.7 to 5.3 kPa)
 pH: 7.35 to 7.45 (SI, 7.35 to 7.45)
 O2CT: 15% to 23% (SI, 0.15 to 0.23)
 SaO2: 94% to 100% (SI, 0.94 to 1)
 HCO3: 22 to 26 mEq/L (SI, 22 to 25
mmol/L).
CRITICAL FACTS ABOUT ABG
 Remember the Normal Values
 Look at the pH. Does it indicate presence
of acidemia or alkalemia or normal ph?
 (pH low)= ACIDOSIS= below 7.35
 (pH high) = ALKALOSIS = above 7.45
3. Look at the PaCO2
 PaCO2 is the RESPIRATORY
INDICATOR
 CO2 acts as an ACID when CO2 combines
with plasma, CARBONIC ACID is formed
(CO2 + H2O = H2CO3)
 (PaCO2 low) = RESPIRATORY
ALKALOSIS = below 35mmHg
 (PaCO2 high) = RESPIRATORY
ACIDOSIS = high 45 mmHg
4. Look at the HCO3 (Bicarbonate)
 (HCO3 high) = METABOLIC ALKALOSIS
= above 26mEq/L
 (HCO3 low) = METABOLIC ACIDOSIS =
below 22mEq/L
5. Determine the PRIMARY ACID- BASE
disturbances
 The changes that matches the pH is the
primary acid- base disturbance
  pH and PaCO2- match: Respiratory Acid-
Base Imbalance
 pH (low)
 PaCO2 (high) = RESPIRATORY
ACIDOSIS
 b. pH and HCO3- match: Metabolic Acid-
Base Imbalance
 pH (low)
 PaCO2 (low) = METABOLIC ACIDOSIS
 Therefore, pH and PaCO2 are opposite, pH
and HCO3 are equal.
6. Look at the degree of compensation
 Check the relationship between PaCO2 and
HCO3
 Remember: the lungs and kidneys normally,
attempt to help each other to maintain acid-
base balance
 If the lungs unable to maintain acid- base
balance, the kidneys will attempt to adjust
levels of HCO3
 If the kidneys are unable to maintain acid
base balance, the lungs will attempt to adjust
levels of CO2
 If CO2 and HCO3 levels move towards the
same direction, (both are high or low), then
the acid base imbalance is compensated
When is the acid- base imbalance considered as
partial or complete compensation?
 When the acid- base balance is
compensated, but the pH is still
ABNORMAL; PARTIAL
COMPENSATION
 When the acid- base balance is
compensated, and the pH is NORMAL;
COMPLETE COMPENSATION
When is the acid- base imbalance considered
uncompensated?
 When the CO2 and HCO3 levels move
toward opposite direction (The problem is
worsened)
 Or when PaCO2 is abnormal and HCO3
remains normal and vice versa, the acid-
base imbalance is also uncompensated
FLUID IMBALANCES
HYPEROSMOLAR IMBALANCE
(DEHYDRATION)
 This causes shifting of fluids from the ICF
and ECF. The cell shrink. There is sodium
excess or water deficit
 The initial manifestation of dehydration is
thirst
 The most objective indicator of dehydration
is weight loss, next is decreased urine
output
 Hyperthermia- Tachycardia- Tachypnea-
Hypotension
OTHER SIGNS AND SYMPTOMS
 Dry, mouth and throat
 Warm, flushed, dry skin
 Soft, sunken eyeballs
 Dark, concentrated urine
 Altered LOC
 Increased hematocrit, BUN, serum
electrolyte levels
MANAGEMENT
 Fluid replacement
 Oral care for dry mouth and throat
 Safety measures for altered level of
consciousness
 Identify and treat underlying causes (enteral
feedings, renal failure, DM)
HYPOOSMOLAR IMBALANCE (WATER
INTOXICATION)
 This cause of shifting of fluids from the ECF
to ICF. The cells swell
 There is sodium deficit or water excess
 The most dangerous effects of water
intoxication is increased ICP
 Changes in mental status, (confusion,
incoordination, convulsions)
 Sudden weight gain
 Peripheral edema
MANAGEMENT
 Fluid restriction
 Administration of diuretics as prescribed
 Infusion of hypertonic saline per IV
 Promote safety
 Assess neurologic status
 Identify and treat underlying cause (excess
intake of electrolyte, free fluid, repeated tap
water enema, SIADH, sodium deficit
SODIUM
  Sodium is most abundant electrolyte in the
ECF, its concentration ranges from 135-
145mEq/ L (135-145 mmol/L) and it is
primary determinant of ECF and osmolality.
 Sodium has a major role in controlling water
distribution throughout the body, because it
does not easily cross the cell wall membrane
and because of its abundance and high
concentration in the body.
 Sodium is regulated by ADH, thirst, and
renin angiotensin aldosterone system.
 A loss or gain of sodium by is usually
accompanied by loss or gain of water.
 Sodium also functions in establishing the
electrochemical state necessary for muscle
contraction and the transmission of nerve
impulses
ELECTROLYTE IMBALANCES
SODIUM IMBALANCES
HYPONATREMIA (Sodium Deficit)
 It is caused by sodium loss or water excess
 The causes of hyponatremia are as follows:
diuretics, low sodium diet, decreased
aldosterone secretion (Addison’s disease),
edema, ascites, burns, diaphoresis
 CLINICAL MANIFESTATIONS: These
are due to decreased ECF volume and
increased ICF volume
 Headache
 Muscle weakness, fatigue, apathy
 Anorexia, nausea and vomiting
 Abdominal cramps
 Weight loss
 Postural hypotension
 Seizures, coma
MANAGEMENT
 Administer NaCL 0.9% per IV, plasma
expanders-
 Sodium rich foods in diet
 Safety precautions
b. HYPERNATREMIA (Sodium excess, edema)
 Sodium and water excess results to edema
 Hyperventilation, diarrhea (more water is
lost than sodium)
CLINICAL MANIFESTATIONS
 Extreme thirst
 Dry, sticky mucous membrane
 Oliguria
 Firm, rubbery tissue turgor
 Red, dry, swollen tongue
 Restlessness, tachycardia, fatigue
 Disorientation, hallucination
MANAGEMENT
 Monitor intake and output
 Restrict sodium in diet
 Increase oral fluids or administer D5W as
prescribed
 Administer diuretics as ordered
 Dialysis as indicated
 Promote safely, monitor and behavior
chnaes
POTASSIUM
 Potassium is the major intracellular
electrolyte. In fact, 98% of body’s potassium
is inside the cells.
 The remaining 2% is in the ECF and is
important in neuromuscular function.
 Potassium influences both skeletal and
cardiac muscle activity.
 The normal serum potassium is 3.5 to
5.0mEq/L (3.5 to 5mmol/L), and even
minor variations are significant. potassium
imbalances are commonly associated with
various diseases, injuries, medications,
(NSAIDS, and ACE inhibitors), and acid-
base imbalances.
HYPOKALEMIA (POTASSIUM DEFICIT)
CAUSES of HYPOKALEMIA
 Decreased food and fluid intake (starvation)
 Increased loss of potassium (hypersecretion
of aldosterone, gastrointestinal losses,
potassium- wasting diuretics)
 shifting of potassium into cells (treatment of
DKA, metabolic alkalosis)
CLINICAL MANIFESTATION
 Gastrointestinal: anorexia, nausea and
vomiting, abdominal distention, paralytic
ileus
 CNS: lethargy, diminished deep tendon
reflexes, confusion, mental depression
CLINICAL MANIFESTATION
 Muscles: weakness, flaccid paralysis,
weakness of respiratory muscles, respiratory
arrest
 Cardiovascular: hypotension,
dysrhythmias, myocardial damage, cardiac
arrest
 Kidneys: water loss, thirst, renal damage
MANAGEMENT
 Potassium rich foods (ABC of fruits and
vegetables)
 Potassium Supplementation (Oral or IV
incorporation)
 NURSE ALERT!!!! NEVER TO
ADMINISTER POTASSIUM VIA IV
PUSH!!!- CARDIAC ARREST
HYPERKALEMIA (POTASSIUM EXCESS)
CAUSES of HYPERKALEMIA
 Excess dietary intake of potassium rich
foods
 Excess parenteral administration of
potassium
 Decreased excretion of potassium
 Renal failure
 Adrenal insufficiency
 Shifting of potassium out of cells (extensive
trauma, crushing injuries, metabolic acidosis
CLINICAL MANIFESTATION
 Gastrointestinal: nausea, vomiting,
diarrhea, colic
 CNS: numbness, tingling
CLINICAL MANIFESTATION
 Muscles: irritability (early), weakness (late),
flaccid paralysis
 Cardiovascular: ventricular fibrillation,
cardiac arrest
 Kidneys: oliguria, anuria
MANAGEMENT
 Low potassium diet
 Dextrose 10% in water with regular insulin
per IV as prescribed.
 Polysterene Sulfonate (exchange resin
Kayexalate) per mouth or enema as
prescribed
 Calcium Gluconate per IV
 Dialysis as indicated
CALCIUM
 More than 99% of the body’s calcium is
located in the skeletal system; it is a major
component of bones and teeth.
 About 1% of skeletal calcium is rapidly
exchangeable with blood calcium, and the
rest is more stable and only slowly
exchanged.
 The small amount of calcium is located
outside the bone circulates in the serum,
partly bound to protein and partly ionized.
 Calcium plays a major role in transmitting
nerve impulses and helps regulate muscle
contraction and relaxation, including cardiac
muscle.
 Calcium is instrumental in activating
enzymes that stimulate many essential
chemical reactions in the body, and it also
plays a role in blood coagulation.
 Because many factors affect calcium
regulation, both hypocalcemia and
hypercalcemia are relatively common
disturbances
 The normal total serum calcium level is
8.6 to 10.2mg/dL.
 Calcium exists in plasma three forms:
ionized, bound and complexed. About 50%
of the serum calcium exists in a
physiologically active ionized form that is
important neuromuscular activity and blood
coagulation; this is the only physiologically
and clinically significant form.
 The normal ionized serum calcium level is
4.5 to 5.1mg/dL. Less than half of the
plasma calcium is bound to serum proteins,
primarily albumin.
 The remainder is combined with nonprotein
anions; phosphate, citrate, and carbonate.
HYPOCALCEMIA (CALCIUM DEFICIT)
CAUSES of HYPOCALCEMIA
 Decreased ionized calcium
 Excess loss of calcium
 Inadequate dietary intake of calcium
 Decreased calcium absorption
(hypoparathyroidism, hyperthyroidism,
hypermagnesemia, decreased Vitamin D)
CLINICAL MANIFESTATION
 Gastrointestinal: increased peristalsis,
nausea and vomiting, diarrhea
 CNS: tingling, convulsions
CLINICAL MANIFESTATION
 MUSCLES: increased peristalsis, nausea
and vomiting, diarrhea
 Sensations of tingling may occur in the tips
of the fingers, around the mouth, and less
commonly in the feet. Spasms of the
muscles of the extremities and face may
occur (Chvostek’s Sign)
 Trousseau’s sign can be elicited by inflating
a blood pressure cuff on the upper arm to
about 20mmHg above systolic pressure,
within 2 to 5 minutes, carpal spasm (an
adducted thumb, flexed wrist and
metacarpophalangeal joints, extended
interphalangeal joints with fingers together)
will occur as ischemia of the ulnar nerve
develops.
CLINICAL MANIFESTATION
 Tetany, the most characteristic
manifestations of hypocalcemia and
hypomagnesemia, refers to the entire
symptom complex induced by increased
neural excitability. These symptoms are
caused by spontaneous discharges of both
sensory and motor fibers in peripheral
nerves
MANAGEMENT
 High calcium diet
 Oral calcium salts as prescribed
 Vitamin D and parathormone supplements as
ordered
 Amphogel (Aluminum Hydroxide) as
prescribed, this is a phosphate binder. As it
lowers phosphate levels, calcium levels will
increase
 Calcium gluconate 10% as per IV
prescribed. This is indicated if hypocalcemia
is severe
 Promote safety
 Protect from trauma
 Monitor breathing. Laryngospasm will occur
HYPERCALCEMIA (CALCIUM EXCESS)
CAUSES of HYPERCALCEMIA
 Calcium loss from bones (immobilization,
carcinoma with bone metastases)
 Excess intake of calcium (high calcium diet,
calcium containing antacids)
 Hyperparathyroidism, hypervitaminosis D,
steroid therapy
CLINICAL MANIFESTATION
 Gastrointestinal: decreased peristalsis
(constipation, paralytic ileus)
 CNS: diminished deep tendon reflexes
CLINICAL MANIFESTATION
 MUSCLES: muscle fatigue, hypotonia
 CARDIOVASCULAR: depressed electrical
activity (dysrhythmias), cardiac arrest
 KIDNEYS: polyuria, dehydration, stones,
renal damage
MANAGEMENT
 Increased fluid intake
 Provide acid- ash diet
 Protect the client from I jury
 Administer normal saline (NaCl 0.9%) per
IV as prescribed
 Mithracin (Mithramycin)- to reduce serum
calcium levels
MAGNESIUM
 Magnesium is the most abundant
intracellular cation after potassium.
 It acts an activator for many intracellular
enzyme systems and plays a role in both
carbohydrate and protein metabolism.
 The normal serum magnesium level is 1.3 to
2.3mg/dL (0.62 to 0.95mmol/L).
 Approximately one third of serum
magnesium is bound to protein; the
remaining two thirds exists as free cations-
the active component.
 Magnesium balance is important in
neuromuscular function.
 Because magnesium acts directly on the
Myoneural junction, variations in the serum
level affect neuromuscular irritable and
contractility.
 Magnesium produces its sedative effect at
the neuromuscular junction, probably by
 inhibiting the release of neuromuscular
acetylcholine. It also increases the stimulus
threshold in nerve fibers.
 Magnesium also affects the cardiovascular
system, acting peripherally to produce
vasodilation and decreased peripheral
resistance
 Magnesium predominantly found in bone
and soft tissues and eliminated by the
kidneys.
 Magnesium produces its sedative effect at
the neuromuscular junction, probably by
inhibiting the release of neuromuscular
acetylcholine.
 It also increases the stimulus threshold in
nerve fibers.
 Magnesium also affects the cardiovascular
system, acting peripherally to produce
vasodilation and decreased peripheral
resistance
 Magnesium predominantly found in bone
and soft tissues and eliminated by the
kidneys.
HYPOMAGNESIMIA
CAUSES of HYPOMAGNESEMIA
 Prolonged malnutrition or starvation
 Malabsorption syndrome
 Hypercalcemia
 Alcohol withdrawal syndrome
 Draining fistulas
CLINICAL MANIFESTATION
 CNS: convulsions, paresthesia, tremors,
ataxia
 MENTAL CHANGES: agitation,
depression, confusion
 MUSCLES: cramps, spasticity, tetany
 CARDIOVSACULAR: tachycardia,
hypertension, dysrhythmias
MANAGEMENT
 Provide rich foods rich in magnesium (milk,
fruits, green vegetables, whole grain cereals,
nuts, seafoods
 Promote safety, protect the client from injury
 Monitor for laryngeal stridor
 Administer magnesium supplement oral or
parenteral as prescribed
HYPERMAGNESEMIA
CAUSES of HYPERCALCEMIA
 Excessive intake of magnesium containing
antacids
 Renal failure
 DKA
CLINICAL MANIFESTATION
 Decreased BP
 Thirst, nausea and vomiting
 Drowsiness
 Diminished or loss of deep tendon reflexes
MANAGEMENT
 Calcium gluconate per IV as prescribed
 Dialysis
 Correct the underlying cause
ACID BASE IMBALANCES
RESPIRATORY ACIDOSIS (CARBONIC ACID
EXCESS)
 It is caused by the failure of the respiratory
system to remove carbon dioxide from the
body fluid as it is produced in the tissues
 Disorders that lead to hypoventilation
result to retention of carbon dioxide
CAUSES
 Respiratory acidosis is caused by primary
defects in the function of the lungs or
changes in normal respiratory system
 Any condition that causes obstruction of the
airway or depresses the respiratory system
that can cause respiratory acidosis
 Asthma: spasms resulting from allergens,
irritant or emotions cause the smooth
muscles of the bronchioles to constrict,
resulting in ineffective gas exchange
 Atelectasis: excessive mucus collection,
with the collapse of alveolar sacs caused by
mucous plus, infectious drainage, or
anesthetic medications results in ineffective
gas exchange.
 Brain trauma: excessive pressure on the
respiratory center or medulla oblongata
depresses respirations
  Bronchiectasis: bronchi become dilated as a
result of inflammation, and destructive
changes and weakness in the walls of the
bronchi occur
 Bronchitis: inflammation causes airway
obstruction, resulting in inadequate gas
exchange
 Central Nervous System (CNS)
depressants such as sedatives, opioids and
anesthetics depress the respiratory center,
leading to hypoventilation; carbon dioxide is
retained and the hydrogen ion concentration
increases
 Emphysema: loss of elasticity of alveolar
sacs restricts air flow in and out, primary
out, leading to an increased carbon dioxide
level
 Hypoventilation: carbon dioxide is retained
and the hydrogen ion concentration
increases, leading to the acidic state,
carbonic acid is retained and the pH
decreases
 Pulmonary Edema: extracellular
accumulation of fluid in pulmonary tissue
causes disturbances in alveolar diffusion and
perfusion
 Pneumonia: excess mucus production and
lung congestion cause airway obstruction,
resulting in inadequate gas exchange
 Pulmonary Emboli: emboli cause a
pulmonary artery and airway obstruction,
resulting in inadequate gas exchange
CLINICAL MANIFESTATIONS
 Neurological: Drowsiness, disorientation,
dizziness, headache, coma
 Cardiovascular: Decreased blood pressure,
ventricular fibrillation (related to
hyperkalemia from compensation), warm,
flushed skin (related to peripheral
vasodilation)
 Gastrointestinal: No abnormal findings
 Neuromuscular: Seizures
 Respiratory: Hypoventilation with hypoxia
(lungs are unable to compensate when there
is a respiratory problem)
MANAGEMENT
 Administer bronchodilators as prescribed
 Perform postural drainage as ordered
 If the client develops hyperkalemia or
ventricular fibrillation, sodium bicarbonate
per IV is prescribed
RESPIRATORY ALKALOSIS (CARBONIC
ACID DEFICIT)
 It is caused by loss of carbon dioxide from
the lungs at a faster rate than it is produced
in the tissues.
 Hyperventilation result to excess loss of
carbon dioxide
CAUSES
 Respiratory Alkalosis results from
conditions that cause overstimulation of the
respiratory system
 Fever: causes increased metabolism,
resulting in overstimulation of the
respiratory system
 Hyperventilation: rapid respirations caused
the blowing off CO2 leading to a decrease in
carbonic acid
 Hypoxia: stimulates the respiratory center in
the brainstem, which causes an increase in
the respiratory rate in order to increase
oxygen; this causes hyperventilation, which
results in decrease in the CO2 level
 Hysteria: is often is neurogenic and related
to psychoneurosis; however, this condition
leads to vigorous breathing and excessive
exhaling of CO2
 Overstimulation by mechanical
ventilators: The over administration of O2
and the depletion of CO2 can occur from
mechanical ventilation, causing the client to
be hyperventilated
 Pain: overstimulation of the respiratory
center in the brainstem results in a carbonic
acid deficit
CLINICAL MANIFESTATIONS
 Initially the hyperventilation and respiratory
stimulation cause abnormal rapid
respirations (tachypnea); in an attempt to
 compensate, the kidneys excrete excess
circulating bicarbonate into the urine
 Neurological: lethargy, lightheadedness,
confusion
 Cardiovascular: tachycardia, dysrhythmias
(related to hypokalemia from compensation)
 Gastrointestinal: Nausea, Vomiting,
epigastric pain
 Neuromuscular: tetany, numbness, tingling
of extremities, hyperreflexia, seizures
 Respiratory: Hyperventilation (lungs are
unable to compensate when there is a
respiratory problem)
MANAGEMENT
 Monitor for signs of respiratory distress
 Provide emotional support and reassurance
to the client
 Encourage appropriate breathing patterns
 Assist with breathing techniques and
breathing aids as prescribed
 Encourage voluntary holding of the breath if
appropriate
 Provide use of a rebreathing mask as
prescribed
 Provide carbon dioxide breaths as prescribed
(rebreathing into a paper bag)
MANAGEMENT
 Provide cautious care with ventilator clients
so that they are not forced to take breaths too
deeply or rapidly
 Monitor electrolyte values, particularly
potassium and calcium levels
 Administer medications as prescribed
 Prepare to administer calcium gluconate for
tetany as prescribed
METABOLIC ACIDOSIS (BICARBONATE
DEFICIT)
 It is caused by abnormal accumulation of
fixed acids or loss of base
 Hyperventilation result to excess loss of
carbon dioxide
 CAUSES
 Diabetes Mellitus or Diabetic
Ketoacidosis: an insufficient supply of
insulin increased fat metabolism, leading to
an excess accumulation of ketones or other
acids; the bicarbonate then ends up being
depleted
 Excessive ingestion of acetylsalicylic acid
(aspirin) causes an increase in the hydrogen
ion concentration
 High- fat diet: a high intake of fat causes a
much too rapid accumulation of the waste
products of fat metabolism, leading to a
buildup of ketones and acids
 Insufficient metabolism of carbohydrates:
when the O2 supply is not sufficient for the
metabolism of carbohydrates, lactic acid is
produced and lactic acidosis results
 Malnutrition: improper metabolism of
nutrients causes fat catabolism, leading to an
excess buildup of ketones and acids
 Renal insufficiency or renal failure results in
the following:
o Increased waste products of protein
metabolism are retained
o Acid increase, and bicarbonate is
unable to maintain acid- base
balance
 Severe diarrhea: intestinal and pancreatic
secretions are normally alkaline; therefore
excessive loss of base leads to acidosis
CLINICAL MANIFESTATIONS
 to compensate for the acidosis, hyperpnea
with Kussmaul’s respiration occurs as the
lungs attempt to exhale the excess CO2
 Neurological: drowsiness, confusion,
headache, coma
 Cardiovascular: decreased blood pressure,
dysrhythmias (related to hyperkalemia from
compensation), warm, flushed skin (related
to peripheral vasodilation)
 Gastrointestinal: nausea, vomiting,
diarrhea, abdominal pain
 Neuromuscular: no significant findings
  Respiratory: deep, rapid respirations
(compensatory action by the lungs)
MANAGEMENT
 Monitor for signs of respiratory distress
 Assess level of consciousness for central
nervous system depression
 Monitor intake and output and assist with
fluid and electrolyte replacement as
prescribed
 Prepare to administer solutions
intravenously as prescribed to increase the
buffer base
 Initiate safety and seizure precautions
 Monitor the serum potassium level closely;
as metabolic acidosis resolves, potassium
moves back into the cell and the serum
potassium level decreases
METABOLIC ALKALOSIS (BICARBONATE
EXCESS)
 A deficit of carbonic acid and a decrease in
hydrogen ion concentration that results from
the accumulation of base or from a loss of
acid without a comparable loss in the body
fluids.
CAUSES
 Metabolic Alkalosis results from a
dysfunction of metabolism that causes an
increased amount of available base solution
in the blood or a decrease in available acids
in the blood
 Diuretics: the loss of hydrogen ions and
chloride from diuresis causes a
compensatory increase in the amount of
bicarbonate in the blood
 Excessive vomiting or gastrointestinal
suctioning leads to an excessive loss of
hydrochloric acid
 Hyperaldosteronism: increased renal
tubular reabsorption of sodium occurs, with
the resultant loss of hydrogen ions
 Ingestion of and/ or infusion of excess
sodium bicarbonate causes an increase in the
amount of base in the blood
 Massive transfusion of whole blood: the
citrate anticoagulant used for storage of
blood is metabolized to bicarbonate
CLINICAL MANIFESTATIONS
 Neurologic: lethargy, irritability, confusion,
headache
 Cardiovascular: low blood pressure,
tachycardia, dysrhythmias
 Gastrointestinal: anorexia, nausea,
vomiting
 Neuromuscular: tremors, hypertonic
muscles, muscle cramps, tetany, tingling of
extremities, seizures
 Hypoventilation (compensatory action by
the lungs)
MANAGEMENT
 Monitor for signs of respiratory distress
 Monitor potassium and calcium serum levels
 Institute safety precautions
 Prepare to administer medications as
prescribed to promote the kidney excretion
of bicarbonate
 Prepare to replace potassium chloride as
prescribed
 Treat the underlying cause of alkalosis
INTRAVENOUS THERAPY
PURPOSES AND USES
 Used to sustain clients who are unable to
make substances orally
 Replaces water, electrolytes, and nutrients
more rapidly than oral administration
 Provides immediate access to the vascular
system for the rapid delivery of specific
solutions without the time required for
gastrointestinal tract absorption
 Provides a vascular support route for
administration of medication and blood
components
TYPES OF SOLUTIONS
ISOTONIC SOLUTIONS
 Have the same osmolality as body fluids
 Increase extracellular fluid volume
 Do not enter the cells because no osmotic
force exists to shift the fluids
HYPOTONIC SOLUTIONS
  Are more dilute solutions and have a lower
osmolality than body fluids
 Cause the movement of water into cells by
osmosis
 Should be administered slowly to prevent
cellular edema
HYPERTONIC SOLUTIONS
 Are more concentrated solutions and have a
higher osmolality than body fluids
 Concentrate extracellular fluid and cause
movement of water from cells into the
extracellular fluid by osmosis
COLLOIDS
 Also called plasma expanders
 Pull fluid from the interstitial compartment
into the vascular compartment
 Used to increase the vascular volume
rapidly, such as in hemorrhage or severe
hypovolemia
IV CANNULAS
BUTTERFLY SETS
 The set is a wing-tip needle with a metal
cannula, plastic or rubber wings, and a
plastic catheter or hub.
 The needle is 0.5 to 1.5 inches in length,
with needle gauge sizes from 16 to 26.
 Infiltration is more common with these
devices.
 The butterfly infusion set is used commonly
in children and older clients, whose veins
are likely to be small or fragile
PLASTIC CANNULAS
 Plastic cannulas may be an over-the-needle
device or an in-needle catheter and are used
primarily for short-term therapy.
 The over-the-needle device is preferred for
rapid infusion and is more comfortable for
the client.
 The in-needle catheter can cause catheter
embolism if the tip of the cannula breaks
IV GAUGES
 The gauge refers to the diameter of the
lumen of the needle or cannula
 The smaller the gauge number, the larger the
diameter of the lumen; the larger the gauge
number, the smaller the diameter of the
lumen.
 The size of the gauge used depends on the
solution to be administered and the diameter
of the available vein.
 Large-diameter lumens (smaller gauge
numbers) allow a higher fluid rate than
smaller diameter lumens and allow the
administration of higher concentrations of
solutions.
 For rapid emergency fluid administration,
blood products, or anesthetics,
preoperative and post-operative clients,
large-diameter lumen needles or cannulas
are used, such as an 18- or 19-gauge lumen
or cannula
 For peripheral fat emulsion (lipids)
infusions, a 20- or 21-gauge lumen or
cannula is used.
 For standard IV fluid and clear liquid IV
medications, a 22- or 24-gauge lumen or
cannula is used.
 If the client has very small veins, a 24- to
25-gauge lumen or cannula is used
IV CONTAINERS
 Container may be glass or plastic.
 Squeeze the plastic bag to ensure intactness
and assess the glass bottle for any cracks
before hanging.
 Reconstitute any medications per agency
protocol and pharmacy instruction
IV TUBINGS
 IV tubing contains a spike end for the bag or
bottle, drip chamber, roller clamp, Y site,
and adapter end for attachment to the
cannula or needle that is inserted into the
client’s vein.
 Shorter, secondary tubing is used for
piggyback solutions, connecting them to the
injection sites nearest to the drip chamber
 Special tubing is used for medication that
absorbs into plastic (check specific
medication administration guidelines when
administering IV medications).
 Vented and non vented tubing are available.
 A vent allows air to enter the IV container as
the fluid leaves.
  A vented adapter can be used to add a vent
to a non vented IV tubing system.
 Use non vented tubing for flexible
containers
 Use vented tubing for glass or rigid plastic
containers to allow air to enter and displace
the fluid as it leaves; fluid will not flow from
a rigid IV container unless it is vented
DRIP CHAMBERS
MACRODRIP CHAMBERS
 The chamber is used if the solution is thick
or is to be infused rapidly.
 The drop factor varies from 10 to 20 drops
(gtt)/mL, depending on the manufacturer.
 Read the tubing package to determine how
many drops per milliliter are delivered (drop
factor)
MICRODRIP CHAMBERS
 Normally, the chamber has a short vertical
metal piece (stylet) where the drop forms.
 The chamber delivers about 60 gtt/mL.
 Read the tubing package to determine the
drop factor (gtt/mL).
 Microdrip chambers are used if fluid will be
infused at a slow rate (less than 50 mL/hour)
or if the solution contains potent medication
that needs to be titrated, such as in a critical
care setting or in pediatric clients
FILTERS
 Filters provide protection by preventing
particles from entering the client’s veins.
 They are used in IV lines to trap small
particles such as undissolved substances, or
medications that have precipitated in
solution.
 Check the agency policy regarding the use
of filters.
 A 0.22-µm filter is used for most solutions; a
1.2- µm filter is used for solutions
containing lipids or albumin; and a special
filter is used for blood components.
 Change filters every 24 to 72 hours
(depending on agency policy) to prevent
bacterial growth.
NEEDLESS INFUSION DEVICES
 Needleless infusion devices include recessed
needles, plastic cannulas, and 1-way valves;
these systems decrease the exposure to
contaminated needles.
 Do not administer parenteral nutrition or
blood products through a 1-way valve.
INTERMITTENT INFUSION DEVICES
 Intermittent infusion devices are used when
intravascular accessibility is desired for
intermittent administration of medications
by IV push or IV piggyback.
 Patency is maintained by periodic flushing
with normal saline solution (sodium chloride
and normal saline are interchangeable
names).
 Depending on agency policy, when
administering medication, flush with 1 to 2
mL of normal saline to confirm placement of
the IV cannula; administer the prescribed
medication and then flush the cannula again
with 1 to 2 mL of normal saline to maintain
patency
ELECTRONIC IV INFUSION DEVICES
 IV infusion pumps control the amount of
fluid infusing and should be used with
central venous lines, arterial lines, solutions
containing medication, and parenteral
nutrition infusions.
 Most agencies use IV pumps for the infusion
of any IV solution.
 A syringe pump is used when a small
volume of medication is administered; the
syringe that contains the medication and
solution fits into a pump and is set to deliver
the medication at a controlled rate
PATIENT- CONTROLLED ANALGESIA (PCA)
 A device that allows the client to self
administer IV medication, such as an
analgesic; the client can administer doses at
set intervals and the pump can be set to lock
out doses that are not within the preset time
frame to prevent overdose.
 The PCA regimen may include a basal rate
of infusion along with the demand dosing,
basal rate infusion alone, or demand dosing
alone.
 A bolus dose can be given prior to any of the
settings and should be set based on the
HCP’s prescription.
  PCAs are always kept locked and setup
requires the witness of another registered
nurse (RN).
LATEXT ALLERGY
 Assess the client for an allergy to latex.
 IV supplies, including IV catheters, IV
tubing, IV ports (particularly IV rubber
injection ports), rubber stoppers on
multidose vials, and adhesive tape, may
contain latex.
 Latex-safe IV supplies need to be used for
clients with a latex allergy; most agencies
carry these now, but this still needs to be
checked.
SELECTION OF PERIPHERAL IV SITES
 Veins in the hand, forearm, and antecubital
fossa are suitable sites
 Veins in the lower extremities (legs and feet)
are not suitable for an adult client because of
the risk of thrombus formation and the
possible pooling of medication in areas of
decreased venous return
 Veins in the scalp and feet may be suitable
sites for infants
 Assess the veins of both arms closely before
selecting a site
 Start the IV infusion distally to provide the
option of proceeding up the extremity if the
vein is ruptured or infiltration occurs; if
infiltration occurs from the antecubital vein,
the lower veins in the same arm usually
should not be used for further puncture sites.
 Determine the client’s dominant side, and
select the opposite side for a venipuncture
site.
 Bending the elbow on the arm with an IV
may easily obstruct the flow of solution,
causing infiltration that could lead to
thrombophlebitis.
 Avoid checking the blood pressure on the
arm receiving the IV infusion if possible.
 Do not place restraints over the venipuncture
site.
 Use an arm board as needed when the
venipuncture site is located in an area of
flexion
INITIATION AND ADMINISTRATION OF IV
SOLUTIONS
Check the IV solution against the HCP’s
prescription for the type, amount, percentage
of solution, and rate of flow; follow the 6
rights for medication administration.
 Assess the health status and medical
disorders of the client and identify client
conditions that contraindicate use of a
particular IV solution or IV equipment, such
as an allergy to cleansing solution, adhesive
materials, or latex. Check compatibility of
IV solutions as appropriate
 Check client’s identification and explain the
procedure to the client; assess client’s
previous experience with IV therapy and
preference for insertion site.
 Wash hands thoroughly before inserting an
IV line and before working with an IV line;
wear gloves.
 Use sterile technique when inserting an IV
line and when changing the dressing over
the IV site.
 Change the venipuncture site every 72 to 96
hours in accordance with Centers for
Disease Control and Prevention (CDC)
recommendations and agency policy.
 Change the IV dressing when the dressing is
wet or contaminated, or as specified by the
agency policy.
 Change the IV tubing every 96 hours in
accordance with CDC recommendations and
agency policy or with change of
venipuncture site
 Do not let an IV bag or bottle of solution
hang for more than 24 hours to diminish the
potential for bacterial contamination and
possibly sepsis.
 Do not allow the IV tubing to touch the floor
to prevent potential bacterial contamination.
PRECAUTIONS FOR IV LINES
 On insertion, an IV line can cause initial
pain and discomfort for the client.
 An IV puncture provides a route of entry for
microorganisms into the body.
 Medications administered by the IV route
enter the blood immediately, and any
adverse reactions or allergic responses can
occur immediately.
  Fluid (circulatory) overload or electrolyte
imbalances can occur from excessive or too
rapid infusion of IV fluids.
 Incompatibilities between certain solutions
and medications can occur
IV COMPLICATIONS
AIR EMBOLISM
 A bolus of air enters the vein through an
inadequately primed IV line, from a loose
connection, during tubing change, or during
removal of the IV
SIGNS AND SYMPTOMS
 Tachycardia
 Chest pain and dyspnea
 Hypotension
 Cyanosis
 Decreased level of consciousness
PREVENTION AND INTERVENTIONS
 Prime tubing with fluid before use, and
monitor for any air bubbles in the tubing.
 Secure all connections.
 Replace the IV fluid before the bag or bottle
is empty.
 Monitor for signs of air embolism; if
suspected, clamp the tubing, turn the client
on the left side with the head of the bed
lowered (Trendelenburg position) to trap the
air in the right atrium, and notify the
Physician.
CATHETER EMBOLISM
 An obstruction that results from breakage of
the catheter tip during IV line insertion or
removal
SIGNS AND SYMPTOMS
 Decrease in blood pressure
 Pain along the vein
 Weak, rapid pulse
 Cyanosis of the nail beds
 Loss of consciousness
PREVENTION AND INTERVENTIONS
 Remove the catheter carefully.
 Inspect the catheter when removed.
 If the catheter tip has broken off, place a
tourniquet as proximally as possible to the
IV site on the affected limb, notify the
physician immediately, prepare to obtain a
radiograph, and prepare the client for
surgery to remove the catheter piece(s), if
necessary
CIRCULATORY OVERLOAD
 Also known as fluid overload; results from
the administration of fluids too rapidly,
especially in a client at risk for fluid
overload
SIGNS AND SYMPTOMS
 Increased blood pressure
 Distended jugular veins
 Rapid breathing
 Dyspnea
 Moist cough and crackles
PREVENTION AND INTERVENTIONS
 Identify clients at risk for circulatory
overload.
 Calculate and monitor the drip (flow) rate
frequently.
 Use an electronic IV infusion device and
frequently check the drip rate or setting (at
least every hour for an adult).
 Add a time tape (label) to the IV bag or
bottle next to the volume markings.
 Mark on the tape the expected hourly
decrease in volume based on the mL/hour
calculation
ELECTROLYTE OVERLOAD
 An electrolyte imbalance is caused by too
rapid or excessive infusion or by use of an
inappropriate IV solution
SIGNS AND SYMPTOMS
 Signs depend on the specific electrolyte
overload imbalance
PREVENTION AND INTERVENTIONS
 Assess laboratory value reports.
 Verify the correct solution.
 Calculate and monitor the flow rate.
 Use an electronic IV infusion device and
frequently check the drip rate or setting (at
least every hour for an adult).
 Add a time tape (label) to the IV bag or
bottle
 Place a red medication sticker on the bag or
bottle if a medication has been added to the
IV solution
  Monitor for signs of an electrolyte
imbalance, and notify the physician if they
occur.
HEMATOMA
 The collection of blood in the tissues after
an unsuccessful venipuncture or after the
venipuncture site is discontinued and blood
continues to ooze into the tissue
SIGNS AND SYMPTOMS
 Ecchymosis, immediate swelling and
leakage of blood at the site, and hard and
painful lumps at the site
PREVENTION AND INTERVENTIONS
 When starting an IV, avoid piercing the
posterior wall of the vein.
 Do not apply a tourniquet to the extremity
immediately after an unsuccessful
venipuncture.
 When discontinuing an IV, apply pressure to
the site for 2 to 3 minutes and elevate the
extremity; apply pressure longer for clients
with a bleeding disorder or who are taking
anticoagulants.
 If a hematoma develops, elevate the
extremity and apply pressure and ice as
prescribed.
 Document accordingly, including taking
pictures of the IV site if indicated by agency
policy.
INFECTION
 Infection occurs from the entry of
microorganisms into the body through the
venipuncture site.
 Venipuncture interrupts the integrity of the
skin, the first line of defense against
infection.
 The longer the therapy continues, the greater
the risk for infection.
 Infection can occur locally at the IV
insertion site or systemically from the entry
of microorganisms into the body
AT RISK PATIENTS
 Immunocompromised clients with diseases
such as cancer, human immunodeficiency
virus or acquired immunodeficiency
syndrome, those receiving biologic modifier
response medications for treatment of
autoimmune conditions, or status post organ
transplant are at risk for infection.
AT RISK PATIENTS
 Clients receiving treatments such as
chemotherapy who have an altered or
lowered white blood cell count are at risk for
infection.
 Older clients, because aging alters the
effectiveness of the immune system, are at
risk for infection.
 Clients with diabetes mellitus are at risk for
infection
SIGNS AND SYMPTOMS
 Local—redness, swelling, and drainage at
the site
 Systemic—chills, fever, malaise Headache,
nausea, vomiting, backache, tachycardia
PREVENTION AND INTERVENTIONS
 Assess the client for predisposition to or risk
for infection.
 Maintain strict asepsis when caring for the
IV site.
 Monitor for signs of local or systemic
infection
PREVENTION AND INTERVENTIONS
 Monitor white blood cell counts.
 Check fluid containers for cracks, leaks,
cloudiness, or other evidence of
contamination.
 Change IV tubing every 96 hours in
accordance with CDC recommendations or
according to agency policy; change IV site
dressing when soiled or contaminated and
according to agency policy.
 Label the IV site, bag or bottle, and tubing
with the date and time to ensure that these
are changed on time according to agency
policy.
PREVENTION AND INTERVENTIONS
 Ensure that the IV solution is not hanging
for more than 24 hours.
 If infection occurs, the physician is notified;
discontinue the IV, and place the
venipuncture device in a sterile container for
possible culture.
 Prepare to obtain blood cultures as
prescribed if infection occurs and document
accordingly.
  Restart an IV in the opposite arm to
differentiate sepsis (systemic infection) from
local infection at the IV site.
 Document accordingly, including taking
pictures
INFILTRATION
 Infiltration is seepage of the IV fluid out of
the vein and into the surrounding interstitial
spaces.
 Infiltration occurs when an access device
has become dislodged or perforates the wall
of the vein or when venous backpressure
occurs because of a clot or venospasm
SIGNS AND SYMPTOMS
 Edema, pain, numbness
 coolness at the site; may or may not have a
blood return
PREVENTION AND INTERVENTIONS
 Avoid venipuncture over an area of flexion.
 Anchor the cannula and a loop of tubing
securely with tape.
 Use an arm board or splint as needed if the
client is restless or active.
 Monitor the IV rate for a decrease or a
cessation of flow.
 Evaluate the IV site for infiltration by
occluding the vein proximal to the IV site.
 If the IV fluid continues to flow, the cannula
is probably outside the vein (infiltrated); if
the IV flow stops after occlusion of the vein,
the IV device is still in the vein.
 Lower the IV fluid container below the IV
site, and monitor for the appearance of blood
in the IV tubing; if blood appears, the IV
device is most likely in the vein
PREVENTION AND INTERVENTIONS
 If infiltration has occurred, remove the IV
device immediately; elevate the extremity
and apply compresses (warm or cool,
depending on the IV solution that was
infusing and the Physician prescription) over
the affected area.
 Do not rub an infiltrated area, which can
cause hematoma.
 Document accordingly, including taking
pictures of the IV site if indicated by agency
policy
PHLEBITIS AND THROMBOPHLEBITIS
 Phlebitis is an inflammation of the vein that
can occur from mechanical or chemical
(medication) trauma or from a local
infection.
 Phlebitis can cause the development of a clot
(thrombophlebitis).
SIGNS AND SYMPTOMS OF PHLEBITIS
 Heat, redness, tenderness at the site
 Not swollen or hard
 Intravenous infusion sluggish
SIGNS AND SYMPTOMS OF
THROMBOPHLEBITIS
 Hard and cordlike vein
 Heat, redness, tenderness at site
 Intravenous infusion sluggish
PREVENTION AND INTERVENTIONS
 Use an IV cannula smaller than the vein, and
avoid using very small veins when
administering irritating solutions.
 Avoid using the lower extremities (legs and
feet) as an access area for the IV.
 Avoid venipuncture over an area of flexion.
 Anchor the cannula and a loop of tubing
securely with tape
PREVENTION AND INTERVENTIONS
 Use an arm board or splint as needed if the
client is restless or active.
 Change the venipuncture site every 72 to 96
hours in accordance with CDC
recommendations and agency policy.
 If phlebitis occurs, remove the IV device
immediately and restart it in the opposite
extremity; notify the physician if phlebitis is
suspected, and apply warm, moist
compresses, as prescribed.
 If thrombophlebitis occurs, do not irrigate
the IV catheter; remove the IV, notify the
physician, and restart the IV in the opposite
extremity.
 Document accordingly, including taking
pictures if indicated by agency policy
TISSUE DAMAGE
 Tissues most commonly damaged include
the skin, veins, and subcutaneous tissue.
 Tissue damage can be uncomfortable and
can cause permanent negative effects.
  Extravasation is a form of tissue damage
caused by the seepage of vesicant or irritant
solutions into the tissues; this occurrence
requires immediate physician notification so
that treatment can be prescribed to prevent
tissue necrosis
SIGNS AND SYMPTOMS
 Skin color changes, sloughing of the skin,
discomfort at the site
PREVENTION AND INTERVENTIONS
 Use a careful and gentle approach when
applying a tourniquet.
 Avoid tapping the skin over the vein when
starting an IV.
 Monitor for ecchymosis when penetrating
the skin with the cannula.
 Assess for allergies to tape or dressing
adhesives.
 Monitor for skin color changes, sloughing of
the skin, or discomfort at the IV site.
 Notify the physician if tissue damage is
suspected.
 Document accordingly, including taking
pictures if indicated by agency policy