FLUID AND
ELECTROLYTE
BALANCES
WHY IS IT IMPORTANT
FOR NURSES TO
KNOW ABOUT FLUID
& ELECTROLYTE
BALANCE
INTRODUCTION
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Water is found everywhere on earth including
human body
In an adult 60% of the weight is water
Two third of the body’s water is found in the
cell
DISTRIBUTION OF BODY
FLUIDS
Body fluids are distributed in two distinct
compartments:
1.Extracellular fluids[ECF] Which includes
interstitial fliud & intravascular fluid
2.Intracellular fluids[ICF]
COMPOSITION OF BODY
FLUIDS
The fluids circulating throughout the body in
extracellular and intracellular fluid spaces
contain
1.Electrolytes
2.Minerals
3.Cells
MOVEMENT OF BODY
FLUIDS
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Diffusion
Osmosis
Filtration
Active transport
REGULATION OF BODY
FLUIDS
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Fluid intake
Fluid output
Hormonal influence
Lymphatic influences
Neurologic influences
Renal influences
ACID-BASE BALANCE
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Chemical regulation
Biologic regulation
Physiological regulation
1.Lungs
2.Kidneys
FLUID ,ELCTROLYTE
AND ACID-BASE
IMBALANCES
FLIUD IMBALANCES
The five types of fluid imbalances that may
occur are:
 Extracellular fluid imbalances(EVFVD)
 Extracellular fluid volume excess(ECFVE)
 Extracellular fluid volume shift
 Intracellular fluid vloume excess(ICFVE)
 Intrcellular fluid volume deficit(ICFVD)
EXTRACELULLAR FLUID
VOLUME DEFICIT

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An ECFVD, commonly called as dehydration ,
is a decrease in intravascular and interstitial
fluids
An ECFVD can result in cellular fluid loss if it
is sudden or severe
THREE TYPES OF ECFVD
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Hyperosmolar fluid volume deficit- water loss
is greater than the electrolyte loss
Isosmolar fluid volume deficit – equal
proportion of fluid and electrolyte loss
Hypotonic fluid volume deficit – electrolyte
loss is greater than fluid loss
ETIOLOGY AND RISK
FACTORS
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Severe vomiting
Diaphoresis
Traumatic injuries
Third space fluid shifts
[percardial, pleural,
pertonial and joint cavities]
Fever
Gatrointestinal suction
Ileostomy
Fistulas
Burns
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Hyperventilation
Decresed ADH secretions
Diabetes insipidus
Addison’s disease or adrenal
crisis
Diuretic phase of acute renal
failure
Use of diuretics
ELDERLY ARE HIGH RISK
OF ECFVD DUE TO
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Decreased thirst response
Decreased renal concentration of urine
Altered ADH response
Increased drug – drug interaction
Multiple chronic diseases
Decreased access to fluids due to financial or
transportation barriers
Debilitation
Chemical or physical restraint
Changes in mental status
CLINICAL MANIFESTATION
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In Mild ECFVD, 1to 2 L of water or 2% of the
body weight is lost
In Moderate ECFVD, 3 to 5L of water loss or
5%weight loss
IN Severe ECFVD , 5 to 10 L of water loss or
8% of weight loss
CLINICAL MANIFESTATION
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Thirst
Muscle weakness
Dry mucus membrane;dry
cracked lips or furrowed
tongue
Eyeballs soft and sunken
(severe deficit)
Apprehension ,
restlessness, headache ,
confusion, coma in severe
deficit
Elevated temperature
Tachycardia, weak thready
pulse
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Peripheral vein filling> 5
seconds
Postural systolic BP falls
>25mm Hg and diastolic
fall > 20 mm Hg , with
pulse increases > 30
Narrowed pulse pressure,
decreased CVP&PCWP
Flattened neck veins in
supine position
Weight loss
Oliguria(< 30 mlper hour)
Decreased number and
moisture in stools
LABORATORY FINDINGS
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Increased osmolality(> 295 mOsm/ kg)
Increased or normal serum sodium level (>
145mEq/ L )
Increase BUN (>25 mg / L )
Hyperglycemia ( >120 mg /dl )
Elevated hematocrit (> 55%)
Increased specific gravity ( > 1.030)
MANAGEMENT
Mild fluid volume loss can be corrected with oral
fluid replacement
-if client tolerates solid foods advice to take
1200 ml to 1500ml of oral fluids
-if client takes only fluids, increase the total
intake to 2500 ml in 24 hours
Management of Hyperosmolar
fluid volume deficit

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Administration of hypotonic IV solution ,
such as 5% dextrose in 0.2 %saline
If the deficit has existed for more than 24
hours,avoid rapid correction of fluid [sodium
solution to be infused at the rate of 0.5 to 0.1m
Eq/ L/ hr]
If heamorrhage is the cause for
ECFVD
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Packed red cells followed by hypotonic IV fluids is
administered
In situations where the blood loss is less than 1 L
normal saline or ringer lactate may be used
clients with severe ECFVD accompanied by severe
heart , liver, or kidney disease cannot tolerate large
volumes of fluid and sodium
EXTRACELLULAR FLUID
VOLUME EXCESS

ECFVE is increased fluid retention in the
intravasular and interstitial spaces
ETIOLOGY AND RISK
FACTORS
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Heart failure
Renal disorders
Cirrhosis of liver
Increased ingestion of high sodium foods
Excessive amount of IV fluids containing sodium
Electrolyte free IV fluids
SIADH,Sepsis
decreased colloid osmotic pressure
lymphatic and venous obstruction
Cushing’s syndrome & glucocorticoids
CLINICAL
MANIFESTATION
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Constant irritating cough
Dyspnea & crackles in lungs
Cyanosis, pleural fffusion
Neck vein obstruction
Bounding pulse &elevated BP
S3 gallop
Pitting & sacral edema
Weight gain
Increased CVP& PCWP
Change in level of consiousness
LAB INVESTIGATION
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serum osmolality <275mOsm/ kg
Low , normal or high sodium
Decreased hematocrit [ < 45%]
Specific gravity below 1.010
Decreased BUN [< 8mg/ dl]
MANAGEMENT
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Diuretics [combination of potassium sparing
and potassium depleting diuretics]
In people with CHF, ACE inhibitors and low
dose of beta blockers are used
A low sodium diet
EXTRACELLULAR FLUID
VOLUME SHIFT: THIRD
SPACING
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Fluid that shifts into the interstitial spaces and
remain there is called as third space fluid
Common sites are abdomen , pleural cavity,
peritoneal cavity and pericardial sac
RISK FACTORS
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Crushing injuries, major tissue trauma
Major surgery
Extensive burns
Acid –base imbalances and sepsis
Perforated peptic ulcers
Intestinal obstruction
Lymphatic obstruction
Autoimmune disorders
Hypoalbunemia
GI tract malabsorption
CLINICAL MANIFESTATION
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skin pallor
Cold extremities
Weak and rapid pulse
Hypotension
Oliguria
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Decreased levels of consiousness
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LAB INVESTIGATION
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Elevated hematocrit & BUN level
MANAGEMENT
Treat the cause
1.
For burns and tissue injuries large volume of
isosmolar IV fluid is administered
2.
Albumin is administered for protein deficit
3.
IV fluid intake is maintained after major surgery to
maintain kidney perfusion
4.
Pericardiocentesis if pericarditis is the result
5.
Paracentesis for ascitis
INTRACELLULAR FLUID
VOULME EXCESS:WATER
INTOXICATION

ICFVE is increase in amount of water inside
the cells
ETIOLOGY
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Administration of excessive amount of
hyposmolar IV fluids[0.45%saline or
5%dextrose in water]
Consumption of excessive amount of tap water
without adequate nutritional intake
SIADH
Schizophrenia[compulsive water consumption]
CLINICAL MANIFESTATIONS
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Headaches
Behavioral changes
Apprehension
Irritability, disorientation and confusion
Increased ICP – pupillary changes and decreased
motor and sensory function
Bradycardia, elevated BP, widened pulse pressure &
altered respiratory patterns, Babinski’s response
flaccidity, projectile vomiting, Papilledema, delirium,
convulsions &coma
LABORATORY FINDINGS
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High serum sodium level- 125 mEq/L
decreased hamatocrit
MANAGEMENT
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Early administration of IV fluids containing sodium
chloride cam prevent SIADH
oral fluids such as juices or soft drinks can be given
orally every hour
Perform neurologic checks every hour to see if
cranial changes are present
Monitor fluid intake , IV fluids and fluid output
hourly and weight daily
Administer antiemetics for food and fluid retention
INTRACELLULAR FLUID
VOLUME DEFICIT
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Severe hypernatremia and dehydration can
cause ICFVD
Relatively rare in healthy adults
common in elderly people and in those
conditions that result in acute water loss
Symptoms include confusion, coma, and
cerebral hemorrhage
Sodium
imbalances
Hyponatr
-aemia
Definiti
on
It is
defined
as a
plasma
sodium
level
below
135
mEq/ L
Risk factors/ etiology
Clinical
manifestation
Laboratory
findings
management
Kidney diseases
•Weak rapid pulse
•Hypotension
•Dizziness
•Apprehension
and anxiety
•Abdominal
cramps
•Nausea and
vomiting
•Diarrhea
•Coma and
convulsion
•Cold clammy
skin
•Finger print
impression on the
sternum after
palpation
•Personality
change
•Serum sodium
less than
135mEq/ L
•Identify the cause
and treat
Adrenal insufficiency
Gastrointestinal
losses
Use of diuretics
(especially with
along with low
sodium diet)
Metabolic acidosis
• serum
osmolality less
than
280mOsm/kg
•urine specific
gravity less than
1.010
*Administration of
sodium orally, by
NG tube or
parenterally
*For patients who
are able to eat &
drink, sodium is
easily accomplished
through normal diet
*For those unable
to eat,Ringer’s
lactate solution or
isotonic saline
[0.9%Nacl]is given
*For very low
sodium 0.3%Nacl
may be indicated
*water restriction in
case of
hypervolaemia
Sodium
imbalan
-ce
Definit
ion
causes
Hypernat
-remia
It is
defined
as
plasma
sodium
level
greater
than
145mE
q/L
*Ingestion of
large amount
of
concentrated
salts
*Iatrogenic
administration
of hypertonic
saline IV
*Excess
alderosterone
secretion
Clinical
manifestation

Low grade
fever

Postural
hypertension

Dry tongue
& mucous
membrane

Agitation

Convulsions

Restlessness

Excitability

Oliguria or
anuria

Thirst

Dry
&flushed skin
Lab findings
management
*high serum
sodium
135mEq/L
*Administration of
hypotonic sodium solution
[0.3 or 0.45%]
*high serum
osmolality295m
O sm/kg
*Rapid lowering of
sodium can cause cerebral
edema
*high urine
specificity 1.030
*Slow administration of
IV fluids with the goal of
reducing sodium not more
than 2 mEq/L for the first
48 hrs decreases this risk
*Diuretics are given in
case of sodium excess
*In case of Diabetes
insipidus desmopressin
acetate nasal spray is used
*Dietary restriction of
sodium in high risk clients
Potassium
imbalances
Definition
Causes
Clinical
manifestation
Lab findings
Management
Hypokalemia
It is
defined as
plasma
potassium
level of
less than
3.0
mEq/L
*Use of
potassium
wasting
diuretic
*weak irregular
pulse
* K – less than
3mEq/L results
in ST
depression ,
flat T wave,
taller U wave
Mild hypokalemia[3.3to
3.5] can be managed by
oral potassium
replacement
*shallow
respiration
*diarrhea,
vomiting or
other GI losses
*hypotesion
*Alkalosis
*weakness,
decreased
bowel sounds,
*Cushing’s
syndrome
*Polyuria
heart blocks ,
paresthesia,
fatigue,
*Extreme
sweating
decreased
muscle tone
*excessive use
of potassium
free Ivs
intestinal
obstruction
* K – less than
2mEq/L cause
widened QRS,
depressed ST,
inverted T
wave
Moderate hypokalemia
*K-3.0to 3.4mEq/L need
100to 200mEq/L of IV
potassium for the level to
rise to 1mEq/
Severe hypokalemia K- less
than 3.0mEq/L need 200to
400 mEq/L for the level to
rise to l mEq/L
*Dietary replacement of
potassium helps in
correcting the problem[1875
to 5625 mg/day]
Hyperkal
emia
Definition
Causes
Clinical
manifestation
Lab findings
Management
It is
defined as
the
elevation
of
potassium
level
above
5.0mEq/L
Renal failure ,
Irregular slow
pulse,
*High serum
potassium
5.3mEq/L
results in
peaked T wave
HR 60 to 110
*Dietary restriction of
potassium for potassium
less than 5.5 mEq/L
Hypertonic
dehydration,
hypotension,
Burns& trauma
anxiety,
Large amount of
IV administration
of potassium,
irritability,
Adrenal
insufficiency
Use of potassium
retaining diuretics
&
rapid infusion of
stored blood
paresthesia,
weakness
*serum
potassium of
7mEq/L results
in low broad Pwave
*serum
potassium
levels of
8mEq/L results
in no arterial
activity[no pwave]
*Mild hyperkalemia can be
corrected by improving
output by forcing fluids,
giving IV saline or
potassium wasting diuretics
*Severe hyperkalemia is
managed by
1.infusion of calcium
gluconate to decrease the
antagonistic effect of
potassium excess on
myocardium
2.infusion of insulin and
glucose or sodium
bicarbonate to promote
potassium uptake
3.sodium polystyrene
sulfonate [Kayexalate]
given orally or rectally as
retention enema
Calcium
imbalanc
es
Definitio
n
Causes
Clinical
manifestation
Lab
findings
hypocalc
emia
It is a
plasma
calcium
level
below
8.5
mg/dl
•Rapid
administration of
blood containing
citrate,
•Numbness and
tingling
sensation of
fingers,
•hypoalbuminemia,
•hyperactive
reflexes,
• Positve
Trousseau’s sign,
positive
chvostek’s sign ,
Serum
calcium
less
than 4.3
mEq/L
and
ECG
changes
•Hypothyroidism ,
•Vitamin
deficiency,
•neoplastic
diseases,
•pancreatitis
•muscle cramps,
•pathological
fractures,
•prolonged
bleeding time
Management
1.Asymtomatic hypocalcemia is
treated with oral calcium chloride,
calcium gluconate or calcium
lactate
2.Tetany from acute hypocalcemia
needs IV calcium chloride or
calcium gluconate to avoid
hypotension bradycardia and other
dysrythmias
3.Chronic or mild hypocalcemia
can be treated by consumption of
food high in calcium
Calcium
imbalance
Hypercalc
emia
Definition
Causes
Clinical
manifestation
Lab findings
Management
It is
calcium
plasma
level over
5.5 mEq/l
or 11mg/dl
•Hyperthyro
•idism,
•Decreased
muscle tone,
•High serum
calcium level
5.5mEq/L,
•Metastatic
bone tumors,
•anorexia,
1.IV normal saline, given
rapidly with Lasix
promotes urinary excretion
of calcium
•paget’s
disease,
•nausea,
vomiting,
•weakness ,
lethargy,
•osteoporosis ,
•prolonged
immobalisation
•low back pain
from kidney
stones,
•decreased level
of
consciousness
& cardiac arrest
• x- ray
showing
generalized
osteoporosis,
2.Plicamycin an antitumor
antibiotics decrease the
plasma calcium level
•widened bone
cavitation,
3.Calcitonin decreases
serum calcium level
•urinary stones,
4.Corticosteroid drugs
compete with vitamin D
and decreases intestinal
absorption of calcium
•elevated BUN
25mg/100ml,
•elevated
creatinine1.5mg
/100ml
5. If cause is excessive use
of calcium or vitamin D
supplements reduce or
avoid the same
Acid-Base
imbalance
Definition
Causes
Clinical
manifestation
Lab findings
Management
Respiratory
acidosis
It is a
clinical
disorder in
which the
pH is less
than 7.35
and the
paCO2 is
greater
than
42mmHg
COPD,
neuromuscular
disorder, GuillianBarre syndrome,
Myssthenia gravis,
Respiratory center
depression, Drugs,
late ARDS,
Dyspnea ,
PH lesser than
7.35,
Paco2 greater
than 45mmHg,
Hyperkalemia,
Hypoxemia
1.Treat underlying
cause
It is a
clinical
condition
in which
the arterial
Ph is
greater
than7.45
and the
paCO2 is
less than
38mmHg
Hypoxemia,
impaired lung
expansion,
thickened alveolar
– capillary
membrane,
Chemical
stimulation of
respiratory center,
traumatic
stimulation of
respiratory center
Hypoventilation
& excessive
CO2 production
Respiratory
Alkalosis
Hyperventilation
disorientation,
coma
2.Support ventilation
3.Correct electrolyte
imbalance
4.Intravenous
NaHCO3
Tachypnea,
giddiness,
dizziness,
syncope,
convulsions,
coma,
weakness,
paresthesia,
tetany
PH greater than
7.35
PaCO2 lesser
than 35 mmHg,
Hypokalemia,
Hypocalcemia
Increase CO2
retention
through CO2
rebreathing &
sedation and
mechanical
hypoventilation
Metabolic
Acidosis
Metabolic
Alkalosis
Definition
causes
Clinical
manifestation
Lab findings
Management
It is a
clinical
condition in
which the
HCO3 & pH
is decreased
Renal failure,
Diabetic
ketoacidosis,
Lactic acidosis,
ingested toxins,
renal tubular
acidosis
Hyperventilation
confusion,
drowsiness,
coma, headache
PH< 7.35,
HCO3<
22mEq/L
1.Treat the underlying
cause
Hypokalemia,
gatric fluid loss,
massive
correction of
whole blood,
Overcorrection of
acidosis with
NaCO3
Hypoventilation
Dysrythmias
It is a
clinical
condition in
which PH is
raised
2.Intravenous
NaHCO3
3.correct electrolyte
imbalance
PH >7.45
Hypokalemia
Hypocalcemia
PaCO2 normal
or increased
1.Treat the underlying
cause
2.Administer KCL
3.intravenous
acidifying
salts[NH4CL]
4.Administer
acetazolamide
CONCLUSION