Introduction

To maintain good health, a balance of fluids and electrolytes, acids and bases must be
normally regulated for metabolic processes to be in working state. A cell, together with its environment in
any part of the body, is primarily composed of fluid. Thus fluid and electrolyte balance must be maintained
to promote normal function. Potential and actual problems of fluid and electrolytes happen in all health care
settings, in every disorder and with a variety of changes that affect homeostasis. The nurse therefore needs
to fully understand the physiology and pathophysiology of fluid and electrolyte alterations so as to identify
or anticipate and intervene appropriately.

Body Water Distribution

Water is the largest single constituent of the
body, representing 45% to 75% of the body’s total weight.
About two-thirds of the body fluid is intracellular. The
remaining one-third is extracellular, with one-fourth of this fluid
being intravascular and three-fourths being interstitial fluid.
Bones are made up of nearly one-third water, while the muscles
and brain cells contain 70% water. Body fat is essentially free of
water; therefore, the ratio of water to body weight is greater in
leaner people than in obese people. Water is present in all body
tissues and cells, and serves two main functions: to act as a
solvent for the essential nutrients, so that they can be used by
the body; and to transport nutrients and oxygen from the blood
to the cells and to remove waste material and other substance
from the cells back to the blood so they can be excreted by the
body. Water is also needed by the body to:
• Give shape and form to the cells
• Regulate body temperature
• Act as a lubricant in joints
• Cushion body organs
• Maintain peak physical performance
The body has many regulators that maintain fluid balance, includes:
• Fluid and food intake
• Skin
• Lungs
• Gastrointestinal tract
• Kidneys(ADH, Aldosterone, Renin)
Water loss has a negative effect on the body’s ability to function, because every 2% to 5% of
water loss results in a 30% decrease in work performance (Kloss, 1995; Kleiner, 1999).

Electrolytes
An electrolyte is a compound that, when dissolved in water or another solvent, forms or
dissociates into ions (electrically charged particles). The electrolytes
provide inorganic chemicals for cellular reactions and control Electrolyte Normal values
mechanisms. Electrolytes have special physiological functions in the Sodium 135-148 mEq/L
body, i.e. Potassium 3.5-5.0 mEq/L
• Promote neuromuscular irritability, Calcium 8.4-10.5 mg/dl
• Maintain body fluid osmolarity,
Magnesium 1.3-2.0 mEq/L
• Regulate acid-base balance, and
• Distribute body fluids between the fluid compartments. Phosphate 2.7-4.5 mg/dl
Chloride 96-109 mEq/L
 Electrolytes are measured in terms of their electrical combining power, the quantities of
cations and anions in a solution, expressed as milliequivalents per liter (mEq/L). Because electrolytes
produce either positively charged ions (cations) or negatively charged ions (anions), they are critical
regulators in the distribution of body fluid. The main electrolytes in body fluid are:

• Sodium (Na+)
• Potassium (K+)
• Calcium (Ca2+)
• Magnesium (Mg2+)
The extracellular fluid contains the largest quantities of sodium, chloride, and bicarbonate
ions, but only small quantities of potassium, calcium, magnesium, phosphate, sulfate, and organic acid ions.
The intracellular fluid contains only small quantities of sodium and chloride ions and almost no calcium
ions. Large quantities of potassium and phosphate ions with moderate quantities of magnesium and sulfate
ions are contained within intracellular fluid.
The normal levels, its functions and the dietary sources of these common electrolytes are
listed below:
Distribution in Body
Fluid
Electrolyte Ion Basic Functions Dietary Sources
Extracellular Intracellular
(mEq/L) (mEq/L)

• Regulates fluid volume within

extracellular fluid (ECF)
compartment. Table salt (NaCl),
• Increases cell membrane 40% of which is
permeability. sodium; cheese,
• Regulates osmotic pressure. milk, processed
Sodium (Na+) 135–154 15–20 • Controls water distribution meat, poultry,
between ECF and intracellular shellfish, fish, eggs,
fluid (ICF) compartments. and foods preserved
• Stimulates conduction of with salt (e.g., ham
nerve impulses. and bacon)
• Maintains neuromuscular
irritability.

• Regulates osmolality of ICF.

• Promotes transmission of
nerve impulses.
• Promotes contraction of
skeletal and smooth muscles. Fruits, especially
• Promotes enzymatic action for bananas, oranges,
Potassium (K+) 3.5–5 150–155 cellular energy production by and dried fruits;
transforming carbohydrates vegetables, meats,
into energy and restructuring and nuts
amino acids into proteins.
• Regulates acid-base balance
by cellular exchange of
hydrogen ions.
 • Provides strength and
durability to bones and teeth.
• Establishes thickness and
strength of cell membranes.
• Promotes transmission of
Dairy products (milk,
nerve impulses.
cheese, and yogurt),
• Decreases neuromuscular
Calcium (Ca2+) 4.5–5.5 1–2 sardines, whole
excitability.
grains, and green
• Is essential for blood leafy vegetables
coagulation.
• Promotes absorption and
utilization of vitamin B12.
• Activates enzyme reactions
and hormone secretions.
• Activates enzyme systems,
mainly those associated with
vitamin B metabolism and the
utilization of potassium,
Green leafy
Magnesium calcium, and protein.
4.5–5.5 27–29 vegetables, whole
(Mg2+) • Promotes regulation of serum
grains, fish and nuts
calcium, phosphorus, and
potassium levels.
• Promotes neuromuscular
activity.
Acid-Base Balance
Acid-base balance refers to the homeostasis of the hydrogen ion concentration in
extracellular fluid. The slightest variation in the hydrogen ion concentration causes marked alterations in the
rate of cellular chemical reactions. The pH symbol is used to indicate the hydrogen ion concentration of
body fluids; 7.35 to 7.45 is the normal pH range of extracellular fluid. Hydrogen ions (H+), which carry a
positive charge, are protons. Depending on the number of hydrogen ions present, a solution can be acidic,
neutral, or alkaline.
As the number of hydrogen ions increases, the fluid becomes acidic. Acidity of a solution
increases as the pH value decreases. An acid is a substance that donates hydrogen ions. For example,
hydrochloric acid (HCl) ionizes in water (a solution) to form hydrogen ions and chloride ions. HCl, which is
found in gastric juices, has a strong tendency to form ions, discharging hydrogen ions into the solution;
carbonic and acetic acids are considered weak acids because in a solution they provide a low concentration
of hydrogen ions.
As the number of hydrogen ions decreases, the fluid becomes alkaline. Alkalinity of a
solution increases as the pH value increases. A base is a substance that accepts hydrogen ions (proton
acceptor).
A neutral solution has a pH of 7. In such a solution there are equal numbers of hydrogen ions
(H+) and hydroxyl ions (OH–), which can combine to form water (H2O). When the number of hydrogen
ions is increased, the solution becomes acidic (pH value below 7); a decrease in the number of hydrogen
ions causes the solution to become alkaline (pH value above 7). When the number of free hydrogen ions in a
solution increases to the point that the pH value becomes less than 7.35, the body is in a state of acidosis.
The opposite occurs with alkalosis, in which a pH value higher than 7.45 results from a low hydrogen ion
concentration.
The body has three main control systems that regulate acid-base balance to counter acidosis
or alkalosis:
• The buffer systems,
• Respiration, and
• Renal control of H+ concentration
Fluid changes in the body
A. Disturbances of Volume
If isotonic fluid is lost from or added to the body fluids, only a change in the volume of the
extracellular fluid is observed. A loss of intestinal secretions thus led to a loss of isotonic fluid and to a
depletion of fluid within the extracellular compartment. However the concentration of sodium and chloride
in plasma remain unchanged, and there is no shift of water between the intracellular and extracellular fluid
compartments.
B. Disturbance in Concentration
It produces a change in osmotic activity of the extracellular fluid and the plasma. If water
alone is lost from or added to ECF, the concentration of osmotically active solutes in the compartment will
change. Sodium is the most important osmotically active ion in the ECF. There will be shift from
Intracellular to ECF and vice versa till osmotic equality between the compartments are re-established.
C. Disturbances in volume and concentration
Volume and concentration abnormalities may both arise from because of disease or from
inappropriate fluid replacement therapy. A classic example is the association of a volume deficit together
with a fall in serum sodium concentration that results from a massive loss of gastrointestinal fluid (causing a
volume deficit), where fluid replacement is only through water (producing a fall in sodium concentration).
D. Disturbances in composition
Concentrations of ions other than sodium can be altered within ECF compartment without
much change in the effective osmotic activity of the ECF. This produces a compositional change which may
be comparatively small when it involves an electrolyte like potassium, and yet has disastrous consequences,
if not promptly corrected. Compositional changes also involve disturbances in acid –base balance.

Volume changes
Volume deficit or excess is diagnosed by clinical examination. It is to be stressed that a
severe volume deficit may exist with a normal, low or even high serum sodium level.

Volume Deficit (Hypovolaemia)

Hypovolaemia is a state of decreased blood volume; more specifically, decrease in volume of
blood plasma. It is thus the intravascular component of volume contraction or loss of blood volume due to
things such as hemorrhage or dehydration.
Causes:
• Dehydration • Drugs (diuretics or vasodilators)
• Bleeding • Naso-gastric suction
• Vomiting • Intestinal fistulae
• Severe burns

Clinical Manifestations:
• Anxiety, restlessness
• Tachycardia
• Postural hypotension
• Cold and clammy skin
• Decreased urine output
• Poor tissue perfusion
• Drowsiness and coma

Management:
• Restore circulating volume through infusion of IV fluids
• Once this is satisfactorily achieved, disturbance in electrolytes and acid-base balance if present need to
be rectified.
Nursing Diagnoses:
• Deficient fluid volume related to excessive ECF losses or decreased fluid intake
• Decreased cardiac output related to excessive ECF losses or decreased fluid intake
• Risk for hypovolemic shock related to excessive fluid losses

Volume Excess (Hypervolaemia)

Hypervolaemia, or fluid overload, is the medical condition where there is too much fluid in
the blood. In ICU patients, volume excess is often iatrogenic when the fluid intake has consistently exceeded
the output.
Causes:
• Excess IV infusion of saline • Congestive heart failure
• Excess blood transfusion • Liver diseases
• Renal insufficiency

Clinical Manifestations:
• Oedema • Tachycardia
• Ascites • Warm skin
• Pleural effusion • Bounding pulse
• Pulmonary congestion • Increased CVP

Management:
• Salt restriction
• Restriction of fluid intake
• Administration of diuretics(furosemide)
Nursing Diagnoses:
• Excess fluid volume related to increased sodium and water retention
• Ineffective airway clearance related to sodium and water retention
• Risk for impaired skin integrity related to edema
• Disturbed body image related to altered body appearance secondary to edema
• Potential complications: pulmonary edema, ascites

Electrolyte Disturbances
In health, normal homeostatic mechanisms function to maintain electrolyte and acid-base
balance. In illness, one or more of the regulating mechanisms may be affected, or the imbalance may
become too great for the body to correct without treatment.

Sodium
Sodium is the primary determinant of extracellular fluid concentration because of its high
concentration and inability to cross the cell membrane easily. Alterations in sodium concentration can
produce profound central nervous system effects on cognition and sensory perception and on the circulating
blood volume. When the kidneys reabsorb sodium ions, chloride and water are reabsorbed with the sodium
to maintain the body’s fluid volume.
Hyponatremia :( Serum Sodium < 135 mEq/L)
Hyponatremia is a deficit in the extracellular level of sodium. With hyponatremia, there is
either a sodium deficit or a water excess; a hypo-osmolar state exists because the ratio of water to sodium is
too high. The water moves out of the vascular space into the interstitial space and then into the intracellular
space, causing edema. The low extracellular serum sodium causes water to enter the cells in the brain,
thereby producing cerebral edema as manifested by the cognitive and sensory changes.
Causes:
• Loss of GI secretions (vomiting, diarrhoea, suctioning etc.)
• Loss of ECF sodium (peritonitis, burns etc.)
• ECF sodium dilution (CHF, cirrhosis, nephrosis)
• Advanced renal disorders
• Diuretics, ADH, or SIADH(syndrome of inappropriate ADH)
Manifestations and Nursing Interventions:
Manifestations Nsg. Interventions
 Admn. Comfort measures as needed
Headaches, Apprehension, Lethargy,
 Monitor level of consciousness
Confusion, Depression & convulsion
 Institute safety measures for seizure
Muscular Weakness  Assist with range of motion
Dry, pale skin & mucous  Admn. IV isotonic solution (0.9%NaCl)
 Monitor hourly vital signs & I/O
Tachycardia & Hypotension
 Restrict fluids and Admn. diuretics
Nausea, vomiting, diarrhoea, abdominal  Monitor daily intake of Na & watch for water intoxication
cramps with SIADH (Headache & behavioural changes)
 Monitor serum sodium levels
Biochemical changes  Teach about intake of Na, side effects of diuretics, & other
causes.
Nursing Diagnoses:
• Risk for injury related to altered sensorium and decreased level of consciousness secondary to abnormal
CNS function
Hypernatremia: (Serum Sodium > 146 mEq/L)
Hypernatremia is an excess in the extracellular level of sodium. With an excess of sodium
or a loss of water, a hyperosmolar state exists because the ratio of sodium to water is too high. This ratio
causes an increase in the extracellular osmotic pressure, which pulls fluid out of the cells into the
extracellular space. The symptoms of this increase depend on the cause and the location of the edema.
Causes:
• High sodium intake
• Administration of IV fluids (hypertonic or isotonic saline)
• Hypertonic saline abortions
• Renal dysfunction
• Uncompensated diabetes insipidus
• CHF, Nephrotic syndrome and cirrhosis
Manifestations and Nursing Interventions:
Manifestations Nursing Interventions
Restlessness, Agitation, Delirium,  Monitor level of consciousness
Convulsions, Coma  Institute Safety measures for seizures

Increased muscle tone, hyperreflexia  Maintain body alignment and assist with movement.
Flushed, dry skin, Red, dry tongue &
 Administer oral hygiene hourly.
sticky mucous
Tachycardia  Monitor vital signs hourly
 Admn. oral fluid/parenteral hypotonic soln.(0.3%NaCl) as
Nausea, vomiting, anorexia
ordered
Polyuria  Monitor I/O hourly
 Monitor laboratory findings
Biochemical Changes
 Teach about foods high in Na & about Na-retaining drugs
Nursing Diagnoses:
• Risk for injury related to altered sensorium and seizures secondary to abnormal CNS function
Potassium
The normal range of extracellular potassium is narrow (3.5–5.0 mEq/L). The slightest
decrease or increase can cause serious or life-threatening effects on physiological functions. A reciprocal
relationship exists between sodium and potassium; large sodium intake results in an increased loss of
potassium, and vice versa. When potassium is lost from the cells, sodium enters the cells. Intracellular
potassium deficit may coexist with an excess of extracellular potassium.
Hypokalemia (Serum Potassium < 3.5 mEq/L)
Hypokalemia is a decrease in the extracellular level of potassium. Gastrointestinal-tract
disturbances and the use of diuretics can place the client at risk for hypokalemia and an acid-base imbalance
(metabolic alkalosis). Potassium-wasting diuretics can cause hypokalemia. Besides diuretics, other major
drug groups that can cause hypokalemia are laxatives, corticosteroids, and antibiotics.
Causes:
• Abnormal loss of K+ (K+ depleting diuretics e.g. thiazide, furosemide)
• Inadequate replacement(malnutrition, starvation, NPO & K+ free IV fluids)
• Increased movement into cells (possible when insulin given)
• Adrenal tumor, Cirrhosis, CHF
Manifestations and Nursing Interventions:
Manifestations Nursing Interventions
Abdominal Distention, nausea & vomiting  Admn of K+ replacement therapy as ordered.

 Admn. of Oral potassium should be diluted in 4-8 oz of

Malaise, disorientation, coma, loss of
water or juice
tactile discrimination
 IV potassium 20-40mEq/ 1L of IV fluids
Muscle weakness & hyporeflexia  Protect from injury
Constipation & Polyuria  Monitor I/O hourly
Diminished breath sounds, tachycardia,  Monitor vital signs hourly
Increased sensitivity to digitalis, ST  Monitor heart rate and rhythm
depression, T-wave inverted, heart block,  Monitor closely for signs of digitalis toxicity(premature
cardiac arrest(severe Hypokalemia) atrial & ventricular beats)
 Teach client about K+ rich foods and how to prevent
Biochemical changes
excessive loss( abuse of laxatives and diuretics)
Nursing Diagnoses:
• Risk for injury related to muscle weakness and hyporeflexia
• Potential complications: arrhythmias
Hyperkalemia (Serum Potassium > 5.0 mEq/L)
Hyperkalemia is an increase in the extracellular level of potassium. There are major drug
groups that may cause hyperkalemia:
• Potassium-sparing diuretics
• Central nervous system agents
• Oral and intravenous replacement potassium salts
Hyperkalemia can also inhibit the action of digitalis.
Causes:
• Acute and chronic renal failure
• Cellular damage (K+ released into ECF when cells destroyed)
• Insulin deficiency
• Adrenal deficiency
• Rapid IV infusion of K+
Manifestations and Nursing Interventions:
Manifestations Nursing Interventions
 Restrict oral and parenteral potassium intake as ordered
Abdominal cramps, nausea, diarrhoea
 Admn. of ion exchange resins(Kayexalate)
Muscular weakness, paresthesias, muscle
 Assess for pain and provide comfort measures as indicated
cramps & pain
Oliguria or anuria  Monitor I/O hourly
Bradycardia, T-wave tented, QRS
complex widened, Life-threatening  Monitor vital signs & heart rhythm hourly for ECG changes
dysrhythmias
Biochemical changes  Teach client about K+ rich foods, K+ conserving diuretics etc.
Nursing Diagnoses:
• Risk for injury related to lower extremity muscle weakness and seizures
• Potential complication: arrhythmias

Calcium
Most of the body’s calcium (99%) is deposited in bone as phosphate and carbonate. The
remaining 1% is in the blood plasma (serum). Normally, 50% of the serum calcium is ionized
(physiologically active), with the remaining 50% bound to protein. Free, ionized calcium is needed for cell
membrane permeability. The calcium that is bound to plasma protein cannot pass through the capillary wall
and therefore cannot leave the intravascular compartment.
A stable blood level of calcium is maintained by a negative-feedback system controlled by
vitamin D, parathyroid hormone, calcitonin (thyrocalcitonin), and the serum concentrations of calcium and
phosphate ions. A decreased blood level stimulates the parathyroid gland to secrete parathyroid hormone,
which in turn mobilizes the release of calcium from the bone, increases the renal reabsorption, and increases
intestinal absorption in the presence of vitamin D. Likewise, calcitonin, secreted by the thyroid gland,
reduces the blood calcium concentration.
Calcium ions are never completely absorbed from the gastrointestinal tract. Dietary calcium
absorption and utilization require an adequate amount of protein and vitamin D. Besides being needed by the
body for bone and tooth formation, calcium is an important ion in the blood-clotting mechanism and for
maintaining the integrity of the neuromuscular system.
Hypocalcemia (Serum Calcium < 8.4 mg/dl)
Hypocalcemia is a decrease in the extracellular level of calcium. The rapid administration of
citrated blood, alkalosis, and elevated levels of serum albumin increase the activity of calcium binders,
thereby decreasing the amount of free calcium.
Causes:
• Parathyroid deficiency
• Poor vitamin D intake and absorption
• Some malignancies
• Inadequate dietary intake (e.g. during pregnancy and lactation)
Manifestations and Nursing Interventions:
Manifestations Nursing Interventions
Anxiety, irritability, tingling and  Monitor client’s state of sensorium for safety factors and
numbness of fingers, tetany, convulsions breathing for laryngeal stridor
 Admn. of 10% calcium gluconate
Laryngospasm, abdominal and muscle
 Admn. of calcium lactate orally
cramps, pathologic fractures
 Diet high in Ca2+ with Vit.D supplement
Decreased stroke volume, ST segment
 Monitor ECG for changes
lengthened, prolonged PR interval
Nursing Diagnoses:
• Risk for injury related to tetany and seizures
• Potential complication: fracture, respiratory arrest
Hypercalcemia (Serum Calcium > 10.5 mg/dl)
Hypercalcemia is an increase in the extracellular level of calcium. The clinical symptoms
result from a decrease in neuromuscular activity, reabsorption of calcium from bone, and the kidney’s
response to a high serum calcium concentration.
Causes:
• Bone tumors, immobility
• Overconsumption of milk or dietary salts
• Hyperparathyroidism
• Renal impairment
Manifestations & Nursing Interventions:
Manifestations Nursing Interventions
Depression & Lethargy  Monitor State of sensorium
Decreased muscle tone & deep tendon
 Encourage client movement and exercise
reflexes, osteoporosis, osteomalacia, deep
 Assist client with movement to decrease pain
bone pain
Heart block, Arrest(Hypercalcemia crisis)  Monitor for ECG changes
Nausea, vomiting, anorexia, constipation  Teach to decrease Ca2+ intake & increase fibre
 Encourage oral intake of acid-ash fluids to decrease deposit of
Flank pain from calculi, Polyuria
calcium salts.
Nursing Diagnoses:
• Risk for injury related to neuromuscular and sensorium changes
• Potential complication: arrhythmias

Magnesium
Magnesium plays an important role as a coenzyme in the metabolism of carbohydrates and
proteins and as a mediator in neuromuscular activity. Magnesium has the unique characteristic of being the
only cation that has a higher concentration in cerebrospinal fluid than in extracellular fluid.
Hypomagnesemia (Serum Magnesium < 1.3 mEq/L)
Hypomagnesemia is a decrease in the extracellular level of magnesium and usually occurs
with hypokalemia and hypocalcaemia. It is probably the most undiagnosed electrolyte deficit because it is
asymptomatic until the serum level approaches 1.0 mEq/L; the normal range is 4.5–5.5 mEq/L (Kee &
Paulanka, 2000).
Drugs that may cause hypomagnesaemia include: digitalis, potassium-wasting diuretics,
cortisone, aminoglycosides, and amphotericin B; the chronic use of laxatives may also cause the condition.
Clinical manifestations are related to the neuromuscular, neurologic, or cardiovascular system.
Causes:
• Impaired intake (impaired intestinal absorption)
• Excessive urinary excretion (diuretics and alcoholism)
• Severe renal disease
Manifestations and Nursing Interventions:
Manifestations Nursing Interventions
Disorientation, Confusion, Vertigo,
 Monitor for seizure activity & laryngeal stridor
Tremors, Irritability
Increased tendon reflexes
Increased BP, Tachycardia, T-wave flat or  Monitor for ECG changes
inverted, ST segment depressed  Assess the client for digitalis toxicity
Biochemical changes  Teach to avoid excess use of laxatives
Hypermagnesemia (Serum Magnesium > 2mEq/L)
Hypermagnesemia refers to an increase in the extracellular level of magnesium. It rarely
occurs from excessive dietary ingestion; however, overuse of magnesium containing drugs (antacids,
laxatives, and intravenous magnesium sulfate) can cause hypermagnesemia. The clinical manifestations of
hypermagnesemia are nonspecific.
Causes:
• Renal failure (diabetic ketoacidosis)
• Excessive treatment of magnesium deficit
Manifestation and Nursing Interventions
Manifestations Nursing Interventions
Lethargy, Drowsiness, Coma  Monitor level of consciousness
Muscle weakness, decreased deep-tendon
 Assess patellar reflexes, if absent notify practitioner
reflexes
Decreased Resp. & BP, Bradycardia, QRS  Monitor vital signs q15-30mins & for ECG changes
complex widening, QT interval prolonged  Encourage fluids unless contraindicated

Phosphate
Phosphate is the main intracellular anion; it appears as phosphorus in the serum. Phosphorus
is similar to calcium in that vitamin D is needed for its reabsorption from the renal tubules.
Hypophosphatemia (Serum Phosphate < 1.7 mEq/L)
Hypophosphatemia is a decreased extracellular level of phosphorus. An increase in
parathyroid hormone causes decreased renal reabsorption and increased excretion of phosphates. The aim of
nursing care is to protect the client from injury and to correct the deficit
Causes:
• Inadequate intake: malnutrition, chronic alcoholism
• Prolonged administration of IV solutions that is phosphorus-poor or phosphorus-free
• Acid-base imbalances (e.g., diabetic ketoacidosis and respiratory alkalosis)
• Increased secretion of parathyroid hormone
• Overuse of aluminum-containing antacids
Manifestations and Nursing Interventions
Manifestations Nsg. Interventions
Confusion, seizures, coma, fatigue,  Monitor client’s level of consciousness.
memory loss  Institute safety measures for seizures.
Muscle pain, weakness, paresthesia,  Administer pain medication and other comfort measures
hyporeflexia, bone pain, joint stiffness  Assist the client in maintaining proper body alignment
Tissue hypoxia, hyperventilation, possible
 Monitor for bleeding and respiratory failure
bleeding, weak pulse
Possible infection  Institute precautions to prevent infection
 Teach client about phosphorus rich foods and over-the-
Anorexia, Dysphagia
counter drugs that contain aluminum hydroxide
 Administer IV phosphates with caution: dilute and infuse
Biochemical changes slowly to avoid phlebitis
 Do not infuse with calcium

Hyperphosphatemia (serum phosphate > 4.6mEq/L)

Hyperphosphatemia is an increased extracellular level of phosphorus. Excessive
administration (oral or intravenous) of phosphate-containing substances can cause hyperphosphatemia.
Other causes of hyperphosphatemia are hypoparathyroidism, renal insufficiency, and laxatives containing
phosphate.
Causes:
• Excessive administration of oral and IV solutions containing phosphate substances
• Hypoparathyroidism
• Laxatives containing phosphate
• Renal insufficiency
Manifestations and Nursing Interventions
Manifestations Nsg. Interventions
Tetany, muscle weakness, flaccid
 Monitor for tetany and other signs of hypocalcaemia
paralysis, Hyperreflexia
Tachycardia, ST segment shortened, QT
 Monitor heart rate and assess for ECG changes
interval shortened
 Administer calcium replacement
Nausea, anorexia, vomiting, diarrhoea
 Monitor urinary output
Biochemical changes-  Teach client to avoid foods high in phosphorus, and
Increased phosphate level, decreased excessive use of phosphorus containing laxative and
serum calcium enemas

Chloride
As previously stated, chloride and water move in the same direction as sodium ions,
influencing the osmolality of extracellular fluid. Although chloride losses usually follow sodium losses, the
proportion will differ because a loss of chloride can be compensated for by an increase in bicarbonate.
Therefore, signs and symptoms of a chloride imbalance will be similar to those of a metabolic acid-base
imbalance. A deficit of either chloride or potassium will lead to a deficiency of the other electrolyte.
Hypochloremia
Hypochloremia is a decrease in the extracellular level of chloride. Gastrointestinal tract losses
may cause a decrease in chloride because of the acid content of gastric juices, mainly hydrogen chloride.
Because the bicarbonate ion compensates for the loss of chloride, the client is at risk for developing
metabolic alkalosis. The signs and symptoms of hypochloremia are muscle twitching and slow, shallow
breathing. With a severe loss of chloride and extracellular fluid volume, there may be a drop in blood
pressure.
Hyperchloremia
Hyperchloremia is an increase in the extracellular level of chloride. It usually occurs with
dehydration, hypernatremia, and metabolic acidosis. The signs and symptoms of hyperchloremia are muscle
weakness, deep, rapid breathing, and lethargy progressing to unconsciousness if untreated.

Acid-Base Disturbances
The common types of acid-base imbalances are respiratory acidosis and alkalosis and
metabolic acidosis and alkalosis. The biochemical indicators of acid-base imbalance are assessed by
measurement of arterial blood gases (ABGs). Arterial blood gases measure the levels of oxygen and carbon
dioxide in arterial blood. The levels of blood pH, bicarbonate ion, sodium, potassium, and chloride are also
important in the assessment of acid-base imbalance.
In the determination of whether the acid-base imbalance is caused by a respiratory or a
metabolic alteration, the key indicators are bicarbonate and carbonic acid levels. With respiratory acidosis
and alkalosis, the bicarbonate level is normal and carbonic acid is either increased (acidosis) or decreased
(alkalosis). With metabolic acidosis and alkalosis, the carbonic acid is normal and the bicarbonate level is
either decreased (acidosis) or increased (alkalosis).
Respiratory Acidosis (Carbonic Acid Excess)
Respiratory acidosis is characterized by an increased hydrogen ion concentration, an
increased arterial carbon dioxide pressure (greater than 45 mm Hg), and an excess of carbonic acid.
Respiratory acidosis is caused by hypoventilation or any condition that depresses ventilation (see the
accompanying display). Hypoventilation can begin in the respiratory system, as occurs with respiratory
failure, or outside the respiratory system, as occurs with drug overdose. Common drugs that can cause
central nervous system depression and place the client at risk for respiratory acidosis are narcotics,
barbiturates, and anesthetic agents.
Clients with respiratory acidosis experience neurologic changes resulting from the acidity of
the cerebrospinal fluid and brain cells. Hypoventilation causes hypoxemia (decreased oxygen levels), which
causes further neurologic impairments. Hyperkalemia may accompany acidosis.
Causes:
• CNS disorders
• Drug overdose
• Pneumonia
• Pulmonary edema
• Pneumothorax
• Restrictive lung disease
Manifestations and Nursing Interventions
Manifestations Nsg. Interventions
 Institute safety measures
Disorientation, depression, stupor
 Assist with positioning
 Monitor I/O
Flushed and warm skin
 Administer fluids as ordered
 Administer oxygen and medications as ordered
Dyspnoea, tachycardia, dysrhythmias
 Monitor vital signs and respiratory status hourly
Biochemical changes:
Decreased pH(<7.35),  Monitor arterial blood gases(ABGs), pH, PaCO2, HCO3-
increased PaCO2 (>45mm Hg)

Respiratory Alkalosis (Carbonic Acid Deficit)

Respiratory acidosis is characterized by a decreased hydrogen ion concentration (a blood pH
above 7.45) and a decreased arterial carbon dioxide pressure (less than 35 mm Hg). Respiratory alkalosis is
caused by hyperventilation (excessive exhalation of carbon dioxide) resulting in hypocapnia (decreased
arterial carbon dioxide concentration). Hyperventilation can be triggered by hypoxia at high altitudes,
anxiety, fear, pain, fever, and rapid mechanical ventilation. Other causes of hyperventilation, which involve
overstimulation of the respiratory center, include salicylate poisoning, hyperthyroidism, pneumonia,
atelectasis, asthma, adult respiratory distress syndrome, congestive heart failure, pulmonary edema and
embolus, brain tumors, meningitis, and encephalitis.
Causes:
• Anxiety, fear • Pneumonia, atelectasis
• CNS disorders • Adult respiratory distress syndrome (ARDS)
• Pain • CHF, Pulmonary edema
• Fever • Pulmonary embolus
•
Manifestations and Nursing Interventions:
Manifestations Nursing Interventions
 Institute safety measures for the client with vertigo or the
Hyperactive reflexes, tetany, Vertigo, unconscious client.
unconsciousness  Encourage the anxious client to verbalize the fear.
 Administer sedation as ordered to relax the client.
Sweating(may occur)  Keep the client warm and dry
  Encourage the client to take deep, slow breaths into a
Rapid & shallow breathing, palpitations
brown paper bag(inspire CO2)
Biochemical changes:
Increased pH(>7.45),  Monitor ABGs, primarily PaCO2
decreased PaCO2(<35mm Hg)

Metabolic Acidosis (Bicarbonate Deficit)

Metabolic acidosis is characterized by an increase in hydrogen ion concentration (blood pH
below 7.35) or a decrease in bicarbonate concentration. Causes of metabolic acidosis can be divided into two
categories: loss of base and gain in metabolic acids. Chronic diarrhea causes an excessive loss of
bicarbonate and sodium ions from the small intestines. With the loss of sodium ions, chloride ions are in
excess and combine with hydrogen to produce a strong acid (hydrochloric acid). Clients with certain medical
diagnoses are at risk for metabolic acidosis. Such conditions include:
1. Diabetic ketoacidosis: The cells are deprived of glucose (decrease or absence of insulin) for metabolism;
the liver, in response to the needs of the cells, increases the metabolism of fatty acids, which causes an
increase in ketone bodies, making the extracellular fluid more acidic.
2. Renal failure: The normal mechanism of the kidneys to conserve sodium and water and excrete hydrogen
is compromised.
3. Anaerobic metabolism: Cellular catabolism and acid accumulation occur with starvation, severe
malnutrition, infection, fever, trauma, shock, and excessive exercise.
4. Drug overdose: Acid accumulation results from excessive ingestion of salicylate, paraldehyde, and
methanol.
In response to metabolic acidosis, the respiratory center is stimulated, causing an increase in
the rate and depth of respirations, to lower the acid concentration in extracellular fluid by increasing the
exhalation of carbon dioxide. The respiratory compensatory mechanism is usually ineffective in decreasing
acids, especially if the client has chronic obstructive pulmonary disease or is in ketoacidosis. The renal
compensatory mechanism tries to increase the pH by exchanging sodium ions with hydrogen ions to
increase the excretion of hydrogen.
Causes:
Increased acids:
• Renal failure
• Diabetic ketoacidosis
• Anaerobic metabolism
• Drug overdose (Salicylates, methanol)
Loss of base:
• Diarrhoea
Manifestation and Nursing Interventions
Manifestations Nursing Interventions
 Institute safety measures
Restlessness, disorientation, stupor, coma  Monitor client’s sensorium, report alteration in level of
consciousness.
 Assist the patient with positioning and proper body
Weakness, lethargy
alignment
Warm & flushed skin  Keep the client comfortable
 Monitor vital signs and I/O
Deep & rapid respirations, Bradycardia,  Monitor and report cardiac dysrhythmias
decreased cardiac output, dysrhythmias  Administer sodium bicarbonate and fluid replacement as
ordered.
 Provide comfortable measures
Nausea, vomiting, abdominal pain
 Correct metabolic problem as ordered
Biochemical changes:
 Monitor ABGs and evaluate the metabolic indicators
Decreased pH(<7.35),
(HCO3- & BE)
decreased HCO3-(<24mEq/L)
Metabolic Alkalosis (Bicarbonate Excess)
Metabolic alkalosis is characterized by an increased loss of acid from the body or a gain in
base (increased levels of bicarbonate). The blood pH is above 7.45. A gain in base may result from
excessive ingestion of antacids. These substances neutralize acids, producing alkalosis and hypercalcemia.
The excessive oral or parenteral administration of sodium bicarbonate or other alkaline salts (e.g., sodium or
potassium acetate, lactate, or citrate) increases the amount of base in extracellular fluids. The following
clinical conditions can place clients at risk for metabolic alkalosis:
1. Vomiting and nasogastric suctioning or lavage cause a loss in hydrochloric acid and chloride; with the
loss of the hydrogen and chloride ions, bicarbonate ions are absorbed, unneutralized, into the bloodstream
and the pH of the extracellular fluid rises (alkalosis).
2. Diarrhea, and steroid or diuretic therapy can cause the excessive loss of potassium, chloride, and other
electrolytes; the potassium deficit causes the kidneys to exchange hydrogen ions (instead of potassium ions)
for sodium ions, which promotes the loss of hydrogen, thereby increasing bicarbonate level.
Hydrochlorothiazide, a thiazide diuretic, blocks the reabsorption of sodium in the cortex in the distal tubule
causing sodium to be excreted in greater amounts than water (hyponatremia). Thiazides also cause
hypokalemia because of the loss of urinary potassium. The secondary effects of thiazide lead to metabolic
alkalosis because of a depletion in volume, chloride, potassium, and hydrogen ions (DeJong, 1998).
The respiratory and renal compensatory mechanisms respond to an increased bicarbonate–
carbonic acid ratio. The rate and depth of respirations are decreased in an effort to retain carbon dioxide. The
arterial carbon dioxide concentration rises, creating respiratory acidosis, to counter the pH imbalance of
metabolic alkalosis. A normal serum potassium level is a prerequisite to renal compensation. In alkalosis,
potassium ions enter the cells in exchange for hydrogen ions, causing hypokalemia. Hypokalemia further
potentiates metabolic alkalosis because the kidneys conserve hydrogen ions by excreting potassium ions in
exchange for sodium ions. When hypokalemia is present, the kidneys cannot function as a compensatory
mechanism; therefore, they continue to excrete hydrogen, and bicarbonate excess continues.
Causes:
Gain of base:
• Excess ingestion of antacids
• Excess administration of sodium bicarbonate
Loss of metabolic acids:
• Vomiting
• Nasogastric suction or lavage
• Low potassium or chloride
• Increased Aldosterone
• Administration of steroids or diuretics
Manifestations and Nursing Interventions
Manifestations Nursing Interventions
 Monitor clients sensorium and report increasing mental
Irritability, confusion
confusion
Tetany, hypertonic muscles, hypertonic  Institute safety and comfort measures.
reflexes  Report symptoms of tetany
 Monitor vital signs and report changes in the client’s
Depressed rate and depth of respirations
respiratory status
 Monitor I/O; recording amount of loss from vomiting and
gastric suctioning.
Vomiting
 Administer IV sodium chloride solutions(0.45-0.9%) as
ordered
Biochemical changes:
 Monitor ABGs and evaluate the metabolic
Increased pH(>7.45),
indicators(HCO3- and BE)
increased HCO3-(>28mEq/L)
Nursing Diagnoses for
Respiratory Acidosis:
• Impaired gas exchange related to ventilation perfusion imbalance evidenced by dyspnea with exertion,
tachypnea; changes in mentation, irritability; tachycardia, hypoxia and hypercapnia
Respiratory Alkalosis:
• Impaired gas exchange related to ventilation perfusion imbalance evidenced by dyspnea, tachypnea;
changes in mentation; hypocapnia, tachycardia; hypoxia
Metabolic Acidosis and alkalosis:
Because no current nursing diagnosis speaks clearly for metabolic imbalances, the interventions are
presented in a general format for inclusion in the primary plan of care