This is topic very helpful for understanding fluid therapy and electrolyte balance maintained in human body.

1. MR.JAGDISH SAMBAD
Assistant Professor
Balaji College of Nursing

2.  Fluid and electrolyte balance is a dynamic process that is
crucial for life.
 Potential and actual disorders of fluid and electrolyte
balance occur in every setting, with every disorder, and with
a variety of changes that affect well people (e.g., increased
fluid and sodium loss with strenuous exercise and high
environmental temperature; inadequate intake of fluid and
electrolytes) as well as those who are ill.

3.  Electrolytes in body fluids are active chemicals which are
 The major cations (carry positive charges) - sodium,
potassium, calcium, magnesium, and hydrogen ions.
 The major anions(carry negative charges ) -chloride,
bicarbonate, phosphate, sulfate, and proteinate ions.

5.  Osmosis and Osmolality
fluid shifts through the membrane from the region of low solute
concentration to the region of high solute concentration until the
solutions are of equal concentration
 Tonicity is the ability of all the solutes to cause an osmotic driving
force that promotes water movement from one compartment to
another.
 Osmotic pressure is the amount of hydrostatic pressure needed to
stop the flow of water by osmosis. It is primarily determined by the
concentration of solutes.
 Oncotic pressure is the osmotic pressure exerted by proteins (e.g.,
albumin).
 Osmotic diuresis occurs when the urine output increases due to
the excretion of substances such as glucose, mannitol, or contrast
agents in the urine.

6.  Diffusion is the natural tendency of a substance to move
from an area of higher concentration to one of lower
concentration. It occurs through the random movement of
ions and molecules.
 Filtration
Movement of water and solutes occurs from an area of high
hydrostatic pressure to an area of low hydrostatic pressure.
Filtration allows the kidneys to filter 180 L of plasma per day.

9.  Sodium–Potassium Pump
The sodium concentration is greater in the ECF than in the ICF,
and because of this, sodium tends to enter the cell by
diffusion. This tendency is offset by the sodium–potassium
pump, which is located in the cell membrane and actively
moves sodium from the cell into the ECF. Conversely, the high
intracellular potassium concentration is maintained by pumping
potassium into the cell. By definition, active transport implies
that energy must be expended for the movement to occur
against a concentration gradient.

11. Fluid imbalances

12.  Fluid volume deficit (FVD) occurs when loss of
extracellular fluid volume exceeds the intake of fluid

13.  FVD results from loss of body fluids and occurs more rapidly
when coupled with decreased fluid intake. It includes
 abnormal fluid losses, such as those resulting from vomiting,
diarrhea, GI suctioning, and sweating,
 and decreased intake, as in nausea or inability to gain access to
fluids.
 Additional risk factors include diabetes insipidus, adrenal
insufficiency, osmotic diuresis, hemorrhage, and coma.

14.  acute weight loss
 decreased skin turgor
 oliguria
 concentrated urine
 postural hypotension
 a weak, rapid heart rate
 flattened neck veins
 increased temperature
 decreased central venous
pressure
 cool, clammy skin related to
peripheral vasoconstriction
 thirst
 anorexia
 muscle weakness
 cramps

15.  Hematocrit level is greater than normal because the red blood
cells become suspended in a decreased plasma volume. Serum
electrolyte changes may also exist.
 Hypokalemia occurs with GI and renal losses.
 Hyperkalemia occurs with adrenal insufficiency.
 Hyponatremia occurs with increased thirst and ADH release.
 Hypernatremia results from increased insensible losses and
diabetes insipidus.
 Urine specific gravity is increased in relation to the kidneys’
attempt to conserve water and decreased with diabetes insipidus.
 Urine osmolality is greater than 450 mOsm/Kg, since the kidneys
try to compensate by conserving water.

16.  When the deficit is not severe, the oral route is preferred,
provided the patient can drink.
 When fluid losses are acute or severe, however, the IV route is
required. Isotonic electrolyte solutions (e.g., lactated
Ringer’s or 0.9% sodium chloride) are frequently used.
 As soon as the patient becomes normotensive, a hypotonic
electrolyte solution (e.g., 0.45% sodium chloride) is often
used to provide both electrolytes and water for renal
excretion of metabolic wastes.
 Accurate and frequent assessments of intake and output,
weight, vital signs, central venous pressure, level of
consciousness, breathe sounds, and skin color should be
performed to determine when therapy should be slowed to
avoid volume overload.

17.  To assess for FVD, the nurse monitors and measures fluid intake
and output at least every 8 hours and sometimes hourly.
 Skin and tongue turgor is monitored on a regular basis. The
degree of oral mucous membrane moisture is also assessed; a dry
mouth may indicate either FVD or mouth breathing.
 Urinary concentration is monitored by measuring the urine
specific gravity. In a volume-depleted patient, the urinary specific
gravity should be above 1.020, indicating healthy renal
conservation of fluid.
 Mental function is eventually affected in severe FVD as a result of
decreasing cerebral perfusion. Decreased peripheral perfusion can
result in cold extremities.

18.  To prevent FVD, the nurse identifies patients at risk and
takes measures to minimize fluid losses. For example, if the
patient has diarrhea, diarrhea control measures should be
implemented and replacement fluids administered. These
measures may include administering antidiarrheal
medications and small volumes of oral fluids at frequent
intervals.

19.  Fluid volume excess (FVE) refers to an isotonic expansion of
the ECF caused by the abnormal retention of water and
sodium in approximately the same proportions in which they
normally exist in the ECF. It is always secondary to an
increase in the total body sodium content, which, in turn,
leads to an increase in total body water.

20.  FVE may be related to simple fluid overload or diminished
function of the homeostatic mechanisms responsible for
regulating fluid balance.
 Contributing factors can include heart failure, renal failure,
and cirrhosis of the liver.
 Another contributing factor is consumption of excessive
amounts of table or other sodium salts.

21.  edema,
 distended neck veins,
 and crackles (abnormal lung sounds).
 Other manifestations include
 tachycardia;
 increased blood pressure,
 pulse pressure, and central venous pressure;
 increased weight;
 increased urine output;
 and shortness of breath and wheezing.

23.  BUN
 Hematocrit levels.
 Chest X-ray
 Serum sodium levels.

24.  PHARMACOLOGIC THERAPY
Diuretics
 HEMODIALYSIS
 NUTRITIONAL THERAPY
dietary restriction of sodium and fluid.
Lemon juice, onions, and garlic are excellent substitute
flavorings, although some patients prefer salt substitutes.
Patients may need to use distilled water when the local water
supply is very high in sodium.

26. Electrolytes imbalances

28.  Vomiting
 Diarrhea
 Fistulas
 Sweating
 Dilutional Hyponatremia In water intoxication (dilutional
hyponatremia), the patient’s serum sodium level is diluted by
an increase in the ratio of water to sodium. This causes
water to move into the cell, so that the patient develops an
ECF volume excess.
 SIADH

29.  Poor skin turgor,
 dry mucosa,
 decreased saliva production,
 orthostatic fall in blood pressure,
 nausea, and abdominal cramping
 altered mental status
 anorexia,
 muscle cramps,
 feeling of exhaustion.
 When the serum sodium level drops below 115 mEq/L (115 mmol/L),
signs of increasing intracranial pressure, such as lethargy, confusion,
muscle twitching, focal weakness, hemiparesis, papilledema, and
seizures, may occur

30.  SODIUM REPLACEMENT
 Careful administration of sodium
 In SIADH, the administration of hypertonic saline solution alone
cannot change the plasma sodium concentration. Excess sodium
would be excreted rapidly in highly concentrated urine.
 With the addition of the diuretic furosemide (Lasix), urine is not
concentrated and isotonic urine is excreted to effect a change
in water balance.
 In patients with SIADH, in whom water restriction is difficult,
lithium or demeclocycline can antagonize the osmotic effect of
ADH on the medullary collecting tubule.

32.  Hypernatremia is a higher-than-normal serum sodium level
(exceeding 145 mEq/L [145 mmol/L]).
 causes
 Hyperaldosteronism
 Renal failure
 Corticosteroids
 Increase in oral Na intake
 Na containing IV fluids
 Decreased urine output with increased urine concentration
 Fluid deprivation

33.  thirst.
 dry, swollen tongue and sticky mucous membranes.
 Flushed skin,
 peripheral and pulmonary edema,
 postural hypotension,
 and increased muscle tone and deep tendon reflexes
 restlessness and weakness in moderate hypernatremia
 disorientation, delusions, and hallucinations in severe
hypernatremia.

34.  a gradual lowering of the serum sodium level by the infusion
of a hypotonic electrolyte solution (e.g., 0.3% sodium
chloride) or an isotonic no saline solution (e.g., dextrose 5%
in water [D5W]).

36.  Hypokalemia (below-normal serum potassium concentration)
usually indicates an actual deficit in total potassium stores,
fallen below 3 mEq/L (3 mmol/L).
 Pathophysiology –
 Decrease in K+ causes decreased excitability of cells, therefore
cells are less responsive to normal stimuli

37.  Diuretics
 Shift into cells
 Digitalis
 Water intoxication
 Corticosteroids
 Diarrhea
 Vomiting

39.  In hypokalemia, the serum potassium concentration is less
than the lower limit of normal.
 Electrocardiographic (ECG) changes can include
 flat T waves and/or inverted T waves, suggesting
ischemia, and depressed ST segments. An elevated U wave
is specific to hypokalemia.

40.  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

41.  Fatigue, anorexia, muscle weakness, decreased bowel
motility, paresthesias, and dysrhythmias are signals that
warrant assessing the serum potassium concentration.
 Careful watch for signs.

42.  Hyperkalemia (greater-than-normal serum potassium
concentration) i.e. above 6mEq/L.
 Pathophysiology – An Inc. in K+ causes increased excitability
of cells

43.  Increase in K+ intake
 Renal failure
 K+ sparing diuretics
 Shift of K+ out of the cells

45.  often occurring at a serum potassium level greater than 6
mEq/L (6 mmol/L), are peaked, narrow T waves; ST-segment
depression; and a shortened QT interval.
 If the serum potassium level continues to rise, the PR interval
becomes prolonged and is followed by disappearance of the P
waves. Finally, there is decomposition and prolongation of
the QRS complex.

47.  Need to restore normal K+ balance:
 Eliminate K+ administration either orally or by
retention enema
 Inc. K+ excretion
 Lasix
 Kayexalate (Polystyrene sulfonate)
 Infuse glucose and insulin
 Cardiac Monitoring

48.  The nurse observes for signs of muscle weakness and
dysrhythmias. The presence of paresthesias is noted, as are
GI symptoms such as nausea and intestinal colic.

49.  Hypocalcemia (lower-than-normal serum concentration of
calcium) occurs in a variety of clinical situations.
 Contributing factors:
 Dec. oral intake
 Lactose intolerance
 Dec. Vitamin D intake
 End stage renal disease
 Diarrhea
Acute pancreatitis
Hypophosphatemia
Immobility
Removal or destruction of parathyroid gland

50.  Neuro –Irritable muscle twitches. Tetany.
 Positive Trousseau’s sign.
 Positive Chvostek’s sign.
 Resp. – Resp. failure d/t muscle tetany.
 CV – Dec. HR., Dec. BP, diminished
peripheral pulses
 GI – Inc. motility. Inc. BS. Diarrhea

51.  Trousseau’s sign can be elicited by inflating a blood pressure cuff
on the upper arm to about 20 mm Hg above systolic pressure; within
2 to 5 minutes, carpopedal spasm (an adducted thumb, flexed wrist
and metacarpophalangeal joints, extended interphalangeal joints
with fingers together) will occur as ischemia of the ulnar nerve
develops

52.  Chvostek’s sign consists of twitching of muscles supplied by
the facial nerve when the nerve is tapped about 2 cm
anterior to the earlobe, just below the zygomatic arch.

53.  Drug Therapy
 Calcium supplements
 Vitamin D
 Diet Therapy
 High calcium diet
 Prevention of Injury
 Seizure precautions

54.  Seizure precautions are initiated when hypocalcaemia is
severe. The status of the airway is closely monitored because
laryngeal
 stridor can occur. Safety precautions are taken, as indicated,
if confusion is present.
 People at high risk for osteoporosis are instructed about the
need for adequate dietary calcium intake; if not consumed in
the diet, calcium supplements should be considered.

55.  Hypercalcemia (excess of calcium in the plasma) is a
dangerous imbalance when severe; in fact, hypercalcemic
crisis has a mortality rate as high as 50% if not treated
promptly. The serum calcium level is greater than 10.5 mg/dL
(2.6 mmol/L).
 Causes
 Excessive calcium intake
 Excessive vitamin D intake
 Renal failure
 Hyperparathyroidism
 Malignancy
 Hyperthyroidism

56.  Neuro – Disorientation, lethargy, coma, profound
muscle weakness
 Resp. – Ineffective resp. movement
 CV - Inc. HR, Inc. BP. , Bounding peripheral pulses,
Positive Homan’s sign.
Late Phase – Bradycardia, Cardiac arrest
 GI – Dec. motility. Dec. BS. Constipation
 GU – Inc. urine output. Formation of renal calculi

57.  ECG - Cardiovascular changes may include a variety of
dysrhythmias and shortening of the QT interval and ST
segment. The PR interval is sometimes prolonged.
 X-rays may reveal the presence of osteoporosis, bone
cavitation, or urinary calculi. The Sulkowitch urine test
analyzes the amount of calcium in the urine; in
hypercalcemia, dense precipitation is observed due to
hypercalciuria.

58.  Eliminate calcium administration
 Drug Therapy
 Isotonic NaCL (Inc. the excretion of Ca)
 Diuretics
 Calcium reabsorption inhibitors (Phosphorus)
 Cardiac Monitoring

59.  Increase patient mobility
 encourage fluids
 When encouraging oral fluids, the nurse considers the
patient’s likes and dislikes.
 Fluids containing sodium should be administered unless
contraindicated by other conditions
 encouraged to drink 3 to 4 quarts of fluid daily.
 Adequate fiber should be provided in the diet to offset the
tendency for constipation.
 Safety precautions are taken, as necessary, when mental
symptoms of hypercalcemia are present.

60.  below-normal serum magnesium concentration.
 The normal serum magnesium level - 1.5 to 2.5 mEq/L (or 1.8–
3.0 mg/dL; 0.8–1.2 mmol/L).
 Contributing factors:
 Malnutrition
 Starvation
 Diuretics
 Aminoglycoside antibiotics
 Hyperglycemia
 Insulin administration

61.  Neuro - Positive Trousseau’s sign. Positive Chvostek’s sign.
Hyperreflexia. Seizures , athetoid movements (slow,
involuntary twisting and writhing).
 CV – ECG changes. Dysrhythmias. HTN
 Resp. – Shallow resp.
 GI – Dec. motility. Anorexia. Nausea

62.  Eliminate contributing drugs
 IV MgSO4
 Assess DTR’s hourly with MgSO4
 Diet Therapy

63.  Diet therapy- magnesium rich foods
 Teach to stop contributing drugs- diuretic or laxative
 Provide help for avoidance of alcohol consumption.

64.  Hypermagnesemia is a greater-than-normal serum
concentration of magnesium. The serum magnesium level is
greater than 2.5 mEq/L or 3.0 mg/dL (1.25 mmol/L).
 Contributing factors:
 Increased Mg intake
 Decreased renal excretion

65.  Neuro – Reduced or weak DTR’s. Weak voluntary muscle
contractions. Drowsy to the point of lethargy
 CV – Bradycardia, peripheral vasodilatation, hypotension.
ECG changes- a prolonged PR interval, tall T waves, and a
widened QRS.

66.  Eliminate contributing drugs
 Administer diuretic
 Calcium gluconate reverses cardiac effects
 Diet restrictions

67.  Careful observation
 Check vital signs
 Check DTR

68.  Hypophosphatemia is a below-normal serum concentration of
inorganic phosphorus. The serum phosphorus level is less
than 2.5 mg/dL (0.80 mmol/L) in adults.
 Contributing Factors:
 Malnutrition
 Starvation
 Hypercalcemia
 Renal failure
 Uncontrolled DM

69.  Neuro – Irritability, confusion
 CV – Dec. contractility
 Resp. – Shallow respirations
 Musculoskeletal - Rhabdomyolysis
 Hematologic – Inc. bleeding
Dec. platelet aggregation

70.  Treat underlying cause
 Oral replacement with vit. D
 IV phosphorus (Severe)
 Diet therapy
 Foods high in oral phosphate

71.  Careful observation and monitoring
 Food rich in phosphate.

72.  Hyperphosphatemia is a serum phosphorus level that exceeds
normal. The serum phosphorus level exceeds 4.5 mg/dL (1.5
mmol/L) in adults.
 Rarely occurs.

73.  Tetany
 Anorexia, nausea, vomiting, muscle weakness, hyperreflexia,
and tachycardia may occur.
 Decreasing urine output, impairing vision, and producing
palpitations.

74.  Avoid Vitamin D supplements
 Restriction of dietary phosphate.
 Give calcium binding antacids, phosphate binding gels or
antacids.
 Dialysis.

75.  Low phosphorus diet
 Teach to avoid phosphate binding substances such as
laxatives and enemas.

76.  The normal serum chloride level is 96 to 106 mEq/L (96–106
mmol/L)
 As chloride decreases (usually because of volume depletion),
sodium and bicarbonate ions are retained by the kidney to
balance the loss. Bicarbonate accumulates in the ECF, which
raises the pH and leads to hypochloremic metabolic alkalosis.

78.  Metabolic alkalosis
 Hyper-excitability of muscles, tetany, and hyperactive deep
tendon reflexes, weakness, twitching, and muscle cramps
may result.
 seizures and coma.

79.  correcting the cause of hypochloremia and contributing
electrolyte and acid–base imbalances.
 Normal saline (0.9% sodium chloride) or half-strength saline
(0.45% sodium chloride) solution is administered IV to replace
the chloride.
 Foods high in chloride are provided; these include tomato
juice, salty broth, canned vegetables, processed meats, and
fruits.
 Ammonium chloride, an acidifying agent, may be prescribed
to treat metabolic alkalosis; the dosage depends on the
patient’s weight and serum chloride level.

80.  The nurse monitors intake and output, arterial blood gas
values, and serum electrolyte levels,
 Check patient’s level of consciousness and muscle strength
and movement
 Vital signs are monitored and respiratory assessment is
carried out frequently.
 The nurse teaches the patient about foods with high chloride
content.

81.  Hyperchloremia exists when the serum level exceeds 106
mEq/L (106 mmol/L).

82.  same as those of metabolic acidosis, hypervolemia, and
hypernatremia.
 Tachypnea;
 weakness;
 lethargy;
 deep, rapid respirations;
 diminished cognitive ability;
 hypertension occur.

83.  Lactated Ringer’s solution may be prescribed to convert
lactate to bicarbonate in the liver, which will increase the
base bicarbonate level and correct the acidosis.
 Sodium bicarbonate may be given IV to increase bicarbonate
levels, which leads to the renal excretion of chloride ions as
bicarbonate and chloride compete for combination with
sodium.
 Diuretics may be administered to eliminate chloride as well.
Sodium, fluids, and chloride are restricted.

84.  Monitoring vital signs, arterial blood gas values, and intake
and output is important to assess the patient’s status and the
effectiveness of treatment.
 Assessment findings related to respiratory, neurologic, and
cardiac systems are documented and changes discussed with
the physician.
 The nurse teaches the patient about the diet that should be
followed to manage hyperchloremia.

90.  Acute and chronic metabolic acidosis
 Acute and chronic metabolic alkalosis
 Acute and chronic respiratory acidosis
 Acute and chronic respiratory alkalosis

95.  Metabolic acidosis is a clinical disturbance characterized by a
low pH (increased Concentration) and a low plasma
bicarbonate concentration. It can be produced by a gain of
hydrogen ion or a loss of bicarbonate. Low pH (less than
7.35).
Clinical Manifestations
 Headache, confusion, drowsiness, increased respiratory rate
and depth, nausea, and vomiting. Peripheral vasodilation and
decreased cardiac output occur when the pH falls below 7.
Additional physical assessment findings include decreased
blood pressure, cold and clammy skin, dysrhythmias, and
shock.

97.  Assessment and Diagnostic Findings
 Arterial blood gas measurements.
 Expected blood gas changes include a low bicarbonate level
(less than 22 mEq/L) and a low pH (less than 7.35).
 ECG will detect dysrhythmias caused by the increased
potassium.
 Medical Management
 When necessary, bicarbonate is administered if the pH is less
than 7.1 and the bicarbonate level is less than 10.
 Alkalizing agents may be given if the serum bicarbonate level
is less than 12 mEq/L.
 Treatment modalities may also include hemodialysis or
peritoneal dialysis.

98.  Metabolic alkalosis is a clinical disturbance characterized by
a high pH (decreased H+ concentration) and a high plasma
bicarbonate concentration. It can be produced by a gain of
bicarbonate or a loss of H+. A pH greater than 7.45
Clinical Manifestations
 Alkalosis is primarily manifested by symptoms related to
decreased calcium ionization, such as tingling of the fingers
and toes, dizziness, and hypertonic muscles. The ionized
fraction of serum calcium decreases in alkalosis as more
calcium combines with serum proteins.

100.  Assessment and Diagnostic Findings
 Evaluation of arterial blood.
 The urine chloride concentration should be less than 15 mEq/L when
decreased chloride levels and hypovolemia occur.
 Medical Management
 Sufficient chloride must be supplied for the kidney to absorb sodium
with chloride (allowing the excretion of excess bicarbonate).
 In patients with hypokalemia, potassium is administered as KCl to
replace both K+ and Cl−losses. Histamine-2 receptor antagonists,
such as cimetidine (Tagamet), reduce the production of gastric HCl.
Carbonic anhydrase inhibitors are useful in treating metabolic
alkalosis in patients who cannot tolerate rapid volume expansion
(e.g., patients with heart failure).

101.  Respiratory acidosis is a clinical disorder in which the pH is
less than 7.35 and the PaCO2 is greater than 42 mm Hg. It
may be either acute or chronic.
 Clinical Manifestations
Increased pulse and respiratory rate, increased blood pressure,
mental cloudiness, and feeling of fullness in the head.
Intracranial pressure may increase, resulting in papilledema
and dilated conjunctival blood vessels.

103.  Assessment and Diagnostic Findings
 Arterial blood gas evaluation reveals a pH less than 7.35, a
PaCO2 greater than 42 mm Hg
 Serum electrolyte levels
 Chest x-ray for determining any respiratory disease
 ECG to identify any cardiac involvement as a result of chronic
obstructive pulmonary disease
 Medical Management
 Treatment is directed at improving ventilation
 Pharmacologic agents are used as indicated. For example,
bronchodilators help reduce bronchial spasm, antibiotics are
used for respiratory infections, and thrombolytic or
anticoagulants are used for pulmonary emboli.

104.  Respiratory alkalosis is a clinical condition in which the arterial
pH is greater than 7.45 and the PaCO2 is less than 38 mm Hg. As
with respiratory acidosis, acute and chronic conditions can occur.
Respiratory alkalosis is always due to hyperventilation, which
causes excessive “blowing off” of CO2 and, hence, a decrease in
the plasma carbonic acid concentration.
 Clinical Manifestations
Clinical signs consist of lightheadedness due to vasoconstriction and
decreased cerebral blood flow, inability to concentrate, numbness
and tingling from decreased calcium ionization, tinnitus, and at
times loss of consciousness. Cardiac effects of respiratory alkalosis
include tachycardia and ventricular and atrial dysrhythmias.

106.  Assessment and Diagnostic Findings
 Analysis of arterial blood gases
 Evaluation of serum electrolytes is indicated to identify any
decrease in potassium as hydrogen is pulled out of the cells
in exchange for potassium; decreased calcium
 Medical Management
 If the cause is anxiety, the patient is instructed to breathe
more slowly to allow CO2 to accumulate or to breathe into a
closed system (such as a paper bag).
 A sedative may be required to relieve hyperventilation in
very anxious patients.

107. Thank you