MEDICAL AND SURGICAL NURSING

solute the substance dissolved

solvent substance in which the solute is dissolved
usually water (universal solvent)
molar solution (M) - # of gram-molecular weights of solute
per liter of solution
osmolality concentration of solute per kg of water
normal range = 275-295 mOsm/kg of water
osmolarity concentration of solute per L of solution
* since 1kg=1L, & water is the solvent of the human
body, osmolarity & osmolality are used interchangeably

Fluids and Electrolytes

IV.

FLUIDS & ELECTROLYTES

I. Fluid Status of Human Body
A. Homeostasis: state of the body when
maintaining a state of balance in the
presence of constantly changing conditions
B. Includes balance of fluid, electrolytes, and
acid- base balance
C. Body water intake and output
approximately equal (2500 mL/24 hr.)
Adult body: 40L water, 60% body weight
2/3 intracellular
1/3 extracellular (80% interstitial, 20%
intravascular)
Infant: 70-80% water
Elderly: 40-50% water
II. Body Fluid Composition
A.
Water: 60% of body weight
B.
Electrolytes: substances that become charged
particles in solution
1. Cations: positively charged (e.g.
Na+,
K+)
2. Anions: negatively charged (e.g.
Cl-)
3. Both are measured in milliequivalents
per liter (mEq/L)
C.
Balance of hydrostatic pressure and
osmotic pressure regulates movement of
III. Body Fluid Distribution:
water
A.
2 body compartments:
between
intravascular and
interstitial
spaces
1. Intracellular
fluids
(ICF): fluids

2.

B.

within cells of body [major

intracellular electrolytes: Potassium
(K+), Magnesium (Mg +2)]
Extracellular fluids (ECF): fluid
outside cells; [major extracellular
electrolytes: Sodium (Na+),
Chloride(Cl-)]; this is where
transportation of nutrients,
oxygen, and waste products occurs

Locations of ECF:
1. Interstitial: fluid between most cells
2. Intravascular: fluid within blood
vessels; also called plasma
3. Transcellular: fluids of body
including urine, digestive
secretion,
cerebrospinal, pleural,
synovial, intraocular, gonadal,
pericardial

MS: Fluids and Electrolyte

Mechanisms of Body Fluid Movement (i.e. movement

of solutes, solvents across different extracellular
locations)
A.
Osmosis: water is mover; water moves from
lower concentration to higher concentration
1. Normal Osmolality of ICF and ECF:
275 295 mOsm/kg
2. Types of solutions according to
osmolality
Isotonic: all solutions with osmolality
same as that of plasma .Body cells placed
in isotonic fluid: neither shrink nor swell
Hypertonic: fluid with greater
concentration of solutes than plasma
Cells in hypertonic solution: water in
cells moves to outside to equalize
concentrations: cells will shrink
Hypotonic: fluid with lower concentration
of solutes than plasma Cells in hypotonic
solution: water outside cells moves
to inside of cells: cells will swell and
3. Different
intravenous
eventually
burst solutions,
(hemolyze)used
to correct some abnormal conditions,
categorized according to osmolality:
B.

C.

D.

Diffusion: solute molecules move from higher

concentration to lower concentration
1. Solute, such as electrolytes, is the
mover; not the water
2. Types: simple and facilitated
(movement of large water-soluble
molecules)
Filtration: water and solutes move from area
of higher hydrostatic pressure to lower
hydrostatic pressure
1. Hydrostatic pressure is created by
pumping action of heart and gravity
against capillary wall
2. Usually occurs across capillary
membranes
Active Transport: molecules move across
cell membranes against concentration
gradient; requires energy, e.g. Na K pump

Hydrostatic pressure -pushes fluid out of vessels into tissue

space; higher to lower pressure
due to water volume in vessels; greater in arterial end
swelling: varicose veins, fluid overload, kidney
failure
& CHF
Osmotic pressure -pulls fluid into vessels; from weaker
concentration to stronger concentration
- from plasma proteins; greater in venous end
- swelling: liver problems, nephrotic syndrome

Abejo

Mechanisms that Regulate Homeostasis:

How the body adapts to fluid and electrolyte
changes?
A.
Thirst: primary regulator of water intake
(thirst center in brain)
B.
Kidneys: regulator of volume and
osmolality by controlling excretion of
water and electrolytes
C.
Renin-angiotension-aldosterone
mechanism: response to a drop in blood
pressure; results from vasoconstriction
and sodium regulation by aldosterone
D.
Antidiuretic hormone: hormone to
regulate water excretion; responds to
osmolality and blood volume
E.
Atrial natriuretic factor: hormone
from
atrial heart muscle in response to fluid
excess; causes increased urine output
by blocking aldosterone
Fluid Balance Regulation
V.

Thirst reflex triggered by:

1. decreased salivation & dry mouth
2. increased osmotic pressure stimulates
osmoreceptors in the hypothalamus
3. decreased blood volume activates the
renin/angiontensin pathway, which simulates
the thirst center in hypothalamus
Renin-Angiotensin
1. drop in blood volume in kidneys = renin released
2. renin = acts on plasma protein angiotensin
(released by the liver) to form angiotensin I
3. ACE = converts Angiotensin I to
Angiotensin II in
the lungs
4. Angiotensin II = vasoconstriction &
MS: Fluids and Electrolyte
aldosterone release

ADH produced by hypothalamus, released by

posterior pituitary when osmoreceptor or
baroreceptor is triggered in hypothalamus
Aldosterone produced by adrenal cortex; promotes Na
& water reabsorption
Sensible & Insensible Fluid Loss
Sensible:
Insensible:

urine, vomiting, suctioned

secretions lungs , skin, GI and
evaporation

Normal Fluid Intake and Loss in Adults

Intake:

Output:

Water in food
1,000 mls
300 mls
Water from oxidation
Water
TOTALin liquid
2,500 mls1,200 mls
Skin
Lungs
Feces
Kidneys
TOTAL

500 mls
300 mls
150 mls
1,500 mls
2,500 mls

Abejo

IV Fluids
Isotonic

Hypotonic

Hypertonic

LR
PNSS (0.9%NSS)
NM
D5W
- isotonic in bag
- dextrose=quickly
metabolized=hypotonic
D2.5W
0.45% NSS
0.3% NSS
0.2% NSS
D50W
D10W
D5NSS
D5LR
3%NSS

Colloids (usually CHONs) & Plasma expanders

Dextran synthetic polysaccharide, glucose solution
increase concentration of blood, improving
blood volume up to 24 hrs
contraindicated: heart failure, pulmonary edema,
cardiogenic shock, and renal failure
Hetastarch like Dextran, but longer-acting
expensive
derived from corn starch
Composition of Fluids
Saline solutions water, Na, Cl
Dextrose solutions water or saline, calories
Lactated Ringers water, Na, Cl, K, Ca, lactate
Plasma expanders albumin, dextran, plasma
protein
(plasmanate)
- increases oncotic pressure, pulling
fluids into circulation
Parenteral hyperalimentation fluid, electrolytes,
amino acids, calories
A.

FLUID VOLUME DEFICIT or HYPOVOLEMIA

Definition: This is the loss of extra cellular fluid

volume that exceeds the intake of fluid. The loss
of water and electrolyte is in equal proportion. It
can be called in various terms- vascular, cellular or
intracellular dehydration. But the preferred term is
hypovolemia.
Dehydration refers to loss of WATER alone, with
increased solutes concentration and
sodium concentration

Pathophysiology of Fluid Volume Deficit

Etiologic conditions
include:
a.
Vomiting
b. Diarrhea
c. Prolonged GI suctioning
d. Increased sweating
e. Inability to gain access to fluids
f. Inadequate fluid intake
g. Massive third spacing

MS: Fluids and Electrolyte

Risk factors are the following:

a. Diabetes Insipidus
b. Adrenal insufficiency
c. Osmotic diuresis
d. Hemorrhage
e. Coma
f. Third-spacing conditions like
ascites, pancreatitis and burns
PATHOPHYSIOLOGY:

Risk Factors --- inadequate fluids in the body ---- decreased

blood volume ----- decreased cellular hydration ---- cellular
shrinkage ---- weight loss, decreased turgor, oliguria,
hypotension, weak pulse, etc.

ASSESSMENT:
Physical examination

Weight loss, tented skin turgor, dry mucus membrane

Hypotension
Tachycardia
Cool skin, acute weight loss
Flat neck veins
Decreased CVP

Subjective cues

Thirst
Nausea, anorexia
Muscle weakness and cramps
Change in mental state

Laboratory findings
1.

Elevated BUN due to depletion of fluids or

decreased renal perfusion
2. Hemoconcentration
3. Possible Electrolyte imbalances: Hypokalemia,
Hyperkalemia, Hyponatremia, hypernatremia
4. Urine specific gravity is increased (concentrated
urine) above 1.020
NURSING MANAGEMENT
1.
2.
3.
4.

5.
6.
7.
8.

Assess the ongoing status of the patient by doing

an accurate input and output monitoring
Monitor daily weights. Approximate weight loss 1
kilogram = 1liter!
Monitor Vital signs, skin and tongue turgor,
urinary concentration, mental function and
peripheral circulation
Prevent Fluid Volume Deficit from occurring by
identifying risk patients and implement
fluid replacement therapy as needed
promptly
Correct fluid Volume Deficit by offering fluids orally
if tolerated, anti-emetics if with vomiting, and foods
with adequate electrolytes
Maintain skin integrity
Provide frequent oral care
Teach patient to change position slowly to
avoid sudden postural hypotension

B.

FLUID VOLUME EXCESS: HYPERVOLEMIA

Definition : Refers to the isotonic expansion
of the ECF caused by the abnormal retention of
water and sodium
There is excessive retention of water and
electrolytes in equal proportion. Serum
sodium concentration remains NORMAL

4.

Teach patient about edema, ascites, and fluid

therapy. Advise elevation of the extremities,
restriction of fluids, necessity of paracentesis,
dialysis and diuretic therapy.
Instruct patient to avoid over-the-counter
medications without first checking with the health
care provider because they may contain sodium

5.

Pathophysiology of Fluid Volume Excess

Etiologic conditions and Risks factors

a. Congestive heart failure
b. Renal failure
c. Excessive fluid intake
d. Impaired ability to excrete fluid as in
renal disease
e. Cirrhosis of the liver
f. Consumption of excessive table salts
g. Administration of excessive IVF
h. Abnormal fluid retention
PATHOPHYSIOLOGY

Excessive fluid --- expansion of blood volume ----- edema,

increased neck vein distention, tachycardia, hypertension.

The Nursing Process in Fluid Volume Excess

ASSESSMENT
Physical Examination
Increased weight gain
Increased urine output
Moist crackles in the lungs
Increased CVP
Distended neck veins
Wheezing
Dependent edema

ELECTROLYTES

Sources of electrolytes

IMPLEMENTATION
ASSIST IN MEDICAL INTERVENTION
1.
2.
3.

Administer diuretics as prescribed

Assist in hemodialysis
Provide dietary restriction of sodium and
water
NURSING MANAGEMENT
1.

2.
3.

Continually assess the patients condition by

measuring intake and output, daily weight
monitoring, edema assessment and breath sounds
Prevent Fluid Volume Excess by adhering to
diet prescription of low salt- foods.
Detect and Control Fluid Volume Excess by closely
monitoring IVF therapy, administering
medications,
providing rest periods, placing in semi-fowlers
position for lung expansion and providing
frequent skin care for the edema

MS: Fluids and Electrolyte

Foods and ingested fluids, medications; IVF

and TPN solutions

Functions of Electrolytes
Maintains fluid balance
Regulates acid-base balance
Needed for enzymatic secretion and activation
Needed for proper metabolism and effective
processes of muscular contraction, nerve
transmission
Types of Electrolytes
CATIONS- positively charged ions; examples are
sodium, potassium, calcium
ANIONS- negatively charged ions; examples are
chloride and phosphates]
The major ICF cation is potassium (K+);
the major ICF anion is Phosphates
The major ECF cation is Sodium (Na+); the
major ECF anion is Chloride (Cl-)

ELECTROLYTE IMBALANCES

Subjective cue/s
Shortness of breath
Change in mental state
Laboratory findings
1. BUN and Creatinine levels are LOW because of
dilution
2. Urine sodium and osmolality decreased (urine
becomes diluted)
3. CXR may show pulmonary congestion

Electrolytes are charged ions capable of

conducting electricity and are solutes found in all
body compartments.

SODIUM

The most abundant cation in the ECF

Normal range in the blood is 135-145 mEq/L
A loss or gain of sodium is usually accompanied by
a loss or gain of water.
Major contributor of the plasma Osmolality
Sources: Diet, medications, IVF. The minimum daily
requirement is 2 grams
Functions:
1.
2.
3.
4.
5.
6.
7.

8.

Participates in the Na-K pump

Assists in maintaining blood volume
Assists in nerve transmission and muscle
contraction
Primary determinant of ECF
concentration.
Controls water distribution throughout
the body.
Primary regulator of ECF volume.
Sodium also functions in the establishment of
the electrochemical state necessary for muscle
contraction and the transmission of nerve
impulses.
Regulations: skin, GIT, GUT,
Aldosterone increases Na retention in the
kidney

SODIUM DEFICIT: HYPONATREMIA

In summary:

Physical Examination
Altered mental status
Vomiting
Lethargy
Muscle twitching and convulsions (if sodium level
is below 115 mEq/L)
Focal weakness

Definition : Refers to a Sodium serum level of less

than 135 mEq/L. This may result from excessive
sodium loss or excessive water gain.

Pathophysiology
Etiologic Factors
a. Fluid loss such as from Vomiting and nasogastric
suctioning
b. Diarrhea
c. Sweating
d. Use of diuretics
e. Fistula
Other factors
a. Dilutional hyponatremia
Water intoxication, compulsive water
drinking where sodium level is
diluted with increased water intake
b. SIADH
Excessive secretion of ADH causing
water retention and dilutional
hyponatremia
PATHOPHYSIOLOGY
Decrease sodium concentration --- hypotonicity of plasma -- water from the intravascular space will move out and go to
the intracellular compartment with a higher concentration --cell swelling --Water is pulled INTO the cell because of
decreased extracellular sodium level and increased
intracellular concentration

The Nursing Process in HYPONATREMIA

Subjective Cues
Nausea
Cramps
Anorexia
Headache
Laboratory findings
1. Serum sodium level is less than 135 mEq/L
2. Decreased serum osmolality
3. Urine specific gravity is LOW if caused by sodium loss
4. In SIADH, urine sodium is high and specific gravity
is HIGH
IMPLEMENTATION
ASSIST IN MEDICAL INTERVENTION
1. Provide sodium replacement as ordered. Isotonic
saline is usually ordered.. Infuse the solution very
cautiously. The serum sodium must NOT be increased
by greater than 12 mEq/L because of the danger of
pontine osmotic demyelination
2. Administer lithium and demeclocycline in SIADH
3. Provide water restriction if with excess volume
NURSING MANAGEMENT
1.

ASSESSMENT
Sodium Deficit (Hyponatremia)
Clinical Manifestations
Clinical manifestations of hyponatremia depend on
the cause, magnitude, and rapidity of onset.
Although nausea and abdominal cramping occur, most
of the symptoms are neuropsychiatric and are
probably related to the cellular swelling and cerebral
edema associated with hyponatremia.
As the extracellular sodium level decreases, the cellular
fluid becomes relatively more concentrated and
pulls water into the cells.
In general, those patients having acute decline in
serum sodium levels have more severe symptoms and
higher mortality rates than do those with more slowly
developing hyponatremia.
Features of hyponatremia associated with sodium loss
and water gain include anorexia, muscle cramps, and
a feeling of exhaustion.
When the serum sodium level drops below 115
mEq/L (SI: 115 mmol/L), thee ff signs of increasing
intracranial pressure occurs:
lethargy
Confusion
muscular twitching
focal weakness
hemiparesis
papilledema
convulsions
MS: Fluids and Electrolyte

Provide continuous assessment by doing an

accurate intake and output, daily weights, mental
status examination, urinary sodium levels and GI
manifestations. Maintain seizure precaution
2. Detect and control Hyponatremia by encouraging
food
intake with high sodium content, monitoring patients
on lithium therapy, monitoring input of fluids like
IVF, parenteral medication and feedings.
3. Return the Sodium level to Normal by restricting
water
intake if the primary problem is water retention.
Administer sodium to normovolemic patient and
elevate the sodium slowly by using sodium
chloride solution
SODIUM EXCESS: HYPERNATREMIA

Serum Sodium level is higher than 145 mEq/L

There is a gain of sodium in excess of water or a
loss of water in excess of sodium.

Pathophysiology:
Etiologic factors
a. Fluid deprivation
b. Water loss from Watery diarrhea, fever, and
hyperventilation
c. Administration of hypertonic solution
d. Increased insensible water loss
e. Inadequate water replacement, inability to
swallow
f. Seawater ingestion or excessive oral
ingestion of salts

Other factors
a. Diabetes insipidus
b. Heat stroke
c. Near drowning in ocean
d. Malfunction of dialysis

IMPLEMENTATION
ASSIST IN THE MEDICAL INTERVENTION
1.
2.

PATHOPHYSIOLOGY
Increased sodium concentration --- hypertonic plasma ---water will move out form the cell outside to the interstitial
space ----- CELLULAR SHRINKAGE ----- then to the
blood ---- Water pulled from cells because of increased
extracellular sodium level and decreased cellular fluid
concentration

The Nursing Process in HYPERNATREMIA

Sodium Excess (Hypernatremia)
Clinical Manifestations
primarily neurologic
Presumably the consequence of cellular dehydration.
Hypernatremia results in a relatively concentrated ECF,
causing water to be pulled from the cells.
Clinically, these changes may be manifested by:
o restlessness and weakness in moderate
hypernatremia
o disorientation, delusions, and
hallucinations in severe
Dehydration (hypernatremia)
hypernatremia.is often overlooked as
the primary reason for behavioral changes in the
elderly.
If hypernatremia is severe, permanent brain damage
can occur (especially in children). Brain damage is
apparently due to subarachnoid hemorrhages that
result from brain contraction.
Thirst
is so strong
a defender of hypernatremia
serum sodium levels
in
A primary
characteristic
is thirst.
normal people that hypernatremia never occurs unless
the person is unconscious or is denied access to water;
unfortunately, ill people may have an impaired thirst
mechanism. Other signs include dry, swollen tongue and
sticky mucous membranes. A mild elevation in body
temperature may occur, but on correction of the
hypernatremia the body temperature should return to
normal.
ASSESSMENT
Physical Examination
Restlessness, elevated body temperature
Disorientation
Dry, swollen tongue and sticky mucous membrane,
tented skin turgor
Flushed skin, postural hypotension
Increased muscle tone and deep reflexes
Peripheral and pulmonary edema
Subjective Cues
Delusions and hallucinations
Extreme thirst
Behavioral changes
Laboratory findings
1. Serum sodium level exceeds 145 mEq/L
2. Serum osmolality exceeds 295 mOsm/kg
3. Urine specific gravity and osmolality INCREASED
or elevated
MS: Fluids and Electrolyte

3.

Administer hypotonic electrolyte solution slowly

as ordered
Administer diuretics as ordered
Loop diuretics (thiazides ok)
Desmopressin is prescribed for diabetes insipidus

NURSING MANAGEMENT
1.

Continuously monitor the patient by assessing

abnormal loses of water, noting for the thirst and
elevated body temperature and behavioral
changes
2. Prevent hypernatremia by offering fluids regularly
and plan with the physician alternative routes if oral
route is not possible. Ensure adequate water for
patients with DI. Administer IVF therapy
cautiously
3. Correct the Hypernatremia by monitoring the
patients response to the IVF replacement.
Administer
the hypotonic solution very slowly to prevent
sudden cerebral edema.
4. Monitor serum sodium level.
5. Reposition client regularly, keep side-rails up, the
bed in low position and the call bell/light within
reach.
6. Provide teachingPOTASSIUM
to avoid over-the counter
medications without consultation as they may
contain sodium
The most abundant cation in the ICF
Potassium is the major intracellular electrolyte; in fact,
98% of the bodys potassium is inside the cells.
The remaining 2% is in the ECF; it is this 2% that
is all-important in neuromuscular function.
Potassium is constantly moving in and out of cells
according to the bodys needs, under the influence
of
the sodium-potassium pump.
Normal range in the blood is 3.5-5 mEq/L
Normal renal function is necessary for maintenance of
potassium balance, because 80-90% of the potassium
is excreted daily from the body by way of the kidneys.
The other less than 20% is lost through the bowel and
sweat glands.
Major electrolyte maintaining ICF balance
Sources- Diet, vegetables, fruits, IVF, medications
Functions:
1.
2.
3.
4.
5.

6.

Maintains ICF Osmolality

Important for nerve conduction and
muscle contraction
Maintains acid-base balance
Needed for metabolism of carbohydrates, fats
and proteins
Potassium influences both skeletal and cardiac
muscle activity.
( For example, alterations in its concentration change
myocardial irritability and rhythm )
Regulations: renal secretion and excretion,
* Aldosterone promotes renal excretion
* Acidosis promotes K exchange for hydrogen

POTASSIUM DEFICIT: HYPOKALEMIA

Condition when the serum concentration of

potassium is less than 3.5 mEq/L

Pathophysiology

Etiologic Factors
a. Gastro-intestinal loss of potassium such
as diarrhea and fistula
b. Vomiting and gastric suctioning
c. Metabolic alkalosis
d. Diaphoresis and renal disorders
e. Ileostomy

Other factor/s
a. Hyperaldosteronism
b. Heart failure
c. Nephrotic syndrome
d. Use of potassium-losing diuretics
e. Insulin therapy
f. Starvation
g. Alcoholics and elderly
PATHOPHYSIOLOGY

Decreased potassium in the body impaired nerve

excitation and transmission signs/symptoms such as
weakness, cardiac dysrhythmias etc..

IMPLEMENTATION
ASSIST IN THE MEDICAL INTERVENTION
1.
2.

The Nursing Process in Hypokalemia

Clinical Manifestations
Potassium deficiency can result in widespread
derangements in physiologic functions and
especially nerve conduction.
Most important, severe hypokalemia can result in
death through cardiac or respiratory arrest.
Clinical signs rarely develop before the serum
potassium level has fallen below 3 mEq/L (51:
3
mmol/L) unless the rate of fall has been rapid.
Manifestations of hypokalemia include fatigue,
anorexia, nausea, vomiting, muscle weakness,
decreased bowel motility, paresthesias, dysrhythmias,
and increased sensitivity to digitalis.
If prolonged, hypokalemia can lead to impaired
renal concentrating ability, causing dilute urine,
polyuria, nocturia, and polydipsia
ASSESSMENT
Physical examination
Muscle weakness
Decreased bowel motility and abdominal distention
Paresthesias
Dysrhythmias
Increased sensitivity to digitalis
Subjective cues
Nausea , anorexia and vomiting
Fatigue, muscles cramps
Excessive thirst, if severe
Laboratory findings
1. Serum potassium is less than 3.5 mEq/L
2. ECG: FLAT T waves, or inverted T waves,
depressed ST segment and presence of the U wave
and prolonged PR interval.
3. Metabolic alkalosis
MS: Fluids and Electrolyte

3.

Provide oral or IV replacement of potassium

Infuse parenteral potassium supplement. Always
dilute the K in the IVF solution and administer with a
pump. IVF with potassium should be given no faster
than 10- 20-mEq/ hour!
NEVER administer K by IV bolus or IM

NURSING MANAGEMENT
1.
2.

3.
4.

5.

Continuously monitor the patient by assessing

the cardiac status, ECG monitoring, and digitalis
precaution
Prevent hypokalemia by encouraging the patient to
eat potassium rich foods like orange juice, bananas,
cantaloupe, peaches, potatoes, dates and apricots.
Correct hypokalemia by administering prescribed IV
potassium replacement. The nurse must ensure that
the kidney is functioning properly!
Administer IV potassium no faster than 20 mEq/hour
and hook the patient on a cardiac monitor. To
EMPHASIZE: Potassium should NEVER be given
IV bolus or IM!!
A concentration greater than 60 mEq/L is not
advisable
for peripheral veins.

POTASSIUM EXCESS: HYPERKALEMIA

Serum potassium greater than 5.5 mEq/L
Pathophysiology

Etiologic factors
a. Iatrogenic, excessive intake of potassium
b. Renal failure- decreased renal excretion of
potassium
c. Hypoaldosteronism and Addisons
disease
d. Improper use of potassium supplements
Other factors
1. Pseudohyperkalemia- tight tourniquet and
hemolysis of blood sample, marked
leukocytosis

2.
3.
4.

Transfusion of old banked

blood
Acidosis
Severe tissue trauma

PATHOPHYSIOLOGY
Increased potassium in the body ---- Causing irritability of
the cardiac cells --- Possible arrhythmias!!

The Nursing Process in Hyperkalemia

Clinical Manifestations
By far the most clinically important effect of
hyperkalemia is its effect on the myocardium.
Cardiac effects of an elevated serum potassium level
are usually not significant below a concentration of
7
mEq/L (SI: 7 mmol/L), but they are almost always
present when the level is 8 mEq/L (SI: 8 mmol/L)
or greater.
As the plasma potassium concentration is increased,
disturbances in cardiac conduction occur.
The earliest changes, often occurring at a serum
potassium level greater than 6 mEq/ L (SI: 6
mmol/L), are peaked narrow T waves and a shortened
QT interval.
If the serum potassium level continues to rise, the
PR interval becomes prolonged and is followed by
disappearance of the P waves.
Finally, there is decomposition and prolongation
of the QRS complex. Ventricular dysrhythmias
and cardiac arrest may occur at any point in this
progression.
Note that in Severe hyperkalemia causes muscle
weakness and even paralysis, related to a
depolarization block in muscle.
Similarly, ventricular conduction is
slowed.
Although hyperkalemia has marked effects on the
peripheral neuromuscular system, it has little effect
on the central nervous system.
Rapidly ascending muscular weakness leading to
flaccid quadriplegia has been reported in patients
with
very high serum potassium levels.
Paralysis of respiratory muscles and those required
for phonation can also occur.
Gastrointestinal manifestations, such as nausea,
ASSESSMENT
intermit
tent intestinal colic, and diarrhea, may
Physical
Examination
Diarrhea
occur in hyperkalemic patients.
Skeletal muscle weakness
Abnormal cardiac rate
Subjective Cues
Nausea
Intestinal pain/colic
Palpitations
Laboratory Findings
1. Peaked and narrow T waves
2. ST segment depression and shortened QT
interval
3. Prolonged PR interval
4. Prolonged QRS complex
5. Disappearance of P wave
6. Serum potassium is higher than 5.5 mEq/L
and Electrolyte
7.MS: Fluids
Acidosis

IMPLEMENTATION
ASSIST IN MEDICAL INTERVENTION
1. Monitor the patients cardiac status with cardiac
machine
2. Institute emergency therapy to lower potassium
level by:
a. Administering IV calcium gluconateantagonizes action of K on cardiac
conduction
b. Administering Insulin with dextrose-causes
temporary shift of K into cells
c. Administering sodium bicarbonatealkalinizes plasma to cause temporary shift
d. Administering Beta-agonists
e. Administering Kayexalate (cation-exchange
resin)-draws K+ into the bowel
NURSING MANAGEMENT
1.
2.
3.
4.
5.

6.
7.

8.

Provide continuous monitoring of cardiac

status, dysrhythmias, and potassium levels.
Assess for signs of muscular weakness, paresthesias,
nausea
Evaluate and verify all HIGH serum K levels
Prevent hyperkalemia by encouraging high risk
patient to adhere to proper potassium restriction
Correct hyperkalemia by administering carefully
prescribed drugs. Nurses must ensure that clients
receiving IVF with potassium must be always
monitored and that the potassium supplement is
given correctly
Assist in hemodialysis if hyperkalemia cannot be
corrected.
Provide client teaching. Advise patients at risk
to avoid
eating potassium rich foods, and to use potassium
salts sparingly.
Monitor patients for hypokalemia who are receiving
potassium-sparing diuretic
CALCIUM
Majority of calcium is in the bones and teeth
Small amount may be found in the ECF and
ICF
Normal serum range is 8.5 10.5 mg/dL
Sources: milk and milk products; diet; IVF
and medications

Functions:
Needed for formation of bones and
teeth
2. For muscular contraction and relaxation
3. For neuronal and cardiac function
4. For enzymatic activation
5. For normal blood clotting
Regulations:

HYPOCALCEMIA
Low levels of calcium in the blood

1.

1.
2.
3.

GIT- absorbs Ca+ in the intestine; Vitamin D helps

to increase absorption
Renal regulation- Ca+ is filtered in the glomerulus
andreabsorbed in the tubules:
Endocrine regulation:

Parathyroid hormone from the parathyroid

glands is released when Ca+ level is low. PTH
causes release of calcium from bones and
increased retention of calcium by the kidney but
PO4 is excreted
Calcitonin from the thyroid gland is released
when the calcium level is high. This causes
excretion of
both calcium and PO4 in the kidney and
promoted deposition of calcium in the bones.

Risk Factors
a. Hypoparathyroidism (idiopathic or
postsurgical)
b. Alkalosis (Ca binds to albumin)
c. Corticosteroids (antagonize Vit D)
d. Hyperphosphatemia
e. Vit D deficiency
f. Renal failure (vit D deficiency)
Clinical Manifestation
Decreased cardiac contractility
Arrhythmia
ECG: prolonged QT interval, lengthened
ST segment
Trousseaus sign (inflate BP cuff 20mm
above
systole for 3 min = carpopedal spasm)

Chvosteks sign (tap facial nerve anterior to

the ear = ipsilateral muscle twitching)

Tetany
Hyperreflexia, seizures
Laryngeal spasms/stridor
Diarrhea, hyperactive bowel sounds
Bleeding

Collaborative Management
1. Calcium gluconate 10% IV
2. Calcium chloride 10% IV
3. both usually given by Dr, very slowly; venous irritant;
cardiac probs
4. Oral: calcium citrate, lactate, carbonate; Vit D
supplements
5. Diet: high calcium
6. Watch out for tetany, seizures, laryngospasm, resp &
cardiac arrest
7. Seizure precautions
Sources:
milk, yogurt, cheese, sardines, broccoli, tofu, green
leafy vegetables
MS: Fluids and Electrolyte

HYPERCALCEMIA

HYPOMAGNESEMIA

is an elevated calcium level in the blood

usually from bone resorption

Risk Factors / Causes

a. Hyperparathyroidism (eg adenoma)
b. Metastatic cancer (bone resorption as tumors
ectopic PTH effect) eg. Multiple myeloma
c. Thiazide diuretics (potentiate PTH effect)
d. Immobility
e. Milk-alkali syndrome (too much milk or antacids
in aegs with peptic ulcer)

Clinical Manifestation
groans (constipation)
moans (psychotic noise)
bones (bone pain, especially if PTH is elevated)
stones (kidney stones)
psychiatric overtones (including depression
and confusion)

Arrhythmia
ECG: shortened QT interval, decreased ST
segment
Hyporeflexia, lethargy, coma

Collaborative Management
1. If parathyroid tumor = surgery
2. Diet: low Ca, stop taking Ca Carbonate antacids,
increase fluids
3. IV flushing (usually NaCl)
4. Loop diuretics
5. Corticosteroids
6. Biphosphonates, like etidronate (Calcitonin)
& alendronate (Fosamax)
7. Plicamycin (Mithracin) inhibits bone
resorption
8. Calcitonin IM or intranasal
10. Watch out for digitalis toxicity
9. Dialysis (severe case)
11. Prevent fractures, handle gently
MAGNESIUM

2nd most abundant intracellular cation

50% found in bone, 45% is intracellular
ATP (adenosine triphosphate), the main source
of energy in cells, must be bound to a magnesium ion
in order to be biologically active.
competes with Ca & P absorption in the GI
inhibits PTH
Normal value : 1.5-2.5 mEq/L

Functions:
1. important in maintaining intracellular activity
2. affects muscle contraction, & especially relaxation
3. maintains normal heart rhythm
4. promotes vasodilation of peripheral arterioles
Sources:
green leafy vegetables, nuts, legumes, seafood, whole
grains, bananas, oranges, cocoa, chocolate

MS: Fluids and Electrolyte

is an electrolyte disturbance in which there is an

abnormally low level of magnesium in the
blood.
Risk Factors and Cause
a. Chronic alcoholism (most common),
Alcohol stimulates renal excretion of
magnesium,
b. Inflammatory bowel disease
c. Small bowel resection
d. GI cancer
e. chronic pancreatitis (poor absorption)
f. Loop and thiazide diuretic use (the most
common cause of hypomagnesemia)
g. Antibiotics (i.e. aminoglycoside, amphotericin,
pentamidine, gentamicin, tobramycin, viomycin)
block resorption in the loop of Henle.
h.
Excess calcium
i. Excess saturated fats
j. Excess coffee or tea intake
k. Excess phosphoric or carbonic acids (soda pop)
l. Insufficient water consumption
m. Excess salt or sugar intake
n. Insufficient selenium,vitamin D, sunlight
exposure or vitamin B6
Clinical
Manifestation
o. Increased
levels of stress
Weakness
muscle cramps
cardiac arrhythmia
increased irritability of the nervous system with
tremors, athetosis, jerking, nystagmus and an
extensor plantar reflex. Confusion
disorientation
hallucinations
depression
epileptic fits
hypertension, tachycardia and tetany.

* Like hypocalcemia,
hypokalemia
Potentiates digitalis toxicity
Collaborative Management
1. Magnesium sulfate IV, IM (make sure renal
function is ok) may cause flushing
2. Oral: Magnesium oxide 300mg/day,
3. Mg-containing antacids (SE diarrhea)
4. Diet: high magnesium (fruits,green vegetables,
whole grains cereals, milk, meat, nuts and sea
foods )
5. Promotion of safety, protect from injury
HYPERMAGNESEMIA

Etiologic Factors
a. Magnesium treatment for pre-eclampsia
b. Renal failure
c. Diabetic Ketoacidosis
d. Excessive use of Mg antacids/laxatives

PATHOPHYSIOLOGY
Increase Mg. ----- Blocks acetylcholine release ---- decrease
excitability of muscle

Clinical Manifestation
Hyporeflexia
Hypotension, bradycardia, arrhythmia
Flushing
Weakness, lethargy, coma
Decreased RR & respiratory paralysis
Loss of DTRs

HYPERPHOSPHATEMIA

Risk Factors
a. Acidosis (Ph moves out of cell)
b. Cytotoxic agents/chemotherapy in cancer
c. Renal failure
d. Hypocalcemia
e. Massive BT (P leaks out of cells during storage
of blood)
f. Hyperthyroidism

Clinical Manifestation
Calcification of kidney, cornea, heart
Muscle spasms, tetany, hyperreflexia

*like hypercalcemia
Collaborative Management
1. Diuretics
2. Stop Mg-containing antacids & enemas
3. IV fluids rehydration
4. Calcium gluconate (antidote,
antagonizes cardiac & respiratory effects
of Mg)
5. Dialysis if RF
PHOSPHORUS

primary intracellular anion

part of ATP energy
85% bound with Ca in teeth/bones, skeletal muscle
reciprocal balance with Ca
absorption affected by Vit D, regulation affected by
PTH (lowers P level)
Normal value : 2.5-4.5 mg/dL

*like hypocalcemia
Collaborative ManagementM
1. Aluminum antacids as phosphate binders: Al
carbonate (Basaljel), Al hydroxide (Amphojel)
2. Ca carbonate for hypocalcemia
3. Avoid phosphate laxatives/enemas
4. Increase fluid intake
5. Diet: low Phos, no carbonated drinks
CHLORIDE

Functions:
1. bone/teeth formation & strength
2. phospholipids (make up cell membrane
integrity)
3. part of ATP
4. affects metabolism, Ca levels
Sources:
red & organ meats (brain, liver, kidney), poultry, fish, eggs,
milk, legumes, whole grains, nuts, carbonated drinks

HYPOPHOSPHATEMIA

Sources:
salt, canned food, cheese, milk, eggs, crab, olives

Risk Factors
a. Decreased Vit D absorption, sunlight exposure
b. Hyperparathyroidism (increased PTH)
c. Aluminum & Mg-containing antacids (bind P)
d. Severe vomiting & diarrhea
Clinical Manifestation
Anemia, bruising (weak blood cell membrane)
Seizures, coma
Muscle weakness, paresthesias
Constipation, hypoactive bowel sounds

Functions:
1. helps regulate BP, serum osmolarity
2. part of HCl
3. acid/base balance (exchanges with HCO3)

HYPOCHLOREMIA

Risk Factors
a. Diuresis
b. Metabolic alkalosis
c. Hyponatremia, prolonged D5W IV
d. Addisons

Clinical Manifestation
Slow, shallow respirations (met. Alkalosis)
Hypotension (Na & water loss)

*Like hypercalcemia
Collaborative Management
1. Sodium phosphate or potassium phosphate
IV (give slowly, no faster than 10 mEq/hr)
2. Sodium & potassium phosphate orally
(NeutraPhos, K-Phos) give with meals to prevent
gastric irritation
3. Avoid Phos-binding antacids
4. Diet: high Mg, milk
5. Monitor joint stiffness, arthralgia,
fractures, bleeding

MS: Fluids and Electrolyte

extracellular anion, part of salt

binds with Na, H (also K, Ca, etc)
exchanges with HCO3 in the kidneys (& in RBCs)
Normal value: 95 -108 mEq/L

Collaborative Management
1. Administer IV or Oral : KCl, NaCl
2. Diet: high Cl (& usually Na)
HYPERCHLOREMIA

Risk Factors / Cause

a. Metabolic acidosis
b. Usually noted in hyperNa, hyperK

Clinical Manifestation
Deep, rapid respirations (met. Acidosis)
hyperK, hyperNa S/S
Increased Cl sweat levels in cystic fibrosis

Collaborative Management
1. Diuretics
2. Hypotonic solutions, D5W to restore
balance
3. Diet: low Cl (& usually Na)
4. Treat acidosis

Acid-Base Balance Mechanisms

Buffer - prevents major changes in ECF by releasing

or accepting H ions
Buffer mechanism: first line (takes seconds)
1. combine with very strong acids or bases
to convert them into weaker acids or bases
2. Bicarbonate Buffer System
most important
- uses HCO3 & carbonic acid/H2CO3 - (20:1)
- closely linked with respiratory & renal
mechanisms
3. Phosphate Buffer System
- more important in intracellular fluids, where
concentration is higher
- similar to bicarbonate buffer system, only uses
phosphate
4. Protein Buffer System
- hemoglobin, a protein buffer, promotes
movement of chloride across RBC membrane
in exchange for HCO3
Respiratory mechanism: 2nd line (takes minutes)
1. increased respirations liberates more CO2 =
increase pH
2. decreased respirations conserve more CO2
= decrease pH
carbonic acid (H2CO3) = CO2 + water
Renal mechanism: 3rd line (takes hours-days)
1. kidneys secrete H ions & reabsorb bicarbonate ions
= increase blood pH
2. kidneys form ammonia that combines with H ions
to form ammonium ions, which are excreted in the
urine
in exchange for sodium ions
Review: Acid-Base Imbalance
pH 7.35-7.45
pCO2 measurement of the CO2 pressure that is
being exerted on the plasma
3545mmHg
PaO2amount of pressure exerted by O2 on the
80plasma
100mmHg
SaO2percent of hemoglobin saturated with O2
Base excess amount of HCO3 available in the
-3 to
ECF +3

MS: Fluids and Electrolyte

Interpretation Arterial Blood Gases

Step 1

Step 2

Step 3

If acidosis the pH is down

If alkalosis the pH is up
The respiratory function indicator is the
PCO2
The metabolic function indicator is the HCO3
Look at the pH
Is it up or down?
If it is up - it reflects alkalosis
If it is down - it reflects acidosis
Look at the PCO2
Is it up or down?
If it reflects an opposite response as the pH,
then you know that the condition is
a respiratory imbalance
If it does not reflect an opposite response as
the
pH - move to step III
Look at the HCO3
Does the HCO3 reflect a corresponding
response with the pH
If it does then the condition is a
metabolic imbalance

FACTORS AFFECTING BODY FLUIDS,

ELECTROLYTES AND ACID-BASE BALANCE
AGE

Infants have higher proportion of body water

than adults
Water content of the body decreases with age
Infants have higher fluid turn-over due to
immature kidney and rapid respiratory rate

GENDER AND BODY SIZE

Women have higher body fat content but
lesser water content
Lean body has higher water content
ENVIRONMENT AND TEMPERATURE
Climate and heat and humidity affect fluid balance
DIET AND LIFESTYLE
Anorexia nervosa will lead to nutritional
depletion
Stressful situations will increase metabolism,
increase ADH causing water retention and
increased blood volume
Chronic Alcohol consumption causes
malnutrition
ILLNESS
Trauma and burns release K+ in the blood
Cardiac dysfunction will lead to edema
and congestion
MEDICAL TREATMENT, MEDICATIONS AND
SURGERY
Suctioning, diuretics and laxatives may
cause
imbalances

ACID-BASE BALANCE PROBLEMS

RESPIRATORY ACIDOSIS
pH < 7.35
pCO2 > 45 mm Hg (excess carbon dioxide in
the blood)
Respiratory system impaired and retaining CO2;
causing acidosis
Common Stimuli
a. Acute respiratory failure from airway obstruction
b. Over-sedation from anesthesia or narcotics
c. Some neuromuscular diseases that affect ability to
use chest muscles
d. Chronic respiratory problems, such as Chronic
Obstructive Lung Disease
Signs and Symptoms
Compensation: kidneys respond by generating and
reabsorbing bicarbonate ions, so HCO3 >26 mm Hg
Respiratory: hypoventilation, slow or shallow
respirations
Neuro: headache, blurred vision,
irritability, confusion
Respiratory collapse leads to
unconsciousness and
cardiovascular collapse
Collaborative Management
1. Early recognition of respiratory status and
treat cause
2. Restore ventilation and gas exchange; CPR for
respiratory failure with oxygen supplementation;
intubation and ventilator support if indicated
3. Treatment of respiratory infections with
bronchodilators, antibiotic therapy
4. Reverse excess anesthetics and narcotics with
medications such as naloxone (Narcan)
5. Chronic respiratory conditions
Breathe in response to low oxygen levels
Adjusted to high carbon dioxide level
through metabolic compensation
(therefore, high CO2 not a breathing
trigger)
Cannot receive high levels of oxygen, or
will have no trigger to breathe; will develop
carbon dioxide narcosis
Treat with no higher than 2 liters O2 per
6. Continue respiratory assessments, monitor
cannula
further arterial blood gas results
RESPIRATORY ALKALOSIS
pH < 7.35
pCO2 < 35 mm Hg.
Carbon dioxide deficit, secondary
to hyperventilation
Common Stimuli
a. Hyperventilation with anxiety from
uncontrolled fear, pain, stress (e.g. women in
labor, trauma victims)
b. High fever
c. Mechanical ventilation, during anesthesia

MS: Fluids and Electrolyte

Signs and Symptoms

Compensation: kidneys compensate by
eliminating bicarbonate ions; decrease
in bicarbonate HCO3 < 22 mm Hg.
Respiratory: hyperventilating: shallow,
rapid breathing
Neuro: panicked, light-headed, tremors, may
develop tetany, numb hands and feet (related to
symptoms of hypocalcemia; with elevated pH
more Ca ions are bound to serum albumin and
less ionized active calcium available for nerve
and muscle conduction)
May progress to seizures, loss of
consciousness (when normal breathing pattern
returns)
Cardiac: palpitations, sensation of chest
Collaborative
Management
tightness
1.
2.

3.
4.

Treatment: encourage client to breathe slowly in

a paper bag to rebreathe CO2
Breathe with the patient; provide emotional
support and reassurance, anti-anxiety
agents, sedation
On ventilator, adjustment of ventilation settings
(decrease rate and tidal volume)
Prevention: pre-procedure teaching,
preventative emotional support, monitor blood
gases as
indicated

METABOLIC ACIDOSIS
pH <7.35
Deficit of bicarbonate in the blood NaHCO3
<22 mEq/L
Caused by an excess of acid, or loss of
bicarbonate from the body
Common Stimuli
a. Acute lactic acidosis from tissue hypoxia (lactic
acid produced from anaerobic metabolism with
shock, cardiac arrest)
b. Ketoacidosis (fatty acids are released and
converted to ketones when fat is used to supply
glucose needs as in uncontrolled Type 1
diabetes
or starvation)
c. Acute or chronic renal failure (kidneys unable
to regulate electrolytes)
d. Excessive bicarbonate loss (severe diarrhea,
intestinal suction, bowel fistulas)
e. Usually results from some other disease and is
often accompanied by electrolyte and fluid
imbalances
f. Hyperkalemia often occurs as the hydrogen ions
enter cells to lower the pH displacing the
intracellular potassium; hypercalcemia and
may occur
Signs andhypomagnesemia
Symptoms
Compensation: respiratory system begins to
compensate by increasing the depth and rate of
respiration in an effort to lower the CO2 in the blood;
this causes a decreased level of carbon dioxide: pCO2
<35 mm HG.
Neuro changes: headache, weakness, fatigue
progressing to confusion, stupor, and coma
Cardiac: dysrhythmias and possibly cardiac
arrest from
hyperkalemia
GI: anorexia, nausea, vomiting
Skin: warm and flushed
Abejo

Respiratory: tries to compensate by

hyperventilation: deep and rapid respirations known
as Kussmauls respirations

Diagnostic test findings:

1. ABG: pH < 7.35, HCO3 < 22
2. Electrolytes: Serum K+ >5.0 mEq/L
3. Serum Ca+2 > 10.0 mg/dL
4. Serum Mg+2 < 1.6 mg/dL
Collaborative Management
1. Medications: Correcting underlying cause
will often improve acidosis
2. Restore fluid balance, prevent dehydration
with IV fluids
3. Correct electrolyte imbalances
4. Administer Sodium Bicarbonate IV, if acidosis is
severe and does not respond rapidly enough to
treatment of primary cause. (Oral bicarbonate is
sometimes given to clients with chronic metabolic
acidosis) Be careful not to overtreat and put client
into alkalosis
5. As acidosis improves, hydrogen ions shift out of
cells and potassium moves intracellularly.
Hyperkalemia may become hypokalemia and
potassium replacement will be needed.
6. Assessment
Vital signs
Intake and output
Neuro, GI, and respiratory status;
Cardiac monitoring
Reassess repeated arterial blood gases and
electrolytes
METABOLIC ALKALOSIS
pH >7.45
HCO3 > 26 mEq/L
Caused by a bicarbonate excess, due to loss
of acid, or a bicarbonate excess in the body
Common Stimuli
a. Loss of hydrogen and chloride ions
through excessive vomiting, gastric
suctioning, or excessive diuretic therapy
Response to hypokalemia
b. Excess ingestion of bicarbonate rich antacids
or excessive treatment of acidosis with Sodium
Bicarbonate
Signs and Symptoms
Compensation: Lungs respond by decreasing the
depth and rate of respiration in effort to retain
carbon dioxide and lower pH
Neuro: altered mental status, numbness and tingling
around mouth, fingers, toes, dizziness, muscle
spasms
(similar to hypocalcemia due to less ionized calcium
levels)
Respiratory: shallow, slow breathing
Diagnostic test findings
1. ABGs: pH> 7.45, HCO3
+
>26 Electrolytes: Serum K < 3.5 mEq/L
2. Electrocardiogram: as with hypokalemia
3.

Collaborative Management
MS: Fluids and Electrolyte

1.
2.
3.
4.

Correcting underlying cause will often improve

alkalosis
Restore fluid volume and correct electrolyte
imbalances (usually IV NaCl with KCL).
With severe cases, acidifying solution may be
administered.
Assessment
Vital signs
Neuro, cardiac, respiratory assessment
Repeat arterial blood gases and electrolytes

Selected Water and Electrolyte

Solutions

Isotonic Solutions
A. 0.9% NaCl (isotonic, also called NSS)
Na+ 154 mEq/L
Cl- 154 mEq/L
(308 mOsm/L)
Also available with varying concentrations of dextrose
(the most frequent used is a 5% dextrose concentration

An isotonic solution that expands the ECF

volume, used in hypovolemic states,
resuscitative efforts, shock, diabetic ketoacidosis,
metabolic alkalosis, hypercalcemia, mild Na
deficit
Supplies an excess of Na and Cl; can cause fluid
volume excess and hyperchloremic acidosis if
used in excessive volumes, particularly in
patients with compromised renal function, heart
failure or edema
Not desirable as a routine maintenance
solution, as it provides only Na and Cl (and
these are provided in excessive amounts)
When mixed with 5% dextrose, the resulting
solution becomes hypertonic in relation to
plasma, and in addition to the above described
electrolytes, provides 170cal/L
Only solution that may be administered with
blood products

B. Lactated Ringers solution (Hartmanns solution)

Na+ 130 mEq/L
K+ 4 mEq/L
Ca++ 3 mEq/L
Cl- 109 mEq/L
Lactate (metabolized to bicarbonate) 28 mEq/L
(274 mOsm/L)
Also available with varying concentration of
dextrose (the
most common is 5% dextrose)
An isotonic solution that contains multiple
electrolytes in roughly the same concentration
as found in plasma (note that solution is lacking
in Mg++) provides 9 cal/L
Used in the tx of hypovolemia, burns, fluid lost
as bile or diarrhea, and for acute blood loss
replacement
Lactate is rapidly metabolized into HCO3- in the
body. Lactated Ringers solution should not
be used in lactic acidosis because the ability to
convert lactate into HCO3- is impaired in this
disorder.

Not to be given with a pH > 7.5 because

bicarbonates is formed as lactate breaks down
causing alkalosis
Should not be used in renal failure because it
contains potassium and can cause
hyperkalemia
Similar to plasma

C. 5% Dextrose in Water (D5W)

No electrolytes
50 g of glucose

An isotonic solution that supplies 170 cal/L

and free water to aid in renal excretion of
solutes
Used in treatment of hypernatremia, fluid loss
and
dehydration
Should not be used in excessive volumes in
the early post-op period (when ADH secretion
is increased due to stress reaction)
Should not be used solely in tx of fluid
volume deficit, because it dilutes plasma
electrolyte concentrations
Contraindicated in head injury because it may
cause increased intracranial pressure
Should not be used for fluid resuscitation
because it can cause hyperglycemia
Should be used with caution in patients with
renal
or cardiac dse because of risk of fluid overload
Electrolyte-free solutions may cause peripheral
circulatory collapse, anuria in pt. with sodium
deficiency and increased body fluid loss
Converts to hypotonic solution as dextrose is
metabolized by body. Overtime D5W without
NaCl can cause water intoxication (ICF vol.
Hypotonic
Solutions
excess bec. solution is hypotonic)
D. 0.45% NaCl
half-strength saline)
Na+ 77 mEq/L
Cl- 77 mEq/L
(154 mOsm/L)
Also available with varying concentration of dextrose
(the most common is 5% dextrose)

Provides Na, Cl and free water

Free water is desirable to aid the kidneys
in elimination of solute
Lacking in electrolytes other than Na and
Cl
When mixed with 5% dextrose, the solution
becomes slightly hypertonic to plasma and
in addition to the above-described
electrolytes provides 170 cal/L
Used in the tx of hypertonic dehydration, Na
and Cl depletion and gastric fluid loss
Not indicated for third-space fluid shifts or
increased intracranial pressure
Administer cautiously, because it can cause fluid
shifts from vascular system into cells, resulting in
cardiovascular collapse and increased
intracranial pressure

MS: Fluids and Electrolyte

Hypertonic Solutions
E. 3% NaCl (hypertonic saline)
Na+ 513 mEq/L
Cl- 513 mEq/L
(1026 mOsm/L)

Used to increase ECF volume, decrease cellular

swelling
Highly hypertonic solution used only in critical
situations to treat hyponatremia
Must be administered slowly and
cautiously, because it can cause
intravascular volume overload and
pulmonary edema
Supplies no calories
Assists in removing ICF excess
F. 5% NaCl (hypertonic solution)
Na+ 855 mEq/L
Cl- 855 mEq/L
(1710 mOsm/L)

Highly hypertonic solution used to

treat symptomatic hyponatremia
Administered slowly and cautiously, because
it can cause intravascular volume overload and
pulmonary edema
Supplies no calories

Colloid Solutions
G. Dextran in NS or 5% D5W
Available in low-molecular-weight (Dextran 40) and
high- molecular-weight (Dextran 70) forms

Colloid solution used as volume/plasma

expander for intravascular part of ECF
Affects clotting by coating platelets and
decreasing ability to clot
Remains in circulatory system up to 24
hours
Used to treat hypovolemia in early shock to
increase pulse pressure, CO, and arterial
BP
Improves microcirculation by decreasing
RBC
aggregation
Contraindicated in hemorrhage,
thrombocytopenia, renal dse and
severe dehydration
Not a substitute for blood or blood
products