Lecture Notes on Fluids and Electrolytes
Prepared By: Mark Fredderick R Abejo R.N, MAN
STI COLLEGE GLOBAL CITY
College of Nursing
MEDICAL AND SURGICAL NURSING
Fluids and Electrolytes
Lecturer: Mark Fredderick R. Abejo RN, MAN
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 water
between intravascular and interstitial spaces
III. Body Fluid Distribution:
A. 2 body compartments:
1. Intracellular fluids (ICF): fluids
within cells of body [major
intracellular electrolytes: Potassium
(K+), Magnesium (Mg +2)]
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
B. 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
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
IV. 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
eventually burst (hemolyze)
3. Different intravenous solutions, used to
correct some abnormal conditions,
categorized according to osmolality:
B. 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)
C. 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
D. 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
Lecture Notes on Fluids and Electrolytes
Prepared By: Mark Fredderick R Abejo R.N, MAN

V. Mechanisms that Regulate Homeostasis:

How the body adapts to fluid and electrolyte changes?
ADH – produced by hypothalamus, released by posterior
pituitary when osmoreceptor or baroreceptor is
A. Thirst: primary regulator of water intake
triggered in hypothalamus
(thirst center in brain)
B. Kidneys: regulator of volume and
Aldosterone – produced by adrenal cortex; promotes Na &
osmolality by controlling excretion of
water reabsorption
water and electrolytes
C. Renin-angiotension-aldosterone
mechanism: response to a drop in blood
Sensible & Insensible Fluid Loss
pressure; results from vasoconstriction and
sodium regulation by aldosterone
Sensible: urine, vomiting, suctioned secretions
D. Antidiuretic hormone: hormone to
Insensible: lungs , skin, GI and evaporation
regulate water excretion; responds to
osmolality and blood volume
E. Atrial natriuretic factor: hormone from Normal Fluid Intake and Loss in Adults
atrial heart muscle in response to fluid
excess; causes increased urine output by Intake:
blocking aldosterone Water in food 1,000 mls
Water from oxidation 300 mls
Fluid Balance Regulation Water in liquid 1,200 mls

Thirst reflex triggered by: TOTAL 2,500 mls

1. decreased salivation & dry mouth
2. increased osmotic pressure Output:
stimulates osmoreceptors in the  Skin 500 mls
hypothalamus
3. decreased blood volume activates the  Lungs 300 mls
renin/angiontensin pathway, which simulates the  Feces 150 mls
thirst center in hypothalamus  Kidneys 1,500 mls
TOTAL 2,500 mls
Renin-Angiotensin
1. renin
2. drop in blood
= acts onvolume
plasmainprotein
kidneys = renin released
angiotensin
(released by the liver) to form angiotensin I
3. ACE = converts Angiotensin I to Angiotensin II in
the lungs
4. Angiotensin II = vasoconstriction &
aldosterone release
MS: Fluids and Electrolyte Abejo
Lecture Notes on Fluids and Electrolytes
Prepared By: Mark Fredderick R Abejo R.N, MAN

IV Fluids  Risk factors are the following:

Isotonic LR a. Diabetes Insipidus
PNSS (0.9%NSS) b. Adrenal insufficiency
NM c. Osmotic diuresis
d. Hemorrhage
Hypotonic D5W e. Coma
- isotonic in bag f. Third-spacing conditions like ascites,
- dextrose=quickly pancreatitis and burns
metabolized=hypotonic
D2.5W
0.45% NSS PATHOPHYSIOLOGY:
0.3% NSS
0.2% NSS Risk Factors --- inadequate fluids in the body-----decreased
Hypertonic D50W blood volume ----- decreased cellular hydration------cellular
D10W shrinkage------weight loss, decreased turgor, oliguria,
D5NSS hypotension, weak pulse, etc.
D5LR
3%NSS
ASSESSMENT:

Colloids (usually CHONs) & Plasma expanders

Physical examination
 Weight loss, tented skin turgor, dry mucus membrane
Dextran – synthetic polysaccharide, glucose solution  Hypotension
- increase concentration of blood, improving blood  Tachycardia
volume up to 24 hrs  Cool skin, acute weight loss
- contraindicated: heart failure, pulmonary edema,  Flat neck veins
cardiogenic shock, and renal failure  Decreased CVP

Hetastarch – like Dextran, but longer-acting

Subjective cues
- expensive
- derived from corn starch  Thirst
 Nausea, anorexia
Composition of Fluids  Muscle weakness and cramps
 Change in mental state
Saline solutions – water, Na, Cl
Dextrose solutions – water or saline, calories
Lactated Ringer‟s – water, Na, Cl, K, Ca, Laboratory findings
lactate
Plasma expanders – albumin, dextran, plasma protein 1. Elevated BUN due to depletion of fluids or
(plasmanate) - increases oncotic pressure, pulling fluids decreased renal perfusion
into circulation 2. Hemoconcentration
Parenteral hyperalimentation – fluid, electrolytes, amino 3. Possible Electrolyte imbalances: Hypokalemia,
acids, calories Hyperkalemia, Hyponatremia, hypernatremia
4. Urine specific gravity is increased (concentrated
A. FLUID VOLUME DEFICIT or HYPOVOLEMIA urine) above 1.020

 Definition: This is the loss of extra cellular fluid NURSING MANAGEMENT

volume that exceeds the intake of fluid. The loss
of water and electrolyte is in equal proportion. It 1. Assess the ongoing status of the patient by doing an
can be called in various terms- vascular, cellular or accurate input and output monitoring
intracellular dehydration. But the preferred term is 2. Monitor daily weights. Approximate weight loss 1
hypovolemia. kilogram = 1liter!
 Dehydration refers to loss of WATER alone, 3. Monitor Vital signs, skin and tongue turgor, urinary
with increased solutes concentration and sodium concentration, mental function and peripheral
concentration circulation
4. Prevent Fluid Volume Deficit from occurring by
Pathophysiology of Fluid Volume Deficit identifying risk patients and implement fluid
replacement therapy as needed promptly
 Etiologic conditions include: 5. Correct fluid Volume Deficit by offering fluids orally
a. Vomiting if tolerated, anti-emetics if with vomiting, and foods
b. Diarrhea with adequate electrolytes
c. Prolonged GI suctioning 6. Maintain skin integrity
d. Increased sweating 7. Provide frequent oral care
e. Inability to gain access to fluids 8. Teach patient to change position slowly to avoid
f. Inadequate fluid intake sudden postural hypotension
g. Massive third spacing

MS: Fluids and Electrolyte Abejo

Lecture Notes on Fluids and Electrolytes
Prepared By: Mark Fredderick R Abejo R.N, MAN

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
Pathophysiology of Fluid Volume Excess
4. Teach patient about edema, ascites, and fluid
therapy. Advise elevation of the extremities,
restriction of fluids, necessity of paracentesis,
dialysis and diuretic therapy.
5. Instruct patient to avoid over-the-counter medications
without first checking with the health care provider
because they may contain sodium

 Etiologic conditions and Risks factors ELECTROLYTES

a. Congestive heart failure
b. Renal failure  Electrolytes are charged ions capable of conducting
c. Excessive fluid intake electricity and are solutes found in all body
d. Impaired ability to excrete fluid as in renal compartments.
disease Sources of electrolytes
e. Cirrhosis of the liver
f. Consumption of excessive table salts  Foods and ingested fluids, medications; IVF and
g. Administration of excessive IVF TPN solutions
h. Abnormal fluid retention
Functions of Electrolytes
 Maintains fluid balance
PATHOPHYSIOLOGY  Regulates acid-base balance
 Needed for enzymatic secretion and activation
Excessive fluid --- expansion of blood volume------edema,  Needed for proper metabolism and
increased neck vein distention, tachycardia, hypertension. effective processes of muscular contraction,
nerve transmission
The Nursing Process in Fluid Volume Excess Types of Electrolytes
 CATIONS- positively charged ions; examples
ASSESSMENT
are sodium, potassium, calcium
Physical Examination
 ANIONS- negatively charged ions; examples
 Increased weight gain
are chloride and phosphates]
 Increased urine output
 The major ICF cation is potassium (K+); the
 Moist crackles in the lungs
major ICF anion is Phosphates
 Increased CVP
 The major ECF cation is Sodium (Na+); the
 Distended neck veins
major ECF anion is Chloride (Cl-)
 Wheezing
 Dependent edema

Subjective cue/s ELECTROLYTE IMBALANCES

 Shortness of breath
 Change in mental state
SODIUM
Laboratory findings
1. BUN and Creatinine levels are LOW because  The most abundant cation in the ECF
of dilution  Normal range in the blood is 135-145 mEq/L
2. Urine sodium and osmolality decreased (urine  A loss or gain of sodium is usually accompanied by
becomes diluted) a loss or gain of water.
3. CXR may show pulmonary congestion  Major contributor of the plasma Osmolality
IMPLEMENTATION  Sources: Diet, medications, IVF. The minimum daily
requirement is 2 grams
ASSIST IN MEDICAL INTERVENTION Functions:
1. Administer diuretics as prescribed 1. Participates in the Na-K pump
2. Assist in hemodialysis 2. Assists in maintaining blood volume
3. Provide dietary restriction of sodium and water 3. Assists in nerve transmission and
NURSING MANAGEMENT muscle contraction
4. Primary determinant of ECF concentration.
1. Continually assess the patient‟s condition by
measuring intake and output, daily weight 5. Controls water distribution throughout the body.
monitoring, edema assessment and breath sounds 6. Primary regulator of ECF volume.
2. Prevent Fluid Volume Excess by adhering to diet 7. Sodium also functions in the establishment of the
prescription of low salt- foods. electrochemical state necessary for muscle
3. Detect and Control Fluid Volume Excess by closely contraction and the transmission of nerve
monitoring IVF therapy, administering impulses.
medications, providing rest periods, placing in
8. Regulations: skin, GIT, GUT, Aldosterone
semi-fowler‟s position for lung expansion and
increases Na retention in the kidney
providing frequent skin care for the edema

MS: Fluids and Electrolyte Abejo

Lecture Notes on Fluids and Electrolytes
Prepared By: Mark Fredderick R Abejo R.N, MAN
SODIUM DEFICIT: HYPONATREMIA
 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
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
In summary:
Physical Examination
 Altered mental status
 Vomiting
 Lethargy
 Muscle twitching and convulsions (if sodium level
is below 115 mEq/L)
 Focal weakness
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. 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
Abejo
Lecture Notes on Fluids and Electrolytes
Prepared By: Mark Fredderick R Abejo R.N, MAN
Other factors
a. Diabetes insipidus
b. Heat stroke
c. Near drowning in ocean
d. Malfunction of dialysis
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
hypernatremia.
 Dehydration (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.
A primary characteristic of hypernatremia is thirst.
Thirst is so strong a defender of serum sodium levels in
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
IMPLEMENTATION
ASSIST IN THE MEDICAL INTERVENTION
1. Administer hypotonic electrolyte solution slowly
as ordered
2. Administer diuretics as ordered
Loop diuretics (thiazides ok)
3. 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
patient‟s 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 teaching to avoid over-the counter
medications without consultation as they may
contain sodium
POTASSIUM
 The most abundant cation in the ICF
 Potassium is the major intracellular electrolyte; in
fact, 98% of the body‟s 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 body‟s 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. Maintains ICF Osmolality
2. Important for nerve conduction and
muscle contraction
3. Maintains acid-base balance
4. Needed for metabolism of carbohydrates, fats
and proteins
5. Potassium influences both skeletal and cardiac
muscle activity.
( For example, alterations in its concentration change
myocardial irritability and rhythm )
6. Regulations: renal secretion and excretion,
* Aldosterone promotes renal excretion
* Acidosis promotes K exchange for hydrogen
Abejo
Lecture Notes on Fluids and Electrolytes
Prepared By: Mark Fredderick R Abejo R.N, MAN

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..
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
IMPLEMENTATION
ASSIST IN THE MEDICAL INTERVENTION
1. Provide oral or IV replacement of potassium
2. 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!
3. NEVER administer K by IV bolus or IM
NURSING MANAGEMENT
1. Continuously monitor the patient by assessing the
cardiac status, ECG monitoring, and digitalis
precaution
2. Prevent hypokalemia by encouraging the patient to eat
potassium rich foods like orange juice, bananas,
cantaloupe, peaches, potatoes, dates and apricots.
3. Correct hypokalemia by administering prescribed IV
potassium replacement. The nurse must ensure that the
kidney is functioning properly!
4. 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!!
5. 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 Addison‟s disease
d. Improper use of potassium supplements
 Other factors
1. Pseudohyperkalemia- tight tourniquet and
hemolysis of blood sample, marked
Abejo
Lecture Notes on Fluids and Electrolytes
Prepared By: Mark Fredderick R Abejo R.N, MAN

leukocytosis

MS: Fluids and Electrolyte Abejo

Lecture Notes on Fluids and Electrolytes
Prepared By: Mark Fredderick R Abejo R.N, MAN

2. Transfusion of “old” banked blood 7. Acidosis

3. Acidosis
4. 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,
intermit tent intestinal colic, and diarrhea, may
occur in hyperkalemic patients.

ASSESSMENT
Physical Examination
 Diarrhea
 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
MS: Fluids and Electrolyte Abejo
Lecture Notes on Fluids and Electrolytes
Prepared By: Mark Fredderick R Abejo R.N, MAN

IMPLEMENTATION

ASSIST IN MEDICAL INTERVENTION

1. Monitor the patient‟s cardiac status with
cardiac machine
2. Institute emergency therapy to lower potassium
level by:
a. Administering IV calcium gluconate-
antagonizes action of K on cardiac
conduction
b. Administering Insulin with dextrose-
causes temporary shift of K into cells
c. Administering sodium bicarbonate-
alkalinizes plasma to cause temporary
shift
d. Administering Beta-agonists
e. Administering Kayexalate (cation-
exchange resin)-draws K+ into the
bowel
NURSING MANAGEMENT
1. Provide continuous monitoring of cardiac
status, dysrhythmias, and potassium levels.
2. Assess for signs of muscular weakness,
paresthesias, nausea
3. Evaluate and verify all HIGH serum K levels
4. Prevent hyperkalemia by encouraging high risk
patient to adhere to proper potassium restriction
5. 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
6. Assist in hemodialysis if hyperkalemia
cannot be corrected.
7. Provide client teaching. Advise patients at risk to
avoid eating potassium rich foods, and to use
potassium salts sparingly.
8. 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
MS: Fluids and Electrolyte Abejo
Lecture Notes on Fluids and Electrolytes
Prepared By: Mark Fredderick R Abejo R.N, MAN

Functions: HYPOCALCEMIA
 Low levels of calcium in the blood
1. Needed for formation of bones and teeth
2. For muscular contraction and relaxation  Risk Factors
3. For neuronal and cardiac function a. Hypoparathyroidism (idiopathic or postsurgical)
4. For enzymatic activation b. Alkalosis (Ca binds to albumin)
5. For normal blood clotting c. Corticosteroids (antagonize Vit D)
d. Hyperphosphatemia
Regulations: e. Vit D deficiency
f. Renal failure (vit D deficiency)
1. GIT- absorbs Ca+ in the intestine; Vitamin D helps to
increase absorption  Clinical Manifestation
2. Renal regulation- Ca+ is filtered in the glomerulus  Decreased cardiac contractility
andreabsorbed in the tubules:  Arrhythmia
3. Endocrine regulation:  ECG: prolonged QT interval, lengthened ST
segment
 Parathyroid hormone from the parathyroid glands  Trousseau’s sign (inflate BP cuff 20mm
is released when Ca+ level is low. PTH causes above systole for 3 min = carpopedal spasm)
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.

 Chvostek’s 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 Abejo

Lecture Notes on Fluids and Electrolytes
Prepared By: Mark Fredderick R Abejo R.N, MAN
HYPERCALCEMIA
 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
tumor‟s 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
9. Dialysis (severe case)
10. Watch out for digitalis toxicity
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
HYPOMAGNESEMIA
 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
o. Increased levels of stress
 Clinical Manifestation
 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
Abejo
Lecture Notes on Fluids and Electrolytes
Prepared By: Mark Fredderick R Abejo R.N, MAN

 Clinical Manifestation
HYPERPHOSPHATEMIA
 Hyporeflexia
 Hypotension, bradycardia, arrhythmia
 Risk Factors
 Flushing a. Acidosis (Ph moves out of cell)
 Weakness, lethargy, coma b. Cytotoxic agents/chemotherapy in cancer
 Decreased RR & respiratory paralysis c. Renal failure
 Loss of DTR‟s d. Hypocalcemia
e. Massive BT (P leaks out of cells during storage
*like hypercalcemia of blood)
f. Hyperthyroidism
Collaborative Management
1. Diuretics  Clinical Manifestation
2. Stop Mg-containing antacids & enemas  Calcification of kidney, cornea, heart
3. IV fluids rehydration  Muscle spasms, tetany, hyperreflexia
4. Calcium gluconate – (antidote,
antagonizes cardiac & respiratory effects
*like hypocalcemia
of Mg)
5. Dialysis – if RF
Collaborative ManagementM
1. Aluminum antacids as phosphate binders: Al
PHOSPHORUS carbonate (Basaljel), Al hydroxide
(Amphojel)
 primary intracellular anion 2. Ca carbonate for hypocalcemia
 part of ATP – energy 3. Avoid phosphate laxatives/enemas
 85% bound with Ca in teeth/bones, skeletal muscle 4. Increase fluid intake
 reciprocal balance with Ca 5. Diet: low Phos, no carbonated drinks
 absorption affected by Vit D, regulation affected by
PTH (lowers P level)
 Normal value : 2.5-4.5 mg/dL
CHLORIDE
Functions:
 extracellular anion, part of salt
1. bone/teeth formation & strength
 binds with Na, H (also K, Ca, etc)
2. phospholipids (make up cell membrane integrity)
 exchanges with HCO3 in the kidneys (& in RBCs)
3. part of ATP
 Normal value: 95 -108 mEq/L
4. affects metabolism, Ca levels
Functions:
Sources:
1. helps regulate BP, serum osmolarity
red & organ meats (brain, liver, kidney), poultry, fish, eggs, 2. part of HCl
milk, legumes, whole grains, nuts, carbonated drinks
3. acid/base balance (exchanges with HCO3)

HYPOPHOSPHATEMIA Sources:
salt, canned food, cheese, milk, eggs, crab, olives
 Risk Factors
a. Decreased Vit D absorption, sunlight exposure
b. Hyperparathyroidism (increased PTH)
HYPOCHLOREMIA
c. Aluminum & Mg-containing antacids (bind P)
d. Severe vomiting & diarrhea
 Risk Factors
a. Diuresis
 Clinical Manifestation
b. Metabolic alkalosis
 Anemia, bruising (weak blood cell membrane)
c. Hyponatremia, prolonged D5W IV
 Seizures, coma
d. Addison‟s
 Muscle weakness, paresthesias
 Constipation, hypoactive bowel sounds
 Clinical Manifestation
 Slow, shallow respirations (met. Alkalosis)
*Like hypercalcemia  Hypotension (Na & water loss)
Collaborative Management
Collaborative Management
1. Sodium phosphate or potassium phosphate
1. Administer IV or Oral : KCl, NaCl
IV (give slowly, no faster than 10 mEq/hr)
2. Diet: high Cl (& usually Na)
2. Sodium & potassium phosphate orally (Neutra-
Phos, K-Phos) – give with meals to prevent
gastric irritation
HYPERCHLOREMIA
3. Avoid Phos-binding antacids
4. Diet: high Mg, milk
 Risk Factors / Cause
5. Monitor joint stiffness, arthralgia,
a. Metabolic acidosis
fractures, bleeding
b. Usually noted in hyperNa, hyperK

MS: Fluids and Electrolyte Abejo

Lecture Notes on Fluids and Electrolytes
Prepared By: Mark Fredderick R Abejo R.N, MAN
 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
- 35-45mmHg
PaO2- amount of pressure exerted by O2 on the plasma
- 80-100mmHg
SaO2- percent of hemoglobin saturated with O2
Base excess – amount of HCO3 available in the ECF
- -3 to +3
MS: Fluids and Electrolyte
Interpretation Arterial Blood Gases
 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
Step 1
 Look at the pH
 Is it up or down?
 If it is up - it reflects alkalosis
 If it is down - it reflects acidosis
Step 2
 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
Step 3
 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
Abejo
Lecture Notes on Fluids and Electrolytes
Prepared By: Mark Fredderick R Abejo R.N, MAN
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
cannula
6. Continue respiratory assessments, monitor 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 tightness
Collaborative Management
1. Treatment: encourage client to breathe slowly in a
paper bag to rebreathe CO2
2. Breathe with the patient; provide emotional
support and reassurance, anti-anxiety agents,
sedation
3. On ventilator, adjustment of ventilation settings
(decrease rate and tidal volume)
4. 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
hypomagnesemia may occur
Signs and 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
 Lecture Notes on Fluids and Electrolytes
Prepared By: Mark Fredderick R Abejo R.N, MAN
 Respiratory: tries to compensate by hyperventilation:
deep and rapid respirations known as Kussmaul‟s
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. ABG‟s: pH> 7.45, HCO3 >26
2. Electrolytes: Serum K+ < 3.5 mEq/L
3. Electrocardiogram: as with hypokalemia
Collaborative Management
MS: Fluids and Electrolyte
1. Correcting underlying cause will often improve
alkalosis
2. Restore fluid volume and correct
electrolyte imbalances (usually IV NaCl
with KCL).
3. With severe cases, acidifying solution may
be administered.
4. 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 Ringer’s solution (Hartmann’s 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 Ringer‟s solution should not be
used in lactic acidosis because the ability to
Abejo
Lecture Notes on Fluids and Electrolytes
Prepared By: Mark Fredderick R Abejo R.N, MAN

convert lactate into HCO3- is impaired in

this disorder.

MS: Fluids and Electrolyte Abejo

Lecture Notes on Fluids and Electrolytes
Prepared By: Mark Fredderick R Abejo R.N, MAN
 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. excess bec. solution is hypotonic)
Hypotonic Solutions
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
Abejo