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 bodys 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 bodys 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 dissociates into ions (electrically charged particles). The electrolytes provide inorganic chemicals for cellular reactions and control mechanisms. Electrolytes have special physiological functions in the body, i.e. Promote neuromuscular irritability, Maintain body fluid osmolarity, Regulate acid-base balance, and Distribute body fluids between the fluid compartments. water or another solvent, forms or Electrolyte Sodium Potassium Calcium Magnesium Phosphate Chloride Normal values 135-148 mEq/L 3.5-5.0 mEq/L 8.4-10.5 mg/dl 1.3-2.0 mEq/L 2.7-4.5 mg/dl 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: Electrolyte Ion Distribution in Body Fluid Extracellular Intracellular (mEq/L) (mEq/L) Basic Functions Dietary Sources

Sodium (Na+)

135154

1520

Regulates fluid volume within extracellular fluid (ECF) compartment. Increases cell membrane permeability. Regulates osmotic pressure. Controls water distribution between ECF and intracellular fluid (ICF) compartments. Stimulates conduction of nerve impulses. Maintains neuromuscular irritability.

Table salt (NaCl), 40% of which is sodium; cheese, milk, processed meat, poultry, shellfish, fish, eggs, and foods preserved with salt (e.g., ham and bacon)

Potassium (K+)

3.55

150155

Regulates osmolality of ICF. Promotes transmission of nerve impulses. Promotes contraction of skeletal and smooth muscles. Promotes enzymatic action for cellular energy production by transforming carbohydrates into energy and restructuring amino acids into proteins. Regulates acid-base balance by cellular exchange of hydrogen ions.

Fruits, especially bananas, oranges, and dried fruits; vegetables, meats, and nuts

Calcium (Ca2+)

4.55.5

12

Provides strength and durability to bones and teeth. Establishes thickness and strength of cell membranes. Promotes transmission of nerve impulses. Decreases neuromuscular excitability. Is essential for blood 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, calcium, and protein. Promotes regulation of serum calcium, phosphorus, and potassium levels. Promotes neuromuscular activity.

Dairy products (milk, cheese, and yogurt), sardines, whole grains, and green leafy vegetables

Magnesium (Mg2+)

4.55.5

2729

Green leafy vegetables, whole grains, fish and nuts

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 Bleeding Vomiting Severe burns Clinical Manifestations: Anxiety, restlessness Tachycardia Postural hypotension Cold and clammy skin Drugs (diuretics or vasodilators) Naso-gastric suction Intestinal fistulae

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 Excess blood transfusion Renal insufficiency Clinical Manifestations: Oedema Ascites Pleural effusion Pulmonary congestion Congestive heart failure Liver diseases

Tachycardia Warm skin Bounding pulse 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 bodys 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 Headaches, Apprehension, Lethargy, Confusion, Depression & convulsion Muscular Weakness Dry, pale skin & mucous Tachycardia & Hypotension Nausea, vomiting, diarrhoea, abdominal cramps Biochemical changes Nsg. Interventions Admn. Comfort measures as needed Monitor level of consciousness Institute safety measures for seizure Assist with range of motion Admn. IV isotonic solution (0.9%NaCl) Monitor hourly vital signs & I/O Restrict fluids and Admn. diuretics Monitor daily intake of Na & watch for water intoxication with SIADH (Headache & behavioural changes) Monitor serum sodium levels 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 Restlessness, Agitation, Delirium, Convulsions, Coma Increased muscle tone, hyperreflexia Flushed, dry skin, Red, dry tongue & sticky mucous Tachycardia Nausea, vomiting, anorexia Polyuria Biochemical Changes Nursing Interventions Monitor level of consciousness Institute Safety measures for seizures Maintain body alignment and assist with movement. Administer oral hygiene hourly. Monitor vital signs hourly Admn. oral fluid/parenteral hypotonic soln.(0.3%NaCl) as ordered Monitor I/O hourly Monitor laboratory findings 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 (3.55.0 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 Abdominal Distention, nausea & vomiting Malaise, disorientation, coma, loss of tactile discrimination Muscle weakness & hyporeflexia Constipation & Polyuria Diminished breath sounds, tachycardia, Increased sensitivity to digitalis, ST depression, T-wave inverted, heart block, cardiac arrest(severe Hypokalemia) Biochemical changes Nursing Interventions Admn of K+ replacement therapy as ordered. Admn. of Oral potassium should be diluted in 4-8 oz of water or juice IV potassium 20-40mEq/ 1L of IV fluids Protect from injury Monitor I/O hourly Monitor vital signs hourly Monitor heart rate and rhythm Monitor closely for signs of digitalis toxicity(premature atrial & ventricular beats) Teach client about K+ rich foods and how to prevent 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 Abdominal cramps, nausea, diarrhoea

Nursing Interventions Restrict oral and parenteral potassium intake as ordered 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 bodys 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 clients 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 kidneys response to a high serum calcium concentration. Causes: Bone tumors, immobility Overconsumption of milk or dietary salts Hyperparathyroidism Renal impairment Manifestations & Nursing Interventions: Manifestations Depression & Lethargy Decreased muscle tone & deep tendon reflexes, osteoporosis, osteomalacia, deep bone pain Heart block, Arrest(Hypercalcemia crisis) Nausea, vomiting, anorexia, constipation Flank pain from calculi, Polyuria Nursing Interventions Monitor State of sensorium Encourage client movement and exercise Assist client with movement to decrease pain Monitor for ECG changes Teach to decrease Ca2+ intake & increase fibre Encourage oral intake of acid-ash fluids to decrease deposit of 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 4.55.5 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 Lethargy, Drowsiness, Coma Muscle weakness, decreased deep-tendon reflexes Decreased Resp. & BP, Bradycardia, QRS complex widening, QT interval prolonged Nursing Interventions Monitor level of consciousness Assess patellar reflexes, if absent notify practitioner Monitor vital signs q15-30mins & for ECG changes 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 Confusion, seizures, coma, fatigue, memory loss Muscle pain, weakness, paresthesia, hyporeflexia, bone pain, joint stiffness Tissue hypoxia, hyperventilation, possible bleeding, weak pulse Possible infection Anorexia, Dysphagia Biochemical changes Nsg. Interventions Monitor clients level of consciousness. Institute safety measures for seizures. Administer pain medication and other comfort measures Assist the client in maintaining proper body alignment Monitor for bleeding and respiratory failure Institute precautions to prevent infection Teach client about phosphorus rich foods and over-thecounter drugs that contain aluminum hydroxide Administer IV phosphates with caution: dilute and infuse 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 Tetany, muscle weakness, flaccid paralysis, Hyperreflexia Tachycardia, ST segment shortened, QT interval shortened Nausea, anorexia, vomiting, diarrhoea Biochemical changesIncreased phosphate level, decreased serum calcium Nsg. Interventions Monitor for tetany and other signs of hypocalcaemia Monitor heart rate and assess for ECG changes Administer calcium replacement Monitor urinary output Teach client to avoid foods high in phosphorus, and excessive use of phosphorus containing laxative and 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 Disorientation, depression, stupor Flushed and warm skin Dyspnoea, tachycardia, dysrhythmias Biochemical changes: Decreased pH(<7.35), increased PaCO2 (>45mm Hg) Nsg. Interventions Institute safety measures Assist with positioning Monitor I/O Administer fluids as ordered Administer oxygen and medications as ordered Monitor vital signs and respiratory status hourly

Monitor arterial blood gases(ABGs), pH, PaCO2, HCO3-

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 Adult respiratory distress syndrome (ARDS) CNS disorders 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

Rapid & shallow breathing, palpitations Biochemical changes: Increased pH(>7.45), decreased PaCO2(<35mm Hg)

Encourage the client to take deep, slow breaths into a brown paper bag(inspire CO2) Monitor ABGs, primarily PaCO2

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 Restlessness, disorientation, stupor, coma Weakness, lethargy Warm & flushed skin Deep & rapid respirations, Bradycardia, decreased cardiac output, dysrhythmias Nausea, vomiting, abdominal pain Biochemical changes: Decreased pH(<7.35), decreased HCO3-(<24mEq/L) Nursing Interventions Institute safety measures Monitor clients sensorium, report alteration in level of consciousness. Assist the patient with positioning and proper body alignment Keep the client comfortable Monitor vital signs and I/O Monitor and report cardiac dysrhythmias Administer sodium bicarbonate and fluid replacement as ordered. Provide comfortable measures Correct metabolic problem as ordered Monitor ABGs and evaluate the metabolic indicators (HCO3- & BE)

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 Irritability, confusion Tetany, hypertonic muscles, hypertonic reflexes Depressed rate and depth of respirations Nursing Interventions Monitor clients sensorium and report increasing mental confusion Institute safety and comfort measures. Report symptoms of tetany Monitor vital signs and report changes in the clients respiratory status Monitor I/O; recording amount of loss from vomiting and gastric suctioning. Administer IV sodium chloride solutions(0.45-0.9%) as ordered Monitor ABGs and evaluate the metabolic indicators(HCO3- and BE)

Vomiting Biochemical changes: Increased pH(>7.45), 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