FLUID AND ELECTROLYTE BALANCE

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Transcript FLUID AND ELECTROLYTE BALANCE

FLUID
AND
ELECTROLYTE
BALANCE
HOMEOSTASIS



Normal hydration balance
– Intake equals output
» Quantities of water and electrolytes entering
body are equivalent to quantities exiting
Intake
– All water entering into body
» Digestive system (liquids, solids, metabolic
sources)
Output
– All water excreted from the body
» Lungs, kidneys, skin, intestines
HOMEOSTASIS (CONT.)



Maintaining a constant stable internal environment
Fluid levels decrease:
– ADH secreted
– Kidney tubules reabsorb more water back into
blood and excrete less urine
– Thirst sensation stimulates one to drink
– Restoration of fluid volumes to normal values
Fluid levels rise
– Kidneys activated to excrete more urine
– Water shifts from one compartment to another
maintaining balance
BODY WATER





Most abundant substance in human body
– 60% of total body weight in adult male
– 52% of total body weight in adult female
Acts as universal solvent for bodily solutes
Solvent
– Fluid in which another substance will dissolve
Solute
– Substance that is dissolved in a solution
Solution
– Liquid containing dissolved substances
FLUID COMPARTMENTS

Two major fluid compartments
– Intracellular fluid compartment
» Includes all water (and electrolytes) enclosed
by cell membrane
» Constitutes 75% of all body water
» 40-45% of body weight
– Extracellular fluid compartment
» Composed of all fluids found outside of the
cell
» Constitutes 25% of all body water
» 15-20% of body weight
FLUID COMPARTMENTS
(CONT.)

Divisions of extracellular fluid compartment
– Interstitial fluid
» Fluid between the cells and outside of the blood
vessels
» Constitutes 17.5% of extracellular fluid
– Intravascular fluid
» Fluid found within circulatory system
» Water within blood vessels
» Constitutes 7.5% of extracellular fluid
FLUID COMPARTMENTS
(CONT.)

Transcellular fluid
– Specialized fraction of extracelluar fluid
– Seperated from other extracellular fluids by
layer of epithelium
– Includes:
» Cerebrospinal fluid
» Intraoccular fluid
» Synovial fluid
» Serous fluid within body cavities
DEHYDRATION
Definition
– Loss of water and electrolytes
 Etiology:
– Gastrointestinal losses
»Vomiting
»Diarrhea
»Malabsorption disorders

DEHYDRATION
(CONT.)

Etiology:
– Increased insensible loss
»Fever
»Hyperventilation
»High environmental temperatures
– Increased sweating
»Medical conditions
»High environmental temperatures
DEHYDRATION (CONT.)

Etiology:
– Internal losses
» Third spacing
» Peritonitis, Pancreatitis, Bowel obstruction
» Poor nutritional states
– Plasma losses
» Burns
» Surgical drains
» Fistulas
» Open wounds
DEHYDRATION

Management
– Ensure adequate airway
and ventilation
– Administer oxygen and
monitor delivery with
oximetric monitoring
– Monitor cardiac rate and
rhythm
– Establish IV isotonic
crystalloid solution
» LR/NS
» 100-200ml/hr
» Fluid challenge
Edema


Edema is the accumulation of water in the interstitial
space due to disruption in the forces and mechanisms
that normally keep net filtration at zero.
Mechanisms of edema
–
–
–
–
A decrease in plasma oncotic force
An increase in hydrostatic pressure
Increased capillary permeability
Lymphatic channel obstruction
Edema

Can be local or within a certain organ system
– Sprained ankle vs. pulmonary edema


May be generalized
Water in interstitial spaces is not available for metabolic
processes in the cells.
OVERHYDRATION
Clinical Presentation
– Peripheral edema
– Heart failure
– Pulmonary congestion
 Management
– Remove excess fluid
– Diuretic therapy

ELECTROLYTES

General Information
– Substance that dissociate into charged particles
when placed in water
– Ions
» Molecules that possess a positive or negative
charge
» Total number of positve ions equals total number
of negative ions
 Electrical neutrality law
» Cations have positive charge
» Anions have negative charge
» Electrolytes measured in milliquivalents per liter
(mEq/L)
NONELECTROLYTES
Solutes that dissolve in water, but have
no electrical charge
 Nonelectrolytes do not release ions
 Solid molecules are usually measured in
grams and milligrams
 Examples:

– Glucose
– Amino acids
– Urea
ESSENTIAL CATIONS

Sodium (Na+)
– Most abundant extracellular cation
– Regulates water distribution
– Helps transmit nerve impulses
– Normal value: 135-148mEq/L
– Hypernatremia: elevated serum
sodium
– Hyponatremia: reduced serum sodium
ESSENTIAL CATIONS
(CONT.)

Potassium (K+)
– Most abundant intracellular cation
– Mediates electrical impulses in nerves and
muscles
– Helps transmit nerve impulses
– Normal value: 3.5-5.0mEq/L
– Hyperkalemia: elevated serum potassium
– Hypokalemia: decreased serum potassium
ESSENTIAL CATIONS
(CONT.)

Calcium
– Most abundant cation
– Function:
» Bone development
» Blood clotting
» Muscular contraction
» Aids in nerve impulse transmission
– Normal value: 8.5-10.5mEq/L
– Hypercalcemia: elevated serum calcium
– Hypocalcemia: decreased serum calcium
ESSENTIAL CATIONS
(CONT.)

Magnesium (Mg+)
– Necessary for biochemical functions
– Coenzyme in protein and carbohydrate
metabolism
– Aid in transport of sodium and potassium
across cell membranes
– Normal value: 1.3-2.1mEq/L
– Hypermagnesemia: elevated serum
potassium
– Hypomagnesemia: reduced serum potassium
ESSENTIAL ANIONS


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Chloride (Cl-)
– Regulates fluid balance and renal function
– Follows sodium
– Participates in acid/base balance
– Normal value: 98-106mEq/L
Bicarbonate (HC03-)
– Chief buffer in body
– Neutralizes hydrogen (H+) ion and other organic acids
– Normal value: 21-25mEq/L
Phosphate (HP04-)
– Important for energy stores
– Intracellular buffer, aids renal function
Dispatch Information

Your paramedic rescue is dispatched to a bus stop for
a reported “sick person.”
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Initial Impression
46 y/o female
 Sitting on bench
 Appears weak, looks
“ill”
 Pale, dry skin

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Assessment

Your partner performs a verbal assessment, as you
take vital signs.
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Assessment
Patient states that she has been ill for the past week
and has missed dialysis three times.
 She was on her way to the dialysis center when she
felt “too weak to continue.”
 Vital signs:

–
–
–
–
HR = 102
RR = 22 regular
BP = 156/110
SpO2 = 97% room air
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Discussion

Considering the limited information you have, what
is at the top of your differential diagnosis?

What additional information would you like to
have?

What are your immediate concerns?
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Assessment/Treatment


The patient is placed on O2
via nasal cannula at 4 Lpm.
You and your partner assist
the patient to the stretcher
and move her to the
ambulance.
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Assessment

Patient states past medical history of:
– Hypertension
– Renal failure
» Dialysis 3X week

Medications
– Verapamil (Calan, Isoptin)

No known drug allergies
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Detailed Assessment


PEARL
Lung sounds
– Rales/Crackles to the bases
bilaterally



Positive pitting edema to
periphery
Noticeable ascites
Muscle weakness to
extremities
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Detailed Assessment

You place the patient on the cardiac monitor.
Figure 3.5-1
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Treatment/Assessment

IV access
– 20 g angiocatheter
– 1000 mL bag of normal
saline
– Macrodrip set
» Keep vein open

Blood glucose
– 172 mg/dL
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Detailed Assessment

You and your partner prepare the patient for a 12Lead ECG.
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Detailed Assessment
Interpretation?
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Discussion

How has the information provided affected your
differential diagnosis?

What information strongly suggests the presence of
hyperkalemia?

Do paramedics carry medications that can be used
for the treatment of hyperkalemia?
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Treatment
Your partner begins transport to the ED.
 You contact medical control and inform the
receiving physician of your findings.

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Treatment

ED attending agrees with your suspicion of
hyperkalemia and orders you to administer:
–
–
–
–
CaCl2: 5–10 mL IV
50 mEq of sodium bicarbonate
1 mg/kg of lasix
Albuterol 1 unit dose
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Discussion

How do the administration of these medications
help the hyperkalemic patient?
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Treatment

You administer the medications as ordered.
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Ongoing Assessment

Vital signs after
medication
administration
–
–
–
–
HR = 102
RR = 22 regular
BP = 154/102
SpO2 = 99% now on 10
Lpm via albuterol mask
inhalation
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ED Treatment and Beyond
ALS continued
 Blood chemistry

– Acidosis present

Blood labs
– Potassium returns 7.6 mEq/L
Patient immediately dialyzed
 Admitted for observation

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Epidemiology
In U.S. hyperkalemia is diagnosed in up to 8% of
hospitalized patients.
 Mortality rate for severe hyperkalemia is as high as
67% if not treated rapidly.

– Primary cause of death is impaired cardiac function.
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A & P Review
Potassium is an important ion.
 98% of potassium (K+) in body is
intracellular.

– Ratio of intracellular to extracellular K+ is
important in creating cellular membrane
potential.
– Small changes in extracellular K+ can have
profound effects on cardiovascular and
neurological function.
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A & P Review
Cardiac depolarization possible because of
concentration gradients that exist between
intracellular and extracellular K+ and
sodium (Na+)
 This electrical and concentration gradient
maintained by the Na+/K+-ATPase
exchange pump

– Pump controlled by insulin and -2 receptors
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A & P Review

Na+/K+-ATPase pump
– Moves 3 Na+ out for every
2 K+ in
– Creates:
» Chemical concentration
gradient
» Electrical concentration
gradient
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Figure 3.5-3
A & P Review

Action potential in cardiac muscle cells
– Polarization (resting potential)
» Na+/K+-ATPase creates chemical and electrical
gradients across myocardial cell membrane.


More K+ inside, more Na+ outside cell
Greater positive charge outside, greater negative charge
inside cell
» Resting, or membrane, potential of myocardial cell
about -90mV
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A & P Review

Action potential in cardiac muscle cells
– Depolarization (action potential)
» Stimulus results in change of resting potential and
depolarization
» Initially, Na+ fast channels open, allowing Na+ ions
to rush into cell


Inside of cell rapidly becomes more positive, about +30
mV
Na K pump starts pumping Na out of cell
» Na ion channels close, Ca+ slow channels open,
increasing intracellular Ca+, roughly balancing the
loss of + sodium ions.
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A & P Review

Action potential in cardiac muscle cells
– Repolarization
» Slow Ca+ channels close, slow K+ channels open
» + Potassium ions move out of cell, resulting in rapid
repolarization and restoration of resting potential to
-90 mV
– After repolarization, Na+/K+-ATPase pump
begins exchanging the extracellular K+ for
intracellular Na+
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A & P Review

Action potential in cardiac muscle cells
– Refractory period
» Period between depolarization and repolarization where
myocardial membrane will not respond to another stimulus
– Relative refractory period
» Strong enough stimulus can result in depolarization.
» Adequate K+ and Na+ ions have been exchanged to allow
depolarization.

Gradients have been reestablished.
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A & P Review
Fig 3.5-4
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A & P Review

Myocardial electrical conduction system
does not have the Ca+ influx typical of
myocardium action potential.
– No “plateau”
– Shorter absolute refractory period
– Allows for rapid discharge rates
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A & P Review
Total body K+ stores approximately 50
mEq/kg
 Normal serum K = 3.5–5.0 mEq/L

– Serum K+ via blood chemistry used to
determine presence of hyperkalemia
– Hyperkalemia defined as serum K+ > 5.5
mEq/L
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Pathophysiology

Causes of hyperkalemia:
– Decreased excretion
» Renal failure: most common cause
» K-sparing diuretics
» Urinary obstruction
» Addison disease
» Sickle cell disease
» Lupus
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Pathophysiology

Causes of hyperkalemia:
– Extracellular shift of K+
» Acidosis
» Cell necrosis
» Insulin insufficiency
» Medication effects



Digitalis toxicity
Succinycholine
-blockers
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Pathophysiology

Causes of hyperkalemia:
– Additions into extracellular space
» Hemolysis




Venipuncture
Blood transfusion
Burns
Tumor lysis
» Increased intake


IV, PO administration
Rarely a cause of hyperkalemia
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Pathophysiology
Resting membrane potential related to ratio
of intracellular:extracellular K+
 Hyperkalemia partially depolarizes the cell
membrane and altered cellular function

– Cardiac muscle cells: dysrhythmia
– Neurons: altered mental status
– Skeletal muscle cells: weakness
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Pathophysiology
Cardiac toxicity is the most serious effect of
hyperkalemia and does not necessarily correlate with
serum levels.
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Clinical Assessment

History
– History of renal failure?
» Acute, chronic
– Other significant medical history?
» Addison’s, lupus, sickle cell disease, TI diabetes
– Medications?
» K supplements, K-sparing diuretics, -blockers, insulin, digitalis
– Recent trauma?
» Rhabdomyolysis, burns, tumors, venipunctures
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Clinical Assessment
Any patient with a history of renal failure who presents
with cardiac dysrhythmia should be considered
hyperkalemic until proven otherwise.
Especially if they’ve missed dialysis!
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Clinical Assessment

Signs and symptoms
– General malaise, weakness, paralysis,
paresthesias
– Palpitations
– Edema, skin changes typical of Addison’s,
lupus
– ECG changes
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Clinical Assessment

ECG changes in hyperkalemia
–
–
–
–
–
≥ 5.5 mEq/L: T wave abnormalities
≥ 6.5 mEq/L: intervals widen
≥ 7.0 mEq/L: P waves flatten, QRS widens
≥ 8.8 mEq/L: P waves disappear
≥ 10 mEq/L: sine wave pattern
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Clinical Assessment

Consider the following ECG:
Figure 3.5-5
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Clinical Assessment

Note:
– No P waves
– Wide QRS
Figure 3.5-6
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Clinical Assessment
Take-home point:
There are many other ECG changes associated with
hyperkalemia other than peaked T waves!
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Treatment

Three goals for treatment of hyperkalemia:
– Stabilize the myocardial membrane.
– Move K+ from the intravascular space to the
intracellular space.
– Remove K+ from the body.

Treatment is individualized, determined by
patient presentation, potassium level, and
ECG.
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Treatment

Ensure adequate oxygenation and
ventilation.
– High-flow, 100% oxygen
– BVM ventilation, intubation if necessary

IV access
– Large bore angiocatheter
– Withhold fluid administration in patients with
renal failure.
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Treatment

ECG monitoring
– Rule out dysrhythmia

12-Lead ECG
– Rule out AMI
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Treatment
Based on patient history, physical exam findings, and
ECG, medical control may order the administration
of specific medications available in most paramedic
formularies to achieve the three goals of treating
hyperkalemia.
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Treatment
Goal: stabilize the myocardial membrane.
 Administer calcium.

– CaCl2: 5–10 mL IV
» 27.2 mg Ca++/mL
– Ca gluconate 10–20 mL IV
» 9 mg Ca ++/mL

Ca++ potentiates the toxic cardiac side
effects of digitalis, withhold in suspected or
known dig toxicity!
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Treatment
Goal: promote an intracellular K+ shift.
 NaHCO3: 50–100 mEq IV

– Alkalosis, or correction of acidosis drives K+
intracellular

Insulin/glucose
– 10 units regular insulin
– 50 g glucose

Albuterol: 15–20 mg nebulized
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Treatment
Goal: promote excretion of K+
 Furosemide: 40 mg IV

– Only administer if patient can produce urine
– Not effective in cases of complete renal failure
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Treatment: Hospital
Continued airway maintenance and ventilation with
100% oxygen
 Cardiac monitoring
 12-Lead ECG
 Labs

– Serum potassium determination
– Digitalis levels, if appropriate

Blood chemistry
– Resolve acid-base disturbances
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Treatment: Hospital


Specific treatment, if not provided in field
Stabilize the myocardial membrane.
– Calcium

Promote an intracellular K+ shift.
– Sodium bicarbonate
– Insulin and glucose
– Albuterol

Promote K+ excretion.
– Furosemide
– Dialysis
– Kayexalate
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OSMOSIS

Definition and description
– Fluid compartments are seperated by semipermeable
membranes (pores)
– Semipermeable membranes
» Specialized biological membrane that surrounds cell
and encloses blood vessel walls
– Certain materials are allowed to pass through freely
» Oxygen
» Carbon dioxide
» Water
– Larger compounds are restricted
» Proteins
» Large sugars
OSMOSIS (Cont.)

Definition and description
– Movement of a solvent (H20) through a
semipermeable membrane from an
area of lesser (solute) concentration to
an area of greater solute concentration
in an attempt to equalize the
concentration on both sides of a
membrane
– Form of diffusion
OSMOSIS (Cont.)

Description
– If one side of membrane has a higher
solute concentrate than the other, a
pressure gradient exists (pulling force)
and water moves from the side of lower
concentration to higher concentration
until both sides are equal
– Concentration of water to solute
molecules should remain balanced on
both sides of membrane
OSMOTIC PRESSURE

Definition and description
– Pressure established as a result of unequal
solute concentration across a semipermeable
membrane

Osmotic pressure control
– Chief factor controlling water distribution
– Water moves toward the highest solute
concentration
– Sodium is most prevalent extracellular
cation exerting osmotic force
OSMOTIC PROPERTIES



Determined by number of particles in solution
– Not by weight or molecular charge
Greater number of solute particles in solution
– Greater osmotic pressure of that solution
– Greater difference of dissolved particles on
opposite sides of membrane
Osmolarity
– Concentation of osmotically active particles in
solution
– Measured in milliosmoles
– Plasma contains 300 milliosmoles/liter
COLLOID OSMOTIC PRESSURE
(ONCOTIC PRESURE)
Fraction of total osmotic pressure exerted
by colloids (proteins)
 Proteins are large molecules that do not
readily cross capillary walls or cell
membranes
 Colloid osmotic pressure is immensely
important in maintaining fluid within
vascular space
 Albumin/Chief plasma protein

TONICITY OF BODY FLUIDS




Definition Tonicity
– Number of particles present per unit volume
Isotonic solution
– Solution containing same concentration of
dissolved particles
Hypotonic solution
– Solution having a solute concentration lower
than that of bodily cells
Hypertonic solution
– Solution having a concentration greater than
that of bodily cells
ACTIVE TRANSPORT
 Movement
of molecules against a
concentration gradient
 Faster than diffusion
 Requires energy and utilizes
carrier molecules
 Example: Sodium/Potassium
pump
DIFFUSION


Definition and description
– Molecules or ions in solutions move from
regions of higher concentration to regions of
lower concentration until both sides of
membrane are equal
– Process results in uniform distribution of
diffusing substance
– Movement is opposite that of water movement
Facilitated diffusion
– Requires “helper proteins” to cross the
membrane
– Requires energy and must follow a gradient
– Example: Insulin/glucose relationship
Intravenous Therapy

The introduction of fluids and other substances
into the venous side of the circulatory system
– Replaces blood lost through hemorrhage
– Electrolyte or fluid replacement
– Introduction of medications directly into the vascular
system
Blood and Blood Components

Plasma
– Mostly water with
proteins and other
dissolved elements

Formed Elements
– Erythrocyte
– Leukocyte
– Thrombocyte
Fluid Replacement

The most desirable fluid for blood loss
replacement is whole blood.
– Blood is often fractionated
» Packed cells and plasma

Blood must be typed and cross-matched to
prevent a severe allergic reaction.
Fluid Replacement

Transfusion reaction
– Occurs when there is a discrepancy between the
blood type of the patient and donor
– Signs and symptoms of a transfusion reaction
» Chills, hives, hypotension, palpitations, tachycardia,
flushing of the skin, headaches, loss of consciousness,
nausea, vomiting, or shortness of breath
Fluid Replacement

Transfusion reaction (cont.)
– Treatment
» IMMEDIATELY stop the transfusion
» Save the substance being transfused
» Rapid IV infusion crystalloid solution
» Administration of mannitol (Osmotrol), diphenhydramine
(Benadryl), or furosemide (Lasix)
– Be alert for signs of fluid overload and congestive
heart failure.
Intravenous Fluids
 Hemoglobin-based
 Colloids
 Crystalloids
oxygen-carrying solutions
Hemoglobin-Based OxygenCarrying Solutions (HBOCs)

Commonly referred to as “blood substitutes”
– Compatible with all blood types
– Do not require blood typing, testing, or cross-matching
– HBOCs do not contain RBCs, so there is no concern for Rh
incompatibility because the Rh factor of blood is found on the
outer surface of the RBC.

Initial studies on HBOCs have been disappointing
Colloids

Colloids remain in intravascular spaces for an
extended period of time and have oncotic force.
–
–
–
–
Plasma protein fraction (Plasmanate)
Salt-poor albumin
Dextran
Hetastarch (Hespan)
Crystalloids
Crystalloid solutions are the primary compounds
used in prehospital care
 Non-protein solutions

– Normal Saline
– Lactated Ringers

Classified according to tonicity
– Isotonic solutions
– Hypertonic solutions
– Hypotonic solutions
Crystalloids
 Awareness
of the
effects of hypertonic,
isotonic, and
hypotonic solutions
on red blood cells.
Thank you!