1

S.No Table of Content Page No

1 Body Fluids Compartments 2
2 Composition of Body Fluids 3
3 Electrolyte Composition of Body Fluids 3
4 Extracellular and Intracellular Fluids 3
5 Fluid Movement Among Compartments 4
6 Fluid Shifts, Regulation of Fluids And Electrolytes 4
7 Water Balance and ECF Osmolality 4
8 Water Output 4
9 Regulation of Water Output 5
10 Primary Regulatory Hormones 5
11 Disorders of Water Balance 6
12 Electrolyte Balance 7
13 Sodium in Fluid and Electrolyte Balance 7
14 Sodium balance 8
15 Potassium Balance 9
16 Regulation of Potassium Balance 9
17 Regulation of Calcium 9
18 Regulation of Anions 10
19 Acid-Base Balance 10
20
Factors affecting body fluid, electrolyte and acid base
balance
11
21 Electrolyte imbalance 11
22 Acid base imbalance 15
23 Nursing diagnosis 18
24 References 20
2

FLUID AND ELECTROLYTE IMBALANCE
Introduction
Electrolytes are minerals in your body that have an electric charge. They are in your blood,
urine and body fluids. Maintaining the right balance of electrolytes helps your body's blood
chemistry, muscle action and other processes. Sodium, calcium, potassium, chlorine, phosphate
and magnesium are all electrolytes. You get them from the foods you eat and the fluids you
drink.
Levels of electrolytes in your body can become too low or too high. That can happen when the
amount of water in your body changes, causing dehydration or overhydration. Causes include
some medicines, vomiting, diarrhea, sweating or kidney problems. Problems most often occur
with levels of sodium, potassium or calcium.
Fluid Balance- The amount of water gained each day equals the amount lost
Electrolyte Balance - The ions gained each day equals the ions lost
Acid-Base Balance - Hydrogen ion (H
+
) gain is offset by their loss
Body Fluids Compartments
Intracellular Fluid (ICF) - fluid found in the cells (cytoplasm, nucleoplasm) comprises
60% of all body fluids.
Extracellular Fluid (ECF) - all fluids found outside the cells, comprises 40% of all body
fluids
1. Interstitial Fluid - 80% of ECF is found in localized areas: lymph, cerebrospinal
fluid, synovial fluid, aqueous humor and vitreous body of eyes, between serous
and visceral membranes, glomerular filtrate of kidneys.
2. Blood Plasma - 20% of ECF found in circulatory system







3

Composition of Body Fluids
Water is the main component of all body fluids making up 45-75% of the total body
weight.
Sources of water include
o Ingested foods and liquids (preformed water)
o Metabolic water produced during dehydration synthesis of anabolism.
Solutes are broadly classified into
o Electrolytes are inorganic salts, all acids and bases, and some proteins
o Nonelectrolytes examples include glucose, lipids, creatinine, and urea
o Electrolytes have greater osmotic power than nonelectrolytes
o Water moves according to osmotic gradients
Electrolyte Composition of Body Fluids
Each fluid compartment of the body has a distinctive pattern of electrolytes
o Extracellular Fluids
ECFs are similar except for the high protein content of plasma
Sodium (Na
+
) is the major cation
Chloride (Cl
-
)is the major anion
o Intracellular Fluids
Have low sodium and chloride, Potassium (K
+
) is the chief cation,
Phosphate (PO4
-
) is the chief anion
Extracellular and Intracellular Fluids
Sodium and potassium concentrations in extra- and intracellular fluids are nearly opposites
This reflects the activity of cellular ATP-dependent sodium-potassium pumps
Electrolytes determine the chemical and physical reactions of fluids
Ion fluxes are restricted and move selectively by active transport
Nutrients, respiratory gases, and wastes move unidirectionally
Plasma is the only fluid that circulates throughout the body and links external and internal
environments
Osmolalities of all body fluids are equal; changes in solute concentrations are quickly
followed by osmotic changes.








4

Fluid Movement among Compartments
Compartmental exchange is regulated by osmotic and hydrostatic pressures
Net leakage of fluid from the blood is picked up by lymphatic vessels and returned to the
bloodstream
Exchanges between interstitial and intracellular fluids due to the selective permeability of
the cellular membranes
Regulation of Fluids and Electrolytes
Homeostatic mechanisms respond to changes
in ECF
No receptors directly monitor fluid or
electrolyte balance
Response is to changes in plasma volume or
osmotic concentrations
All water moves passively in response to osmotic gradients
Body content of water or electrolytes rises if intake exceeds outflow
Water Balance and ECF Osmolality
To remain properly hydrated,
water intake must equal water
output
Water intake sources
o Ingested fluid (60%) and
solid food (30%)
o Metabolic water or water
of oxidation (10%)
Water Output
Urine (60%)
Feces (4%)
Insensible losses through the
skin and lungs (28%)
Sweat (8%)
Increases in plasma osmolality trigger thirst and release of antidiuretic hormone (ADH)
Fluid Shifts
If ECF becomes hypertonic relative to
ICF, water moves from ICF to ECF
If ECF becomes hypotonic relative to
ICF, water moves from ECF into cells
5

Activation of stomach and intestinal stretch
receptors.
Regulation of Water Output
Obligatory water losses include:
o Insensible water losses from lungs and skin
o Water that accompanies undigested food residues in feces
Obligatory water loss reflects the fact that:
o Kidneys excrete 900-1200 mOsm of solutes to maintain blood homeostasis
o Urine solutes must be flushed out of the body in water
Primary Regulatory Hormones
1. Antidiuretic hormone (ADH) (also called vasopressin)
Is a hormone made by the hypothalamus, and stored and released in the posterior
pituitary gland
Primary function of ADH is to decrease the amount of water lost at the kidneys (conserve
water), which reduces the concentration of electrolytes
ADH also causes the constriction of peripheral blood vessels, which helps to increase
blood pressure
ADH is released in response to such stimuli as a rise in the concentration of electrolytes
in the blood or a fall in blood volume or pressure. These stimuli occur when a person
sweats excessively or is dehydrated.
1. Sweating or dehydration increases the blood osmotic pressure.
2. The increase in osmotic pressure is detected by osmoreceptors within the
hypothalamus that constantly monitor the osmolarity ("saltiness") of the blood
Regulation of Water Intake
The hypothalamic thirst center is stimulated by:
Decline in plasma volume of 10%15%
Increases in plasma osmolality of 12%
Baroreceptor input, angiotensin II, and other stimuli
Thirst is quenched as soon as we begin to drink water
Feedback signals that inhibit the thirst centers
include:Moistening of the mucosa of the mouth and
throat
6

3. Osmoreceptors stimulate groups of neurons within the hypothalamus to release ADH
from the posterior pituitary gland.
4. ADH travels through the bloodstream to its target organs:
a. ADH tavels to the collecting tubules in the kidneys and makes the membrane more
permeable to water (that is it increases water reabsorption) which leads to a decrease in
urine output.
b. ADH also travels to the sweat glands where it stimulates them to decrease perspiration
to conserve water.
c. ADH travels to the arterioles, where it causes the smooth muscle in the wall of the
arterioles to constrict. This narrows the diameter of the arterioles which increases blood
pressure.
Alcohol inhibits the production of ADH which is one of the reasons a person has increased fluid
excretion after drinking alcohol!
2. Aldosterone
Is a hormone made by cells in the adrenal cortex (zona glomerulosa)
Controls the levels of Na
+
and K
+
ions in extracellular fluids such as the blood
Net result of its action is to reabsorb Na
+
ions into the blood and simultaneously excrete
K
+
ions into the urine; because "water follows the ions," as Na
+
is reabsorbed, water is
also reabsorbed.
3. Natriuretic Peptides (Atrial Natriuretic Peptide and Brain Natriuretic Peptide)
Atrial natriuretic peptide (ANP) is a hormone made by cells in the right atrium whenever
blood volume increases (atria are stretched)
Brain natriuretic peptide (BNP) is a hormone made by cells in the ventricles in response
to excessive stretching of the ventricles
In general, the effects of ANP and BNP are opposite to those of angiotensin II
Both ANP and BNP promote the loss of sodium ions and water at the kidneys in the
urine, inhibit rennin release, and inhibit the secretion of ADH and aldosterone
By inducing blood vessels to dilate and water to be excreted in the urine, ANP and BNP
reduce both blood volume and blood pressure.
Disorders of Water Balance
Dehydration:
Water loss exceeds water intake and the body is in negative fluid balance
Causes include: hemorrhage, severe burns, prolonged vomiting or diarrhea, profuse
sweating, water deprivation, and diuretic abuse
7

Signs and symptoms: cottonmouth, thirst, dry flushed skin, and oliguria (decreased
production of urine)
Hypotonic Hydration:
Renal insufficiency or an extraordinary amount of water ingested quickly can lead to
cellular overhydration, or water intoxication
ECF is diluted sodium content is normal but excess water is present resulting
hyponatremia promotes net osmosis into tissue cells
These events must be quickly reversed to prevent severe metabolic disturbances,
particularly in neurons
Electrolyte Balance
Electrolytes are salts, acids, and bases, but electrolyte balance usually refers only to salt
balance
Salts are important for:
o Essential minerals
o Controls osmosis between fluid compartments
o Help maintain acid-base balance
o Carry electrical (ionic) current for action potentials
Sodium in Fluid and Electrolyte Balance
Sodium holds a central position in fluid and electrolyte balance
Sodium is the single most abundant cation in the ECF
o Accounts for 90-95% of all solutes in the ECF
o Contribute 280 mOsm of the total 300 mOsm ECF solute concentration
The role of sodium in controlling ECF volume and water distribution in the body is a
result of:
o Sodium being the only cation to exert significant osmotic pressure
o Sodium ions leaking into cells and being pumped out against their
electrochemical gradient
Sodium concentration in the ECF normally remains stable
o Rate of sodium uptake across digestive tract directly proportional to dietary intake
o Sodium losses occur
through urine and
perspiration
Changes in plasma sodium levels
affect:
o Plasma volume, blood
pressure
o ICF and interstitial fluid
volume
Large variations in sodium are
corrected by homeostatic
mechanisms.
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If sodium levels are too high, atrial natriuretic peptide (ANP) is secreted.
If sodium levels are too low, antidiuretic hormone (ADH) and aldosterone are
secreted.
Sodium balance
Regulation of Sodium Balance: Aldosterone
A decrease in Na
+
levels in the plasma stimulates aldosterone release
The kidneys detect the decrease in Na
+
levels and cause a series of reactions referred to as
the renin-angiotensin-aldosterone mechanisms.
This is mediated by the juxtaglomerular apparatus, which releases renin in response to:
o Sympathetic nervous system stimulation
o Decreased filtrate osmolality
o Decreased stretch (due to decreased blood pressure)
Sodium reabsorption
o 65% of sodium in filtrate is reabsorbed in the proximal tubules
o 25% is reclaimed in the loops of Henle
When aldosterone levels are high, all remaining Na
+
is actively reabsorbed
Water follows sodium if tubule permeability has been increased with ADH
Atrial Natriuretic Hormone (ANH)
Is released in the heart atria as a response to stretch (elevated blood pressure),
It has potent diuretic and natriuretic effects
It promotes excretion of sodium and water, inhibits angiotensin II production












9


Potassium Balance
Potassium ion concentrations in ECF are low
Not as closely regulated as sodium
Potassium ion excretion increases as ECF concentrations rise, aldosterone secreted, pH
rises
Potassium retention occurs when pH falls
Regulation of Potassium Balance
Relative ICF-ECF potassium ion concentration affects a cells resting membrane
potential
Potassium controls its own ECF concentration via feedback regulation of aldosterone
release
An increase in K
+
levels stimulates the release of aldosterone through the renin-
angiotensin-aldosterone mechanism or through the direct release of aldosterone from the
adrenal cortex cells
Aldosterone stimulates potassium ion excretion from the kidneys
In cortical collecting ducts, for each Na
+
reabsorbed, a K
+
is excreted
When K
+
levels are low, the amount of secretion and excretion is kept to a minimum
Excessive ECF potassium (hyperkalemia) decreases membrane potential
Too little potassium (hypokalemia) causes hyperpolarization and nonresponsiveness
Hyperkalemia and hypokalemia can
o Disrupt electrical conduction in the heart
o Lead to sudden death
Hydrogen ions shift in and out of cells lead to corresponding shifts in potassium in the
opposite direction and interferes with activity of excitable cells
Regulation of Calcium
Ionic calcium in ECF is important for blood clotting, cell membrane permeability, and
secretory behavior
Hypocalcemia increases excitability and causes muscle tetany
Hypercalcemia inhibits neurons and muscle cells and may cause heart arrhythmias
Two hormones regulate blood calcium levels:
1. Parathyroid Hormone (PTH) (made by the parathyroid glands)
2. Calcitonin (CT) (made by the thyroid glands)
As calcium-rich foods are ingested, blood calcium levels rise. The thyroid gland releases
calcitonin (CT).
o CT binds to receptors on osteoblasts (bone-forming cells).
o This triggers the osteoblasts to deposit calcium salts into bone throughout the
skeletal system.
o This causes the blood calcium levels to fall.
o CT stops being produced when blood calcium levels return to normal.
When blood calcium levels fall, the parathyroid glands (located on posterior surface of the
thyroid gland) release PTH.
o PTH binds to receptors on osteoclasts (bone-degrading cells) within the skeletal
system
o The osteoclasts decompose bone and release calcium into the blood.
o The blood calcium level rises
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o PTH stops being produced when blood calcium levels return to normal.
Calcium re-absorption and phosphate excretion go hand in hand
o Filtered phosphate is actively reabsorbed in the proximal tubules
o In the absence of PTH, phosphate reabsorption is regulated by its transport
maximum and excesses are excreted in urine
o High or normal ECF calcium levels inhibit PTH secretion
o Release of calcium from bone is inhibited
o Larger amounts of calcium are lost in feces and urine
o More phosphate is retained
Regulation of Anions
Chloride (Cl-) is the major anion accompanying sodium in the ECF
99% of chloride is reabsorbed under normal pH conditions
When acidosis occurs, fewer chloride ions are reabsorbed
Other anions have transport maximums and excesses are excreted in urine
Acid-Base Balance
Acid is the substance releases hydrogen ions (H) and a base (alkalis) which can accept
hydrogen ions. pH is the relative acidity or alkalinity of a solution: higher hydrogen ions more
acidic which is low pH. And less hydrogen ions more alkaline which is high pH.
- Body fluids are slightly alkaline.
- normal pH of arterial blood is 7.35-7.45
- several body systems including buffers, the respiratory system, and the renal system are
maintaining the narrow pH
- a drop in pH is called acidosis
- a rises in pH is called alkalosis
Regulating acid-base
Buffers: major buffers system in ECF is the bicarbonate ( HCO
3
-
) and carbonic acid ( H2CO3).
Besides bicarbonate and carbonic acid buffers, plasma proteins, hemoglobin and phosphates also
function as buffers in body fluids.
Respiratory Regulation:
It regulates acid-base balance by eliminating or retaining carbon dioxide (CO
2
) through
altering the rate and depth of respirations.
- if the blood level of carbonic acid increase the rate and depth of respirations increase to excrete
carbon dioxide to fall the level of carbonic acid
- if the blood level of bicarbonate increase the rate and depth of respirations decrease to retained
the carbon dioxide and rise the level of carbonic acid.
- PCO
2
refer to pressure of carbon dioxide in venous blood
-PaCO
2
refers to pressure of carbon dioxide in arterial blood. Normal PaCO2 is 38-40 mmHg
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Renal Regulation: kidneys maintain acid-base balance by excreting or conserving bicarbonate
and hydrogen ions
- if acidity increased the kidneys reabsorb and regenerate bicarbonate and excrete H
- in the case of alkalosis excess bicarbonate is excreted and H ion is retained
- normal serum bicarbonate level is 22-26 mEq/L.
Factors Affecting Body Fluid, Electrolytes and Acid-Base Balance
Age: infant has immature kidneys, rapid respiration and more body surface area than adult which
make the infant losses the fluid rapidly. In elderly people the thirst response often is blunted and
kidney becomes less able to conserve water that will affect the fluid balance.
Gender and Body Size: people with a higher percentage of body fat have less fluid.
Environmental Temperature: both salt and water are lost through sweating in hot climate
Lifestyle: diet, exercise, stress and alcohol consumption all affect the fluid and electrolyte
balance
Disturbances in Fluid Volume, Electrolyte, and Acid-Base Balances
Many factors affect the fluid and electrolyte balance such as illness, surgery, medications, burns,
vomiting, diarrhea and nasogastric suction. The majority of childhood illnesses that caused
imbalances they occur secondary to vomiting and diarrhea.
The imbalances can be:
a) Total body deficit or excess of fluid and electrolyte and the osmolality of the body is not
affected.
b) When relationship between fluid and electrolyte has been altered and the osmolality is altered.
III) or both a and b.
Electrolyte Imbalances
Potassium (95% of K of body in IC fluid)
Hypokalemia: K < 3.5 mEq/L caused by vomiting, diarrhea and gastric suction diuretics,
alkalosis. The K shifts from EC to IC space and also insulin promotes K to enter skeletal muscles
and hepatic cells. CLINICAL MANIFESTATION are; cardiac arrhythemia, muscle weakness,
shallow breathing, polyuria.
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Hyperkalemia : K > 5.0 : most commonly occur in children as a result of too rapid
administration of IV potassium chloride, and caused by renal failure, shift of K from IC to EC by
tissue damage, and metabolic acidosis. Clinical manifestation is malaise, muscle weakness,
oliguria to anuria, abnormal cardiac function and diarrhea
Calcium (requires for activation of numerous enzymes, cardiac and neural and muscular
functions)
Hypocalcaemia: Ca < 4.0 mEq/L, caused by hypoparathyroidism, Vit D deficiency,burns,
infections diarrhea, renal failure. CLINICAL MANIFESTATION is tetany, when giving cows
milk early in infancy so that the milk is high conc of phosphate which drops the Ca level,
laryngospasm, numbness and seizures.
Hypercalcemia: Ca > 5.5 mEq/L, caused by increase administration of Vit Aand D, prolonged
immobilization and hyperparathyroidism. CLINICAL MANIFESTATION is nausea, vomiting,
constipation and flank pain.
Signs and symptoms of a fluid and electrolyte imbalance are often subtle blood chemistry tests
help diagnose and evaluate electrolyte imbalance.
ELECTROLYTE
IMBALANCES
SIGNS AND SYMPTOMS DIAGNOSTIC
TEST RESULTS
HYPONATREMIA
Muscle twitching and
weakness due to osmotic
swelling of cells
*Lethargy, confusion,
seizures,and coma due to
altered neurotransmission
*Hypertension and tachycardia
due to decreased extracellular
circulating volume
*Nausea,vomiting, and
abdominal cramps due to edema
affecting receptors in the brain or
vomiting center of the brain stem
*Oliguria or anuria due to renal
dysfunction
*Serum sodium <135 mEa/l
*Decreased urine specific
gravity
*Decreased serum osmalality
*Urine sodium > 100 mEq/24
hours
*Increased red blood cell count
HYPERNATREMIA
*Agitation, restlessness, fever,
and decreased level of
consciousness due to altered
cellular metabolism
*Hypertension, tachycardia,
pitting edema, and excessive
weight gain due to water shift
from intracellular to
extracellular fluid
*Serum sodium > 145 mEq/l
*Urine sodium <40 mEq/24
hours
*High serum osmolality
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*Thirst, increased viscosity of
saliva, rough tongue due to fluid
shift
*Dyspnea, respiratory arrest,
and death from dramatic
increase in in osmotic pressure
HYPOKALEMIA
*Dizziness, hypotension,
arrhythmias, electrocardiogram
(ECG) changes, and cardiac
arrest due to changes in membrane
excitability
*Nausea, vomiting, anorexia,
diarrhea, decreased peristalsis,
and abdominal distention due to
decreased bowel motility
*Muscle weakness, fatigue, and
leg cramps due to decreased
neuromuscular excitability
*Serum potassium < 3.5 mEq/l
*coexisting low serum calcium
and magnesium levels not
responsive to treatment for
hypokalemia usually suggest
hypomagnesemia
*metabolic alkalosis
*ECG changes include flattened
Waves, elevated U waves,
Depressed ST segment
HYPERKALEMIA
*Tachycardia changing to
bradycardia,ECG changes, and
cardiac arrest due to
hypopolarization and alterations
in repolarization
*Nausea, diarrhea, and
abdominal cramps due to
decreased gastric motility
*Muscle weakness and flaccid
paralysis due to inactivation of
membrane sodium channels
*Serum potassium > 5mEq./l
*Metabolic acidosis
*ECG changes include tented
and elevated T waves, widened
QRS complex,
prolonged PR interval, flattened
or absent P waves, depressed
ST segment
HYPOCHLOREMIA
*Muscle hypertonicity and
tetany
*Shallow, depressed breathing
*Usually associated with
hyponatremia and its
characteristic symptoms, such
as muscle weakness and
twitching
*Serum chloride <98 mEq/l
*Serum pH > 7.45 (supportive
value)
*Serum CO2 >32 mEq/l
(supportive value)
HYPERCHLOREMIA
*Deep, rapid breathing
*Weakness
*Diminished cognitive ability,
possibly leading to coma
*Serum chloride > 108 mEq/l
*Serum pH < 7.35, serum CO2
<22 mEq/l (Supportive values)
HYPOCALCEMIA
*Anxiety, irritability, twitching
around the
mouth,laryngospasm,seizures,
Chvostek's and Trousseau's
signs due to enhanced
*Serum calcium <8.5 mg/dl
*Low platelet count
*ECG shows lengthened QT
interval, prolonged ST segment,
arrhythmias
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neuromuscular irritability
*Hypotension and arrhthmeas
due to decreased calcium influx
*Possible changes in serum
protein because half of serum
calcium is bound to albumin
HYPERCALCEMIA
*Drowsiness, lethargy,
headaches, irritability,
confusion, depression, or apathy
due to decreased neuromuscular
irritability ( increased threshold)
*Weakness and muscle
flaccidity due to depressed
neuromuscular irritability and
release of acetylcholine of the
myonearal junction
*Bone pain and pathological
fractures due to calcium loss
from bones
*Heart block due to decreased
neuromuscular irritability
*Anorexia, nausea, Vomiting,
constipation, and dehydration
due to kidney stone formation
*Serum calcium > 10.5 mg/dl
*ECG shows signs of heart
block and shortened QT interval
*Azotemia
*Decreased parathyroid
hormone level
*Sulkowitch urine test shows
increased calcium precipitation
HYPOMAGNESEMIA
*Nearly always coexists with
hypokalemia and hypocalcemia
*Hyperirritability, tetany, leg
and foot cramps, positive
Chvostek's and Trousseau's signs
confusion in neuromuscular
transmission
*Arrhythmias, vasodilation, and
hypotension due to enhanced
inward sodium current or
concurrent effects of calcium
and potassium imbalance
*Serum magnesium < 1.5
mEq/l
*Coexisting low serum
potassium and calcium levels
HYPERMAGNESEMIA
*Hypermagnesemia is
uncommon, caused by
decreased renal excretion (renal
failure) or increased intake of
magnesium
*Diminished reflexes, muscle
weakness to flaccid paralysis
due to suppression of acetylcholine
release of the myoneural
junction, blocking cell excitability
*respiratory distress secondary
to respiratory muscle paralysis
*Heart block, bradycordia due
*Serum magnesium > 2.5
mEq/l
*Coexisting elevated potassium
and calcium levels
15

to decreased
inward sodium current
*Hypotension due to relaxation
of vascular smooth muscle and
reduction of vascular wall surface
HYPOPHOSPHATEMIA
*Muscle weakness, tremor, and
paresthesia due to deficiency of
adenosine triphasphate
*Peripheral hypoxia due to 2,3 -
diphosphoglycerate deficiency
*Serum phosphates < 2.5mg/dl
*Urine phosphate > 1.3 g/24
hours
HYPERPHOSPHATEMIA
*Usually asymptomatic unless
leading to hypocalcemia, with
tetany and seizures
*Serum phosphates > 4.5 mg/dl
*Serum calcium < 9mg/dl
*Urine phosphorus < 0.9 g per
24 hours
ACID BASE IMBALANCE
The abnormalities in PCO
2
increase or decrease is called respiratory alkalosis or acidosis because
PCO
2
regulated by respiration
i. Increase in PCO
2
- respiratory acidosis
ii. Decrease in PCO
2
-respiratory alkalosis.
The abnormalities of plasma bicarbonate concentration refer to metabolic process
I) Increase in HCO
3
metabolic alkalosis
II) Decrease in HCO
3
- metabolic acidosis
1- Respiratory Acidosis
Hypoventilation and CO2 retention cause carbonic acid level to increase which will drop the pH
level below 7.35. This can be caused by
I) Asthma,
II) Central nervous system depression
III) Anesthesia, alcohol,
IV) Aspiration of foreign body.
V) Pneumonia
When respiratory acidosis occur the kidneys will retain bicarbonate to restore the normal ratio of
bicarbonate:carbonic acid (20:1) in order to restore the normal pH.
Signs and symptoms
I) Headache
II) Blurred vision
16

III) Restlessness
IV) Anxiety
V) Tremors
2- Respiratory Alkalosis
Hyperventilation the CO2 is exhaled causing the carbonic acid to fall and raise the pH above
7.45. This can be caused by
I) Tetany
II) fever,
III) anxiety,
IV) respiratory infection.
With respiratory alkalosis the kidneys will excrete bicarbonate to return normal pH.
Signs and symptoms
I) increase irritability of central and peripheral nervous system.
II) Light headache
III) Altered consciouness
IV) Paresthesia of extremities
V) arrhythmias
3-Metabolic Acidosis (diarrhea)
When bicarbonate is low in relation to the carbonic acid in the body , causing the pH to fall. This
can be caused by
I) renal failure
II) Inability of the kidneys to excrete H ions.
III) Increase of anaerobic metabolism
IV) Decrease in blood volume causing the kidney to function less effectively
Metabolic acidosis will stimulate the respiratory center causing the rate and depth of respiration
to increase (in which the CO
2
is eliminated and the carbonic acid is fall).
Signs and symptoms
I) Increase depth of respiration
II) Arrhythmia
III) Lethargy-coma
IV) Impaired growth (rickets)
17

V) Wt loss
VI) Anorexia
VII) Muscle weakness and listlessness.
4- Metabolic Alkalosis (vomiting)
When the amount of bicarbonate in the body exceeds the normal 20:1 ratio, which can be caused
with ingestion of antacid, vomiting which causing losing in H
+
ions.
Causes are
I) Muscles hypertonic
II) vomiting
III) nasogastric suctioning
IV) diuretics; decrease the ECF leaving HCO
3
uncharged
V) Hypokalemia The metabolic alkalosis will stimulate the respiratory center to slow and
shallow the breathing (causing to retain CO
2
which will increase the carbonic acid level).
VI) HCO
3
retention may result from, massive blood transfusion, excessive administration of
sodium bicarbonate
Signs and symptoms
i. Weakness
ii. Muscle cramp
iii. Dizziness
Respiratory alkalosis is a common result of hyperventilation.
















18

NURSING DIAGNOSIS: fluid and electrolyte imbalance
A. Fluid volume deficit related to restricted oral fluid intake before, during, and after
surgery; blood loss; and loss of fluid associated with vomiting, nasogastric tube drainage,
and/or profuse wound drainage;
B. Hypokalemia, hypochloremia, and metabolic alkalosis related to loss of electrolytes and
hydrochloric acid associated with vomiting and nasogastric tube drainage;
C. Fluid volume excess or water intoxication related to vigorous fluid therapy during and
immediately following surgery and an increased secretion of antidiuretic hormone (output
of ADH is stimulated by trauma, pain, and anesthetic agents).
Nursing Actions and Selected Purposes/Rationales
A. Assess for and report signs and symptoms of:
1. Fluid volume deficit:
a. decreased skin turgor, dry mucous membranes, thirst
b. sudden weight loss of 2% or greater
c. postural hypotension and/or low B/P
d. weak, rapid pulse
e. capillary refill time greater than 3 seconds
f. neck veins flat when client is supine
g. change in mental status
h. continued low urine output 48 hours after surgery with a change in specific
gravity (the specific gravity will usually increase with an actual fluid volume
deficit but may be decreased depending on the cause of the deficit)
i. elevated BUN
2. hypokalemia (e.g. cardiac dysrhythmias, postural hypotension, muscle weakness,
nausea and vomiting, continued abdominal distention and hypoactive or absent
bowel sounds, low serum potassium)
3. hypochloremia and metabolic alkalosis (e.g. dizziness, irritability, paresthesias,
muscle twitching or spasms, hypoventilation, low serum chloride, elevated pH
and TCO
2
).
B. Implement measures to prevent or treat fluid volume deficit, hypokalemia,
hypochloremia, and metabolic alkalosis:
1. perform actions to prevent nausea and vomiting (see Diagnosis 8, action b)
2. if a nasogastric tube is present and needs to be irrigated frequently and/or with
large volumes of solution, irrigate it with normal saline rather than water
3. perform actions to reduce fever if present (e.g. administer antipyretics as ordered,
sponge client with tepid water, remove excessive clothing or bedcovers) in order
to prevent diaphoresis and subsequent loss of fluid
4. carefully measure drainage (e.g. wound, nasogastric) and administer replacement
fluids as ordered
5. administer fluid and electrolyte replacements if ordered
6. maintain a fluid intake of at least 2500 ml/day unless contraindicated
19

7. when oral intake is allowed and tolerated, assist client to select foods/fluids high
in potassium (e.g. bananas, orange juice, potatoes, raisins, apricots, cantaloupe,
tomato juice).
C. Consult physician if signs and symptoms of fluid volume deficit and electrolyte
imbalances persist or worsen.
Nursing Actions and Selected Purposes/Rationales
A. Assess for and report signs and symptoms of fluid volume excess and water intoxication:
1. weight gain of 2% or greater over a short period
2. elevated B/P (B/P may not be elevated if fluid has shifted out of vascular space)
3. presence of an S
3
heart sound
4. full, bounding pulse
5. intake that continues to be greater than output 48 hours postoperatively (for the
first 48 hours after surgery, output is expected to be less than intake due to
increased secretion of ADH)
6. change in mental status
7. crackles (rales), diminished or absent breath sounds
8. low serum sodium and osmolality (indicates water intoxication)
9. decreased BUN and Hct (low Hct could also indicate blood loss)
10. dyspnea, orthopnea
11. edema (peripheral edema reflects fluid volume excess; cellular edema reflects
water intoxication)
12. distended neck veins
13. delayed hand vein emptying time (longer than 5 seconds)
14. elevated CVP (use internal jugular vein pulsation method to estimate CVP if
monitoring device not present)
15. Chest x-ray results showing pulmonary vascular congestion, pleural effusion, or
pulmonary edema.
B. Implement measures to prevent or treat fluid volume excess and water intoxication:
1. administer fluid replacement therapy judiciously, especially within first 48 hours
after surgery
2. maintain fluid restrictions if ordered
3. if client is receiving intravenous fluids that contain sizable amounts of sodium
(e.g. 0.9% NaCl, lactated Ringer's), consult physician about a change in the
solution or a decrease in the rate of infusion
4. if client is receiving numerous and/or large volume intravenous medications,
consult pharmacist about ways to prevent excessive fluid administration (e.g. stop
primary infusion during administration of intravenous medications, dilute
medication in the minimum amount of solution)
5. administer diuretics if ordered to increase excretion of water.
C. Consult physician if signs and symptoms of fluid volume excess or water intoxication
persist or worsen.

20

References
1. Kozier & Erbs, Fundamental of Nursing 8
th
Edition, Dorling Kindasley publication, Page
1424 1437.
2. Potter.Perry Basic Nursing Essential for practice, 6
th
Edition, Elsevier Publication, Page No.
428 438.
3. Taylor et al., Fundamental of Nursing, 7
th
Edition, Wolters Kluwer Publication, Page No.
1415-1429.
4. Needham, A. Comparative and Environmental Physiology. Acidosis and Alkalosis.
5. Yeomans, ER; Hauth, JC; Gilstrap, LC, Strickland DM. "Umbilical cord pH, PCO2, and
bicarbonate following uncomplicated term vaginal deliveries (146 infants)". Am J Obstet
Gynecol 151, Page No. 798800.
6. Pomerance, Jeffrey. Interpreting Umbilical Cord Gases: For Clinicians Caring for the Fetus
or Newborn. Pasadena, CA: BNMG.