A patient complains of having

muscle twitching ,decreased

skin turgor,BP-80/50 mmhg
lethargy and headache for
one week. Her serum sodium
level was 120 mEq /L,
potassium 3.6 mEq /L on
investigation.
Fluid & Electrolyte
Imbalance
MANISHA
MSC NURSING
1ST YEAR STUDENT
COLLEGE OF NURSING
ILBS HOSPITAL
Help maintain body
temperature and
cell shape
Helps transport
nutrients gases
and wastes
 Mechanism for fluid and
electrolyte movement

osmosis
filtration

diffusion
diffusion
diffusion
osmosis
filtration
 FLUID BALANCE

The desirable amount of fluid intake and loss in

adults ranges from 1500 to 3500 mL each 24
hours. Ave= 2500 mL
Normally INTAKE = OUTPUT
FLUID VOLUME
DISTURBANCES
It is an abnormally decreased or
increased fluid volume or rapid shift
from one compartment of body fluid
to another
Hypovolemia
Hypervolemia
 Fluid
volume deficit

hypovolemia
 FLUID DEFICIT/HYPOVOLEMIA
May occur as a result of:
Reduced fluid intake
Loss of body fluids
Sequestration (compartmentalizing) of body fluids
Pathophysiology
DECREASED FLUID VOLUME

Stimulation of thirst ADH Secretion Renin-Angiotensin-

center in hypothalamus Aldosterone System
Activation
Water resorption
Person complains of thirst
Sodium and
Urine Output
Water Resorption

Urine specific gravity except

with osmotic diuresis
Clinical manifestations
Acute Weight loss

Decreased skin turgor

Concentrated urine

flattened neck veins

Postural hypotension
 Weak, rapid, heart rate

Oliguria

Increased temperature

Decreased central venous pressure

Treatment/Interventions (FVD)
Fluid Management
Oral rehydration therapy Solutions containing
glucose and electrolytes. E.g., Plasmoalyte,
Rehydralyte.

IV therapy Type of fluid ordered depends on the

type of dehydration and the clients cardiovascular
status.

Diettherapy Mild to moderate dehydration.

Correct with oral fluid replacement.
NURSING MANAGEMENT
Monitor& measures fluids at least every 8
hourly and sometimes hourly.
Monitor daily body weight.
Monitor vital signs.
Observefor weak, rapid pulse and
orthostatic hypotension.
Monitorurine concentration by measuring
urine specific gravity.
Assess
degree of oral and mucous
membrane moisture.
PREVENTING HYPOVOLEMIA

To prevent hypovolemia, the nurse

identifies patient at risk and takes
measures to minimize fluid loss. For ex:
the patient has diarrhoea, measures
should be implemented to control
diarrhoea and replacement fluid
administered. This includes antidiarrheal
medication and small volume of oral fluids
at frequent intervals
 Nursing Diagnosis
Fluid volume Deficit r/t
Insufficient intake, vomiting, diarrhea,
haemorrage, manifested by dry mucous
membranes
 Fluid
volume excess

hypervolemia
HYPERVOLEMIA

It refers to an isotonic expansion of

the ECF caused by abnormal
retention of water and sodium in
approximately the same proportion
in which they normally exist in the
ECF.
It is most often secondary to an
increase in total body water.
Fluid Volume Excess
Common Causes:
Congestive Heart Failure
Early renal failure
IV therapy
Excessive sodium ingestion
SIADH
Corticosteroid
 Clinical manifestations

Edema

Distended neck veins

Tachycardia

Increased blood
Pressure
Increased weight

crackles
MEDICAL MANAGEMENT
Pharmacological therapy
Diuretics such as thiazide diuretics and
loop diuretics
Thiazide diuretics: hydrochlorothiazide
Loop diuretics: furosemide, torsemide
Potassium supplement.
NURSING MANAGEMENT

I/O chart at regular intervals to

identify excessive fluid retention
Breath sound are assessed at regular
intervals in at risk patient particularly
if parenteral fluid are being
administered
Monitor the degree of edema in most
dependent parts of body such as feet
& ankles
DIALYSIS
If renal function is so severely impaired that
pharmacologic agents cannot act
efficiently, other modalities are considered
to remove sodium and fluid from the body.
Haemodialysis or peritoneal dialysis may be
used to remove nitrogenous wastes and
control potassium and acid base balance
and to remove sodium and fluid. Continuous
renal replacement therapy may also be
required
CONTROLLING HYPERVOLEMIA
IF it is important to detect FVE before the
condition become severe. Intervention include
promoting rest, restricting sodium intake ,
monitoring parenteral fluid therapy and
administering appropriate medications
Regular rest periods may be beneficial because
bed rest favours diuresis of fluid
Sodium and fluid restriction should be
instituted as indicated
Fowlers position should be maintain to
promote lung expansion
 Nursing Diagnosis
Fluid volume excess r/t
CHF, excess sodium intake, renal failure
WHAT DO ELECTROLYTES DO?
cations
sodium potassium

calcium magnesium
 most abundant cat ion in the extracellular
fluid
sodium is regulated by

Salt intake Aldosterone

Urinary output
functions
Maintain balance of extracellular fluid, thereby
it controls the movements of the water between
fluid compartments

Transmission of nerve impulses

Neuro muscular and myocardial impulse

transmission
PATHOPHYSIOLOGY OF HYPONATREMIA
Sodium loss from the intravascular compartment

Diffusion of water into the interstitial spaces

Sodium in the interstitial space is diluted

Decreased osmolarity of ECF

Water moves into the cell as a result of sodium loss

Water moves into the cell as a result of sodium loss

Extracellular compartment is depleted of water

CLINICAL SYMPTOMS
 CLINICAL MANIFESTATIONS OF HYPONATREMIA

Muscle APATHY
Weakness

Postural Nausea and

hypotensi Abdominal Weight
on Cramps Loss
In severe hyponatremia: mental confusion, delirium, shock and coma
Hyponatremia (<135mEq/L)

Contributing Factors
Excessive diaphoresis
Wound Drainage
NPO
CHF
Low salt diet
Renal Disease
Diuretics
Hyponatremia (<135mEq/L)
Assessment findings:
Neuro- Generalized skeletal muscle
weakness. Headache / personality
changes.
Resp.- Shallow respirations
CV- Cardiac changes depend on fluid
volume
GI Increased GI motility, Nausea,
Diarrhea (explosive)
GU - Increased urine output
Hyponatremia (<135mEq/L)
Interventions/Treatment
Restore Na levels to normal and prevent
further decreases in Na.
Drug Therapy
(FVD) - IV therapy to restore both fluid
and Na. If severe may see 2-3% saline.
(FVE) Administer osmotic diuretic
(Mannitol) to excrete the water rather
than the sodium.
Increase oral sodium intake and restrict oral
fluid intake.
 HYPERNATREMIA

A serum sodium level above 145 mEq/L is termed

hypernatremia
May occur as a result of fluid deficit or sodium
excess
Frequently occurs with fluid imbalance
Develops when an excess of sodium occurs
without a proportional increase in body fluid or
when water loss occurs without proportional loss
of sodium
Risk Factors: excess dietary or parenteral sodium
intake, watery diarrhea, diabetes insipidus,
damage to thirst center, too young, too old, those
with physical or mental status compromise, and
people with hypothalamic dysfunction
PATHOPHYSIOLOGY OF HYPERNATREMIA
Increased Sodium concentration in ECF

Osmolarity rises

Water leaves the cell by osmosis and enters the

the extracellular compartments

Dilution of fluids in ECF Cells are water depleted

CLINICAL SYMPTOMS

Suppression of aldosterone Sodium is exreted in the

secretion urine
CLINICAL MANIFESTATIONS

Dry, sticky mucous Firm, rubbery

membranes tissue turgor

DEATH
Tachycardia
Manic excitement
Hypernatremia (>145mEq/L)
Assessment findings:
Neuro - Spontaneous muscle twitches.
Irregular contractions. Skeletal muscle
wkness. Diminished deep tendon reflexes
Resp. Pulmonary edema
CV Diminished CO. HR and BP depend on
vascular volume.
GU Dec. urine output. Inc. specific
gravity
Skin Dry, flaky skin. Edema r/t fluid
volume changes.
Hypernatremia (>145mEq/L)
Interventions/Treatment
Drug therapy
Lowering of serum sodium level by
infusion of hypotonic electrolyte solution
Diuretics also may be prescribed to treat
sodium gain
Desmopressin acetate to treat diabetes
insipidus if it is cause of hypernatremia
Diet therapy
Mild Ensure water intake
NURSING MANAGEMENT
The nurse should assess for abnormal looses of
water or low water intake and for large gains
of sodium as might occur with ingestion of OTC
medication that have high sodium content
The nurse should obtain a medication history,
because some prescription medications have a
high sodium content
The nurse also notes the patients thirst or
elevated body temperature and evaluates it in
relation to other clinical sign and symptoms
 Main intracellular cat ion
Helps in maintaining fluid balance of the
intracellular fluid
Potassium is regulated by
 functions
Regulates neuromuscular excitability and muscle
contraction

Needed for glycogen formation and protein sunthesis

Correction of acid base imbalances. Potassium

ion can be exchanged with hydrogen ion (H+)
The more K, the less Na. The less K, the more Na
Plays a vital role in such processes such as transmission of
electrical impulses, particularly in nerve, heart, skeletal,
intestinal and lung tissue; CHON and CHO metabolism; and
cellular building; and maintenance of cellular metabolism and
excitation
Assists in regulation of acid-base balance by cellular
exchange with H
Sources: bananas, peaches, kiwi, figs, dates, apricots,
oranges, prunes, melons, raisins, broccoli, and potatoes,
meat, dairy products
Normal value: 3.5 5 mEq/L
Hypokalemia

Serum level is below 3.5 meq/l

(3.5 mmol/L) usually indicates
a deficit in potassium store
PATHOPHYSIOLOGY OF HYPOKALEMIA

= Action Potential

Nerve and Muscle Activity

Increase in The cell

Low
resting becomes less
Extracellular
membrane excitable
K+
potential
 Aldosterone is secreted

Sodium is retained in the body through resorption by

the kidney tubules

Potassium is excreted

Use of certain diuretics such as thiazides and furosemide, and

corticosteroids

Increased urinary output

Loss of potassium in urine

Clinical manifestations
MEDICAL MANAGEMENT
Administrationod 40- 80 meq/day of
potassium is adequate in adult if there
are no abnormal losses of potassium
Dietary intake of potassium in average
adult is 50-100meq/day
When dietary intake is inadequate for
any reason, oral or IV potassium
supplements may be prescribed
NURSING MANAGEMENT
Thenurse needs to monitor for its early
presence in patients at risk
Fatigue,
anorexia, muscle weakness,
decreased bowel motility, paraesthesia
and dysrhythmias are signal that
warrant assessing the serum potasium
concentration
Hypokalemia (<3.5mEq/L)
Interventions
Assess and identify those at risk
Encourage potassium-rich foods
K+ replacement (IV or PO)
Monitor lab values
D/c potassium-wasting diuretics
Treat underlying cause
HYPERKALEMIA

Serum potassium level greater than

5meq/L
Less common than hypokalaemia ,
but it is usually dangerous
Hyperkalemia (>5.0mEq/L)

Contributing factors:
Increase in K+ intake
Renal failure
K+ sparing diuretics
Shift of K+ out of the cells
Clinical manifestations
MEDICAL MANAGEMENT
In non acute situations, restriction of
dietary potassium and potassium containing
medications may correct the imbalance
Administration either orally or by retention
enema of cation exchange resins
EMERGENCY PHARMACOLOGIC THERAPY
If serum potassium level are dangerously
elevated, it may be necessary to adm. IV
calcium gluconate
Monitor blood pressure
NURSING MANAGEMENT
Patients at risk for potassium excess need to
be identified and closely monitored for signs
of hyperkalemia
Nurse should monitor I/O and observe for
signs of muscle weakness and dysrythmias
Serum potassium level as well as BUN ,
creatinine, glucose & arterial blood gas values
are monitored for patient at risk for
developing hyperkalemia
Hyperkalemia (>5.0mEq/L)
Interventions
Need to restore normal K+ balance:
Eliminate K+ administration
Inc. K+ excretion
Lasix
Kayexalate (Polystyrene sulfonate)
Infuse glucose and insulin
Cardiac Monitoring
 Calcium is the most abundant element in the
body
Calcium is extracellular fluid
Regulated by the action of
Thyroid gland parathyroid gland
 Parathyroid hormone (PTH) controls the
balance among bone calcium,
gastrointestinal absorption and kidney
excretion of calcium.

Thyrocalcitoninfrom the thyroid gland

inhibits the release of calcium from
bones, thus playing a minor role in
determining serum calcium levels.
 functions
Maintenance of cell membrane, its integrity and
structure

Conduction of nerve impulses in the skeletal muscle

Stimulation and depolarization and contraction

of cardiac muscles
functions
Aids in blood coagulation

Growth and formation of bones

Muscle relaxation
CALCIUM IMBALANCES
More than 90% of bodys calcium is
located in the skeletal system
The normal total serum calcium level is
8.6-10.2 mg/dl (2.2 to 2.6 mmol/L)
CALCIUM DEFICIT
(HYPOCALCEMIA)
The serum calcium value lower than
8.6mg/dl
Occurs in variety of clinical situation
Older people and those with disabilities, who
spend on increased amount of time in bed
have an increased risk of hypocalcaemia
because bed rest increases bone resorption
Hypocalcemia (<8.6mg/dL)

Contributing factors:
Dec. oral intake
Lactose intolerance
Dec. Vitamin D intake
End stage renal disease
Diarrhea
Hypocalcemia (<8.6mg/dL)

Contributing factors (contd):

Acute pancreatitis
Hyperphosphatemia
Immobility
Removal or destruction of parathyroid
gland
CLINICAL MANIFESTATION
Numbness
Tingling of finger, toes and circumoral
region
Anxiety
Hyperactive deep tendon reflex
Bronchospasm
diarrhoea
Hypocalcemia (<8.6mg/dL)
Assessment findings:
Neuro Irritable muscle twitches.
Positive Trousseaus sign.
Positive Chvosteks sign.
Resp. Resp. failure d/t muscle tetany.
CV Dec. HR., dec. BP, diminished
peripheral pulses
GI Inc. motility. Inc. BS. Diarrhea
Positive Trousseaus Sign
Positive Chvosteks Sign
Hypocalcemia (<8.6mg/dL)

Interventions/Treatment
Drug Therapy
Calcium supplements
Vitamin D
Diet Therapy
High calcium diet
Prevention of Injury
Seizure precautions
NURSING MANAGEMENT
Status of airway is clearly monitored
Safety precaution to be taken if
confusion is present
Educate the patient about
hypocalcemia, and calcium containing
foods like milk, yogurt, cheese, sea
fruit, legumes, fruits
Avoid overuse of laxatives and antacids
HYPERCALCEMIA
serum calcium value greater than 10.2
mg/dl
It is a dangerous imbalance when
severe infact, hypercalcemic crisis has
a mortality rate as high as 50% if not
treated promptly
Hypercalcemia (>10.2mg/dL)
Contributing factors:
Excessive calcium intake
Excessive vitamin D intake
Renal failure
Hyperparathyroidism
Malignancy
Hyperthyroidism
CLINICAL MANIFESTATION
Muscular weakness
Constipation
Anorexia
Nausea & vomiting
Dehydration
Hypoactive deep tendon reflexes
Calcium stones
Hypercalcemia (>10.2mg/dL)

Assessment findings:
Neuro Disorientation, lethargy, coma, profound
muscle weakness
Resp. Ineffective resp. movement
CV - Inc. HR, Inc. BP. , Bounding peripheral pulses,
Positive Homans sign.
Late Phase Bradycardia, Cardiac arrest
GI Dec. motility. Dec. BS. Constipation
GU Inc. urine output. Formation of renal calculi
Hypercalcemia (>10.2mg/dL)
Interventions/Treatment
Eliminate calcium administration
Drug Therapy
Isotonic NaCL (Inc. the excretion of Ca)
Diuretics
Calcium reabsorption inhibitors
(Phosphorus)
Cardiac Monitoring
NURSING MANAGEMENT
Increasing patient mobility and
encouraging fluids
Encourage to drink 2.8 to 3.8L of
fluid daily
Adequate fiber in diet is
encouraged
Safety precaution are implemented
 Magnesium is the second most
important cat ion in the
intracellular fluid

It has an inhibitory effect on

skeletal muscles.
functions
Precipitation of metabolic activities of cells

Enzyme activity

Neuro chemical activity

Muscular excitability
MAGNESIUM IMBALANCE
HYPOMAGNESEMIA
Refers to below normal serum
magnesium concentration 1.3mg/dl
(0.62 mmol/L)
Itis frequently associated with
hypokalemia
Hypomagnesemia
(<1.3mEq/L)
Contributing factors:
Malnutrition
Starvation
Diuretics
Aminoglcoside antibiotics
Hyperglycemia
Insulin administration
CLINICAL MANIFESTATION

Neuromuscular irritability
Mood changes
Anorexia
Vomiting
Increased bp
Increased deep tendon reflex
insomnia
Hypomagnesemia
(<1.3mEq/L)
Assessment findings:
*Neuro - Positive Trousseaus sign. Positive
Chvosteks sign. Hyperreflexia. Seizures
*CV ECG changes. Dysrhythmias. HTN
*Resp. Shallow resp.
*GI Dec. motility. Anorexia. Nausea
MEDICAL MANAGEMENT

Mild magnesium deficiency can be corrected

by diet alone
Magnesium salt can be administered orally in
an oxide or gluonate form
Vital signs must be assessed frequently
Calcium gluconate must be readily available
to treat
IV.mgso4
NURSING MANAGEMENT

Observe for its sign and symptom

Safety precaution are institued
Due to dysphagia, patient should be
screened
Health education
HYPERMAGNESEMIA
Serum magnesium level higher than
2.3 mg/dl
It is a rare electrolyte abnormality
because kidney efficiently excrete
magnesium
Hypermagnesemia
(>2.3mEq/L)
Contributing factors:
Increased Mag intake
Decreased renal excretion
CLINICAL MANIFESTATION

Flushing
Hypotension
Muscle weakness
Drowsiness
Depressed respiration
Cardiac arrest
diaphoresis
Hypermagnesemia
(>2.3mEq/L)
Assessment findings:
serum magnesium level is greater than
2.3mg/dl
creatinine clearance decreases to less than
3.0ml/min
ECG finding: prolonged PR interval
: Tall T waves
: widened QRS
MEDICAL MANAGEMENT

Administration of magnesium
Ventilatory support
IV calcium gluconate
Administration of loop diuretics and
sodium chloride
Administration of lactated ringers IV
solution
NURSING MANAGEMENT

Risk for hypermagnesemia are identified and

assessed
Monitor vital signs, noting hypotension and
shallow respiration
Observe for decreased deep tendon reflex
and changes in level of consciousness
Caution is essential when preparing and
medicating magnesium containing fluid
parenterally
anions
 chloride
phosphate

bicarbonate
 Phosphate is a buffer anion in extracellular and
intracellular fluid

Phosphate absorption is through gastrointestinal

tract.

Calcium and phosphate are inversely proportional.

When one rises the other falls

Serum phosphate is regulated by

kidneys

Parathyroid hormone
functions
Development and maintenance of bones and
teeth

Promotes normal neuromuscular action

Participates in carbohydrate metabolism

Assist in acid base regulation

Maintains levels of ATP ( Adenosine

Triphosphate) and thus energy levels
PHOSPHORUS DEFICIT
(HYPOPHOSPHATEMIA)

Itis indicated by value

below 2.5 mg/dl
Hypophosphatemia
(<2.5mg/L)
Contributing Factors:
Malnutrition
Starvation
Hypercalcemia
Renal failure
Uncontrolled DM
CLINICAL MANIFESTATION

Paresthesia
Muscle weakness
Bone pain & tenderness
Chest pain
Confusion
Cardiomyopathy
Seizures
Tissue hypoxia
Hypophosphatemia
(<2.5mg/L)
Assessment findings:
On lab analysis, serum phosphate level is
less than 2.5 mg/L
Serum magnesium may be decreased due to
increased urinary excretion of magnesium
X-ray may show skeletal changes of rickets
Hypophosphatemia
(<2.5mg/L)
MANAGEMENT
Treat underlying cause
Oral replacement with vit. D
IV phosphorus (Severe)
Serumphosphate level should be closely
monitored
Diet therapy
Foods high in oral phosphate
NURSING MANAGEMENT

Identify the patient at risk for

hypophosphatemia
Close monitoring of patient
Vital signs and monitor serum
phosphorous level
Check the level of consciousness
Health education
HYPERPHOSPHATEMIA

Serum phosphorus level

that exceeds 4.5mg/dl
(1.45 mmol/L)
CLINICAL MANIFESTATION
Tetany
Tachycardia
Anorexia
Nausea & vomiting
Muscle weakness
Hyperactive reflexes
MEDICAL MANAGEMENT
Administration of Vit.D such as calcitriol which
is available both oral ( Rocaltrol) & parenteral
( Calajex, paricalcitol forms)
Calcium binding antacids
Administration of amphojel with meals
Restriction of dietary phosphate, forced
diuresis with loop diuretics volume
replacement with saline
Continued

Surgery may be indicated for removal of

large calcium and phosphorus deposits
Dialysis may also lower phosphorus
NURSING MANAGEMENT
The nurse monitor patient at risk for
hyperphosphatemia
If low phosphorus diet is prescribed, patient
is instructed to avoid phosphorus rich food
such as hard cheese, cream, nuts, meats etc
Nurse instruct patient to avoid phosphate
containing laxatives and enemas
Monitoring for chnages in urine output
 Chlorides are found in extracellular and
intracellular fluids

The chloride ion balances the cations within

the extracellular fluid

The ion exchange helps to maintain the

electrical neutrality

Chloride is regulated through kidneys

Normal concentration
of chloride

100 to 106
mEq/L
CHLORIDE DEFICIT
HYPOCHLOREMIA

HYPOCHLOREMIA is a serum
chloride level below 97meq/L
(97mmol/L)
CLINICAL MANIFESTATION

Irritability
Tremors
Muscle cramps
Hyperactive deep tendon reflexes
Slow shallow respiration
Coma
seizures
MEDICAL MANAGEMENT
Correcting the cause of hypochloremia
and contributing electrolytes and acid-
base imbalances
Normal saline (0.9% sodium chloride) or
half strength saline(0.45% sodium
chloride) solution is administered by IV to
replace the chloride
NURSING MANAGEMENT
Monitor the patient I/O, arterial blood gas
values and serum electrolyte levels
Changes in pts level of consciousness,
muscle strength and movement and
reported to the physician promptly
Vital signs are monitored and respiratory
assessment is carried out frequently
Educate the pt about food with high
chloride content which include tomato
juice, banana, eggs, cheese etc
HYPERCHLOREMIA

Serum level of chloride exceeds 107

meq/L
Hypernatremia, bicarbonate loss and
metabolic acidosis can occur with high
chloride levels
CLINICAL MANIFESTATION
Tachypnea
Weakness
Lethargy
Deep and rapid respiration
Hypertension
Dimnished cognitive ability
If untreated it leads to:
Decrease in cardiac output,
dysrhythmias and coma
MEDICAL MANAGEMENT
Correcting the cause of underlying cause of
hyperchloremia and restoring electrolyte fluid
and acid base balance are essential
Hypotonic IV solution may be administered to
restore balance.
Lactated ringers solution may be prescribed to
convert lactate to bicarbonate in liver.
Diuretics may be administered to eliminate
chloride as well
Sodium chloride and fluid are restricted
NURSING MANAGEMENT
Monitoring vital sign , arterial blood gas
values and I/O is important to assess the
patients status and the effectiveness of
treatment
Assessment findings related to respiratory,
neurologic and cardiac systems are
documented and changes are discussed
with physician
Educate about the diet
 Bicarbonate is found in extracellular and
intracellular fluids

It is a major chemical buffer in the body

Regulation is through kidneys

Itis an essential component of the carbonic

acid-bicarbonate buffering system essential
to acid base balance
Normal arterial
bicarbonate value

22 to 26
mEq/L
Normal venous
bicarbonate value
24 to 30
mEq/L
In venous blood, bicarbonate
is measured as
carbondioxide content
BICARBONATE DISTURBANCES

METABOLIC
ACIDOSIS

METABOLIC
ALKALOSIS
METABOLIC ACIDOSIS

Primary decrease in serum bicarbonate (HCO3 )

concentration to below 24 mmol/L and a
compensatory decrease in the CO2
concentration.
It occurs from either loss of bicarbonate
(HCO3 - ) or addition of hydrogen ion (H+ ).
CONTRIBUTING FACTORS
Diabetes
Starvation
cardiac arrest
Shock
Severe dehydration
Renal insufficiency
severe diarrhea
Addison's disease or administration of acidifying
salts (e.g. excessive sodium chloride, calcium
chloride, ammonium chloride).
DIAGNOSTIC FINDINGS

ABG studies
Electrolytes
Anion gap
ECG
MANAGEMENT

Eliminating the source.

Administer Bicarbonate.
Increase alkalizing agents.
Haemodialysis and peritoneal dialysis
may help.
METABOLIC ALKALOSIS

Characterized by high pH and a high

plasma bicarbonate concentration.
Can be produced by the gain of
bicarbonate or a loss of H+ ions.
CONTRIBUTING FACTORS

Vomiting
Gastric suction
Pyloric stenosis
Diuretic therapy
Hyperaldosteronism
Cushing syndrome
CLINICAL MANIFESTATIONS

Tingling of the fingers and toes

Dizziness
Symptoms of hypocalcemia
Decreased respirations
Atrial tachycardia may develop
In chronic conditions: k+ decreases cause
frequent premature ventricular contractions or U
waves appearance.
DIAGNOSTIC TESTS

ABG analysis
Serum Bicarbonate levels
Urine chloride levels
MANAGEMENT
Sufficient chloride must be provided to
excrete bicarbonate ions.
Administer fluids.
Potassium administered in hypokalemia
cases.
Carbonic anhydrase inhibitors.
RECENT STUDIES

Highmaternal calcium, magnesium

and potassium intake is reflected in
lower infant blood pressure.
RECENT STUDIES

Fluid and electrolytes disorders are

among the most common disorders in ICU
such as severe burns, trauma, sepsis,brain
damage and heart failure lead to reduced
perfusion to kidney due to hypovolemia or
hypotension etc.
EVALUATION
What is Chvosteks sign?

What is Trousseaus sign?

Normal value of S. calcium?

ANY QUESTION????