FLUID AND ELECTROLYTE IMBALANCE

Introduction:
 Our body consists of two types of fluid intracellular and extracellular fluid. These fluids
help to maintain our body homeostasis.
 The body contains lots of fluid and electrolytes which are the transports cations, anions as
well as solvents and solutions for various reactions in our body.

Definitions and Terminologies

Homeostatic
The ability or tendency of an organism or cell to maintain internal equilibrium by
adjusting its physiological process.
Hydrostatic pressure
It is pertaining to the liquid in the state of equilibrium or the pressure exerted by a
stationary fluid.
Osmosis
Diffusion of fluid through a semi permeable membrane from a solution with a low solute
concentration to a solution with a higher solute concentration until there is an equal
concentration of fluid on both sides of the membrane.
Osmolarity
The concentration of solution in terms of osmoles of solutes per litre of solution.
Diffusion
The process by which solutes move from an area of higher concentration to one of the
lower concentration, without any expending extra energy.
Isotonic
A solution with the same osmolality as serum and other body fluid.
Osmolality
The number of osmosis(standard unit of osmotic pressure) per kilogram of solution.
Hypotonic Solution
A solution with an osmolality lower than that of the serum.

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Hypertonic solution
A solution with an osmolality higher than that of the serum.
Active Transport
The physiologic pump that moves fluid form an area of lower concentration to one of
higher concentration active transport requires ATP (Adenosine Triphosphate) for energy.
Filtration
Passage through a filter or through a material that prevents passage of certain molecules.
Eg: Capillary wall blood-brain barrier, radiographic grid.
Body fluids
 The total body water in adults of average built is about 60% of body weight.
 This proportion is higher in young people and in adults below average weight.
 It is lower in the elderly and in obese of all age groups.
Fluid Compartments
Body water is located in two major fluid compartments.
1. Intracellular fluid (ICF) compartment.
2. Extracellular fluid (ECF) compartment.
Extracellular Fluid
 The ECF is composed of interstitial fluid (tissues) and the intra vascular fluid (plasma)
interstitial fluid lies outside the vascular fluid and cells comprises 28% of total body
water.
 Approximately 60% of body weight is water.2/3 of water is 1CF, 1/3 of water is ECF.
 ECF consists of blood, plasma, lymph, cerebrospinal fluid and fluid in the interstitial
spaces of the body.
Intracellular fluid
 The composition of ICF therefore very different from ECF.
 Sodium levels are nearly ten times higher in the ECF than in the ICF.
 The substances are found inside the cell in significantly higher amounts than outside.
Eg: Adenosine, Triphosphate, Protein and Potassium.

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Regulators of Fluid balance
Thirst, Hormones, the lymphatic system, the nervous system and the kidneys assist the
regulation of body fluids.
Thirst
 The Thirst Centre is located in the hypothalamus and is activated by an increase in ECF
osmolality (Concentration).
 Thirst may result from hypotension, polyuria or fluid volume depletion.
Lymphatic system
The lymphatic system plays an important role in resuming excess fluid and protein from
the interstitial spaces to the blood.
Kidney
The kidneys maintain fluid volume and the concentration of urine by filtration the ECF
through the glomerulus.
Osmosis
It is the movement of water down its concentration gradient across a semi-permeable
membrane.
Functions of Fluid and Water
1. Kidney Functions
 Kidneys play an important role in the regulation of fluid and electrolyte balance.
 The kidneys normally filter 170L of plasma everyday in an adult, while excreting only
1.5l of urine.
 Regulation of pH of the ECF by retention of hydrogen ions.
 Excretion of metabolic wasted and toxic substance.
2. Heart and Blood Vessel Functions
 The pumping action of the heart circulates blood through the kidneys under sufficient
pressure to allow for urine formation.
3. Lung Function
 Through exhalation the lungs remove 300ml of water daily in the normal adult.
4. Pituitary Function
Functions of ADH include maintaining the osmotic pressure of the cell by controlling the
retention or excretion of water by the kidney and by regulation blood volume.

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5. Adrenal Function
Increased secretion of aldosterone causes sodium retention and potassium loss.
Other functions of fluid & water:
 Water provides the aqueous medium to the organism which is essential by the various bio
chemical reactions to occur.
 Water directly participates as a reactant in several metabolic reactions and chemical
reactions.
 It serves as a vehicle for transport of solutes.
 Waters is closely associated with the regulation of body temperature.

Movement of Body Fluids & Electrolytes

The body fluid compartments are separated from one another by cell membrane and the
capillary membrane. Although these membranes are completely permeable in water. They are
considered to be selectively permeable to solutes.

Small particles such as ions, oxygen and carbon dioxide move easily across these
membranes, but larger molecules such as glucose and proteins have more difficulty moving
between fluid compartments.

Solutes are substances dissolved in a liquid.

Eg: When sugar added to coffee.

The sugar is the solute. Coffee is the solvent. In the body water is solvent. The solutes
include electrolytes gasses such as oxygen and carbon dioxide, glucose, urea, amino acids and
proteins.

Methods of Movement of Body Fluid

 Diffusion
 Osmosis
 Active Transport
 Filtration

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Diffusion

Diffusion occurs when two solutes of different concentrations are separated by a semi
permeable membrane. The rate of diffusion of a solute varies according to the size of the
molecules, the concentration of the solution and the temperature of the solution. Large molecules
moves less quickly than smaller ones, molecules move from a solution of higher concentration to
a solution of lower concentration and increases in temperature increases the rate of motion of
molecules and therefore the rate of diffusion.

Osmosis

Osmosis is a specific kind of diffusion in which water moves across cell membranes,
from the less concentrated solution to the more concentrated solution.Osmosis is an important
mechanism for maintaining homeostasis and fluid balance.

Active Transport

An example of active transport Energy (ATP) is used to move sodium and potassium
molecules across a semi permeable membrane against sodium's and potassium's concentration
gradients(i.e. from areas of lesser concentration to areas of greater concentration).

This process differs from diffusion and osmosis. In this particular importance in
maintaining the differences in sodium and potassium ion concentrations of ECF and ICF under
normal conditions sodium concentrations are higher in ECF and potassium concentrations are
higher in ICF. To maintain the proportions, an active transport mechanism (The sodium-
potassium pump) is activated moving sodium from cells in to plasma and potassium from plasma
into cells. Active transport moves and holds sodium & potassium against their diffusion
gradients.

Filtration

Filtration is the transport of water and dissolved materials through a membrane from an
area of high pressure to an area of lower pressure. Passage through a filter or through a material
that prevents passage of certain molecules.

Eg: Capillary Wall, Blood-Brain Barrier, Radio Graphic Grid

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Fluid movement among compartments

1. Intra cellular fluid (ICF)

2. Extra cellular fluid (ECF)

Intra cellular fluid (ICF)

 The ICF provides the cell with the internal aqueous medium necessary for its chemical
functions.
 Thus sodium levels are nearly the times higher in the ECF than in the ICF. This
concentration gradient is essential for the function of excitable cells.
Eg: Mainly Nerve & Muscle
 Many substances are found inside the cell in significantly higher amounts than outside.
Eg: Adenosine Triphosphate, Protein and Potassium
 It includes all the water and electrolytes inside the cells of the body.
 It contains high concentration of
 Potassium
 Phosphate
 Magnesium
 Sulphate Ions & Along with most of the proteins in the body.

Extracellular Fluid compartment

 It includes all the fluid outside the cells

 Intestinal fluid, plasma, lymph, secretions of gland, fluid with in sub compartments are
separated by epithelial membranes.
 It contains high concentration of
 Sodium
 Chloride and
 Bicarbonate
 One third of the ECF is in plasma extracellular fluid osmolality.

The extra cellular fluid consists of blood, plasma, lymph, cerebrospinal fluid and fluid in the
interstitial spaces of the body.

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Fluid Imbalances

1. Extracellular Fluid Volume Deficit(ECFVD)

2. Extracellular Fluid Volume Excess(ECFVE)
3. Extracellular Fluid Volume Shift(ECFVS)
4. Intracellular Fluid Volume Excess(ICFVE)

1. Extracellular fluid volume Deficit (ECFVD)[Hypovolemia]

An ECFVD is a decrease in intravascular and interstitial fluids. ECFVD is a common and

serious fluid imbalance that results in vascular fluid volume loss (Hypovolemia). ECFVD can
lead to cellular fluid loss owing to fluid shifting from the cells to the vascular fluid to restore
fluid balance.

Etiology
 Commonly occurs with severe vomiting or diarrhea, traumatic injuries with excessive
blood loss.
 Third space fluid shifts & insufficient water or fluid intake.

Clinical Manifestations:

 Mild ECFVD- 1 to 22 of water & 2% of body weight is lost

 Moderate ECFVD- 3 to 5L of water loss & 5% of weight loss
 Severe ECFVD- 5 to 10L of water loss & 8% weight loss
 Thirst
 Decreased Skin Turgor
 Dry Mucus Membrane
 Dry cracked Lips or tongue
 Eye Balls sunken & soft
 Restlessness, Coma in severe deficit
 Elevated Temperature
 Systolic blood pressure >15mm Hg & Diastolic fall<10mm Hg
 Weight loss
 Oliguria (<30ml/hr)

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Laboratory Findings

 Increased Osmolality
 Increased or Normal serum sodium level
 BUN (>25mg/dL) (Blood Urea Nitrogen)
 Hyperglycemia (>120mg/dL)
 Elevated Hematocrit (>55%) value
 Increased Specific gravity

Risk Factors

 Diabetic Ketoacidosis
 Loosing large volume of blood
 Experiencing severe vomiting or diarrhea
 Having difficulty swallowing
 Elderly confused persons

Medical Management

An intravenous solution of 5% dextrose in water may be prescribed. If hemorrhage is the

cause of ECFVD blood replacement may be necessary if blood losses greater than 1 Lit. In that
situation in which the blood losses are less than 1Lit normal saline & lactated Ringers Solution
may be used to restore fluid volume. Urine output, Body weight and laboratory levels of sodium,
bilirubin, urea and nitrogen osmolality and potassium are closely monitored for both types
underlying problems can be treated with antiemetic, antidiarrheal agents, antibiotics and
antipyretics.

Dietary Management

Clients experiencing fluid loss from diarrhea should avoid fatty or fried foods and milk
products.

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2. Extra Cellular Fluid Volume Excess (ECFVE) [Hypervolemia]

Definition: Increased fluid retention in the intravascular & interstitial spaces.

Etiology

 Increase in the total body sodium content

 Heart failure
 Renal disorders
 Cirrhosis of liver
 Excessive amount of IV fluids contain sodium
 Increased ingestion of foods that contain high amount of sodium

Clinical Manifestations

a. Respiratory
 Constant irritating cough
 Dyspnea
 Cyanosis
 Crackles lungs

b. Cardio Vascular
 Neck vein engorgement in semi fowlers position
 Head vein engorgement
 Elevated blood pressure
 Pitting edema of Lower Extremities
 Sacral edema
 Weight gain

c. Neurological
 Change in level of consciousness

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Laboratory Findings

 Serum Osmolality < 275mosm/kg

 Serum Sodium <135 mag/L
 Decreased hematocrit value
 Specific gravity below 1.010

Medical Management

Pharmacological Management

 Loop & potassium sparing diuretics and digitalis preparation are frequently prescribed by
doctor.
 These potent diuretics cause potassium to be excreted along with the sodium &water.
 To preserve potassium a combination of potassium wasting and potassium sparing
diuretics is frequently prescribed.
 Digoxin, a digitalis preparation is ordered to increase the force of myocardial contraction
or to slow the heart failure is the cause of ECFVE.

Dietary Management

A low sodium diet is prescribed in order to reduce fluid retention.

NSG Diagnosis

Fluid volume excess related to compromised regulatory mechanisms of kidneys.

3. Extracellular Fluid Volume Shift (Third Space Fluid)

A fluid volume shift is basically a change in the location of extra cellular fluid between
the intravascular and the interstitial spaces. Vascular fluid to interstitial space fluid that shifts in
to the interstitial space and remains there is referred to as third space fluid.

Third space fluid occurs in case of tissue injury resulting from altered capillary
permeability (Eg: Inflammation, traumatic injury).

From increased vascular fluid volumes, increased vascular fluid volume appears in the
abdomen (Ascites), peritoneal cavity and pericardial sac.

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Etiology

 Simple blister or Sprain

 Crushing injuries
 Extensive burns
 Perforated peptic ulcer
 Intestinal obstruction
 Large venous thrombosis
 Lymphatic obstruction

Risk Factors

Major trauma or major surgery

Pathophysiology

Tissue injury causes

Relax of Histamine & Bradykinin

Increases Capillary Permeability

Allowing fluid, protein and other solutes to shift to interstitial spaces

The first phase fluid shift from vascular to interstitial spaces

Leading to fluid volume deficit (Hypovolemia)

II phase is shift from interstitial to vascular space

Leading to a fluid volume excess (Hypervolemia)

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Clinical Manifestations

 Skill pallor, cold extremities

 Weak and rapid pulse
 Hypotension
 Oliguria
 Decreased level of consciousness

Diagnostic Assessment

 Elevated Haemotocit
 BUN (Blood Urea Nitrogen)
 After fluid return to blood stream
 Decreased Haematocrit and BUN Levels

Medical Management

When hypovolemia results from tissue injury such as burns or crush injury a large
volume of intravenous need to be administrated.

The amount of fluid infusion may be three times greater than the urinary output.

During second phase, fluid administration and intake may need to be limited because of
fluid influx the tissue spaces to the vessels.

If third space fluid has occurred as a result of other process such as pericarditis and bowel
obstructions, the fluid may have to be removed in order for the organ to retain its function.

Nursing Management

 Vital signs should be recorded out.

 IV fluids replacement should be monitored if IV fluids are administered too rapidly,
hypervoleic (fluid overload) may occur.
 Frequently checks for difficulty breathing and neck vein engorgement are essential to
prevent pulmonary edema with fluid volume excess.
 The abdominal girth of clients with ascites should be measured every 8 hours.
 The level of consciousness should be monitored and precautious taken for seizures.

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  Frequent skin care to edematous areas during fluid shift is essential to prevent skin
breakdown.
 As fluid shifts back with the repair of tissue damage IV fluid replacement is decreased.
 Urine output should be monitored every hour to ensure at least 25ml/hr. Urine output is
usually reduced after tissue injury because of decreased renal circulation and the fluid
shift into the injured tissue spaces.
 The serum levels of BUN(Blood Urea Nitrogen) and ammonia should be monitored in
clients with ascites.

4. Intra cellular fluid volume Excess (ICFVE)

Water intoxication hypo osmolality disorders result from either water excess or solute
deficit and are mainly due to sodium loss.

The most common cause of ICFVE is the administration of excessive amount of hypo
osmolar fluids such as 5% Dextrose.

In those with brain injury that causes an increased production of ADH which increase
water re-absorption from renal tubules.

Clinical Manifestations

 Head ache, nausea, vomiting

 Pupillary changes
 Behavioral changes, irritability, disorientation
 Confusion, drowsier, decreased co-ordination
 Weight gain
 Bradycardia with increased systolic BP
 Increased respiration, projectile vomiting convulsions

Laboratory Findings

 Serum sodium level <125MG/LT

 Decrease Hematocrit value

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Management

 ICFVE is treated by the addition of solutes to IV fluids.

 Use of DS 0.45% Nacl will help to correct ICFVE when the cause is water excess.
 Oral fluids such as juices and soft drinks should be given in addition to water and ice
chips.
 Reflexes are pupillary response should be amended.
 Monitor vital signs and intake and output.
 Weight should be checked daily to measure fluid gain or loss.
 Administrated prescribed antiemetic as need to allow food and fluids to be ingested.
 Safety measures are necessary when the client displays behavioral changes.

Dehydration

It occurs when water is lost from the body leaving the client with excess sodium.

Because water is lost while electrolytes particularly sodium, are retained. The serum osmolality
and serum sodium levels increase.

Water is drawn in to the vascular compartment from the interstitial space and cells resulting in
cellular dehydration

Types

1. Hypotonic- loss of electrolytes

2. Hypertonic – loss of water

3. Isotonic – equal loss of water

Daily Fluid Requirement

Up to 10kg = 100ml/kg

10 to 20 kg= 50ml/kg

>20 kg = 20ml/kg

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Deficient Replacement

 75ml/kg
 ORS to be given over 4 hrs

Edema

In fluid volume excess both intravascular and interstitial spaces have an increased water and
sodium content. Excess interstitial fluid is knows as edema.

Types

1. Localized
2. Generalized

Localized

 Lymphatic edema
 Inflammatory edema
 Allergic edema
 Upto 70% of our body is water
 Muscle is made up of approximately 75% water
 Fat consists of about 50% water
 Bones are made up of about 50% water

Generalized

 Renal Edema
 Cardiac Edema
 Nutritional Edema

Pitting Edema

It is the edema that leaves a small depression or pit after finger pressure is applied to the
swollen area. The pit is caused by movement of fluid to adjacent tissue away from the point of
pressure. Within 10 to 30seconds the pit normally disappears.

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ELECTROLYTES

 Electrolytes are substances found in extracellular and intracellular fluid that dissociate
into electrically charged particles known as ions.
 Cations are that carry a positive charge and anions are ions that carry a negative charge.
 The positively charged electrolytes (cations) are sodium, potassium, calcium and
magnesium.
 The negatively charged electrolytes (anions) are chloride, phosphate and bicarbonate.

Functions of Electrolytes

1. Body water regulations

2. Acid base regulation
3. Enzyme reactions
4. Neuromuscular activity
5. Sodium concentration in the extra cellular fluid assists in the main tenance of fluid
balance

Factors that influence Electrolyte Balance

1. Active transport
2. The sodium pump
3. Diffusion
4. Aldosterone feedback mechanism
5. Parathyroid regulation of calcium

1. Active transport
The use of energy to move ions across a semi permeable membrane against a
concentration, chemical or electrical gradient.
2. Sodium Pump
 It maintains homeostasis of the electrolytes sodium (Na+) and potassium (K+).
 It may utilize upto 30% of ATP required for cellular metabolism.
 Homeostasis is maintained as excess Na+ is pumped across the cell membrane in change
for K+.

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3. Diffusion
 The process in which particles in a fluid move across a semi permeable membrane from
an area of greater concentration to an area of lesser concentration
4. Aldosterone Feedback Mechanism
 Adrenal cortex secretes the steroid hormone aldosterone when extracellular fluid sodium
concentrations decrease or potassium concentrations increases.
 Aldosterone stimulates kidney tubules to reabsorb sodium, potassium reabsorption
decreases as sodium re-absorption increases.
 This mechanism helps preserve normal sodium and potassium concentrations in
extracellular fluid.

5. Parathyroid regulation of calcium

Parathyroid Gland secretes parathormone when extracellular fluid calcium concentration

decreases

Parathormone stimulates the release of calcium form bone

Calcium re- absorption in the small intestine (Vitamin D required)

& Calcium re-absorption in kidney tubules

Increased extracellular fluid calcium concentration results

Decreased secretion of parathormone and gradual loss of excess calcium

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Distributions of Electrolytes in the Body

S. No Test Usual Reference Range

1 Serum Sodium 135-145meq/L

2 Serum Potassium 3.5-4.5meq/L

3 Total Serum Calcium 8.6-10.2meq/L

4 Ionizied Calcium 4.5-5.0mg/dL

5 Serum Magnesium 1.3-2.5meq/dL

6 Serum Chloride 07-107meq/dL

7 Serum Osmalality 275-300 mom/kg

8 Serum Creatinine 0.7-1.4mg/dL

9 Blood Urea Nitrogen 10:1-20:1

10 Burn to Creatinine Ration M:42-52% (OR) F: 35-47%

11 Hematocrit 60-110mg/dL

12 Serum Glucose 1.003-1.030

13 Urine Specific Gravity 60-110mg/dL

14 Urine pH <5-6

15 Urine Osmolarity 250-900mom/kg

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 ELECTROLYTE IMBALANCE

Sodium

 Sodium is the major cation of the extracellular compartment

 It regulated by dietary intake and aldosterone secretion.
 Natrium is the Latin word for sodium.
 Sodium deficit is known as Hyponatremia.
 Sodium excess is known as Hypernatremia.
 Extracellular sodium concentration is normally 135-145mEq/C.
 Intracellular sodium concentration is normally 3-5mEq/C.

Sources of Sodium

 Most of the sodium comes from the dietary intake.

 Sodium intake of 500mg per day is usually sufficient to meet the body’s need.
 The average intake of sodium by an adult is about 6-15 gm/day.
 Recommended dietary allowance for sodium for adults is 500mg or 0.5gm.

Excretion of sodium

Sodium is actively absorbed by the intestines and excreted by the kidneys and skin.

Hyponatremia

Definition: (Decrease in Na+ in ECF)

Hyponatremia is defined as a serum sodium concentration below 135m Eq/L.

Causes

1. Excessive sodium loss

GI losses: Diarrhea, Vomiting, Fistulas, Na suction
Renal losses: Diuretics, Adrenal insufficiency Na+ wasting renal disease
Skin losses: Burns, Wound Drainage
2. Inadequate sodium intake: Fasting diets
3. Excessive water gain(Decrease of sodium concentration)
 Excessive hypotonic and fluids & Primary Polydipsia

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Diseases

 Heart failure
 Primary hypoaldosteronism
 Cirrhosis

C/M

Hyponatremia with decreased ECF volume

 Irritability, apprehension, confusion, dizziness, personality changes, tremors, seizures,

coma.
 Dry mucous membranes.
 Postural hypotension, decrease of CVP, Pulse increase, Thready Pulse and clammy slain.

Hyponatremia with normal or increased ECF volume

 Headache, apathy, confusion, muscle spasms, seizures, come

 Nausea, vomiting, diarrhea, abdominal cranyos
 Weight gain, BP increases, CVP increases

Excretion of sodium

Sodium is actively absorbed by the intestines and excreted by the kidneys and skin.

Etiology

 Renal disease resulting in salt wasting

 Adrenal insufficiency
 GI loss (diarrhea)
 Increased sweating
 Dime tics
 Burns
 Psychogenic Polydypsia
 Liver cirrhosis
 Vomiting
 Excessive perspiration followed by increased water intake

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Clinical Manifestations

a. Muscle Symptoms
 Cramps
 Weakness
 Fatigue
b. Gastro Intestinal
 Nausea
 Vomiting
 Diarrhea
 Bowel sounds
 Abdominal cramps
 Loss of appetite
c. Cardio Vascular
 Decrease in diastolic pressure
 Tachycardia
 Orthostatic hypotension
 Weak pulse
d. Pulmonary
 Changes in rate of respiration
e. Neurologic
 Headache
 Lethargy
 Confusion
 Diminished muscle tone or Extremities
 Weakness and Tremor
f. Intrapulmonary
 Dry skin
 Pale
 Dry mucous membrane

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Laboratory Findings

 Serum sodium <135 mEg/L

 Serum Osmolaltity < 280 mosm / kg

Medical Management

 Determine cause of hyponatremia and to correct it

 Correct body water osmolarity
 If client with moderate hyponatremia 125 meg/L IV saline solution i.e. 0.96% Nacl or RL
solution may be ordered.
 When serum sodium level is 115meq/L or less a concentrated saline solution such as 3%
Nacl is indicated

Dietary Management

 A balanced diet is usually adequate for mild hyponatremia(126-135meq/L).

 More severe hyponatremia may require sodium replacement.
 If the clients have hyponatremia due to excess fluids, a fluid restricted diet may be
prescribed.
 Fluid may be restricted 800 to 1000ml/day.

Nursing Interventions

 Assess the clinical manifestations.

 Monitor fluid intake and output.
 Monitor laboratory findings.
 Assess the client closely if administering hypotonic saline solutions.
 Encourage food and fluid high in sodium.
 Limit water intake as indicated.

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Hypernatremia

Definition:

Hypernatremia is defines as an excess of sodium in the ECF compartment serum sodium

level over 145meq/L.

Causes

1. Excessive sodium intake

Eg: IV fluids
 Hypertonic Nacl.
 Excessive isotonic Nacl IV sodium bicarbonate.
 Hypertonic tube feedings without water supplements.
 Near drowning in salt water.

2. Inadequate water intake

 Unconscious or cognitively impaired individuals

3. Excessive water loss

 Increase of Sodium Concentration
 Increase of insensible water loss(high fever, heart stroke, prolonged hyper
ventilation)
 Osmotic diuretic therapy
 Diarrhea

4. Diseases
 Diabetes Insipidus
 Primary hyper aldosteronism
 Crushing syndrome
 Uncontrolled diabetes mellitus

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Clinical Manifestations

Hypernatremia with decreased ECF volume:

 Restlessness, agitation, lethargy, seizures, coma.

 Intense thirst, dry swollen tongue, sticky mucus membranes, postural hypotension,
decrease CUP, weight loss, increase pulse.
 Weakness, muscle cramps

Hypernatremia with Normal or Increased

ECF volume

 Restlessness, agitation
 Twitching, seizures, coma
 Intense thirst, flushed skin
 Weight gain, peripheral and pulmonary edema increase BP, increase CUP

Renal: Oliguria

Laboratory findings

 Serum sodium >145mEq/L

Medical Management

 To decrease total body sodium and replace fluid loss either a hypo-osmolar electrolyte
solution (0.2% or 0.45% Nacl) or D5W is administrated.
 Hypernatremia caused by sodium excess can be treated with DSW and diacritic such as
furosemide.

Dietary management

 Dietary restrictions of sodium are useful to prevent hypernatemia in high risk clients
 Clients with renal disease may need to have them sodium intake restricted to 500-
2000mg/day.

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Nursing Implementation:

 In primary water deficit, fluid replacement is provided either orally or IV with isotonic
such as 0.9% sodium chloride.
 Monitor serum sodium levels, serum osmolaltiy and the patients response to therapy.
 The serum sodium level should not decrease by more than 8-15meq/L in an 8-h period.
 Quickly reducing levels can cause a rapid shift or water back in to the cells resulting in
cerebral edema and neurologic complications.
 This risk is greatest in the patient who developed hypernatremia over several days or
longer.

Potassium

Potassium has four major roles in the body

As the primary intracellular.

Potassium plays an important role in the action potentials in the nervous system skin and
smooth muscles and the cardiac conduction system.
The normal range of serum potassium is 3.5-5.5mEq/L.
An increase in cellular potassium and increased activity of the distal portion of the
nephron.
Aldosternone is the primary controller of potassium secretion by the kidneys.

Hypokalemia:

Hypokalemia is defines as a potassium deficit in the ECF compartment with a serum potassium
concentration of less than 3.5 mEq/L

Etiology

 Diarrhea, Vomiting, Nasogastric Suctioning

 Malnutrition, starvation, potassium free diet
 Potassium Wanting Diuretics (Thiazide, loop and osmotic dicretics)
 Use of frucimide is most common cause of hypoklaemia
 Diabetic acidosis & Risk of hypokalemic include cushings syndrome, liver disease,
cancer, batter syndrome, chronic electrolyte wasting syndrome.

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Pathophysiology

Potassium levels in the ECF

Require greater than normal stimulus for depolarization of the membrane

Initiate an action potential

All most all manifestations occur with hypokalemioa

Neural excitability

Consequent effect on muscle function

C/M

a. Gastro Intestinal
 Anorexia
 Nausea and vomiting
b. Integumentary
 Dry and flushed skin, muscle membranes dry and sticky, thirst
c. Neurologic
 Restlessness, agitation, irritability, lethargy, coma, tremor, seizures
d. Cardio Vascular
 Tachycardia, hypotension or hyper tension
e. Renal
 Oliguria

26
Laboratory Findings

 Serum sodium > 145meq/L

ECG changes

 Flattened T wave
 Presence of U wave
 ST segment depression
 Prolonged QRS
 Peaked P wave
 Ventricular dysrhythmias
 First and second degree heart block.

Medical management

 Determining and correcting the cause of imbalance.

 Extreme hyokalemia requires cardiac monitoring.
 Oral potassium replacement therapy is usually prescribed for mild hypokalemia(Serum
potassium 3.3-3.5meQ/L).
 Potassium is extremely irritating to gastric mucous. Therefore the drug must be taken
with glass of water or during meals.
 Potassium chloride can be administered intravenously for moderate or severe
hypokalemia and must be diluted in IV fluids.
 Administration of potassium by IV push may result in cardiac arrests
 Potassium can be given in doses of 10-20meq/hour diluted in IV fluid if the client is an
heart monitor
 High concentration of potassium is irritating to heart muscle
 Thus correcting a potassium deficit may take several days.

27
Dietary Management

High potassium foods(approximately 7meq/serving)

Fish
Whole Grains
Nuts
Vegetables:
Broccoli, Brussels Sprouts, Cabbage, Carrots, Celery, Collards, Cucumbers,
Mushrooms, Potatoes with skin, Spinach, Tomatoes.
Fruits:
Apricots, Bananas, Cantaloupe, Guava, Honey Dew Melons, Oranges, Prunes,
Strawberries, Water Melon.
Beverages:
Brewed Coffee, Tomato Juice, Fruit Juices.

Low Potassium Foods (Approximately 3meq/Serving)

Vegetables:
Corn, Sweet Potatoes, Lima Beans, French Fried Potatoes.
Fruits:
Apples, Apples Sauce, Apple Juice, Blue Berries, Cranberries.
Beverages:

Instant Coffee, Cola, Cranberry Juice, Noncarbonated Drinks, Root Beer, Lemon-
Lime Soda.

The adult recommended allowance of potassium is 1875-5625mg.

Nursing Diagnosis

 Hypokalemia related to vomiting diarrhea, Cushing’s syndrome or decreased intake.

 Risk for injury related to muscle weakness ad hypotension.
 Imbalance nutrition less than body requirement related to insufficient intake of foods rich
in potassium.

28
Nursing Interventions

 Monitor heart rate and rhythm.

 Monitor clients receiving digitalis (Eg. Digoxin) closely, because hypokalemia increases
risk of digitalis toxicity.
 Administer oral potassium as ordered with food or fluid to prevent gastric irritation.
 Administer IV potassium solutions at a rate no faster than 10-20meq/hr. Never administer
undiluted potassium intravenously.
 For clients receiving IV potassium monitor for pain and inflammation at the injection
site.
 Teach client about potassium rich foods
 Teach clients how to prevent excess loss of potassium
(Eg. Through abuse of dicretics and laxatives)

Hyperkalemia

Definition

Hyperkalemia is defines as an elevation of the potassium level greater than 5meq/L.

Hyperkalemia is rare in clients with normal kidney function but affects more than half of people
with acute and chronic renal failure

Etiology

 Impaired Potassium Excretion

 Chronic renal failure
 Diuretics
 Urinary obstruction
 Sickle cell disease
 Addison’s disease
 Addition of potassium into extracellular space
 Potassium supplements
 Hemolysis
 Burns

29
  Trans membrane shifts
 Acidosis
 Acute Digitalis Toxicity
 Pseudo hyperkalemia
 Improper blood collection
 Lab error, Leukocytosis
 Other causes
 Fluid volume deficit
 Adrenal insufficiency & Rapid infusion of stored blood
 Excessive IV infusions or oral administration of potassium.

Clinical Manifestations

a. Cardio vascular
 First tachycardia then brady cardiac
 Electro cardiagraphic changes like peaked narrow T waves, wide QRS complex,
depressed ST segment, widened PR interval.
b. Gastro intestinal
 Nausea & Diarrhea
 Hyperactive bowel sounds
c. Neuro muscular
 Muscle weakness
 Muscle gramps
 Tingling sensation(parasthesia)
d. Renal
 Oliguira and later anuria

Laboratory Findings

 Serum Potassium >5.0meq/L

 Serum Osmolaltiy> 295meq/L
 Serum Creatinine> 1.5meq/L
 BUN > 25 mg/dL (Blood Urea Nitrogen)

30
ECG changes

 Tall, peaked T wave

 Prolonged PR interval
 ST segment depression
 Widening QRS
 Loss of P wave
 Ventricular Fibrillation
 Ventricular stand still

Medical management

Oral kayexalate

 It is used to treat high level potassium (Sodium polystyrene sulfonate) powder for
suspension.
 Kayexate is abenzene, diethenyl polymer with ethenly benzene, sulfonated salt and
has the following structural formula.

Indication

 Kayexalate is indicated for the treatment of hyperkalemia.

 Administer kayxalate at least 3hrs before or 3 hrs after other oral medications.
 Patients with gastroparesis may requires a 6 hr separation.

31
Dose

Adult dose 15gm to 60gm one to four times daily.

Rectal

Average adult dose is 30gm to 50gm every six hrs.

Adverse reactions

GI:

Anorexia, constipation, diarrhea, fecal impaction, gastro intestinal concretions, ischemic

colitis, nausea, ulcerations, vomiting, gastric irritations, intestinal obstruction.

Contradictions

 During pregnancy and lactating mother.

 Hypersensitivity to polystyrene sulfonate resins.
 Obstructive bowel disease.
 Neonates with reduces gut molality.
 When serum potassium level is 5.0 to 5.5meq/L restriction of dietary potassium intake.
 If potassium excess is due to metabolic acidosis, correcting the acidosis switch sodium bi
carbonate promotes potassium uptake in to the cells improving urine out putdrcreases
elevated serum potassium level.
 When hyperkalemai is severe immediate actions are needed to be taken to avoid severe
cardiac disturbances.
 Intravenous calcium glucarate infusions to decrease the antagonistic effect of potassium
excess on the myocardium.
 Infusion of insulin &glucose, sodium bicarbonate to promote K+ uptake in to cells.
 In hyperkalemia is secondary to respiratory acidosis enchancing pulmonary funticon is
the primary focus.

Nursing Diagnosis

 Risk for electrolyte imbalance related to excessive retention or cellular release of

potassium.

32
  Risk for activity intolerance related to muscle weakness.
 Risk for injury related to muscle weakness and seizures.
 Potential complication is dysrhythmias.

Nursing implementation

 Eliminate oral and parenteral potassium intake.

 Closely monitor cardiac status and ECG.
 Administer diuretics and other medications such as glucose and insulin as ordered.
 Hold potassium supplements and K+ conserving diuretics.
 Monitor serum potassium levels carefully.
 Teach the clients to avoid foods high in potassium and salt substitutes.

Self care

 Teaching still remains one of the primary interventions to promote and maintain normal
potassium balance for those at high risk for hyperkalemia
 Explain potassium restriction.
 Teaching dietary sources of potassium.
 Avoiding salt substitutes.

Calcium Imbalances

 Calcium along with phosphorus and magnesium plays a critical role in nerve
transmission, bone composition and regulation of enzymatic processes.
 Balance of these three electrolytes is maintained through intestinal absorption and renal
excretion.
 The majority of calcium (98-99%) is stored in the skeleton and teeth remainder is found
in soft tissue and serum.
 Calcium is necessary for metabolic process.
 Calcium place a role in blood clotting, transmission of nerve impulses, myocardial
contractions and muscle contractions.
 The source of calcium is dietary intake calcium absorption require the active form of
Vitamin D.

33
  Vitamin D is obtained from foods or made in the skin by the action of sunlight on
cholesterol.

Hypocalcemia

Definition:

Hypocalcaemia is a decrease in serum calcium levels below 8mg/dL and ionized calcium
levels below 4mg/dL.

Etiology

 Hypoalbuminemia
 Hypoparathroidism
 Hypomagnesemia
 Nutritional Deficiency
 Impaired Absorption
 Hepatic Disease
 Pseudo vitamin D deficiency
 Renal Failure
 Fluoride Poisoning
 Hungry Bone Syndrome
 Acute Pancreatitis
 Critical illness
 Serve Sepsis
 Alkalosis
 Chemotherapy
 Anti Convulsion Therapy
 Citrated blood

Clinical Manifestations

a. Neuro Muscular
 Numbness and tingling
 Muscle cramps

34
  Wheezing
 Dysphasia
 Voice change (Due to Larynges Spasm)
b. Neurologic
 Irritability
 Fatigue
 Seizures
c. Cardiac
 Shortness of breath
 CHF

d. Skin
 Brittle nails
 Psoriasis
 Dry skin
e. Other
 Confusion
 Anxiety
 possible psychosis

ECG changes

 Elongation of ST segment
 Prolonged QT interval
 Ventricular Tacky cardiac

A calcium deficit (hypocalcemia) or magnesium deficit (hypomagnesemia) increases the resting

potential of nerves.The increase allows nerve stimulation and firing with fewer stimuli.

Touching the facial nerve adjacent of the ear produces twitching to the clients upper lip
(Chrostek’s sign). The hand and finger can also go into spasm(Trousseau’s sign or carpal spasm).
These spasms can occur spontaneously or when blood flow is decreased.

Eg: During Blood Pressure Cuff Inflation

35
Management

 Treatment is provided by IV administration of either calcium gluconate (9 ml elemental

calcium/mL)
 The dosage for calcium gluconate is 100 mg/kg.
 Closely monitor and cardio systems.
 Precaution should be taken to protect a confused patient.
 Monitoring of cardiac status and ECG.
 Educate patients at high risk for osteoporosis.

Dietary Management

High Calcium Foods (Greater Than 100 mg/Serving)

Dairy products:
Cheese, Ice Cream, Milk, Yoghurt

Other:
Instant Oatmeal, Rhubarb Spinach, Tofu

Low calcium foods (greater than 25 mg/serving)

 Apples
 Bananas
 Chicken
 Hamburger
 Cooked Oatmeal
 Pasta
 Vegetable Juice

Nursing Diagnosis

 Hypocalcaemia related to diarrhea, pancreatitis, renal failure or decreased intake.

 Risk for injury related to increased neuromuscular irritability from hypocalcemia.
 Altered health Maintenance related knowledge deficit rebounding foods high in calcium.

36
Nursing Interventions

 Closely monitor respiratory and cardiovascular status

 Take precaution to protect a confused client
 Administer for parenteral calcium
 Supplements as ordered
 When administering intravenously, closely cardiac status and ECG during infusion.
 Teach clients at high risk for Osteoporosis about
 Dietary rich in calcium
 Recommendation for 1000-1500mg of calcium per day
 Calcium Supplements
 RegularExercise

Self care

 Reinforce intake of a well balanced diet

 Avoid high protein diet or other non prescribed weight loss diets.
 Encourage weight bearing suggest to prevent bone resorption.

Hypercalcaemia

 Hypercalcemia defined as a plasma calcium level greater than 5.5 meQ/ L or 11 mg/L
 Hypercalcemia can occur in any age group.
 It is a common electrolyte disorder that can have serious physical complications.

Etiology

 Metastatic malignancy- lung breast, ovarian, prostatic,, leukemia kidney

Hyper parathyroidism
 Thiazide Diuretic therapy
 Prolong Immobilization
 Excessive intake of calcium supplements and Vitamin D

37
Clinical manifestations

 Lethargy, weakness, fatigue

 Decreases memory depressive reflectors
 increase of BP
 confusion psychosis
 Anorexia, nausea, vomiting, constipation
 Bone pain, fractures
 Poly Urea, dehydration, kidney stone, renal failure
 Nephrolithiasis
 Seizures, Coma

ECG Changes

 Shortened ST segment
 Shortened QT interval
 Ventricular dysrhythmias
 Increases digitachis effect

Laboratory Findings

 Serum Calcium >5.35meq/L(.11.5mg/dL)

 Aterial Blood Gases pH <7.45 HCO3< 26meq/L

Medical Management

 Treatment consists of correcting the underlying cause.

 Intravenous normal saline (0.9% Nacl) given rapidly with frusemide to prevent fluid
overload, promote urinary calcium excretion.
 Calcitonin decreases serum calcium level by inhibiting the effects of parathyroid
hormone PTH on the osteoclasts and increasing urinary calcium excretion.
 Corticosteroid drugs decrease calcium levels by competing with thus resulting in
decreases intestinal absorption of calcium.

38
  In excessive use of calcium or Vitamin D supplements or calcium containing antacids
this happens should be either avoided or removed in reducer dosages in drug therapy is
acid or not disodium.
 In Drug therapy is ethideonate disodium. This drug reduces serum calcium by reducing
normal and abnormal bone re-absorption of calcium and secondary, by reducing bone
formation.

Nursing Diagnosis

 Risk for electrolyte related to excessive bone destruction

 Risk for activity intolerance related to generalize muscle weakness.
 Risk for injury related to neuromuscular and sensorium changes
 Potential Complications: Dysrhythmia

Nursing Interventions

 Increase client movement and exercise.

 Encourage oral fluids as permitted to maintain a dilute urine.
 Teach clients to liquid intake of food and fluid high in calcium.
 Encourage injection of fiber to prevent constipation.
 Protect a confused client.
 Monitor for pathological features in clients with long term hypercalcemia.
 Encourage intake of acid-ash fluids (Eg: Prune or Cranberry Juice) to counteract deposits
of calcium slats in the urine.

Phosphate Imbalances

 Phosphorus is the primary anion in ICF and the second most abundant element in the
after calcium.
 Most phosphorus sis in bones and teeth as calcium phosphate.
 The remaining phosphorus is metabolically active and essential to the function of muscle,
red blood cells and the nervous system.
 It is involved in acid base buffering system.

39
Hypophosphatemia

Definition:

Low serum phosphate is called Hypo Phosphatemia. In children levels below 3mg/dL
until the level is below 2mg/dL. Levels lower then 1mg/dL may be life threatening.

Causes

 Malabsorption Syndromes
 Chronic Diarrhea
 Malnutrition, Vitamin D Deficiency
 Parenteral Nutrition
 Chronic Alcoholism
 Phosphate Binding Antacids
 Diabetic Ketoacidosis
 Hyperparathyroidism
 Refeeding Syndrome
 Respiratory alkalosis

Manifestations

 CNs Depression (Confusion, Coma)

 Muscle Weakness including respiratory muscle weakness
 Polyneuropathy, seizures
 Cardiac Problems (Dysrhythmias, Heart Failure)
 Osteomalacia, Rickets

Management

 To identify the underlying cause and take steps to correct it.

 Phosphorous administration of 20mg/kg/day divided into several doses to minimize
diarrhea.
 The recommended dose is 0.15-0.33 mmol/kg generally given as a continuous infusion
over at least 6hrs.

40
Hyperphosphatemia

Definition

Hyperphosphatemia is defines as an excess of phosphate in the ECF compartment and

exists when phosphate levels exceed 4.5mg/dL.

Causes

 Renal failure
 Phosphate Enemas
 (Eg: Fleet Enema)
 Excessive Ingestion
 Eg: Phosphate contain laxatives)
 Tumor Lyses Syndrome
 Thyrotoxicosis
 Hypoparathyrodism
 Sickle cell anemia
 Hemolytic Anemia
 Hyperthermia
 Excessive Consumption of Vitamin D metabolites
 Rapid Cell Catabolism

Clinical Manifestations

 Hypocalcaemia
 Numbness and tingling in extremities and region around mouth
 Hyperreflexia, Muscle Cramps
 Tetany Seizures
 Calcium Phosphate Precipitates in skin, soft tissue, cornea, viscera, blood vessels
 Tachy Cardia
 Nausea Diarrhea

41
Management

 Treatment should be directed at both determining the underlying cause and correcting the
imbalance.
 Usually dietary restriction of phosphorus..
 Aluminum antacids may be used.
 Adequate hydration and correction of hypocalcemia also enhance phosphate elimination.
 If increased phosphorus related to renal failure.
 The administration of sodium bicarbonate may be used to enhance renal excretion of
phosphorus.
 For the child with life threatening symptoms, fluids to increased renal phosphate losses.
 Treatment of hypocalcemia
 Dialysis may be indicated.

Magnesium Imbalances

The distribution of magnesium is similar to that of potassium and approximately 60% in

the mineral component of bone, 40% in the body cells and less than 1% in the ECF compartment

Role of Magnesium

Major role is can be divided into three areas enzyme and biochemical activation,
medication of skeletal muscle tension and inhibition of electrical activity at the neuromuscular
junction.

The serum magnesium concentration is regulated by the kidney, GI tract and bones.

Hypomagnesaemia

Definition

Hypomagnesaemia is defined as a plasma magnesium level less than 1.5meq/L or

1.8mg/dL.

Causes

 GI tract fluid losses (E.g. Diarrhea, NG suction)

42
  Chronic alcoholism
 Malabsorption syndrome
 Prolonged malnutrition
 Increase Urine output
 Hyperglycemia
 Proton pump inhibitor therapy

Clinical Manifestation

 Confusion
 Muscle cramps
 Tremors
 Seizures
 Vertigo
 Hyper active deeptondon reflexes
 Chvostek's and trousseau's signs
 Increase of pulse and increase of BP
 Dysrhythmia.
 Convulsion & Tachy cardia

Lab Findings

 Serum magnesium below 1.5 meq/L

43
Management

 It includes oral magnesium replacement in the form of magnesium containing antacids or

parenteral magnesium sulfate.
 Increasing dietary intake of magnesium also helps ensure balance and stability.
 IV magnesium sulphate may be diluted to 10mg/ml and given slowly over 3-5 minutes.
 Carefully monitor serum levels.
 Client is encouraged to eat magnesium rich foods if permitted.

High Magnesium Foods (>75mg/Serving)

 Cashews
 Tofu
 Chili
 Wheat germ
 Halibut
 Swiss chard

Nursing Interventions

 Assess clients receiving digitalis for digitalis toxicity.

 Hypomagnesaemia increases the risk of toxicity take protective measures when there is a
possibility of seizures.
 Assess the clients ability to swallow water prior to initiating oral feeding.
 Initiate safely measures to prevent injury during seizure activity.
 Carefully administer magnesium salts as ordered.
 Encourage clients to eat magnesium rich foods if permitted.
Eg: whole grains, meat seafood and green leafy vegetables
 Refer clients to alcohol treatment programs as indicated

Hypermagnesaemia

Definition

Hypomagnesaemia, a plasma magnesium level greater than 2-5meq/L or 3mg/dL is called

Hypermagnesaemia is a rare disorder.

44
Causes

 Renal insufficiency
 Excessive use of magnesium containing antacids or laxatives
 Administration of potassium sparing diuretics
 Many potassium sparing diuretics conserve magnesium
 Severe dehydration from ketoacidosis
 Adrenal insufficiency

Clinical Manifestation

 Peripheral vasodilatation
 Nausea vomiting
 Muscle weakness, paralysis
 Hypotension, bradycardia
 Depressed deep-tendon reflexes
 Lethargy, drossiness
 Respiratory depression, coma
 Respiratory and cardiac arrest if hypermagnesemia is sever

Laboratory Findings

 Serum magnesium >2-5meq/L

 ECG showing prolongeed QT interval
 Prolonged PR interval
 Widened QRS complexes
 Tall T waves

Management

 Treat the underlying cause

 Calcium gluconate or other calcium salts may be administered because calcium is an
antagonist to magnesium and often reverses the cardiac manifestations of
hypermagnesemia.
 Vital signs monitored

45
  Monitored level of consciousness
 The presence of severe respiratory distress requires ventilator assistance
 If renal failure is present, hemodialysis may be necessary

Dietary Management

Low magnesium food (<25mg/serving)

 Chicken
 Eggs
 Fruits
 Green Peas
 Hamburger
 White Bread

Nursing Interventions

 Monitor vital signs and level of consciousness when clients are at risk.
 If patellar reflexes are absent notify the primary care provider.
 Advise clients who have renal disease to contact theri primary care provider before taking
over the counter drugs.

Chloride

Chloride is the most abundant anion found in the ECF compartment. Its major role is as a
buffer in the maintenance of acid base balance.

Chloride along with sodium maintains serum osmolality. Chloride ions are highly
concentrated in gastric secretions and perspiration.

Normal serum chloride levels in children are 95-108meq/L.

46
Hypochloremia

Definition:

Hypochloremia occurs when serum chloride levels are below 95meq/L

Causes

 Renal losses
 Loss of chloride through excessive sweating
 Clinical manifestations
 Hyperirritability
 Agitation
 Muscle weakness
 Tetany
 Slow, shallow respirations

Management

 Treat the underlying cause.

 Correct the electrolyte balance.
 Imbalance usually corrected through the administration of sodium chloride,, potassium
chloride or ammonium chloride.
 3/4 imbalance replaced by sodium chloride.
 1/4 imbalance replaced by potassium chloride.
 0.9% solution of sodium chloride is used to correct the chloride imbalance.
 Usually potassium chloride is given a dose of 0.5-1meq/kg over a 1to 2 hr period.

47
Hyperchloremia

Definition: Hyperchloremia occurs when serum chloride levels excess 108meq/L

Causes

 Excessive chloride intake

 Medication administration
 Lead to metabolic acidosis with excessive loss of bicarbonate ions such as diarrhea, renal
failure and administration of isotonic saline solution.

Clinical Manifestations

 Muscle weakness
 Decreased level of consciousness
 Deep rapid respiration

Management

 Identify the underlying cause and correction of fluid and electrolyte imbalance
 Fluid may be increased to dilute the excess chloride, in emergency sodium bicarbonate
may be administrated to correct the underlying metabolic acidosis.
 Diuretics may be used to eliminate chloride as well as sodium.

48
 ACID-BASE BALANCE

Acid-Base disturbances are commonly encountered in clinical practice. Identification of

the specific acid base imbalance is important in identifying the underlying cause of the disorder
and in determining appropriate treatment.

-Kraut & Madias, 2001

 Plasma pH is an indicator of hydrogen ion (H+) concentration.

 Homeostatic mechanisms consist of buffer systems the kidneys and the lungs.
 Homeostatic mechanisms keep pH within a normal range 7.35-7.45.
 Blood needs the right balance of acidic and basic (alkaline) compounds to function
properly. This is called the acid base balance.
 Kidneys and lungs work to maintain the acid base balance. Even slight variations from
the normal range can have significant effects on vital organs.
 Acid and alkaline levels are measured on pH scale. An increase in acidity causes pH
levels to fall. An increase in alkaline causes pH levels to rise.
 When the levels of acid in blood are too high is called acidosis.
 When blood is too alkaline is called alkalosis.
 Respiratory acidosis and alkalosis are due to a problem with the lungs. Metabolic acidosis
and alkalosis are due to a problem with the kidneys.

Normal ABG Values

PH 7.35-7.45 Potential Hydrogen

PaO2 75-100mm/kg Pulmonary Arterial Oxygen Tension

PaCO2 35-45mmHg Partial pressure at CO2 in atrial blood

HCO3 22-26meq/L Bicarbonate

SAO2 96-100% Saturation of O2

Base Excess 1-2meql

49
Regulation of Acid Base Balance

 A number of mechanism works together to maintain the pH of the body with in the
normal range.
 Three systems work together in the body to maintain the balance. The pH buffers
respiratory system, renal system.

Types of Acid-Base Disturbance

 The two types of acidosis and alkalosis are respiratory and metabolic.
 The major effect of acidosis is depression of CNs, as evidenced by coma.

Acid-Base Imbalance

Acidosis - occurs when the hydrogen ion concentration increases normal pH.

Alkalosis - occurs when hydrogen ion concentration fall below normal (pH above 7.45).

Respiratory Acidosis

Carbonic acid excess

 It occurs due to the retention of CO2 in the lungs because of hypoventilation of alveoli
and results in the fall in the blood Ph.
 Hypoventilations of alveoli can be a cause of airway obstruction and pulmonary
disorders.
 Respiratory acidosis is CO2 accumulation (hypercapnia) form a decrease in respiratory
rate, respiratory volume.

Causes

 Lung Disorders
 Hyaline Membrane Disease
 Obstructive Sleep apnea
 Emphysema
 Severe Asthma
 Chronic Bronchitis

50
  COPD
 Overdoes of drugs
 Guillain barre syndrome
 Myasthenia gravis
 CNS depression
 Neuromuscular disease
 Chest muscles disorders
 Pneumothorax
 Poliomyelitis
 Atelectasis

Risk Factors for Respiratory Acidosis

 Acute lung conditions that impair alveoli gas exchange.

(Eg: Pneumonia, acute pulmonary edema, aspiration of foreigh body, near-drowning)
 Chronic lung disease.
(Eg: Asthma, Cystic fibrosis or emphysema)
 Overdose of narcotics or sedatives that depress respiratory rate and depth.
 Bear injury that affects the respiration center.
 Airway obstruction.

Symptoms

 Headache, Dizziness
 Constricted Pupils
 Confusion
 Pulmonary Hypertension
 Anxiety
 Cyanosis
 Drowsiness
 Flushed Skin, Warm
 Stupor
 Gait Disturbance

51
  Sleep Disturbance
 Azotemia
 Myoclonic Jerks
 Breathlessness
 Hypercapnia
 Convulsions
 Increased pulse and respiratory rate
 Decreased level of Consciousness

Laboratory Findings

 Arterial blood pH < 7.35

 PaCO2 > 45mm Hg
 HCO3 normal or slightly elevated in Acute
 >26meq/L in chronic

Nursing Interventions

 Frequently assess respiratory status and lungs sounds.

 Monitor airway and ventilation.
 Insert artificial airway and prepare for mechanical ventilation as necessary.
 Administer pulmonary therapy measure such as inhalation therapy, percussion and
postural drainage, bronchodilators and antibiotics as ordered.
 Monitor fluid intake and output vital signs and arterial blood gases.
 Administer narcotic antagonists as indicated.
 Maintain adequate hydration (2-3L of fluid per day).

Expected Patient Outcome

 To maintain patent airway and adequate breath rate and rhythms.

 To cope with anxiety.
 To exhibit effective coping and awareness support.
 To maintain adequate rate and depth of respiration.

52
Respiratory Alkalosis

 It is due to hyperventilation of alveoli, which results in fall in PCO2 of arterial blood.

 Low PCO2 leads to decreased H+ ion secretion in kidney, which in turn reduces the re-
absorption of filtered bicarbonate and increases its excretion in the urine.
 Common cause of respiratory alkalosis is hyperventilation.

Causes

 Pulmonary Embolism
 Panic disorder
 Heat stroke
 Anxiety disorder
 Hypoxia
 Pain
 Pulmonary edema
 Pneumonia
 Hepatic Failure
 Fever
 Functional Disorder
 Hyperventilation Syndrome
 Cerebra vascular accident

Signs & Symptoms

 Dizziness
 Fainting
 Numbness
 Tetany
 Light Headache
 Confusion
 Seizures

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  Chest Pain
 Laryngeal spasm
 Muscle cramps
 Reduced ICP
 Parasthecia in extremities
 Brain tumor

Risk Factors

 Hyper ventilation due to extreme anxiety

 Elevated body temperature
 Over ventilation with a mechanical ventilator
 Hypoxia
 Salicylate over dose
 Brain stem injury fever
 Increased basal metabolic rate

Laboratory Findings

 Arterial blood pH > 7.45

 PCO2 < 35mm of Hg

Management

1. Treat the underlying cause is the primary approach

Replacement of lost fluids and electrolytes (potassium and magnesium) and
support of renal function.
2. Administration of Acetazolamide
Acetazolamide (Diamox) is a diuretic that inhibits CA and promotes loss of
bicarbonate in the urine. Losses of potassium and phosphate are also greater with the use
of acetazolamide, however and may lead to manifestations of electrolyte imbalance.
3. Administration of Exogenous Acid
In severe alkalemia, the intravenous administration of acid (Hcl) or Hcl precursors
may be warranted to enhance physiologic compensation

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Nursing Assessment

A. History
 Age
 Post medical history
 Illness, Surgery, Burns, Respiratory Disorders, Head Injury, Cardiovascular Disease,
Renal Disorders
Environmental factors
Diet
Life style
Medications
B. Physical Assessment
C. Maintained I/O Chart
D. Assess the Laboratory Diagnosis
Serum electrolyte level, hematocrit, blood creatinine, BUN level, Urine Specific
Gravity, ABG Readings

Nursing Diagnosis

 Risk for imbalance body temperature

 Ineffective breathing pattern
 Decreased cardiac output
 Deficient fluid volume
 Impaired gas exchange
 Deficient knowledge regarding disease managemnt
 Impaired skin integrity
 Ineffective tissue perfusion

Intervention

 Monitor vital signs and ABGs

 Assist client to breathe more slowly
 Help client breathe in a paper bag or apply a rebreather mask(to inhale CO2)
 Health promotion by client teaching

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  Daily weights
 Parenteral replacement of fluid and electrolytes
 Assess skin color, temperature, moisture and turgor
 Assess the level of consciousness, orientation, motor function
 Assess reflexes
 Identify clients at risk
 Monitor I/o chart calculate fluid balance
 Maintain quiet environment
 Provide safety and seizure precautions

Expected Outcomes

 Reduce the anxiety

 Provide anti anxiety drugs
 Position the patient

Metabolic Acidosis

 When bicarbonate levels are low in relation to the amount of carbonic acid in the body
pH falls and metabolic acidosis develops.
 This may occur because of renal failure and the inability of the kidneys to excrete
hydrogen ions and produce bicarbonate.
 It also may occur when too much acid is produced in the body.
 Eg: Diabetic ketoacidosis or starvation when fat tissue is broken down for energy.
 Metabolic acidosis stimulated the respiratory center and the rate and depth of respiration
increase.
 Carbon dioxide is eliminated and carbonic acid levels fall minimizing the change in pH.
 This respiratory compensation occurs within minutes of the outset of the ph imbalance.

Causes

 Increase in the generation of H+ from endogenous or exogenous acids.

 Inability of kidneys to excrete the hydrogen from dietary protein intake
 The loss of bicarbonate due to wasting through the kidney or GIT
 The kidney's response to a respiratory alkalosis

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Others

 Diabetic acidosis
 Excessive loss of sodium bicarbonate
 Lactic acidosis (due to alcohol, cancer, liver failure, hypoglycemia)
 Renal disorders
 Renal tubular acidosis
 Aspirin poisoning
 Dehydration (Drugs)

Risk Factors

 Conditions that increase nonvolatile acids in the blood

(Eg: renal impartment, diabetes milletus and starvation)
 Conditions that decrease bicarbonate
(Eg: prolonged diarrhea)
 Excessive infusion of chloride containing IV fluids
(Eg: Nacl)
 Excessive ingestion of acids such as salicylates
 Cardiac Arrest

Signs & Symptoms

 Kussmaul's respirations (deep rapid respirations)

 Lethargy, Confusion
 Headache
 Weakness
 Nausea and Vomiting
 Coma

Laboratory Findings

 Arterial blood pH < 7.35

 Serum bicarbonate less than 22meq/L
 PCO2 < 38mm Hg with respiratory compensation

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Management

1. Treatment of underlying disorder

 Electrolyte imbalance is treated only if it is life threatening because it normally
resolves with correction of the underlying disorder.
2. Respiratory support
 Assisted mechanical ventilation may be indicated for clients whose ability to
hyperventilate in compensation is limited.
 Administration of exogenous alkali to treat metabolic acidosis.
 Administration of intravenous sodium bicarbonate or other alkalinizing.
 Substances to minimize the effects of acidosis until the underlying disorder is
resolved or until physiologic compensation is effective.

Nursing Interventions

 Monitor ABG values

 Maintain intake and output chart
 Administer IV sodium bicarbonate carefully if ordered
 Treat underlying problem as ordered
 Monitor Vital Signs
 Provide Comfort
 Fluid and electrolyte replacement
 Instruct the patient for deep breathing and coughing exercise
 Hemodialysis

Metabolic Alkalosis

 In metabolic alkalosis the amount of bicarbonate in body exceeds the normal 20:1 ratio.
 Ingestion of bicarbonate of soda s antacid is one cause o metabolic alkalosis is prolonged
vomiting with loss of hydrochloric acid from the stomach.
 The respiratory center is depressed in metabolic alkalosis and respirations slow and
become shallower.
 Carbon Dioxide is retained and carbonic acid levels increased helping the balance the
excess bicarbonate.

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Causes

 Diuretics
 Loss of gastric secretion
 Ingestion of large doses of non absorbable antacids
 Hypokalemia
 Hypomagnesaemia
 Poly Hypercapnic
 Sweat loss in cystic fibrosis
 Milk alkali syndrome
 Intravenous penicillin
 Massive Blood Transfusion
 Vomitings

Risk Factors

a. Excess acid losses due to

 Vomiting
 Gastric Suction
b. Excessive use of potassium losing diuretics
c. Excessive adrenal corticoid hormones due to
 Cushing’s syndrome
 Hyper aldosteronism
d. Excessive bicarbonate intake form
 Antacids
 Parenteral NaHCO3

Signs & Symptoms

 Decreased respiratory rate

 Dizziness
 Parasthesia
 Numbness and tingling of the extremities
 Hypertonic muscles, Tetany

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  Hypertension
 Hypoventilation
 Irritability
 Confusion
 Nausea and vomiting
 Diarrhea
 Atreal tachycardia
 Cyanosis
 Apnea

Laboratory Findings

 Atrial blood pH >7.456

 Serum bicarbonate > 26meq/L
 PaCO2 > 45mmHg with respiratory compensation

Management

 Treat the cause

 Administration of ammonium chloride and Hcl
 Electrolyte Replacement

Nursing Interventions

 Monitor intake and output closely.

 Monitor vital signs, especially respiration and LOC (Level of Consciousness).
 Administer ordered IV fluids carefully.
 Treat underlying problem.

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 Acid – Base Imbalance

Arterial Blood
Acid Base
Compensatory Mechanism
Disturbance
PCO2 pH HCO3

Respiratory Kidneys conserve bicarbonate and

Acidosis excrete hydrogen ions in urine.

Kidneys increase bicarbonate

Respiratory
excretion and plasma bicarbonate
Alkalosis
concentration decreases.

Metabolic Acidosis Increased CO2 excretion by lungs.

Decrease in respiratory rate and renal

Metabolic Alkalosis
loss of bicarbonate.

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 Focused Physical Assessment for fluid, Electrolyte or Acid-Base Imbalances

System Assessment Focus Technique Possible Abnormal Findings

Colour, Temperature Inspection Flushed, Warm very dry or cool
Skin
Moisture Palpation and pale
Gently pinch up a fold
of skin over sternum Poor Turger
inner aspect of thigh Skin remains tended for several
Turgor
for adults on the seconds instead of immediately
abdomen or medial returning to normal position
thigh for children
Inspect for Visible
Skin around eyes in puffy lids
Swelling around Eyes,
Edema appear swollen. Rings are tight
In finger and in lower
shoes leave impressions on feet
extremities
Mucus membrane dry, dull in
Mucous
Colour Moisture Inspection appearance
Membrane
Tongue dry & cracked
Gently Palpate eye
Eyes Firmness Eyeballs feels soft to palpation
ball with lid closed
Inspect & Gently
Fontanel bulging firm fontanel
Fontanels(Infant) Firmness Level Palpate Anterior
sunken and soft
Fontanel
Cardio Vascular Auscultation Cardiac Tachy Cardia, Brady Cardia
Heart Rate
system monitor Irregular Dysarhythmias
Peripheral Pulse Palpation Weak and Thready
Blood Pressure Auscultation Hypotension
Capillary Refill Palpation Slowed Capillary Refill
Jugular Veins distention
Inspection of Jugular
Venous Filling Flat Jugular veins
veins and Land Veins
Poor venous refill

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 Respiratory rate and Increased or decreased rate and
Respiratory Inspection
pattern depth of respiration
Lung sounds Auscultation Crackles or moist Rales
Level of Observation Decreased LOC
Neurologic
consciousness (LOC) Stimulation Lethargy, Stuper or Coma
Disoriented, Confused
Orientation Cognition Questioning
Difficulty Concentrating
Weakness, Decreased Motor
Motor Function Strength Testing
Strength
Deep Tendon Reflex Hyperactive or Depressed
Reflexes
(DTR) Testing DTR’s
Chvostek’s Sign:
Tap over facial nerve
Weakness,, Decreased Motor
about 2cm anterior to
Strength, Hyperactive
tragus of ear
Depressed DTR
Traousseau’s Sign:
Abnormal Reflexes Facial Muscle Twitching
Inflate blood pressure
Corpal muscle contraction of
cuff on the upper ear
hand and fingers on affected
to 20mm Hg> the
side
systolic pressure leave
in place 2-5mts

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 CONCLUSION

It is to conclude that the knowledge of all above discussed fluid and electrolyte imbalance

So that by utilizing this knowledge we can update our knowledge and can taking the
profession to the higher standards.

SUMMARY

So far we are discusses introduction, definitions, terminologies, fluid and water functions,
fluid components, regulation of water, fluid compartments, fluid imbalance, electrolytes, factors
affecting the fluid and electrolyte imbalance, acid base balances respiratory acidosis, alkalosis,
metabolic acidosis, alkalosis.

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 BIBILOGRAPHY

1. Shabeer, P.Basheer "The text book of Advance Nursing Practice" Emmess Medical
Publications, 1st Edition, Page No: 212-223.

2. Navdeepkawe "A text book of Medical & Surgical Nursing" 13th Edition Volume-I, Page
No: 237-284.

3. Lippincolt Manual of Medical Surgical Nursing 10th edition Page No:115-123.

4. JOYCE m.BLACK JANE Hokanson Hawks "A text book of Medical Surgical Nursing"
published by Elsevir India Pvt. Ltd. 8th Edition, Volume I, Page No: 127-178.

5. Koziers & Erb's fundamentals of Nursing, 10th Edition, Page No: 1346-1399.

6. Lewis's A text book of Medical Surgical Nursing, 2nd Edition Volume I Page No: 222-245

7. V. Sathyanarayana and Chakrapani" A text book of Biochemistry" Elsever Publications, 4th

Edition, Page No: 468-484

Net References

https://emmwikipedia.org>wikifluidbalance

https://studer10H>academy>fluidvolume

https://www.msdmanvav.com>volume

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