Transcript NURS 2140 Fluid and Electrolytes Acid Base and IV

NURS 2140
Fluid and Electrolytes Acid Base
and IV Therapy
Teresa Champion, RN MSN
Metropolitan Community College
Winter 2012
BODY COMPOSITION AND FUNCTION
• PRIMARY FLUID = Water
– 60% total body weight (1 L = 2.2 lbs)
– 2 – 2.5 L of water per day
• TWO PRIMARY FLUID COMPARTMENTS
– Intracellular (ICF)
– Extracellular (ECF)
• FUNCTIONS:
–
–
–
–
–
Transporting
Removing
Regulation
Lubricating
Food Digestion
Intake = Output
Regulation of Body Fluid
• Osmosis – movement of water from lower
particle concentration to higher particle
concentration
• Diffusion – movement of molecules from higher
to lower concentration (simple or facilitated)
• Filtration – movement of molecules through a
semi-permeable membrane from higher
concentration to lower concentration as a result
of hydrostatic pressure
There are two ways
in which substances
can enter or leave a
cell:
1) Passive
a) Simple
Diffusion
b) Facilitated
Diffusion
(carrier)
c) Osmosis (water
only)
2) Active
a) Molecules
b) Particles
Oncotic vs Hydrostatic Pressure
• Filtration is directly opposed by the oncotic pressure of
plasma proteins, especially Albumin in the blood stream.
• Arteriole – high hydrostatic pressure - (~32mmHg)
• Venus – low hydrostatic pressure – (~15 mmHg)
• Plasma oncotic pressure – (~22mmHg)
• http://www.youtube.com/watch?v=VMvD29-Agtg
• http://www.youtube.com/watch?v=mpg7ON2CfFE
• http://www.youtube.com/watch?v=dAO8igIysaA
• Homeostasis - thus in a steady state ECF = ICF
OSMOLALITY
• Number of molecules of solute per kg of water
• NORMAL OSMOLALITY of blood is 275 – 295
milliosmoles per kg (mOsm/kg) of body weight
– Isotonic Fluids - same osmolality as blood plasma)
– Hypotonic Fluids - less concentration than blood plasma
(< 275 mOsm/kg)
– Hypertonic Fluids - greater concentration than blood
plasma (>295 mOsm/kg)
Homeostatic Mechanisms
• Fluid Balance - regulated by:
– Osmoreceptors of the hypothalamus - stimulates release
of ADH and stimulates thirst.
– Baroreceptors (pressure sensitive cells) in carotids and
aorta also stimulate the release of ADH
– Baroreceptors in glomerular arterioles in kidney will
secrete Renin and start the Renin-Angiotension (RAA)
cascade thus resulting in release of aldosterone from
the adrenal glands and cause sodium retention = fluid
retention (water follows sodium)
Role of the Heart
• Atrial Natriuretic Peptide: (ANP): secreted
from atrial cells of heart (in response to too
much volume in the blood)
– acts as diuretic
– inhibits thirst mechanism
– suppresses the RAA cascade
Role of the Kidneys
• Filter approx 180 Liters of blood per day; GFR
(glomerular filtration rate)
• Produces urine between 1-2 Liters/day
• If loss of 1% to 2% of body water, will conserve
water by reabsorbing more water from
filtrate; urine will be more concentrated
• If gain of excess body water, will excrete more
water from filtrate; urine will be more diluted
Lab Tests for Evaluating Fluid Balance
SERUM
Normal Levels
Osmolality
275-295 mOsm/kg of
water
Hematocrit
40-50%*
BUN
5-20 mg/dl
URINE
Normal
Levels
Specific Gravity
1.005 – 1.030
Osmolality
50-1200 mOsm/kg
of water
Sodium
135 – 145 mEq/L
Potassium
3.5 – 5.0 mEq/L
Sodium
40-220 mEq/day
Chloride
95-108 mEq/L
Potassium
25-100 mEq/day
Bicarbonate
(CO2)
22-28 mEq/L -Arteriole
24-30 mEq/L -Venous
Evaluation of Fluid Status
• Normal serum hematocrit
– 40 – 50%
• Dilute serum
– Low hematocrit and electrolyte levels
• Concentrated serum
– Elevated hematocrit and electrolyte levels
Clinical Manifestations of
Overhydration and Dehydration
OVERHYDRATION
DEHYDRATION
Crackles in lungs
Dry mouth and tongue, mucous membranes
S3 Heart Sound
Tachycardia
Dyspnea
Severe thirst (maybe not in elderly)
Reduced blood oxygen levels and increased
CO2 levels – respiratory acidosis
Increased temperature (may rise 1 or 2 degrees)
Bounding pulses
Weak pulses
Increased blood pressure
Orthostatic Hypotension, systemic hypotension
Increased edema, ascites
“tenting” skin
Increased neck swelling – jugular vein
distension
Flat neck veins
Decreases in HCT, Serum Osmolality, Serum
Sodium, Potassium, Chloride, Bicarbonate,
BUN; Urine Specific Gravity < 1.005; Urine
Osmolality >1,200 mOsm/kg
Increases in HCT, Serum Osmolality, Serum
Sodium, Potassium, Chloride, Bicarbonate, BUN,
Creatinine; Urine specific Gravity >1.030; Urine
Osmolality < 50 mOsm/kg
Nursing Considerations
•
•
•
•
•
•
•
Assess for headache, dizziness, syncope
CHF-SOB, dyspnea, activity intolerance
Maintaining accurate I & O
Daily weights
Monitoring Lab values
Frequency and consistency of stools
Meals include adequate fluid intake
Dehydration in the Elderly
Increased risks for dehydration:
•Decrease in thirst
•Lack of fluid replacement
•Use of diuretic medications for
high BP
•Susceptibility to contagious
diseases
Nursing Care Plan
Dehydration
• Risk for imbalanced Fluid
Volume Related to excessive
fluid loss/inability to take in
fluids AEB ….
Overhydration
• Risk for Imbalanced Fluid
Volume Related to excessive
fluid intake/decreased
urination AEB ….
Electrolytes
– Substance that develops an electrical charge when
dissolved in water
• Cation - positive charged
• Anion - negative charged
• Examples of cations: Sodium, Potassium,
Magnesium, Calcium
• Examples of anions: Chloride, Bicarbonate,
Phosphorous
Sodium
Normal serum values
135-145 mEq/L
• Most abundant cation in ECF
• Functions
– ECF volume – water balance
– Acid-base balance
– Nerve impulse control – sodium potassium pump
– Levels below 115 mEq/L – brain damage, seizures
– Sodium is primarily excreted through the kidneys, but
other avenues are GI Secretions and sweat.
Sodium Deficit - Levels < 135 mEq/L
Hyponatremia
• Loss through GI tract, skin or kidneys
• An increased amount of sodium shift into the
cells when there is a potassium deficit
• An excessive ADH release (SIADH) causing
Water retention and sodium deficit
• Inadequate sodium intake, increased water
intake
• Excessive use of 5% dextrose solution
• Levels below 115 mEq/L – brain damage
Pathophysiology of decreased sodium
imbalances
• CNS – excess water moves into the cerebral
tissues – increased intracranial pressure
• GI – loss causes acid base imbalances
• Kidneys – renal dysfunction promotes sodium
and water retention resulting in diluted
sodium level (fluid overload)
• Cellular activity - decrease in Na-K pump
Causes of Hyponatremia
• Dietary changes – low sodium intake, excessive water
intake, “fad diets”/fasting, anorexia nervosa, prolonged
use of IV D5W
• GI Losses – vomiting, diarrhea, GI Suctioning, Tap water
enemas, GI surgery, Bulimia.
• Renal Loses – Salt wasting kidney disease, diuretics.
• Hormonal Influences - ADH, SIADH.
• Decreased adrenocortical hormone: Addison’s disease.
• Altered Cellular Function – Hypervolemic state: heart
failure, cirrhosis
• Burns
• Skin
Sodium Excess - Levels > 145 mEq/L
Hypernatremia
•
•
•
•
•
Excessive secretion of aldosterone or cortisol
Excessive sodium intake
Decreased water intake
GI disorders
Decreased renal function
Pathophysiology of increased sodium
imbalances
• Overproduction of adrenal hormones –
excessive secretions of aldosterone and
cotrisol promote an increase in the sodium
level
• Cellular activity – increases the sodium pump
action, causes cellular irritability.
Causes of Hypernatremia
• Dietary Changes – Increased sodium intake, decreased
water intake, Administration of 3% saline solutions
• GI Disorders – severe vomiting, Diarrhea
• Decreased Renal Function – reduced glomerular
filtration
• Environmental Changes – Increased temperature and
humidity, water loss
• Hormonal Influence – Increased adrenocortical
hormone production: oral or IV cortisone or Cushing's
syndrome.
• Altered Cellular Function – Heart Failure, Renal
Diseases
• Trauma – Head injury
Clinical Manifestations of Sodium
Imbalances
Hyponatremia
• Nausea, vomiting, diarrhea,
abdominal cramps
• Tachycardia, hypotension
• Headaches, apprehension,
lethargy, confusion, depression,
seizures
• Muscle weakness
• Dry skin, pale dry mucus
membranes
• Serum Na <135 mEq/L
• Serum osmolality < 275 mOsm/kg
• Urine Specific Gravity <1.005
• Urine Sodium >220 mEq/day
Hypernatremia
•
•
•
•
•
•
•
•
•
•
Nausea, vomiting, anorexia
Rough, dry tongue
Tachycardia, possible hypertension
Restlessness, agitation, stupor,
elevated body temperature
Muscular twitching, tremor,
hyperreflexia
Flushed, dry skin and dry sticky
membranes
Serum Na >145 mEq/L
Serum osmolality > 295 mOsm/kg
Urine Specific Gravity >1.030
Urine Sodium < 40 mEq/day
Chloride
Normal Levels
95-108 mEq/L
• Primary extracellular anion
• Creates electrical neutrality when combined with
sodium
• Body Water Balance
• Hydrochloric acid
• Buffers carbonic acid
• Anion gap - calculated AG = (Na + K) – (Cl + HC03
(metabolic acidosis)
Hypochloremia <95 mEq/L
• Causes
– Loss of gastric fluid
– Osmotic diuresis
• Manifestations
– Reflects alkalosis
– Paresthesias, muscle spasms, slow respirations
– Dehydration
Hyperchloremia > 108 mEq/L
• Causes
– Hyperparathyroidism, dehydration
– Respiratory acidosis
• Manifestations
– Lethargy, disorientation
– Increased rate and depth of respirations
Chloride
• Primary extracellular anion
• Creates electrical neutrality when combined
with sodium
• Hydrochloric acid
• Buffers carbonic acid
• Anion gap - calculated AG = (Na + K) – (Cl +
HC03 (metabolic acidosis)
Potassium
Normal serum values
3.5- 5.0 mEq/L
• Most abundant cation in ICF
• Functions
– Transmission and conduction of nerve impulses and the
contraction of skeletal, cardiac and smooth muscles (na-K
pump)
– Assists with regulation intracellular osmolality
– Enzyme production for cellular metabolism
– Maintains Acid-base Balance
– Levels less than 2.5 mEq/L and greater than 7.0 mEq/L can
cause cardiac arrest
– Potassium is excreted through the kidneys (80-90%) and
feces (10-20%)
Potassium Deficit - Levels < 3.5 mEq/L
Hypokalemia causes
• Dietary changes – decrease in dietary intake
• Cellular Potassium Loss – Tissue Injury, Muscle
contraction
• GI losses – vomiting, diarrhea, GI suctioning, intestinal
fistula, laxative abuse, bulimia, enemas
• Hormonal Influences – Aldosterone (Cushing
syndrome), licorice, Stress
• Drugs – adrenergic, epinephrine, decongestants,
amphotericin B, beta2 –adrenergic agonist,
aminoglycosides, large doses of penicillins, potassium
wasting diruetics, steroids
• Redistribution - Insulin, alkalotic states
• Electrolyte loss - Magnesium
Potassium Excess - Levels > 5.0 mEq/L
Hyperkalemia causes
• Dietary – excessive intake, supplements, salt
substitutes, herbal juices
• IV Potassium replacements – with poor renal function
• Decreased renal function – acute and chronic renal
failure
• Altered Cellular Function – injury, metabolic acidosis,
stored blood >1-3 weeks old
• Hormonal Deficiency – Addison’s disease
• Drugs – K-sparing diuretics, ACE inhibitors, beta
blockers
• Pseudohyperkalemia – poor blood samples
Clinical Manifestations of Potassium
Imbalances
Hypokalemia
• GI – anorexia, N/V, diarrhea,
abdominal distention, decreased
peristalsis or ileus
• Cardiac – dysrhythmias, vertigo
(dizziness), cardiac arrest
• ECG – Flat or inverted T waves,
depressed ST
• Renal – polyuria
• Neuromuscular – malaise,
drowsiness, muscular weakness,
confusion, mental depression,
diminished deep tendon reflexes,
respiratory paralysis
• Lab Values - <3.5 mEq/L
• Alkalosis
Hyperkalema
• GI – Nausea, Diarrhea, Abdominal
Cramps
• Cardiac – tachycardia, then
bradycardia and then cardiac
arrest
• ECG - Peaked T waves, shortened
QT interval, prolonged PR followed
by a disappearance of the P wave,
Prolonged QRS.
• Renal - oliguria or anuria
• Neuromuscular – weakness,
numbness or tingling sensation,
muscle cramps
• Lab Values - > 5.0 mEq/L
• Acidosis
Hypokalemia – flattened, inverted T
wave with a U wave sometimes
present
Hyperkalemia – peaked T Wave
CLINICAL MANAGEMENT OF
POTASSIUM IMBALANCES
Hypokalemia
• Oral supplements (tablets,
capsules, liquid)
– Oral potassium is very irritating to
the gastric mucosa and should be
given diluted and not on an empty
stomach
• IV Potassium DILUTED in an IV
Solution
– Never more than 10mEq of KCL per
hour
– Never given undiluted as a bolus
injection
– For life threatening hypokalemia
(<2.6 mEq/L) 30-40 mEq of KCL can
be diluted in 100 – 150 ml of IV
Fluid and administered in a central
Hyperkalemia
• Potassium Restriction
• IV Sodium bicarbonate (NaHCO3)
– moves K back into the cells –
temporary tx
• 10% Calcium gluconate
– decreases irritability of myocardium,
does not promote K loss, use
cautiously with patients on digitalis
• Insulin and glucose – (10 units of
Insulin and 50% dextrose)
– Moves K back into the cells
• Kayexalate (sodium polystyrene)
and sorbitol 70%
– Cation exchange
• Dialysis
Drugs that effect Potassium Balances
Hypokalemia
• Laxatives and enemas
• Corticosteroids
• Antibiotics
• Potassium-wasting diuretics
• Beta2 agonists
Hyperkalemia
• Oral and intravenous K
• Central nervous system
agents
• Potassium sparing diuretics
• ACE inhibitors
• Beta blockers
• Heparin/Lovenox
• NSAIDS
Calcium
Normal serum values 8.5- 10.5 mg/dL
Ionized Calcium 4.0 – 5.0 mg/dL
•
•
•
•
•
•
•
•
Cation found in both ECF and ICF, but greater concentration in ECF
Maintains cellular membrane stability
98% in bones and teeth, 2% in the serum
Of the 2% in serum - 45% is bound to albumin and 50% is ionized
calcium – physiologically active
Serum pH greatly affects calcium levels – metabolic acidosis
increases ionized calcium levels, alkalosis opposite effect
Normal ionized Ca levels are 4.0 to 5.0 mg/dL
Serum Ca levels are regulated by Vitamin D, calcitonin (thyroid
glad) and parathyroid hormone (PTH) from parathyroid gland
There is a direct relationship between Ca and Phosphorous, when
Ca is low Phosphorous is high and vise versa.
Calcium Regulation
When serum Calcium is low:
• PARATHYROID GLAND
releases PTH. PTH mobilizes
calcium from the bone,
increases renal
reabsorption of calcium and
promotes calcium
absorption in the intestines
in the presence of Vitamin
D to increase serum
Calcium levels
When serum Calcium is High:
• THYROID GLAND – releases
Calcitonin. Calcitonin
increases calcium return to
the bone and decreases
serum Calcium levels
Functions of Calcium
• Neuromuscular
– normal nerve and muscle activity, causes transmission of nerve
impulses and contraction of skeletal muscles.
• Cardiac
– contraction of the myocardium (heart muscle)
• Cellular and Blood
– maintenance of normal cellular permeability - decreased
calcium increases cellular permeability
– Coagulation of blood. Promotes clotting by converting
prothrombin into thrombin
• Bone and teeth construction
– Calcium along with phosphorous forms bones and teeth make
them strong and durable
Calcium Deficit - Levels < 8.5 mg/dL
and Ionized Ca is <4.0 mg/dL
Hypocalemia causes
• Dietary changes – lack of calcium intake (rare), inadequate
Vitamin D, inadequate protein intake, hypoalbuminemia*,
chronic diarrhea
• Hormone and electrolyte influence – decreased PTH (thyroid
surgeries), increased serum phosphorous, decreased
magnesium
• Calcium Binders or Chelators - citrated blood transfusions
• Alkalosis
• Increased serum albumin* (low ionized Ca)
• Renal Failure – decreases phosphorous excretion and results
in excessive Ca Loss
• GI Surgery, Pancreatitis and Small Bowel disease
Calcium Excess - Levels >10.5 mg/dL
and Ionized Ca is >5.0 mg/dL
Hypercalemia causes
• Primary hyperparathyroidism
• Bone malignancy, fractures and immobility
• Drug toxicity (lithium carbonate, vitamin a and d,
thiazides)
• Excessive use of calcium supplements, anti-acids
and calcium salts
• Renal Impairment and diuretics (thiazides)
• Steroid therapy
• Decreased serum phosphorous
Clinical Manifestations of Calcium
Imbalances
HYPOCALCEMIA
• CNS and Muscular
–
–
–
–
–
–
Anxiety, irritability
Tetany, muscle twitching (Chvostek’s sign)
Numbness and tingling
Carpopedal spasm (Trousseau’s sign)
Convulsions
Abdominal and muscle cramps
• Cardiac
– Weak contractions
– ECG/EKG lengthened ST segment and
prolonged QT interval
• Blood
– reduction in prothrombin (reduced
clotting)
• Bone
– With prolonged deficiency – fractures
occur easily
HYPERCALCEMIA
• CNS and Muscular
– Depression/apathy
– Weak, flabby muscles
• Cardiac
– Signs of heart block
– Cardiac arrest in systole
– Decreased or diminished ST
segment and shortened QT interval
• Bone
– Pathologic fracture
– Deep pain over bony areas
– Thinning of bones
• Renal
– Flank pain
– Calcium stones in kidney
Important Clinical tests for
Hypocalemia
Chvotsek’s Sign
• https://www.youtube.com/
watch?v=ep6IEqnyxJU
Trousseau’s Sign
• https://www.youtube.com/
watch?v=H13yn9AwtPY&fe
ature=relmfu
ECG changes with Calcium Imbalances
• Normal ST segment and
QT Interval
• Hypocalcemia – ST
segment is lengthened,
QT interval is prolonged
• Hypercalcemia – ST
segment is shortened,
QT interval is shortened
Clinical Management of Calcium
Imbalances
Hypocalcemia
• Oral supplements and IV
calcium diluted in D5W (not
normal saline)
– IV calcium should be given
slowly at 1-3ml/min
• Vitamin D supplements
Hypercalcemia
• Treat underlying cause
• IV Normal Saline
• Loop Diuretics
• Calcitonin SQ
• IV phosphates
• Others:
– Corticosteroids
– Antitumor antibiotics
MAGNESIUM
Normal serum values
1.4- 2.1 mg/dL
• Intracellular Cation (2nd most)
• Only 1% of body magnesium is in the blood serum the rest is
stored in muscle and bone
• Of the 1% - 2/3 is ionized (free) and 1/3 is bound to plasma
proteins
• When calcium absorption goes up magnesium absorption goes
down
• Alcohol decreases magnesium absorption
• Many of the same foods rich in potassium and also rich in
magnesium (green vegetable, whole grains, fish, seafood and
nuts).
• Mg deficiency is usually asymptomatic until <1.0 mg/dL
Functions of Magnesium
• Neuromuscular activity transmission
• Contracts the heart muscle
• Cellular
– Activates enzymes for carbohydrate and protein
metabolism
– Responsible for proper transportation of sodium and
potassium across cell membranes
– Influences utilization of K, Ca, and proteins
– Magnesium deficits are FREQUENTLY accompanied by
a Potassium and/or Calcium deficit
Magnesium deficit < 1.4 mg/dL
Hypomagnesemia Causes
• Dietary – inadequate intake, mal absorption, GI losses,
TPN, malnutrition, starvation, chronic alcoholism, GI
fistulas, chronic use of laxatives, chronic diarrhea
• Renal Dysfunction – diuresis in diabetic ketoacidosis
and in ARF in the diuretic phase
• Cardiac dysfunction – post MI, prolonged diuretic
therapy with CHF
• Electrolyte and Acid/Base Influences – hypocalcemia,
hypokacemia, metabolic alkalosis
• Drug influence – potassium wasting diuretics,
aminoglycosides, cortisone, amphotericin B, digitalis
Magnesium excess > 2.1 mg/dL
Hypermagnesemia Causes
• Dietary – prolonged use/excessive use of
magnesium-containing anta-acids (Maalox),
laxatives (MOM) and IV magnesium sulfate
• Renal Dysfunction – Renal insufficiency and
failure
• Severe Dehydration – Diabetic ketoacidosis
Clinical Manifestations of Magnesium
Imbalances
Hypomagnesemia
• Neuromuscular –
hyperirritability, tetany-like
symptoms, tremors,
twitching of the face,
spasticity, increased tendon
reflexes
• Cardiac – Hypertension,
cardiac dysrhythmias PVC’s, VT (Torsades), VF, and
flat or inverted T wave, ST
depression (like low K levels)
Hypermagnesemia
• Neuromuscular – CNS
depression, lethargy,
drowsiness, weakness,
paralysis, loss of deep tendon
reflexes
• Hypotension, Complete heart
block (3rd degree), bradycardia,
Widened QRS complex,
prolonged QT interval
• Others: Flushing, respiratory
depression
Hypomagnesemia
Clinical Management of Magnesium
Imbalances
Hypomagnesemia
• Oral or IV replacements
• Diet high in magnesium green vegetables, whole
grains, legumes, nuts
Hypermagnesemia
• Correct the underlying
cause
• IV saline or calcium
• Dialysis
Phosphorous
Normal levels
2.5 – 4.5 mg/dL
• Major Intracellular anion
• Needed for metabolism, nerve and muscle
function
• Part of energy units
• Component of phospholipids (cellular and
organelle membranes)
• Regulated by calcitonin, parathyroid hormone
AND Vitamin D
• Levels vary with acid-base balance
• Glucose, insulin or sugar-containing foods
temporarily shift phosphorous into the cells
Functions of Phosphorous
• Neuromuscular – normal nerve and muscle activity
• Bones and teeth – bone and teeth formation,
strength and durability
• Cellular
– forms high energy compounds (ATP, ADP, AMP), is the
backbone of nucleic acids and stores metabolic energy
– Formation of red blood cell enzyme (2,3diphosphoglycerate) that delivers oxygen to tissues
– Utilization of B vitamins
– Metabolism of fats, carbohydrates and proteins
– Maintenance of ACID BASE balance in body fluids
Phosphorous deficit < 2.5 mg/dL
Hypophosphatemia Causes
• Dietary - Vitamin D deficiency, chronic
alcoholism TPN
• GI – malabsorption, vomiting, diarrhea
• Hormonal Influence – Hyperparathyroidism
(increased PTH)
• Drugs – aluminum containing antacids (binders),
diuretics
• Cellular – Diabetic Ketoacidosis
• Acid-Base disorders – Respiratory alkalosis,
metabolic alkalosis
Phosphorous excess > 4.5 mg/dL
Hyperphosphatemia Causes
• Dietary – excessive administration of
phosphorous containing substances
• Hormonal – lack of PTH
• Renal Insufficiencies – Renal Failure (ARF, CRF)
• Drug – frequent use of phosphate laxatives
• Cellular destruction – chemo, radiation,
rhabdomyolsis (breakdown of striated muscle)
• Acid-Base disorders – Metabolic and Respiratory
Acidosis
Clinical Manifestations of Phosphorous
Imbalances
Hypophosphatemia
•
•
•
•
Hyperphosphatemia
Neuromuscular – muscle
• Neuromuscular – Tetany (with
weakness, tremors,
decreased calcium),
paresthesia, bone pain,
hyporeflexia, seizures,
hyperreflexia, muscular
delirium, hallucinations,
weakness (more common with
ascending motor paralysis
hypophosphatemia), flaccid
Hematologic – tissue hypoxia,
paralysis
possible bleeding, possible
infection
• Cardiopulmonary –
Cardiopulmonary – weak
tachycardia
pulse, hyperventilation,
respiratory weakness
• GI- nausea, diarrhea,
GI – Anorexia, dysphagia
abdominal cramps
Clinical Management of Phosphorous
Imbalances
Hypophosphatemia
• Oral phosphorous
replacements
• Treat underlying causes
• Diet high in phosphorous
• Avoid phosphorous binding
antacids
• IV phosphorous (only when
levels are below 1 mg/dl)
dose 12-15 mmol/L diluted
in IV fluid
Hyperphosphatemia
• Phosphorous binding antacids
• Calcium based antacids are
preferred in renal failure to
avoid hypermagnesemia
• If hyperphosphatemia is
accompanied by hypocalcemia
correcting calcium level will
reduce phosphorous levels
• Administer Insulin and glucose
ACID BASE IMBALANCES
NURS 2140
Winter 2012
Teresa Champion, RN, MSN
ACID BASE BALANCE
• Hydrogen ions - Low concentrations but highly
reactive
– Concentration affects physiological functions, for
example:
• Alters protein and enzyme functioning
• Can cause cardiac, renal, respiratory abnormalities
• Alters blood clotting, metabolization of meds
Acid and Bases
• Acids – compounds that form hydrogen ion in a
solution
– Proton donors
– Strong acids give up their hydrogen ion easily
– Weak acids hold on to their hydrogen ion more tightly
• Bases – compounds that combine with hydrogen
ion in a solution
– Proton acceptors
– Neutralizes
• 20:1 ratio (20 parts bicarbonate to one part
carbonic acid)
The Basics explained:
• pH is a measurement of the acidity or alkalinity of
the blood.
• It is inversely proportional to the number of
hydrogen ions (H+) in the blood.
– The more H+ present, the lower the pH will be.
– The fewer H+ present, the higher the pH will be.
Plasma pH
• Inversely related to hydrogen ion
concentration
– ↑ hydrogen ion concentration, ↓ pH
– ↓ hydrogen ion concentration, ↑ pH
Body Acids
• Respiratory Acid - CO2 – eliminated by lungs (daily
~288L/day)
• Metabolic acids: (either excreted by kidney or
metabolized in liver and Production: 0.1 mol (100
mEq)/day. Eliminated more slowly than respiratory acid
–
–
–
–
–
Lactic acids
Pyruvic acid
Ketoacids (DKA)
Acetoatic acids
Beta-hydrobutyric acids
Normal Blood pH
• The normal blood pH range is 7.35 to 7.45.
– Slightly alkalotic
– Must maintain this range for normal body
functions
• < 7.35 Blood pH is acidotic
• > 7.45 blood pH is alkalotic
• This is the FIRST step in interpretation of
Arterial Blood Gases and plasma pH.
BUFFER SYSTEMS
• Extracellular Buffers
– carbonic acid (lungs) and bicarbonate (kidneys)
• Intracellular Buffers
– Phosphate Buffer System
• Dihydrogen phosphate (H2PO4) – hydrogen donor
• Hydrogen phosphate (HPO4) – hydrogen acceptor
• Protein Buffers
– Plasma Proteins
– Hemoglobin – oxyhemoglobin and deoxygenated Hgb
• Bones
– Carbonate and phosphate salts in bone provide a long term
supply of buffer.
Role of the lungs
• Regulate plasma pH minute to minute by
regulating the level of Carbon Dioxide (CO2)
• Carbon Dioxide is measured as a partial
pressure of carbon dioxide in arterial blood –
PaCO2 35-45mmHg
• Lungs alter rate and depth of ventilations in
order to retain or excrete CO2
Minute Volume – Tidal Volume
• Ventilation is measured by how much air the lungs
move in one minute (minute ventilation)
• Minute Ventilation is the product of respiratory rate
and depth and is referred to as the TIDAL VOLUME
(Vt)
• NORMAL tidal volume at rest is about 500ml.
• Aveolar volume = tidal volume – anatomical dead
space
• Aveolar minute ventilation = respiratory rate x
alveolar volume
Terms for Respiration
• Hypercarbic Drive – increased PaCO2 levels raise
the level of H+ ions, lowering pH. Central
Chemorectptors (in CNS) stimulate the phrenic
nerve, increasing respiration
• Hypoxic Drive – peripheral chemoreceptors in
carotid arteries and arch of aorta are stimulated
by low PaO2 level (<60mmHg) increasing
respiratory rate.
• Hypocapnia – Low PaCO2 (<35)
• Hypercapnia – High PaCO2 (>45)
The role of the Kidneys
• Two main functions to maintain acid/base
– Secrete hydrogen ions
– Restore or reclaim bicarbonate
• Secretion – active process of moving substances from
blood into the tubular fluid against a concentrated
gradient, for example hydrogen ions.
• In high metabolic acidosis, the kidneys can excrete
ammonia as a urinary buffer.
• In alkalosis - the kidneys retain hydrogen ion and
excrete bicarbonate to correct the pH.
• In acidosis - the kidneys excrete hydrogen ion and
conserve bicarbonate to correct the pH.
Assessment of ACID BASE
• Arterial Blood Gases (ABG) most often and the most
accurate to assess acid base balances.
• Serum Electrolytes can help fine tune acid base
analysis
• NORMAL ABG VALUES:
• pH = 7.35 to 7.45
• PaCO2 = 35 – 45 mEq/L (7.40 mEq/L – middle range)
• HCO3 = 22 – 28 mEq/L
Steps to Interpret ABG’s
1. Assess the pH
2. Assess the respiratory component – PaCO2
3. Assess the metabolic component – HCO3,
base excess
4. Evaluate compensation
Respiratory Acidosis
• High PaCo2 (>45 mEq/L) with resultant drop in
in pH (<7.35 - acid)
• Respiratory system fails to eliminate the
appropriate amount of carbon dioxide to
maintain the normal acid-base balance
• Caused by pneumonia, drug overdose, head
injury, chest wall injury, obesity, asphyxiation,
drowning, or acute respiratory failure
• Medical treatment
– Improve ventilation, which restores partial pressure
of carbon dioxide in arterial blood (Paco2) to normal
Respiratory Acidosis
• Nursing care
– Assess Paco2 levels in the arterial blood, and pH.
– Observe for signs of respiratory distress:
restlessness, anxiety, confusion, tachycardia
• Intervention
– Encourage fluid intake
– Position patients with head elevated 30 degrees
Respiratory Alkalosis
• Low PaCO2 (< 35 mEq/L) with a resultant rise in pH
(>7.45 – alkalotic)
– Most common cause of respiratory alkalosis is
hyperventilation – usually caused by pain, anxiety
• Medical treatment
• Major goal of therapy: treat underlying cause of condition; sedation
may be ordered for the anxious patient
• Nursing care
– Intervention
• In addition to giving sedatives as ordered, reassure the patient to
relieve anxiety
• Encourage patient to breathe slowly, which will retain carbon dioxide
in the body
Metabolic Acidosis
• Body retains too many hydrogen ions or loses too
many bicarbonate ions; with too much acid and
too little base, blood pH falls (pH <7.35)
• Causes are starvation, dehydration, diarrhea,
shock, renal failure, and diabetic ketoacidosis
• Signs and symptoms: changing levels of
consciousness, headache, vomiting and diarrhea,
anorexia, muscle weakness, cardiac dysrhythmias
• Medical treatment: treat the underlying disorder
Metabolic Acidosis cont’d
• Nursing care
– Assessment of the patient in metabolic acidosis
should focus on vital signs, mental status, and
neurologic status
– Emergency measures to restore acid-base balance.
Administer drugs and intravenous fluids as
prescribed. Reassure and orient confused patients
Metabolic Alkalosis
• Increase in bicarbonate levels or a loss of hydrogen
ions and increases pH (>7.45)
• Causes:
– Loss of hydrogen ions may be from prolonged
nasogastric suctioning, excessive vomiting, diuretics, and
electrolyte disturbances
• Signs and symptoms:
– headache; irritability; lethargy; changes in level of
consciousness; confusion; changes in heart rate; slow,
shallow respirations with periods of apnea; nausea and
vomiting; hyperactive reflexes; and numbness of the
extremities
• Medical treatment
– Depends on the underlying cause and severity of the
condition
Metabolic Alkalosis
• Nursing care
– Assessment
• Take vital signs and daily weight; monitor heart rate, respirations,
and fluid gains and losses
• Keep accurate intake and output records, including the amount of
fluid removed by suction
• Assess motor function and sensation in the extremities; monitor
laboratory values, especially pH and serum bicarbonate levels
• Intervention
– To prevent metabolic alkalosis, use isotonic saline solutions
rather than water for irrigating nasogastric tubes because
the use of water for irrigation can result in a loss of
electrolytes
Infusion Therapy
NURS 2140
Winter 2012
Teresa Champion, RN, MSN
Infusion Therapy
• PARENTAL – the Gastrointestinal route
(alimentary route) is by-passed.
– Medications and solutions are delivered by
Intravenous (IV) routes
– Non-vascular routes - (i.e. - Subcutaneous
(SQ), Intramuscular (IM), Intraosseous
(IO), Intraspinal, or Intrathecal routes.
Vascular Access Device (VAD)
• Device or catheter introduced through the skin
and into the vascular network.
– Peripheral Vascular Access Devices (PVAD)
• Inserted in upper extremities and/or lower extremities
(per policy) – peripheral vasculature
– Central Vascular Access Devices (CVAD)
• Inserted into a Centrally or Peripherally Located Vein with
the tip residing in the vena cava
Vascular Access Devices (VAD)
• Terminology
– Bevel – the slant or angle at the end of the needle
• Insertion is Bevel up – facilitates puncture and
cannulation of the vascular lumen.
– Flashback chamber – small space in the hub of the
stylet that allows confirmation of the presence of
blood and indicated access to the vascular lumen
– Self-sheathing stylet - the needle to becomes
encased in a protective chamber upon removal
(Needle stick Safety and Prevention Act of 2000)
Images of IV Catheters
Needle Stick Prevention
Types of Peripheral Access Devices
•
•
•
•
Winged Steel
Over-the-needle Peripheral Short Catheters
Through-the-needle Peripheral Short Catheters
Midline Catheters
Peripheral Vascular Access Devices
(PVAD) –Peripheral-Short Catheters
• Most - < 7.5 cm (3.5 inches) in length and Gauge
(needle size) 25 (smallest) to 10 gauge (largest).
• Locations of insertion and length of insertion
time:
– Inserted in upper extremities mostly (lower
extremities - per policy) of adults patients.
– Pediatric patients – insertions are upper extremities,
occipital, superficial temporal, posterior auricular(ear)
and saphenous veins.
– Dwell times are 72 to 96 hours, in most cases.
Short Catheter Sizes
Common Peripheral IV Stick Sites
Winged Steel Infusion Set
• Winged Steel – flexible plastic attachments “wings”
that extend from either side of the steel needle to
facilitate insertion.
– Length – 3/8 to 1.5 inches
– Gauges – 19 to 27 gauge
• Attached to the needle is plastic tubing extending from
several inches to 12 inches with an adaptor attachment
on the end for infusion administration equipment.
• Now manufactured with safety sheaths.
• Complications – infiltration - due to needle rigidity
• Temporary / short term infusions < 4hours – supportive
devices – arm boards/splints
Figure 22.2 Winged steel infusion
set. Winged safety steel infusion
set.
Over-the-needle and Through-theneedle Peripheral Short Catheters
• OVER-THE-NEEDLE – MOST COMMON
– Hollow bore needle (stylet) – inserted through the
lumen of a flexible catheter – needle (stylet) is
then withdrawn as the flexible catheter is
advanced forward into the vein
• THROUGH-THE-NEEDLE
– Allows passage of a catheter through a steel
introducer – introducer needle is then withdrawn
from the vessel lumen-and then protected by a
cover or sleeve to prevent sheering or patient
injury
Through-the-needle short catheter
Complication-catheter shearing
Peripheral VAD - Midline
• Peripherally inserted but is approximately 7.5 cm to 20 cm
(3.1 inches to 8.0 inches)
• Longer dwell periods but not to exceed 4 weeks
• Insertion sites –
– Adults - antecubital fossa
– Pediatrics – antecubital fossa, saphenous, posterior auricular
(ear) superficial temporal
• Distal tip – dwells in basilic, cephalic, or brachial veins –
level with the axilla and distal to the shoulder
• Inserted using an introducer-once vein is canulated the
needle (stylet) is withdrawn and the midline catheter is
threaded though the introducer –then introducer is
peeled apart or separated and withdrawn.
• Therapies for midlines-restricted to pH 5-9, osmolarities of
<500mOsm/L
Peripheral IV Catheter
Insertion/Removal
• RN’s, LPN-C – trained in IV insertion using standard
precautions and aseptic technique, RN’s only may
be specially trained to insert midlines.
• RN’s. LPN-C and LPN – trained in IV removal using
standard precautions and aseptic technique
• Assess/observe for phlebitis, drainage-apply sterile
dressing till hemostasis is observed.
• Inspect cannula, for midline – length of catheter
should be measured and be same length as
insertion.
CENTRAL VASCULAR ACCESS DEVICE
(CVAD)
• Catheter inserted into a centrally located vein
with the tip in residing in the vena cava.
• Tip in vena cave must be confirmed with
radiologic examination (X-Ray)
• Three major CVAD Categories
– Nontunneled and noncuffed
– Tunneled and cuffed
– Implanted Ports
Nontunneled and Noncuffed CVAD
• Inserted percutaneuosly via direct skin puncture with passage
of catheter into the vasculature.
• Single or multiple lumens
• Indentified by insertion site (i.e. – Subclavian, Jugular,
Femoral)
• Inserted by physicians or advanced practice clinicians who are
skilled and competent to perform procedure (certified)
• Insertion requires – sterile technique and maximum barrier
precautions
• Complications – pneumothorax, air embolism, arrhythmias
• Once inserted secured – sutures, stat locks
• Catheters are not tunneled under the skin – less dwell times
than tunneled
• Examples – TRIPLE LUMEN NONCUFFED (ARROW), PICC LINES
Removal of Nontunneled and
Noncuffed CVAD’s (including PICC)
• May be done by a nurse skilled and education in the
procedure
• Standard precaution and aseptic technique
• Recumbent position (preferred)
• Removal of occlusive dressing and securing devices
• Instruct Patient to perform the valsalva maneuver to prevent air from entering – causing air embolism
• Pressure is applied 30 minutes to achieve
hemostasis and sterile occlusive dressing applied
• Post removal catheter length measured and
compared to insertion length (same)
Nontunneled noncuffed CVP – Triple
Lumen (Arrow)
Peripherally Inserted Central Catheter
(PICC)
• Nontunneled and non cuffed
• Long-term catheter – several weeks to one year.
• Therapies with extreme variations in solution pH (>5 and <
9) and osmolarities >600 mOsm/L with irritant and Vesicant
properties
• Therapies – Total Parental Nutrition (TPN), Antineoplastic,
Anti-infective and Inotropic
• Radiologic confirmation (X-Ray) required for tip location –
vena cava
• Complications – device fracture, tip malposition, device
occlusion, thrombus formation
• Removal – same as central insertion central venous access
devices
PICC vs. Midline
Tunneled and Cuffed CVAD
• Cuff – piece of the catheter for stabilization and
reduces migration of organisms
• Anti-thombogenic catheters
• Tunneled under the skin – reduces infection risk
• Inserted in surgical or radiologic suite
• Inserted by physicians, surgeons, vascular surgeons and
advanced practice clinicians trained in procedure
• Long term therapies
• Single or multi-lumens
• Examples: Broviac, Hickman, Raaf, Groshong
Implanted Ports
• Long term – chronic therapies
• Chambered device, double or single reservoirs with an
attached single or double lumen catheter
• Catheter tip dwells in a designated structure depending on
therapy – could be vascular or non-vascular (CVAD PORTS –
Vena Cava)
• Inserted by physicians, surgeons, vascular surgeons and
advanced practice clinicians trained in procedure in a
surgical or radiological suite
• The septum is the access point-damage to the septum could
cause air embolism, infiltration, extravasion, infection
• Access of septum of port requires a noncoring (Huber
needle) needle with opening on the side and preventing
coring of the septum
• Therapies – antineoplastics, inotropics, TPN, Antibiotics
Additional Info on VAD’s
• Tunneled and cuffed and Implanted port removal
only by physicians, advanced clinicians trained in
procedure and not included in the scope of
practice for nurses
• CVP – Central Venous Pressure Monitoring on
CVAD
• CVAD – Lines flushed and patency checked q shift
with 10ml of Normal Saline (Heparin per
institution) whereas PVAD’s are flushed and
checked for patency q shift with 3-5 ml Normal
Saline.
SPECIALIZED INFUSION CATHETERS
•
•
•
•
•
Hemodynamic Monitoring – Swan Ganz
Dialysis and Pheresis Catheters
Arterial – Venous Shunts
Arterial Catheters
Hepatic Artery Catheters
Swan-Ganz Catheter
• Exclusively for cardiac monitoring and
hemodynamic analysis
• Used to measure
– Central Venous Pressure (CVP)
– Pulmonary Artery Pressure (PA)
– Cardiac Output (CO)
– Pulmonary Artery Wedge Pressure (PAWP)
– Temporary Pacing
– Parental Therapy Administrations
Swan-Ganz Catheter
Hemodialsys and Pheresis Catheters
• RARELY considered for infusions
• Used for procedures using large amounts of blood –
Dialysis, Plasmapheresis, Aquapheresis
• Dialysis Catheters – temporary till a shunt can be placed
• Catheters are large (12 to 16 G) for blood to flow in both
directions on dialysis or pheresis machine, dwell in the
vena cava
• Surgical Placement – OR, Radiological suite or at bedside
by vascular or general surgeon or advanced practice
clinician trained in procedure
• Examples – Quinton, Hohn, Tesio, Perma-Cath, and
Trialysis* *(Trialysis-can be used for infusions)
Dialysis and Pheresis Catheters
Arterial-Venous Shunts
•
•
•
•
•
•
Anastomose venous and arterial structures
Arm – radial and cephalic and brachial veins
Dialysis or large blood volume exchanges
Accessed with large bore needle
Can be used for other infusion- rare
Patency assessed by auscultation bruit and
palpating vibration
• No IV sticks, phlebotomy or Blood Pressure on
Arm with AV Shunt
• If AV shunt is damaged – only surgical repair or
replacement is the option
AV Shunt and AV Graft
Arterial Catheters
• Used for ONLY two reasons:
– Invasive Blood Pressure Monitoring
– Blood Draws
• Catheters are made of stiff polyurethane material
to withstand the high pressure of the artery and
blood pressure monitoring attached to pressure
transducers and monitor, and to limiting kinking
of line.
• Inserted in Radial or Femoral Arteries
• Inserted by physician or advanced practice
clinician in OR, or Radiological suite or at
bedside.
Arterial Catheter
Hepatic Artery Catheters
• Specialized Catheter Inserted in Hepatic Artery
• Only for regional anti-neoplastic therapy for
Liver Cancer Patients
Hepatic Artery Catheter
NONVASCULAR ACCESS DEVICES
•
•
•
•
Subcutaneous Infusion Therapy
Intraosseous Therapy
Intraspinal Catheters
Intrathecal Therapy
Subcutaneous Infusion Therapy
• Hypodermoclysis – infusing large amounts of isotonic
solutions in the subcutaneous to be absorbed
• Continuous Subcutaneous Infusion – infusing small amounts
of medications like pain medications and insulin
• Use very small gages of 25-27G and only ½ inch in length
• Needle attached to a adhesive disk of may appear as a
winged steel infusion set
• May be inserted by a nurse in locations of adequate
subcutaneous tissue
• Site is prepared with antiseptic agent, allowed to dry and
then aspirated to confirm absence of blood
• Device is then secured with sterile dressing
• Complications – localized skin irritation, erythemia, itching,
infection and dislodgement of device
Subcutaneous Infusion Pump
Intraosseous therapy
• Insertion of hollow bore needle into the bone
accessing the marrow space
• Screws into long bones of the leg, iliac crest or
sternum
• Allows for rapid infusions of large volumes of
fluids
• Complications – bone fracture, infiltration,
osteomyelitis, cellulitis, occlusions, or needle
breakage
• Ideal for patients with difficult venous access
• Being used more by EMT, Paramedics
INTRAOSSEOUS
Intraspinal Catheters
• Catheters inserted within the spinal spaces – epidural and
intrathecal
• Delivery of anesthesia and infusions
• Diagnostic testing
• 22 to 26 Gauge, 10 to 30 inches in length
• Catheter inserted percutaneously or tunneled
• Infusates, drugs and diluents must be preservative free due to
neurotoxic effects
• Epidural space usually cannot accommodate infusion rates greater
15ml/min
• Cross the dura mater and have direct effect on the CNS
• Complications: malposition and infection
• Sterile technique required
• Usually inserted by anesthesiology or neurology
Intrathecal Therapy
• Administration of medications directly into the
Cerebral Spinal Fluid via an implanted reservoir
• Catheter dwells (terminates) in the ventricular
space of the cerebrum
• Ommaya Reservoir
–
–
–
–
–
–
Delivers preservative free opioids
Antineoplastics
Measures CSF pressures
Drains excess CSF
Obtaining CSF samples for Lab
Surgically places via burr hole in the skull and skin
secured over the device
– Standard precautions and sterile technique
INFUSION DELIVERY
Fluid Containers
• Glass
– Can be heavy
– Requires venting
– Accurate to measure
• Plastic
– Portable, easy to store, inexpensive
– Flexibility may cause volume and dosage
administration to vary
Administration Sets
• The tubing that delivers fluid from the
container to the catheter
• Primary set = main tubing
• Secondary set = tubing that attaches to the
primary set (piggy backed on the primary set)
• Metered-Volume Chambered Set – neonates
and pediatric patients and critical care units
for close observation and monitoring with
fluid control issues
Primary set with
Secondary (Piggy back Set)
Add On Devices
– Flow-control device – controls flow when used
with gravity IV set
– Stopcocks – manually directs flow
– Extension sets – adds length to tubing, provides
additional stopcocks, access sites
– Multi-flow adaptors and Y sets – multiple access
on one catheter
– Injection ports, caps or hub – sites for IV catheter
access
– Filters – remove particulate, precipitate
ADD ON DEVICES
Flow Control Device
Stopcock
Add On Devices
Extension Set
Multiflow Adaptor
Odd On Devices
Injection Port or Cap
Filter
INFUSION DELIVERY DEVICES
• Mechanical infusion devices (MIDs)
–
–
–
–
Do not require an external power source to operate
Elastomeric Balloons (On Q)
Spring coil containers
Spring Coil Syringes
• Electronic infusion devices (EIDs)
– Do require an external power source
– Two types: pumps (positive pressure) and controllers
(gravity and drop sensors attached to drip chamber)
Positive Pressure Infusion Pumps
•
•
•
•
Pressure to overcome vascular resistance
Strict monitoring of medications, fluids
Accurate delivery
PUMP TERMS:
– RATE (R) – amount of ml/hr
– Volume to be infused (VTBI) – volume of infusion
– Volume Infused (VI) – volume that has already been infused
(Used when calculation I&O)
• Alarms:
–
–
–
–
–
AIR IN LINE
OCCLUSION (patient side or pump side)
INFUSION COMPLETE
FREE FLOW
OTHER – LOW BATTERY, DOOR OPEN, PUMP Malfunction
Patient Controlled Analgesia Pumps
(PCA)
• Delivers analgesia medications continuously
(basal rate)
• Delivers analgesia bolus on patient demand
(PCA Mode)
• Time lockout and Maximum Dose settings for
safety
IV SKILLS FOR NURSES
• Nursing skills:
– Basic competencies
– Clinical skill validation
– Policies and procedures – regulatory and nonregulatory agencies
• Nurses must be knowledgeable about the
properties of drugs and solutions ordered by
the prescriber
• Compatibilities
• Rates of Administration
Infusion Practices
• Flow rate determination is used to calculate the
amount of fluid to be delivered over a specific
time period (Calculation: flow rate x gtt factor /
60 (time in minutes) for gravity sets.
• Safe nursing practices when calculations are
consistently applied result in:
– Fewer medication errors
– Increased patient safety
– Positive infusion outcomes
• Smart Pumps – does calculations and keeps a
drug library
Infusion Therapy Orders
• Nurses obtain orders from a health care
provider to initiate and discontinue infusion
therapy. An order includes:
– Type of medication or solution
– Dose
– Volume to be infused
– Duration of therapy
– Frequency, rate, and route of administration
– Five rights
Informed Consent
• An informed consent must be obtained from
the patient
• The nurse provides the patient with accurate
and complete information:
– Description of the procedure
– Potential benefits of such a device
– Possible risks associated with the procedure
– Available alternatives
Infusion Documentation
• Accurate documentation describes the care
rendered and the patient’s response
• It facilitates monitoring care and tracking
outcomes
Managing Infusion Complications
Complication categories:
• Local complications: Bruising, Infiltration,
Extravasation, Phlebitis, Thrombosis,
Infection, Occlusion
• Systemic complications: Air embolism,
Catheter embolism, Pulmonary edema,
Septicemia, Allergic reactions, Needle stick
complications