Fluid electrolyte balance

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Objectives:
Objectives of the seminar are to:
1. Explain Normal Distribution of Fluid
2. Discuss Intake & Output of Fluid
3. Explain Abnormal Water & Electrolyte Metabolism
4. Discuss Types of Fluid Imbalances
5. Enlist Electrolytes
6. Explain Normal Electrolyte Balance
7. Discuss Composition of Electrolytes
8. Explain Regulation of Electrolytes
9. Discuss Electrolyte Imbalances
10. Explain Acidosis & Alkalosis
11. Discuss Arterial Blood Gases

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FLUID
 Normal Distribution of Fluid
 Intake & Output of Fluid
 Abnormal Water & Electrolyte Metabolism
 Types of Fluid Imbalances

DISTRIBUTION OF BODY WATER
• 70% of b.w
• 2 compartments:
 ICF (Intracellular Fluid):- approx 50%
 ECF (Extracellular Fluid):- approx 20%
 Further divided into 2 compartments:-
 Plasma: approx 5% and
 Interstitial Tissue Fluid (ITF):- 15%
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AVERAGE WATER INTAKE & OUTPUT IN AN
ADULT:-
INTAKE:
• Fluid by mouth (as water
& beverages) 1000-1500 ml
• In food 700 ml
• Metabolic water 400 ml
OUTPUT:
• Urine (via kidneys) 1000-1500 ml
• Lungs 400 ml
• Skin 600 ml
• Faeces 100 ml
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ABNORMAL WATER AND ELECTROLYTE
METABOLISM
2 types:
• Dehydration
• Water intoxication
DEHYDRATION
1. Pure water depletion/ primary dehydration
2. Pure salt depletion/ secondary dehydration
3. Mixed type
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1. PRIMARY DEHYDRATION
Definition: Water intake inadequate. No parallel loss of
salt in body secretions.
Causes:
• Patient too weak or too ill to satisfy his/her water needs,
• In mental patients who refuse to drink,
• In case of coma, dysphagia,
• In individuals lost in desert or shipwrecked.
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Pathophysiology of primary dehydration
Decreased intake of water
Depletion of water stores
Continued obligatory losses
Rise in concentration of electrolytes
Flow of water from ICF to ECF
Volume of ECF maintained at the expanse of ICF
Intracellular dehydration

Clinical and biochemical findings:-
• Thirst
• Oliguria
• Normal or slightly increased blood urea
• Normal or slightly reduced blood volume
• No circulatory collapse or fall in BP (as plasma volume
is maintained)
• Urine contains NaCl
• Death(if water loss approx 15% of b.w)
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Clinical Manifestations according to water loss in
primary dehydration
Clinical Phases Clinical Features Estimated Deficit
Early Thirst+ 2% of body weight(approx
1.5 L)
Moderately severe(72 to
96 hrs without water)
Thirst++
Pinched facies, oliguria,
weakness, seriously ill,
early personality changes
6% of body weight(approx
4.2 L)
Very severe Above
features+diminuation of
physical and mental
capabilities, hallucinations
and delirium
7 to 14% of body
weight(approx 5 to 10 L)
Marriott (1946)

2. SECONDARY DEHYDRATION
Definition:- Fluids of high Na+ and Cl- content lost from the
body and replaced by salt-deficient fluids.
Causes:-
 Excessive sweating.
 Loss of GI fluids( as in
diarrhoea,vomiting,pancretic/biliary fistulaes,cholera &
continuous aspirations through intubations,suction).
 Addison`s disease
 Diabetic Acidosis
 Certain instances of chronic renal diseases.
 Vigorous use of Diuretics
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Pathophysiology of secondary dehydration
Sodium depletion
Hypertonicity of ECF
Low osmotic pressure
Inhibition of release of ADH
Kidneys excrete water to maintain extracellular
concentration of Na+
Plasma and interstitial fluid volume decreases
Extracellular hypertonicity allows water to flow into the
cells
Reduction in volume of ECF 12

Clinical Manifestations according to water loss
in secondary dehydration:-
Clinical Phases Clinical Features Estimated
Deficit
Early (slight to
moderate)
Lassitude,
indifference/apathy,
syncope, urine Cl-
reduced
0.5 gm NaCl/Kg=4L
Moderate to severe Above features+ nausea/
vomiting, cramps, B.P.
decreased but > 90 mm
Hg, urinary Cl- absent
0.5 to 0.75 gm (4.0-6.0L)
Severe to very severe Above features+ B.P. <
90 mm Hg, urinary Cl-
absent
0.75 to 1.25 gm/ kg ( 6.0-
12.0L)
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Marriott (1946)

3. MIXED WATER AND SALT (SODIUM) DEPLETION:-
Definition: - Mixed depletion of both water & salt (sodium) is more
common.
Pathophysiology:-
Hypotonic ECF
Water loss outstrips the salt loss
ECF becomes hypertonic
Clinical and Biochemical features:-
• Patient appears dehydrated
• Thirst
• B.P. may be lowered
• Blood urea is raised
• Haemoconcentration
• Diminished urine output
• Reduced salt excretion
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Types of Fluids to Administer:-
• For pure water depletion: - Water by mouth or per
rectum or 5% Glucose by IV/SC or intra-peritoneal routes
depending on the case.
NOTE: - Never give ISOTONIC SALINE, which will
increase hypertonicity.
• Pure sodium depletion: - Corrected by isotonic saline
solution.
• Mixed water and sodium depletion:- treated with a
mixture of saline and 5% Glucose usually,
In the proportion 1:1( half- normal saline) or
In 1 to 2( one- third normal saline)
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NOTE:
• Urinary chloride level to be kept as a general guide.
• Normal saline to be given when chloride is absent from
urine.
• Half normal saline when urinary chlorides are between
2.0 and 5.0 G.and
• Not more than one-third normal saline for maintenance
therapy, when urinary chloride excretion is greater than
5.0 G.per litre.

ESTIMATION OF CHLORIDE CONTENT OF URINE:-
Fantus`s Test:
• Take ten drops of urine into a clean test tube.
• Add one or two drops of 20% solution of potassium
chromate as an indicator.
• Add 2.9% solution of silver nitrate (AgNO3) drop by drop
counting the drops simultaneously
• The test tube being shaken after addition of each drop.
End Point: Sharp color change from canary yellow to
brown-brick red due to formation of silver chromate.
Result: The number of silver nitrate drops required to
produce the change gives Grams of sodium chloride per
litre of urine.
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Precautions:
• Same dropper/ pipette should be used throughout, as the
whole test depends on the volume contained in the drops.
• Test should be repeated with distilled water instead of
urine to ensure that potassium chromate solution is not
contaminated with chlorides.
Interpretations:
• Chloride may be regarded as absent if color changes with
the first drop of AgNO3.
• If the urine contains more than 5.0 gm/ litre, chloride
deficiency is unlikely.
Contd……

WATER INTOXICATION
Causes:
• Renal failure
• Excessive administration of fluids parenterally.
• Hypresecretion of ADH following the administration of
an anaesthesia for surgery
• Administration of narcotic drugs or in stress(including
surgery)
• Excess of aldosterone ( Conn`s Syndrome)
Clinically:
• Headache
• Nausea
• Incoordination of movements
• Muscular weakness
• Delirium 19

Changes: There is decrease in:
• PCV
• Hb concentration &
• Plasma protein concentration
• Plasma electrolytes lowered
• Urinary volume is usually increased
• Specific gravity of urine is lowered
Treatment:
• Withholding fluids by mouth
• Administering 3 to 5% hypertonic saline IV
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Contd……

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FLUID IMBALANCES
FLUID VOLUME DEFICIT (FVD)/HYPOVOLEMIA
• Caused by a deficiency in the amount of both water and
electrolytes in ECF, but the water and electrolytes
proportions remain near normal. Commonly known as
`hypovolemia’.
• Results from the loss of body fluids especially if fluid
intake simultaneously decreased.
The related factors of FVD:
 Loss of water & electrolytes, as in
 Vomiting
 Diarrhea
 Excessive laxative use
 Fistulas
 Gastrointestinal suction
 Polyuria

 Fever
 Excessive sweating
 Third space fluid shifts
 Decreased intake, as in:
 Anorexia
 Nausea
 Depression
 Inability to gain access to fluids
 Inability to swallow fluids
Characteristics of Fluid volume deficit:
• Weight loss over short period.
• Decreased skin and tongue turger.
• Dry mucus membranes.
• Urine output less than 30 ml per hour in adult.
• Altered sensorium.
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Related factors of FVD……….

 Postural hypotension
 Weak, rapid pulse.
 Slow- filling peripheral veins.
 Decreased body temperature, such as 950 to 980 F (350 to
36.70 C) unless infection is present.
 CVP less than 4 cm H2O.
 BUN elevated out of proportion to serum creatinine.
 Specific Gravity ( urine) high
 Haematocrit elevated.
 Flat neck veins in supine position.
 Marked oliguria, late.
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Characteristics of Fluid volume deficit……….

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Fluid volume deficit….
Nursing Interventions:-
 Asses for presence or worsening of FVD.
 Administer oral fluids if indicated.
 Consider the client`s likes and dislikes when
offering fluids.
 If the client is reluctant to drink provide frequent
mouth care & offer fluids at frequent intervals.
 Explain the need for fluid replacement to the client
 Administer medications if nausea is present.

 Interventions for clients with impaired swallowing.
 Assess gag reflex
 Position the client in an upright position with a
head and neck flexed slightly forward during feeding.
 Provide thick fluids or semisolid foods.
 Client unable to eat and drink, discuss possibility of tube
feeding or TPN with the physician.
 Monitor response to fluid intake, either orally or
parenterally.
 Monitor clients with tendency for abnormal fluid
retention for signs of overload.
 Turn client frequently, apply moisturizing agents to skin.
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Contd……

FLUID VOLUME EXCESS/HYPERVOLEMIA
• Excessive retention of water and sodium in ECF in near
normal proportions results in FLUID VOLUME EXCESS.
The common related factors :
 Compromised regulatory mechanisms such as
 Renal Failure
 Congestive heart failure
 Cirrhosis of liver
 Cushing`s syndrome
 Overzealous administration of sodium containing
IV fluids
 Excessive ingestion of sodium containing
substances in diet or sodium containing medication.
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The characteristics of fluid volume excess :
• Weight gain over short period.
• Peripheral edema
• Excess of fluid in interstitial space
• Distended neck veins & peripheral veins
• Slow- emptying peripheral veins
• CVP over 11 cm H2O
• Crackles and wheezes in lungs
• Polyuria (if renal function normal)
• Ascites, pleural effusion (when FVE is severe, fluid
transudes into body cavities)
• Decreased BUN (due to plasma dilution)
• Decreased Haematocrit (due to plasma dilution)
• Bounding, full- pulse
• Pulmonary edema, if severe
Contd……..

Nursing Interventions:-
• Assess the presence or worsening of FVE
• Encourage adherence to sodium restrictions to avoid
over-the-counter drugs.
• When indicated, encourage rest period.
• Monitor the client`s response to diuretics.
• Monitor the rate of parenteral fluids and the client
response.
• Teach self-monitoring of weight and intake and output
measurements (such as in case of CCF, renal failure,
cirrhosis of liver).
• If dyspnoea or orthopnea, position the client in semi-
Fowler`s position.
• Turn and position the client frequently.
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ELECTROLYTES
 Electrolytes
 Composition
 Regulation
 Electrolyte Imbalances
 Treatment
 Nursing Interventions
 Acidosis & Alkalosis
 Arterial Blood Gases

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ELECTROLYTES
Substances whose molecules dissociate or split into ions
when placed in water, found in ECF and ICF that dissociate
into electrically charged particles known as ions.
The organs are constantly regulating the electrolyte levels
are the:
 Intestines &
The Kidneys
The role of electrolytes in cellular functions:
 Regulation of water distribution, and osmolality
 Regulation of acid-base balance
 Transmission of nerve impulses.
 Contraction of muscles
 Clotting of blood
 Enzyme reaction

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ELECTROLYTE COMPOSITION OF ECF
CATIONS mEq/L
PLASMA:
 Na+ 143
 K+ 5
 Ca+ 5
 Mg+ 5
TOTAL 155
TISSUE FLUID:
 Na+ 145
 K+ 5
 Ca+ 3
 Mg+ 2
TOTAL 155

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Anions mEq/L
PLASMA:
 Cl- 103
 HCO3
- 27
 HPO4
-2 2
 SO4
-2 1
 Proteins- 16
 Organic Acids- 6
TOTAL 155
TISSUE FLUID:
 Cl- 116
 HCO3
- 27
 HPO4
-2 3
 SO4
-2 2
 Proteins- 1
 Organic Acids 6
TOTAL 155

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ELECTROLYTE COMPOSITION OF ICF
Cations mEq/L
 K+ 150
 Mg+ 40
 Na+ 5
TOTAL 195
Anions mEq/L
 HPO4
- 110
 Proteins- 50
 SO4
-2 20
 HCO3
- 10
 Cl- 5
TOTAL 195

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Electrolyte composition of various secretions of GI tract:-
Secretions Volume ml/day Electrolytes in mEq/L
Na+ K+ Cl- HCO3
-
 Saliva 1500 ml 33 20 34 --
 Gastric Juice 2500 ml 70 10 90 10
 Bile 500 ml 145 5 100 40
 Pancreatic 700 ml 145 5 70 115
Juice
 Intestinal 3000 ml 140 5 110 25
Juice
 Total 8200 ml 553 45 404 190

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Loss through Feces: Fluid: 100-150 ml
Na+: 10-30 mEq
K+: 10 mEq
KIDNEYS
Glomerular Filtration & Tubular Reabsorption of Water &
Na+:
Substances Filtered/day Excreted/day Reabsorption
Water 180 L 1L 99.4%
Na+ 180x140mEq 100 mEq 99.6%
Contd……….

Regulation of Electrolytes:
Sodium:-
• Chief electrolyte of ECF.
• Moves easily b/w intravascular and interstitial spaces and
moves across cell membrane by active transport.
• Acts as catalyst in reactions particularly in nervous tissue
cells and muscle tissue cells.
Functions :-
• Controls and regulates the volume of body fluids
• Maintains water balance
• Primary regulator of ECF volume
• Influences ICF volume
• Participates in the generation and transmission of nerve
impulses.
• Essential electrolyte in the sodium-potassium pump.
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The sources and losses of sodium are:-
• Average adult intake b/w 6 and 15 g
• RDA for sodium for adults 500 mg or 0.5 g.
• Found particularly in mustard, processed cheese, canned
vegetables, bread, cereal and salted snack food, table salt
(NaCl) (about 46% sodium).
• Sodium excess eliminated primarily by the kidneys. Small
amounts lost in faeces and perspiration.
Regulation of Sodium:-
• Normally maintained within a relatively narrow range.
• Salt intake regulates its concentrations.
• Conserved through reabsorption in the kidneys
• Normal extracellular concentrations 135 to 145
mEq/L(mmol/L)

Potassium:-
Major cation of ICF. Potassium and sodium work
reciprocally.
Functions:-
• Chief regulator of cellular enzyme activity and cellular
water content.
• Plays a vital role in transmission of electric impulses,
particularly in nerve, heart, skeletal, intestinal, and lung
tissue; protein and carbohydrate metabolism and cellular
building.
• Assists in regulation of acid-base balance by cellular
exchange with H+.
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The sources and losses are:
• An intake of 50 to 100 mEq daily maintains potassium
balance.
• Excreted primarily by the kidneys.
• Major sources: bananas, peaches, kiwi, figs, dates,
apricots, oranges, melons, raisins, and potatoes, meat and
dairy products.
• Gastrointestinal secretions, perspiration and saliva
contain potassium.
• Normal range 3.5 to 5 mEq/L.
Regulation of K+:
• Conserved by the sodium pump.
• Kidneys conserve potassium when cellular K+ decreased.
• Aldosterone secretions trigger potassium excretion in
urine.
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Potassium……….

Calcium
• Most abundant electrolyte .
• Upto 99 per cent found in bones and teeth in ionized
form.
Functions :
• Necessary for nerve impulse transmission and blood
clotting.
• Catalyst for muscle contraction.
• Needed for vitamin B12 absorption and for its use by
body cells.
• Acts as a catalyst for many cell chemical activities.
• Necessary for strong bones and teeth.
• Establishes thickness and strength of cell membrane.
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The sources and losses of calcium:
• Average daily requirement about 1 g for adults. Higher
amounts required according to body weight, for children,
for pregnant and lactating women, and postmenopausal
women.
• Found in milk, cheese and dried beans. Some amount in
meats and vegetables.
• Use & absorption stimulated by vitamin D (calcitriol).
• Leaves bones and teeth to maintain normal blood calcium
levels if necessary.
• Excreted in urine, faeces, bile, digestive secretion and
perspiration.
Calcium……..

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Regulation of calcium:
• When ECF calcium level decreases, the parathyroid
glands increase the secretions of PTH.
• A high serum phosphate concentration increases serum
calcium; a low serum phosphate concentration decreases
serum calcium.
• Calcitonin, a hormone secreted by the thyroid gland has
an opposite effect of calcium than PTH
Calcium……..

Magnesium
• Found within heart, bone, nerve, and muscle tissues.
• Second most important cation of ICF.
Functions:
• Important for the metabolism of carbohydrates and
proteins.
• Important for many vital reactions related to the body`s
enzymes.
• Necessary for protein and DNA synthesis, DNA and RNA
transcription, and translation of RNA.
• Maintains normal intracellular levels of potassium.
• Serves to help maintain electric activity in nervous
membranes and muscle membranes.
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The sources and losses of magnesium are:
• The average daily adult requirement about 18 to 30 mEq.
Children require larger amount.
• Found in most foods but especially in vegetables, nuts,
fish, whole grains, peas and beans.
Regulation of Magnesium
• Absorbed by the intestines and secreted by the kidneys.
• Plasma concentration of magnesium range from 1.3 to
2.1 mEq/L with about one-third of that amount bound to
plasma proteins.
Magnesium…….

Chloride
Found in blood, interstitial fluid, and lymph and in minute
amounts in intracellular fluid.
Functions :-
• Acts with sodium to maintain the osmotic pressure of the
blood.
• Vital role in the body`s acid-base balance.
• Buffering action when O2 and CO2 exchange in RBC`s.
• Essential for the production of HCl.
• The average daily requirement of chlorides are unknown.
Regulation of Cl-
• Chloride deficits lead to potassium deficit and vice versa.
• Normal serum chloride levels range from 95 to 105 mEq/L.
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Bicarbonate
• Major chemical buffer.
• Found in both ECF and ICF.
• Essential for acid-base balance.
• Bicarbonate and carbonic acid constitute the body`s
primary buffer systems.
Phosphate
Buffer anion in both ICF and ECF.
Functions:
• Helps maintain acid-base balance.
• Involved in important chemical reactions in the body
• Important for cell division and for the transmission of
heredity traits.
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ELECTROLYTE IMBALANCES
Hyponatremia
Serum sodium below 135 mEq/L
Causes:-
GI system:
• sweating
• vomiting
• diarrhea
• intestinal fistula
• dialysis
• chronic pyelonephritis
• chrome uremia
• diabetic ketoacidosis
• cystic diseases of the kidney
• excessive loss of sodium through urine.
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Hyponatremia……..
Endocrine system:
• Myxedema
• Addison`s disease
• Hyperaldosteronism
• Uncontrolled diabetes mellitus
Integumentory system :
• Extensive burns
• Generalized dermatitis
In children
• cystic fibrosis

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The main characteristics of hyponatremia are:
• Anorexia
• Nausea and vomiting
• Fingerprint and oversternum
• Muscular twitching & weakness
• Tiredness
• Lethargy
• Mental confusion
• Convulsions and coma in severe cases
• Skin cold, pale and inelastic
• Dry tongue
• Reduction in plasma volume
• Eyeballs become soft due to reduced intraocular
pressure
• Urine output reduced and soon oliguria supervenes

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Treatment:
• Mild cases, frequent drink of water with added sodium
chloride or with isotonic (0.9%) saline solution by IV
injection.
• Given IV infusion over 6-12 hours.
• More severe cases, 2-5 liters within 24-48 hours.
• Associated water intoxication, restrict water intake to
500-1000 ml in 24 hours.
In addition, treatment for the underlying condition.

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Nursing interventions:
• Identify clients at risk for hyponatremia.
• Monitor fluid losses and gains.
• Look for loss of sodium containing fluids.
• Monitor presence of anorexia, nausea, vomiting, and
abdominal cramping.
• Monitor laboratory date for serum sodium levels less
than normal.
• Check specific gravity of urine.

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• With clients able to consume a general diet, encourage
foods and fluids with high sodium content.
• Monitor client with cardiovascular disease receiving
sodium-containing fluids closely for sign of circulatory
overload such as moist rales in the lungs.
• Use extreme caution when administering hypertonic
saline solution (3 to 5% NaCl).
• Avoid giving large water supplements to clients receiving
isotonic tube feedings.
Hyponatremia………

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Hyponatremia………
In Children
 Oral Rehydration Therapy for mild to moderate
 ORS containing 75-90 mmol sodium & 111-139 mmol
glucose for first 4-6 hours.
 Oral fluids containing 30-60 mmol sodium & 111-139
mmol glucose for next 18-24 hours at a dose of 45-60
ml/kg for young children & 30-60 ml for older children.
 Continue breast feed if the child is on breast feed.
 Pediatric maintenance solutions s.a. combination of
dextrose(usually 5% or 10%) and sodium chloride(usually
0.22% to 0.3%).
 Any IV solution can be given containing atleast 0.2%
sodium chloride.

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Hypernatremia
Serum sodium more than 145mEq/L
The related factors are:
• Deprivation of water, most common in those unable to
perceive or respond to thirst.
• Hypertonic tube feeding with inadequate water
supplement.
• Increased insensible water loss (as in hyperventilation)
• Ingestion of salt in unusual amounts.
• Excessive parenteral administration of sodium-
containing solution-
 Hypertonic saline (3% or 5% NaCl)
 7.5% sodium bicarbonate
 Isotonic saline

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 Profuse sweating.
 Diabetes insipidus
 Heat stroke
• Drowning in sea water
• Diabetes insipidus
• Hypercalcemia
• Hypokalaemia
• Chronic renal failure, and recovery phase of acute renal
failure.
• Nephrotic syndrome
• Cardiac failure,
• Nutritional or thiamine deficiency
• Cirrhosis of liver
• Drugs such as corticosteroids, androgens,
phenylbutazone, oral contraceptive and carbenoxelone.
Hypernatremia…….

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The main characteristics of hypernatremia are:
• Thirst.
• Elevated body temperature.
• Tongue dry and swollen, sticky mucus membranes.
• In severe hypernatremia
 Disorientation
 Irritable and hyperreactive when stimulated
 Focal or grand mal seizures, coma, low blood
pressure, tachycardia.

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Hypernatremia……
Treatment:
An immediate treatment : within 24-48 hours to avoid
occurrence of cerebral edema.
• Mild cases- IV infusion 5% dextrose solution.
• Other cases- restriction of water and salt by mouth.
• Management of the condition depends upon the
underlying condition.
• Diuretics and other measures-on the advice of the
physician according to condition of patient.

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Nursing Intervention:
• Identify clients at risk of hypernatremia
• Monitor fluid losses and gains. Look for abnormal losses
of water or low water intake, and for large gains of sodium.
• Monitor changes in behaviour such as restlessness,
disorientation and lethargy.
• Look for excessive thirst, and elevated body temperature.
• Monitor serum sodium level.
• Prevent hyponatremia in debilitated clients unable to
perceive or respond to thirst .
• If fluid intake remains inadequate, consult the physician
to plan an alternate route for intake.

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Hypokalaemia
Potassium less than 3.5 mEq/L
The related factors leading to hypokalaemia are:
• Excessive loss of potassium in the urine and stool and
from severe water depletion.
• Use of carbenicillin, sodium penicillin, amphotorecin.
• Poor intakes as in anorexia nervosa, alcoholism,
potassium free parenteral fluids.
• Osmotic diuresis (as occurs in uncontrolled diabetes
mellitus or mannitol administration).

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(Hypokalaemia)
The main characteristics of hypokalaemia are:
• Fatigue
• Anorexia, nausea and vomiting
• Muscle weakness
• Decreased bowel motility (intestinal ileus)-paralytic ileus
• Cardiac arrhythmia
• Increased sensitivity to digitalis
• Mild hyperglycemia
• Paresthesias or tender muscles
• Respiratory hyperventilation

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(Hypokalaemia)
Treatment:
Adequate management of the underlying condition.
• Be aware of clients at risk for hypokalaemia and monitor
for its occurrence.
• Asses closely for symptoms of digitalis toxicity.
• Take measures to prevent hypokalaemia when possible
 Encourage extra potassium intake for at risk
patient.
 If hypokalaemia due to abuse of laxatives or
diuretics educate the client.
• Administer oral potassium supplement when prescribed.
• Clients may not need potassium supplements if they are
using salt substitutes.

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Hyperkalaemia
Serum potassium more than 5.5 mEq/L
• Decreased potassium excretions as in
 Oliguric renal failure
 Potassium-conserving diuretic usage
 Hypoaldosteronism.
• High potassium intake, in presence of renal
insufficiency:-
 Improper use of oral potassium supplements.
 Rapid excessive administration of IV potassium.
 High-dose potassium penicillin.
 Foods high in potassium (such as dried apricots)

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• Shift of potassium out of cells due to acidosis, tissue
trauma, and malignant cell lysis.
• Potassium excess also occurs in
 Acute renal failure,
 Severe crush injuries and
 Burns,
 Severe hemorrhages and
 Adrenal insufficiency.
 Diabetic keto acidosis.
Related factors of hyperkalaemia

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(Hyperkalaemia)
The main characteristics of hyperkalaemia are:-
• Vague muscular weakness.
• Cardiac arrhythmias, bradycardia and heart block.
• Paresthesis of face, feet and hands.
• Flaccid muscle paralysis.
• Gastrointestinal symptoms such as nausea, intermittent
intestinal colic, or diarrhea.
• Cardiac arrest, metabolic acidosis and respiratory
acidosis.

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(Hyperkalaemia)
Treatment:-
• Replacement of water loss and correction of electrolyte
imbalance.
• Diet with restricted protein but with as much as fat and
carbohydrates
• Manage the underlying condition.
Nursing Intervention:-
• Monitor clients at risk for hyperkalaemia.
• Take measures to prevent hyperkalaemia when possible
by following guidelines for administering potassium safely
both intravenously or orally.

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(Hyperkalaemia)
• Follow rules for safe administration of potassium.
• Avoid administration of potassium conserving diuretics,
potassium supplements or salt substitutes to client with
renal insufficiency.
• Caution client to use salt substitute sparingly if they are
taking other supplementary form of potassium or taking
potassium-conserving diuretics.(example,spironolactone,
triamaterine, and amiloride).
• Caution hyperkalaemic clients to avoid coffee, cocoa,
tea, dried fluids, dried beans, wholegrain breads.

67
Research input
A prospective study to assess the prevalence of post
operative complications among CABG patients in HDHI,
Ludhiana, 2008.43 Pp. B.Sc (N) Thesis
Prabhjot Saini, Nitasha etal
A total of 60 subjects who had undergone CABG were
included in study. All the subjects were interviewed and
observed for post operative complications from 1-7 days of
surgery and on day of discharge.
16(26.6%) subjects showed hyponatremia on 1-3 post
operative days and 7(11.6%) showed hyponatremia on 4-7
post operative days.
While 3(5%) subjects were found hyperkalaemic on 1-3
post operative days and 6(10%) subjects were hypokalaemic.

68
Hypocalcaemia
Calcium level below 8.5 mg/dL
• Surgical hypoparathyroidism
• Malabsorption
• Vitamin D deficiency
• Alkalotia states (decreased ionized calcium)
• Hyperphosphataemia
• Medullary carcinoma of thyroid
(as in cirrhosis, nephrotic syndrome and starvation)
• Hypomagnesaemia
• Decreased ultraviolet exposure.

69
The main characteristics are:
• Numbness-tingling fingers, circumoral region and toes
• Cramps in the muscles of extremities
• Hyperactive deep tendon reflexes (such as patellar and
triceps)
• Trousseau`s sign
• Chvostek`s sign
• Mental changes such as confusion and alteration in mood
and memory
• Convulsions, usually generalized but may be focal
• Spasm of muscles of larynx & abdomen.
• Hypocalcemic state eventually cause tetany and death.
Hypocalcaemia………

70
• Usually asymptomatic and the neurological
manifestations develop slowly
• Diffuse encephalopathy, depression and psychosis
• In severe cases there may be laryngiospasm and
generalized convulsions
• It may also give rise to papilloedema and cataract.
Hypocalcaemia……..

71
Hypocalcaemia……
Treatment:
• Most cases respond well to adequate or supplemental
calcium and phosphorus.
• Give calcium carbonate, 2.52 to 3.78 g daily orally or
calcium gluconate 0.5-1.5 g along with calciferol 15.45 µg
daily orally.
• 10 ml of 10% calcium gluconate slow IV.
• Adequate management and control of predisposing
causes.

72
Nursing Interventions:
• Be aware of clients at risk for hypocalcemia and monitor
its occurrence.
• Be prepared to take seizure-precautions.
• Monitor condition of airway closely.
• Safety precautions if confusion is present.
• Be aware of factors related to the safe administration of
calcium replacement salts.
• Educate people in high-risk groups for osteoporosis.
• Educate high risk group about the value of regular
physical exercise.
• Educate young women to ensure adequate calcium
intake.
• Discuss the calcium-losing aspects of alcohol and nicotine
use
Hypocalcaemia……

73
Hypocalcaemia……
In Children:
 Elemental calcium 35-45 mg/kg/day
 Calcium gluconate 10% solution(elemental calcium 9
mg in each 1.0 ml) 1 ml/kg/dose diluted with equal volume
of distilled water, IV 6 hourly for 48-72 hours or till oral
feeds with calcium supplements are started.

74
Research input
Pathogenesis of early neonatal hypocalcemia: Studies of serum
calcitonin, gastrin, and plasma glucagon
The Journal of Pediatrics, Volume 110, Issue 4, Pages 599-603
P. Venkararaman, R. Tsang, I. Chen, M. SperlingIn
64 maternal-infant pairs were studied, Serum Ca declined significantly
in neonates at 24 hours of age, and was inversely correlated with
serum calcitonin. Cord serum calcitonin, gastrin, and plasma glucagon
concentrations rose significantly at 24 hours of age. The study
conclude that (1) serum calcitonin, gastrin, and plasma glucagon
values rise postnatally; serum calcitonin. concentration does not
correlate with the elevated serum gastrin and plasma glucagon values;
and at 24 hours of age, decreased serum Ca is correlated with serum
calcitonin, and hence calcitonin might play a role in the pathogenesis
of early neonatal hypocalcemia.

75
Hypercalcaemia
Serum calcium over 10.5 mg/dL
The related factors that lead to hypercalcaemia are:
• Hyperparathyroidism
• Malignant neoplastic disease
• Prolonged immobilization
• Large doses of vitamin D or vitamin D intoxication
• Overuse of calcium containing antacids or calcium
supplements
• Milk-alkali syndrome
• Sarcoidosis

76
The common features are:
• Muscle weakness
• Tiredness, listlessness, lethargy
• Constipation
• Anorexia, nausea, and vomiting
• Decreased memory span, decreased attention span, and
confusion
• Polyuria, and polydipsia
• Renal stones
• Neurotic behaviour progressing to frank psychosis may
occur
• Cardiac arrest may occur in hypercalcaemic crisis
• Renal failure, shock and death in complication.
Hypercalcaemia……

77
Treatment:
• In mild cases, adequate rehydration, management of the
underlying conditions.
• In other cases, intravenous infusion of isotonic saline to
promote calciuria.
• Give sodium phosphate 1-2 g orally daily & encourage to
take more fluids.
• Monitor clients at risk for hypercalcaemia.
• Increase client mobilizations when feasible.
• Encourage the oral intake of sufficient fluids.

78
• Discourage excessive consumption of milk products and
other high calcium foods.
• Encourage adequate bulk in the diet.
• Take safety precautions if confusion or other mental
symptoms.
• Be prepared to deal with cardiac arrest as an emergency.
• Be aware that bones may fracture more easily in clients
with chronic hypercalcaemia. Transfer clients cautiously.
• Educate clients and their families, to be alert for
symptoms that occur with this condition and to report
them to the health care providers before they become they
become severe.

79
• Be alert for signs of digitalis toxicity when
hypercalcaemia occurs in digitalized clients.
• Help prevent formation of calcium renal stones in clients
with long-standing hypercalcaemia or immobilization by:
 Forcing fluids to maintain dilute urine, thus
avoiding supersaturation of precipitates.
 Encouraging fluids that yield acid ash (prune or
crannberrymilk) because a urinary pH less than 6.5
favors calcium deposits.
• Preventing urinary stasis by turning the immobilized
client, elevating head of the bed and having the client sit up
if tolerable.

80
Research input
Hypercalcemia in childhood acute lymphoblastic leukemia: frequent
implication of parathyroid hormone-related peptide and E2A-HLF
from translocation 17;19
T Inukai , K Hirose et al
Abstract
Clinical data of 22 cases of childhood ALL accompanied by
hypercalcemia reported in Japan from 1990 to 2005 were
retrospectively analyzed. Eleven patients were 10 years and older.
Twenty patients had low white blood cell count. Parathyroid hormone-
related peptide -mediated hypercalcemia was confirmed in 11 of the 16
patients in whom elevated-serum level or positive
immunohistochemistry of PTHrP was observed. Hypercalcemia and
accompanying renal insufficiency resolved quickly, particularly in
patients treated with bisphosphonate. The final outcome of ALL
accompanied by hypercalcemia was similar to that of all childhood ALL
patients, indicating that the development of hypercalcemia itself is not
a poor prognostic factor

81
Hypomagnesemia
Serum magnesium level below 1.3 mEq/L.
• Chronic alcoholism
• Intestinal Malabsorption syndrome
• Diarrhea
• Nasogastric suction-prolonged
• Aggressive refeeding after starvation (as in TPN)
• Prolonged administration of magnesium-free IV fluids
• Uncontrolled diabetes mellitus-diabetic ketoacidosis

82
Hypomagnesemia
• Drugs-prolonged use of
 Diuretics, aminoglycoside, antibiotics (e.g.
gentamycin), cisplatin
 Excessive dose of vitamin-D or calcium
supplements
 Citrate preservative in blood products Pancreatitis,
thyrotoxicosis, hyperparathyroides
• Severe osteotitis fibrosa ,PEM.
The common characteristics of hypomagnesemia are:
• It presents with multiple metabolic and nutritional
deficiency
• It gives rise to anorexia, lethargy, vomiting, weakness,
and tetany

83
Hypomagnesemia
• Neuromuscular irritability
 Increased reflex
 Course tremors
 Positive chvostek`s sign
 Positive trousseau`s sign
 Convulsions.
• Cardiac manifestations will include
 Tachyrrhythmias
 Increased susceptibility to digitalis toxicity
• Mental changes
 Disorientation in memory
 Mood changes
 Intense confusion
 Hallucination

84
Hypomagnesemia….
Treatment:
• Repletion through magnesium sulphate and chloride.
• Give double the amount required because half of
magnesium given excreted by the kidneys.
• The repletion is done gradually and is given orally or
intravenously.
• In severe cases, IV only.
Nursing Intervention:
• Monitor closely for symptoms of digitalis toxicity because
a deficit of magnesium predisposes to toxicity.
• Be prepared to take seizure precautions when
hypomagnesaemia.
• Monitor condition of airway, because laryngeal stridor
can occur.

85
Hypomagnesemia……….
• Take safety precautions if confusion presents.
• Be familiar with magnesium replacement salts and
factors related to these safe administration.
• Be aware that magnesium-depleted clients may
have difficulty in swallowing.
• When magnesium deficit due to abuse of diuretics in
laxatives, educate the client.
• Be aware that most commonly used IV fluids have either
no magnesium or relatively small amount.
• When indicated, discuss the need for magnesium
replacement with physicians.

86
Research input
Hypomagnesemia in infants of diabetic mothers: Perinatal
studies
R. Tsang, R. Strub et al
56 diabetic mothers and their infants were studied
prospectively from birth. Twenty-one of 56 IDM had serum
Mg≤1.5mg/dl, on at least one occasion during the first 3 days.
Serum Mg in these hypomagnesemic infants did not
demonstrate the normal increase with postnatal age that was
present in normomagnesemic infants. Decreased neonatal
serum Mg was related to increased severity of maternal
diabetes, young mothers, mothers of lower gravidity, and
prematurity.

87
Research input(contd…..)
Decreased serum Mg, alone or with decreased ionized or
total Ca, did not correlate with neuromuscular irritability
in the infants. Decreased serum Mg in IDM was
associated with decreased maternal serum Mg, decreased
neonatal ionized and total Ca, increased serum P, and
decreased parathyroid function. Serum Mg was not
related to dietary P intake, or urinary Ca or P excretion.
Thus, transitory neonatal hypomagnesemia occurs in
IDM; it is speculated that factors causing HM might
include maternal HM or neonatal hyperphosphatemia,
and that the HM is related to the hypocalcemia and
functional hypoparathyroidism of IDM.

88
Hypermagnesaemia
Serum mg level above 3 mEq/L.
• Renal failure (particularly when magnesium containing
medication is administered).
• Adrenal Insufficiency.
• Excessive magnesium administration during treatment
of eclampsia.
• Haemodialysis with excessively hard water or with
dialysate inadequately high in magnesium content.

89
(Hypermagnesaemia)
The main characteristics:
• Early signs (serum level of mg of 3 to 5 mEq/L)
 Flushing and a sense of skin warmth (due to
peripheral vasodilation)
 Hypotension (due to blockage of sympathetic
ganglia as well as to direct effect on smooth muscle)
 Depressed respiration
• Drowsiness, hypoactive reflexes and muscular weakness
• Cardiac abnormalities-cardiac arrest
• Weak or absent cry in newborn

90
(Hypermagnesaemia)
Treatment:
• In severe cases and also in other cases cardiac and
respiratory support by IV injection of 10-20 ml of 10%
calcium gluconate to maintain adequate hydration.
• Also give frusemide by IV injection to promote excretion
of magnesium.
• In severe cases haemodialysis.

91
(Hypermagnesaemia)
• Be aware of client at risk for hypermagnesaemia and
assess for its presence. When suspected assess :
 Vital signs: look for low blood pressure and
shallow respirations with periods of apnea.
 Level of consciousness: look for drowsiness,
lethargy and coma.
• Do not give magnesium containing medication to clients
with renal failure or compromised renal function.
• Be particularly careful in following `standing order’ for
bowel preparation for X-ray because some of these include
the use of magnesium citrate.
• Be aware of factors related to safe parenteral
administration of magnesium salts.

92
ECG changes in various electrolyte imbalances
CONDITION CHANGE IN ECG
Hypokalaemia Fattened T waves, ST segment
depressions
Hyperkalaemia Tall, peaked T waves, absent P waves,
widened QRS complex
Hypocalcaemia Prolonged QT interval
Hypercalcaemia Shortened QT interval
Hypomagnesaemia PR and QT interval prolongation,
widened QRS complex, ST
segment depression and T-wave
inversion
Hypermagnesaemia Prolonged PR interval, widened
QRS complex, and elevated T-
wave amplitude

93
Research input
E. Donovan, R. Tsang et al
Twenty pre-eclamptic mothers treated with MgSO, and their
newborn infants were studied prospectively to determine the clinical
and biochemical effects of hypermagnesemia. Maternal serum
magnesium concentration rose to 4.4 at delivery and was
accompanied by a fall in maternal serum calcium concentration
during labor. Neonatal serum Mg concentration remained elevated
for the first 72 hours of life (mean at 72 hours = 3.0 mg/dl). Serum
Mg concentration was higher in premature infants and in babies with
birth asphyxia. Serum Ca concentration was higher and serum PTH
was lower in hypermagnesemic study infants when compared to a
retrospecitively selected, matched group of control infants. Elevated
serum Mg values in these infants result in a shift of Ca from bone to
plasma, and that elevated Mg and Ca concentrations further suppress
neonatal parathyroid function.

94
ACIDOSIS & ALKALOSIS
Clinical disorders owing to disturbances of the body acid-
base balance.
Acidosis:-
Fall in the [HCO3
-]/[H2CO3] ratio of blood below 20, with a
consequent lowering of the blood pH.
Usually accompanied by a rise in serum K+ (hyperkalaemia)
outflow from cells and K+ retention from urine.
2 types :

95
Respiratory acidosis
1. Pulmonary hypoventilation in asthma, respiratory
paralysis and lobar pneumonia.
2.Characterized by CO2 retention in the blood, raising
the pCO2 and H2CO3 concentration in blood with little
change in HCO3
- concentration.
The consequent decrease in the [HCO3
-]/[H2CO3] ratio
leads to the fall in the ratios of other buffer pairs also, and
thereby lowers the blood pH.
TREATMENT:
 Aimed at improving ventilation.
 Pharmacologic agents as needed.
 Pulmonary hygiene as needed.
 Adequate hydration.
 Mechanical ventilation.

96
Metabolic acidosis
caused by
 excessive loss of bases in diabetic ketosis,
 severe diarrhea,
 nephritic acidosis and hypoxic lactic acidosis.
 characterized by a fall in the plasma HCO3
-
concentration with little change in H2CO3 concentration,
lowering the [HCO3
-]/[H2CO3] ratio and the pH of the
blood.
TREATMENT:
 Aimed at correcting the metabolic defect.
 Administer bicarbonate when necessary.
 Hemodialysis or peritoneal dialysis as needed.

97
Alkalosis
Rise in the [HCO3
-]/[H2CO3] ratio of blood above 20, with a
consequent rise in the blood pH.
Accompanied by a fall in serum K+ (hypokalaemia) due to
K+ influx into cells and K+ depletion through urine.
2 types:
1.Respiratory alkalosis
1. Pulmonary hyperventilation in thermal panting, fever,
mountain sickness, hysterical overbreathing and voluntary
hyperpnoea.
2. Characterized by an excessive removal of CO2 from the
blood and a consequent lowering of the blood H2CO3
concentration with little change in HCO3
- concentration,
raising the [HCO3
-]/[H2CO3] ratio in blood, leading to a
rise in the blood pH.

98
Respiratory alkalosis
Treatment:
 Depends upon the underlying cause of respiratory
alkalosis.
 Instruct to breathe more slowly to allow CO2 to
accumulate.
 Sedatives to relieve hyperventilation.
 Treatment according to underlying problem.

99
Metabolic alkalosis
1. Arises from non-respiratory factors such as violent
vomiting, Pyloric Stenosis and high alkali intake like
NaHCO3.
2. Characterized by a rise in the [HCO3
-] with little
change in [H2CO3],raising the ratio of bicarbonate buffer
pair and thereby increases the blood pH.
TREATMENT:
 Aims at reversing the underlying disorder.
 Administer chlorine to allow the excretion of excess
bicarbonate.
 Administer sodium chloride to restore normal fluid
volume.
 Correct the underlying acid-base disorder.

100
Compensation
• In both acidosis and alkalosis, the body tries to restore
the normal [HCO3
-]/[H2CO3] ratio by changing the
pulmonary elimination of CO2 and/or the urinary
elimination of HCO3
-
• If it succeeds in restoring the normal buffer ratio,
acidosis or alkalosis is said to be compensated.
• If the buffer ratio fails either totally or partially to
return to normal, acidosis or alkalosis is accordingly said
to be uncompensated or partially compensated.

101
Arterial Blood Gases(ABG)
• Measurement of blood pH and of arterial oxygen and carbon dioxide
tensions are obtained when managing patients with respiratory
problems and in adjusting oxygen therapy as needed.
• The arterial oxygen tension (PaO2) indicates the degree of
oxygenation of the blood.
• The arterial carbon dioxide tension (PaCO2) indicates the adequacy of
alveolar ventilation.
• Arterial blood gas studies aid in assessing the ability of the lungs to
provide adequate oxygen and remove carbon dioxide and the ability of
the kidneys to reabsorb or excrete bicarbonate ions to maintain normal
body pH.
• Serial blood gas analysis also is a sensitive indicator of whether the
lung has been damaged after chest trauma.
• Arterial blood gas levels are obtained through an arterial puncture
using the radial, brachial, or femoral artery or through an indwelling
arterial catheter.

102
Normal Values: Arterial and Venous Blood
Parameter Arterial Sample Venous Sample
pH 7.35-7.45 7.32-7.38
PaCO2 35-45 mmHg PCO2 42-50 mmHg
PaO2 80-100 mmHg PO2 40 mmHg
Oxygen Saturation 95%-100% 75%
Base excess or deficit +or-2 +or-2
HCO3
- 22-26 mEq/L 23-27 Eq/L

103
Research input
Arterial Blood Gases and Oxygen Content
in Climbers on Mount Everest
Michael P.W. Grocott, M.B., B.S., Daniel S. Martin, M.B., Ch.B.,
Denny Z.H. Levett, B.M., B.Ch., Roger McMorrow, M.B., B.Ch.,
Jeremy Windsor, M.B., Ch.B., and Hugh E.
, M.B.B.S., M.D.,
for the Caudwell Xtreme Everest Research Group
Results
PaO2 fell with increasing altitude. The haemoglobin concentration increased
such that the oxygen content of arterial blood was maintained at or above sea-
level values until the climbers reached an elevation of 7100 m(23,294 ft). In
four samples taken at 8400 m (27,559 ft) — at which altitude the barometric
pressure was 272 mm Hg (36.3 kPa) — the mean PaO2 in subjects breathing
ambient air was 24.6 mm Hg (3.28 kPa), with a range of 19.1 to 29.5 mm Hg
(2.55 to 3.93 kPa). The mean PaCO2 was 13.3 mm Hg (1.77 kPa), with a range
of 10.3 to 15.7 mm Hg (1.37 to 2.09 kPa). At 8400 m, the mean arterial oxygen
content was 26% lower than it was at 7100 m (145.8 ml per litre as compared
with 197.1 ml

104
BIBLIOGRAPHY
1. Das debajyoti. biochemistry. Calcutta :Academic Publishers, 499-504.
2. Phipps Wilma J. et al. Shafer`s Medical-Surgical Nursing. 7th edition. B.I
Publications. 145-151.
3. Basavanthapa BT. Medical-Surgical Nursing. New Delhi:Jaypee brothers
publications. 84-94.
4. Reddy K.R. Medical Biochemistry for nurses. New Delhi:Jaypee
publishers. 616-621.
5. Chatterjea M.N. Textbook of Biochemistry. Jaypee publishers. 496-504.
6. Suzane c. smeltzer. Brenda g. bare. Textbook of Medical-Surgical Nursing.
Lippincott publishers.313.
7. Hockenberry marliya J. Wilson David. Wong`s nursing care of Infants
and Children. Eighth edition. Mosby`s publishers. 1141-1158.
8. Singh meharban. Care of the Newborn. Sixth edition. Sagar
publications.353-363.

105
Summarization
• Distribution of fluid in body
• Distribution of electrolytes in the body
• Normal water balance
• Normal electrolyte balance
• Abnormal water and electrolyte balance
• Types of fluid imbalances
• Types of electrolyte imbalances
• Acidosis and alkalosis
• Arterial blood gases
• Research inputs
• Bibliography

Fluid electrolyte balance

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