1. 2 3. 4. 5. 6. 7. 8.

Introduction Distribution of Body Fluid Composition of Body Fluid Movement of body Fluid Regulation of Body Water Regulation of Electrolytes Regulation of Acid-base Balance Fluid Imbalance 1.Fluid Volume Deficit 2.Fluid Volume Excess

P.No .
1 1 1-2 2 3-4 4 4-5 6-10 10-12 12 13-14 14-17 17 17-20 20-22 22 23-25 25-27 27-28 28-30 30-32


Electrolyte Imbalance Significance of Sodium 1.Sodium Deficit 2.Sodium Excess Significance of Potassium 1.Potassium Deficit 2.Potassium Excess Significance of Calcium 1. Calcium Deficit 2. Calcium Excess Significance of Magnesium 1.Magnesium deficit 2.Magnesium Excess




Potter 7 perry, fundamentals of nursing, 6th edition, Elsevier publishers,Pp 1136-1152 Smeltzer et al, Textbook of Medical Surgical Nursing, 10th Edition, Lippincott Williams & Wilkins publishers, Pp 250-276

Introduction: Fluid, electrolyte, and acid-base balances within the body are necessary to maintain health & function in al body systems. These balances are maintained by the intake & output of water & electrolytes & regulation by the renal & pulmonary systems. Imbalances may result from many factors, including illnesses, altered fluid intake or prolonged episodes of vomiting & diarrhea. Acid base balance is necessary for many physiological processes, & imbalances can alter respiration, metabolism, & function of CNS. Knowledge & understanding of the mechanisms that contributes to fluid, electrolyte & acid-base imbalances are essential. (Phillips et al, 2003) Water is the largest single component of the body: 60% of the average adult’s weight is fluid. A healthy, mobile, well oriented adult can usually maintain normal fluid, electrolyte & acid-base balances because of the body’s adaptive physiological mechanisms. Distribution of Body Fluid • 2/3 (65%) of TBW is intracellular (ICF) • 1/3 extra-cellular water – 25 % interstitial fluid (ISF) – 5- 8 % in plasma (IVF intravascular fluid) – 1- 2 % in transcellular fluids – CSF, intraocular fluids, serous membranes, and in GI, respiratory and urinary tracts (third space)

Composition of Body Fluids:

As water moves through the compartments of the body, it contains substances that are sometimes called minerals or salts but are technically known as electrolytes. An electrolyte is an element or compound that, when melted or dissolved in water or another solvent, separates into ions & is able to carry an electrical current.


Ionic Extracellular(mEq/L) formula



















22-26(arterial) Bicarbonate HCO324-30(venous)

Movement of body fluids “Where sodium goes, water follows.” Diffusion – It is the movement of particles down a concentration gradient. Osmosis – Osmosis involves the movement of a pure solvent, such as water through a semi permeable membrane, from a area of lesser solute concentration to area of higher solute concentration in an attempt to equalize the concentrations on both sides of the membrane. Solutions are classified as hypertonic, isotonic or hypotonic. A solution with the same osmolarity as plasma is called isotonic.e.g. 0.9% NaCl. A hypertonic solution, a solution of higher osmotic pressure. E.g. Hypotonic solution, a solution of lower osmotic pressure. E.g. 0.45% NaCl.

Active transport –It is movement of particles up a concentration gradient that requires metabolic activity & expenditure of energy to move materials across cell membranes.

Regulation of body water
Body fluids are regulated by fluid intake, hormonal controls & fluid output. This physiological balance is termed as homeostasis (Heitz & Horne, 2001) • Fluid intake: Fluid intake is regulated primarily through the thirst mechanism. The thirst-control center is located within the hypothalamus in the brain. Thirst is the conscious desire for water & is one of the major factors that determine fluid intake (Weldy, 2002). The osmoreceptors continually monitors the serum osmotic pressure & when osmolarity increases the hypothalamus is stimulated. Hormonal regulation: Hormones regulate fluid intake through various mechanisms. Antidiuretic Hormone (ADH) is stored in the posterior pituitary gland & is released in response to changes in blood osmolarity. The osmoreceptors in the hypothalamus are stimulated when there is an increase in the osmolarity to release ADH. The ADH works directly on the renal tubules & collecting ducts to make them more permeable to water. This in turn causes water to return to the systemic circulation, which dilutes the blood & decreases its osmolarity. As the body attempts to compensate the client will experience a decrease in urinary output temporarily. Aldosterone: is released by the adrenal cortex in response to increase plasma potassium levels or as apart of the Renin-Angiotensin aldosterone mechanism to counteract hypovolemia. It acts as the distal portion of the renal tubule to increase the reabsorption of Na+ & the secretion & excretion of K+& H+. Because Na+ retention leads to water retention, the release of aldosterone acts as volume regulators (Heitz & Horne, 2001). Renin: A proteolytic enzyme secreted by the kidneys, responds to decreased renal perfusion secondary to a decrease in extra cellular volume. Renin acts to produce angiotensin1, which causes some vasoconstriction. However, angiotensin1 almost immediately becomes reduced by an enzyme that converts angiotensin1 into angiotensin2. Angiotensin2 then causes massive selective vasoconstriction of many •

blood vessels & relocates & increases the blood flow to the kidney, improving renal perfusion.(Speakman & weldy,2002) • Fluid output regulation: Fluid loss occurs through four organs of the body: the kidney, the skin, the lungs, & the GIT. Kidneys are major regulatory organ of fluid balance. They receive approx. 180L of plasma to filter each day & produce 1200-1500ml of urine. Water loss through skin can be sensible or insensible loss. An average of 500600mL of sensible & Insensible fluid is lost via skin each day( Heitz & Horne, 2001).Lungs expire about 400mL of water daily. The GIT plays an important role in fluid regulation. Approx. 100-200mL of water is loses through feces daily.

Regulation of Electrolytes:
Major cations within the body fluids include Na+, K+, Ca+2, Mg+2. Cations interchange when one cation leaves the cell & is replaced by another. This occurs because cells tend to maintain electrical neutrality. • Sodium Regulation: sodium is the most abundant cation 90% in ECF. Na+ is major contributor to maintaining water balance through their effect on serum osmolarity, water balance through their effect on serum osmolality, nerve impulse transmission, regulation of acid-base balance. (McCance & Huether, 2002).Serum sodium is regulated by dietary intake & aldosterone secretion. • Potassium regulation: Potassium is the major electrolyte & principal cation in Intracellular compartments. It regulates metabolic activities & is necessary for glycogen deposits in liver & skeletal muscles, transmission & conduction of nerve impulses, normal cardiac conduction, and smooth muscle relaxation. Potassium is regulated by dietary intake & renal excretion. • Calcium Regulation: Calcium is stored in bone, plasma, & body cells. 90% of calcium is located in bones & only 1% is located in ECF. Approx.50% calcium in the plasma is bound to protein, primarily albumin & 40% is free ionized calcium. • Magnesium Regulation: Magnesium is essential for enzyme activity, neurochemical activities, and cardiac & skeletal muscle excitability. Serum magnesium is regulated by dietary intake, renal mechanism, & action of parathyroid hormone. Anions: The three main anions of body fluids are chloride, bicarbonate, & phosphate ions. • Chloride Regulation: Chloride is major anion in ECF. The transport of chloride follows sodium. Serum chloride is regulated by dietary intake & the kidneys. • Bicarbonate Regulation: Bicarbonate is the major chemical buffer within the body. The bicarbonate ion is found in ECF & ICF. The bicarbonate ion is an essential component of the carbonic acid-bicarbonate buffering system essential to acid-base balance. • Phosphorous-Phosphate Regulation: Phosphate is a buffer anion found primarily in ICF. It assists in acid-base regulation. Phosphate & calcium helps to develop & maintain bones and teeth. Phosphorous is normally absorbed through GIT. It is regulated by dietary intake, renal excretion, intestinal absorption & parathyroid hormone.

Regulation of Acid-Base Balance:

For optimal functioning of the cells, metabolic processes maintain a steady balance between acids & bases. Arterial pH is inversely proportion to the hydrogen ions concentration. The pH is a reflection of the balance between carbon dioxide which is regulate by lungs, & bicarbonate, a base regulated by kidneys (Heitz & Horne, 2001). The pH scale is used to measure acidity & alkanity of fluids. The three general acid-base regulators in the body are chemical, biological, & physiological buffering systems. A buffer is a substance or a group of substance that can absorb or release H+ to correct an acid-base imbalance. • Chemical Regulation: The largest chemical buffer in ECF is the carbonic acid & bicarbonate buffer system. CO2 + H2O H2CO3 H+ + HCO3

Carbon dioxide + Water carbonic acid hydrogen ion + Bicarbonate When ever the carbon dioxide concentration increases, there is an increase in hydrogen ions produced, there is more carbon dioxide produced (Workman, 2002) • Biological regulation: biological buffering occurs when H+ are released or absorbed by the cells. It occurs after the chemical buffering & takes 2-4 hours. In conditions with excess acid, a H+ enters the cell & K+ leaves the cell & enters the ECF, thus causing an elevated serum level. A second biological buffer is haemoglobin-oxyhaemoglobin system. CO2 diffuses into the RBC & forms carbonic acid. The carbonic acid dissociates into H+ & HCO3 .The H+ attach to hemoglobin & the HCO3 becomes available for buffering by exchanging with extra cellular chloride. Another biological buffer is chloride shift within RBC’s. When blood is oxygenated in the lungs, bicarbonate diffuses into the cells & chloride travels from the hemoglobin to plasma to maintain electrical neutrality.(Groer 2000) Physiological Regulation: The two Physiologic buffers in the body are-lungs & kidneys. The lungs adapt rapidly to an acid-base imbalance: they act to return to normal before action of biological buffers. Increases level of H+ & carbon dioxide provides stimulus for respiration. When H+ concentration is altered, the lungs react to correct the imbalance by altering the rate & depth of respiration. When metabolic acidosis is present, respiration rate is increased, resulting in greater amount of carbon dioxide being exhaled which results in a decrease in the acidic level: when metabolic alkalosis is present, lungs retain carbon-dioxide by decreasing respirations, increasing acidity. (Phillips et al, 2003). Kidneys take from a few hours to several days to regulate acid-base imbalance. They reabsorb bicarbonate in case of acid excess & excrete it in cases of acid deficit.

DISTURBANCES IN FLUID, ELECTROLYTE & ACID_BASE BALANCE: A disturbance in fluid, electrolyte & acid-base balances seldom occurs alone & can disrupt normal body processes. When there is loss of body fluids because of burns, illnesses, or trauma, client is also at risk for electrolyte imbalance. In addition, some untreated electrolyte imbalance results in acid-base imbalances.

Fluid Imbalance:

Fluid volume deficit (FVD) occurs when loss of ECF volume exceeds the intake of fluid. It occurs when water & electrolytes are lost in the same proportion as they exist in normal body fluids. So that the ratio of serum electrolytes to ware remains the same. Fluid volume deficit should not be confused with the term dehydration, which refers to loss of water alone with increased serum sodium levels. FVD may occur alone or in combination with other imbalances. Causes include:

Diarrhea, vomiting. Severe, acute diarrhea — that is, diarrhea that comes on suddenly and violently — can cause a tremendous loss of water and electrolytes in a short amount of time. If vomiting is along with diarrhea, loss may be of more fluids and minerals. Children and infants are especially at risk. Dehydration is a leading cause of death in children worldwide. In the United States, up to 300 children die of dehydration each year. Fever. In general, the higher your fever, the more the dehydration. Excessive sweating. You lose water when you sweat. If you engage in vigorous activity and don't replace fluids as you go along, you can become dehydrated. Hot, humid weather increases the amount you sweat and the amount of fluid you lose. But you can also become dehydrated in winter if you don't replace lost fluids. Preteens and teens who participate in sports may be especially susceptible, both because of their body weight, which is generally lower than that of adults, and because they may not be experienced enough to know the warning signs of dehydration. Increased urination. This is most often the result of undiagnosed or uncontrolled diabetes mellitus, a disease that affects the way your body uses blood sugar and that often causes increased thirst and more frequent urination. Another type of diabetes, diabetes inspidus, also is characterized by excessive thirst and urination, but in this case the cause is a hormonal disorder that makes your kidneys unable to conserve water. Certain medications — diuretics, antihistamines, blood pressure medications and some psychiatric drugs — as well as alcohol also can lead to dehydration. Burns. People with third-degree burns or extensive first- or second-degree burns experience profound fluid loss, and the resulting dehydration can be life-threatening.

 

Risk factors:

Anyone can become dehydrated if the loss of fluids outweighs fluid intake. But certain people are at greater risk, including:

Infants and children. Worldwide, dehydration caused by diarrhea is a leading cause of death in children. Infants and children are especially vulnerable because of their relatively small body weights and high turnover of water and electrolytes. They're also the group most likely to experience diarrhea. In the India, diarrhea remains one of the most common childhood illnesses. Older adults. Older adults are more susceptible to dehydration for several reasons: body's ability to conserve water is reduced; thirst sense becomes less acute and are less able to respond to changes in temperature. Disability or neglect also may prevent them from being well nourished. These problems are compounded by chronic illnesses such as diabetes, by hormonal changes associated with menopause and by the use of certain medications. People with chronic illnesses. Having uncontrolled or untreated diabetes puts people at high risk of dehydration. But other chronic illnesses also make more likely to become dehydrated. These include kidney disease, cystic fibrosis, and alcoholism and adrenal gland disorders. Even having a cold or sore throat makes you more susceptible to dehydration because you're less likely to feel like eating or drinking when you're sick. Endurance athletes. Anyone who exercises can become dehydrated, especially in hot, humid conditions or at high altitudes. But athletes who train for and participate in ultramarathons, triathlons, mountain climbing expeditions and cycling tournaments are at particularly high risk. That's because the longer you exercise, the more difficult it is to stay hydrated. During exercise, your body can absorb about 24 to 32 ounces of water an hour, but you may lose twice that amount in hot weather. People living at high altitudes. Living, working and exercising at high altitudes (generally defined as 8,000 to 12,000 feet, or about 2,400 to 3,600 meters) or very high altitudes (12,000 to 18,000 feet, or about 3,600 to 5,400 meters) can cause a number of health problems. One is dehydration, which commonly occurs when your body tries to adjust to high elevations through increased urination and more rapid breathing — the faster you breathe to maintain adequate oxygen levels in your blood, the more water vapor you exhale.

Signs & MILD sympt. Moderate Severe – Symptoms: General Signs &Drowsy Thirsty, allert, limp, Thirsty, irritable, restlessdrowsy / sweaty or skin cold Radial pulse rate weakfeeble Normal Rapid, Rapid, Respiration Normal Deep & rapid Deep Anterior font. Very sunken Normal Sunken SkinPinchRetracts Poor turgor retracts slowly immediately Eyes Normal Grossly sunken Sunken Tears Present Absent Absent Mucous memb. Very dry Moist Dry Urine flow Dark & NormalOliguria / anuria decreased

Complications FVD can lead to serious complications, including:

Heat injury. Inadequate fluid intake combined with vigorous exercise and heavy perspiration can lead to heat injury, ranging in severity from mild heat cramps to heat exhaustion to potentially life-threatening heatstroke. Swelling of the brain (cerebral edema). Most often, the fluid you lose when you're dehydrated contains the same amount of sodium your blood does (isotonic dehydration). In some instances, though, you may lose more sodium than fluid (hypotonic dehydration). To compensate for this loss, your body produces particles that pull water back into the cells. As a result, your cells may absorb too much water during the rehydration process, causing them to swell and rupture. The consequences are especially grave when brain cells are affected. Seizures. These occur when the normal electrical discharges in your brain become disorganized, leading to involuntary muscle contractions and sometimes to a loss of consciousness. Hypovolemic shock. This is one of the most serious complications of dehydration. It occurs when low blood volume causes a drop in blood pressure and a corresponding reduction in the amount of oxygen reaching your tissues. If untreated, severe hypovolemic shock can cause death in a matter of minutes. Kidney failure. This potentially life-threatening problem occurs when your kidneys are no longer able to remove excess fluids and waste from your blood. Coma and death. When not treated promptly and appropriately, severe dehydration can be fatal.

Assessment & Diagnostic Findings: Laboratory Data useful in evaluating fluid volume status include BUN & its relation to the serum creatinine concentration. A volume-depleted patient has a BUN elevated out of proportion to the serum creatinine level (a ratio greater than 20:1). The cause of hypovolemia may be determined through the health history & physical examination. The BUN can be elevated due to dehydration or decreased renal perfusion & function. Also, the haematocrit level is greater than normal because the RBC becomes suspended in a decresed plasma volume. Serum electrolyte changes may also exist. Potassium & sodium levels can be reduced, or elevated.

• Hypokalemia occur with GI & renal losses • Hyperkalemia occurs with adrenal insufficiency. • Hyponatremia occurs with increased thirst & ADH release. • Hypernatremia results from increased insensible losses & diabetes inspidus. Urine specific gravity is increased in relation to the kidneys attempt to conserve water & decreased with diabetes inspidus. Urine osmalality is greater than 450mosm/kg, since the kidneys try to compensate by conserving water. Gerontologic considerations: Elderly patients have special nursing care needs because of their propensity for developing fluid & electrolyte imbalances (Beck, 2000). Fluid balance in the elderly patient is often marginal at best because of certain physiological changes associated with the ageing process. Some of these changes includes: rduction in toatal body water (associated with increased body fat content & decreased muscle mass), reduction in renal function resulting in decreased ability to concentrate urine, decreased cardio vascular & respiratory function, & disturbances in hormonal regulatory functions. Although these changes are viewed as normal in the ageing process, they must be considered when the elderly person becomes ill because age related changes predispose the person to fluid & electrolyte imbalances. These changes must be considered during assessment of the elderly patient as well as before initiating treatment for fluid & electrolyte imbalances. MEDICAL MANAGEMENT: When planning the correction of fluid loss for the patient with FVD, the health care provider consider the usual maintenance requirements of the Patient &other factors( such as fever) that can influence fluid needs. 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 solution (Lactated ringer, 0.9% NaCl) is frequently used to treat the hypotensive patient with FVD because they expand plasma volume. Accurate & frequent assessment of intake & output, weight, vital signs, central venous pressure, level of consciousness, breath sounds & skin color should be per formed to determine when therapy should be slowed to avoid volume overload. If the patient with sever FVD is not excreting enough urine & is therefore, oliguric, the health care provider needs to determine whether the depressed renal function if the result of reduced renal blood flow secondary to FVD to or more seriously, to acute tubular necrosis from prolonged FVD. The test used in this situation is referred to as a fluid challenge test. During this test volume of fluid are administered at specific rates & intervals while the patients hemodynamic response to this treatment is monitored (i.e. vital signs, breath sounds, sensorium, central venous pressure, urine output) NURSING MANAGEMENT:  To assess for FVD, the nurse monitors and measure fluid intake & output atleast every 8 hours & sometimes hourly. As FVD develops, body fluid losses exceeds fluid intake. This loss may be in the form of excessive urinatin9polyuria), diarrhea, vomiting, & so on. Later, after FVD fully develops the kidneys attempts to conserve needed body fluids leading to a urine output of less then 30Ml/h in an adult. Urine in this instance is concentrated & represents a healthy

renal response. Daily body weights are monitored & acute loss of 0.5kg represents a fluid loss of approx.500mL.  Vital signs are closely monitored. The nurse observes for a weak, rapid pulse & postural hypertension. A decrease in body temperature often accompanies FVD, unless there is a concurrent infection.  Skin & tongue turgor is monitored on a regular basis. In a healthy person pinched skin immediately returns to its normal position when released. When FVD, is severe, the skin may remain elevated for many seconds. The tissue turgor is best measured by pinching the skin over the sternum, inner aspects of the thighs, or forehead.  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. Preventing FVD: To prevent FVD, the nurse identifies patient at risk & takes measures to minimize fluid loses. E.g. if the patient has diarrhea, diarrhea control measures should be implemented & replacement fluid administered. These measures may include administering antidiarrheal medications & small volumes of oral fluids at frequent intervals. Correcting FVD: When possible oral fluids are administered to help, correct FVD, with consideration to the patient’s likes & dislikes. Also, the type of fluid the patient has lost is considered, & attempts are made to select fluids most likely to replace the lost electrolytes. If the patient is reluctant to drink because of oral discomfort, the nurse assists with frequent mouth care & provides non-irritating fluids. The patient may be offered small volumes of fluids at frequent intervals rather than a large volume all at once. If nausea is present, anti-emetics may be needed before oral fluid replacement can be tolerated. If the patient cannot eat & drink, the nurse may need to administer fluid by an alternative route (enteral, or parenteral) prescribed to prevent renal damage related to prolonged FVD. 

Fluid volume excess refers to an isotonic expansion of ECF caused by abnormal retention of water & sodium in approximately the same proportions in which they normally exist in 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. Pathophysiology: 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, & cirrhosis of liver. Another contributing factor is consumption of excessive amounts of table or other sodium salts. Excessive administration of sodium-

containing fluids in a patient with impaired regulatory mechanisms may predispose him or her to a serious FVE as well (Beck, 2000) Clinical Manifestations: Clinical manifestations of FVE stem from expansion of ECF and include edema, distended neck veins, & crackles (abnormal lung sounds). Other manifestations include tachycardia: increased blood pressure: increased weight: increased urine output: and shortness of breath & wheezing. Assessment & Diagnostic Findings: Laboratory data useful in diagnosing FVE include BUN & hematocrit levels. In FVE, both of these values may be decreased because of plasma dilution. Other causes of abnormalities in these values include low protein intake & anemia. In chronic renal failure, both serum osmolality & sodium levels are decreased due to excessive retention of water. The urine sodium level is increased if the kidneys are attempting to excrete excess volume. Chest X-ray may reveal pulmonary congestion. Hypervolemia occurs when aldosterone is chronically stimulated. Urine sodium levels therefore will rise in these conditions. Medical Management: Management of FVE is directed at the causes. When the fluid excess is related to excessive administration of sodium- containing fluids, discontinuing the infusion may be all that is needed. Symptomatic treatment consists of administering diuretics & restricting fluids & sodium.  Pharmacologic therapy: Diuretics are prescribed when dietary restriction of sodium alone is insufficient to reduce edema by inhibiting the reabsorption of sodium & water by kidneys. The choice of diuretics is based on the severity of hypovolemic state, the degree of impairment of renal function & potency of the diuretic.  Hemodialysis: When renal function is so severely impaired that pharmacologic agents cannot act efficiently, other modalities are considered to remove sodium & fluid from the body. Hemodialysis or peritoneal dialysis may be used to remove nitrogenous wastes & control potassium & acid-base balance, and to remove sodium & fluid.  Nutritional Modalities: Treatment of FVE involves dietary restriction of sodium. An average daily diet not restricted in sodium contains 6-15g of salt, whereas low sodium diets can range from a mild restriction to as little as 250mg of sodium per day, depending upon the patients needs. A mild sodium restricted diet allows only light salting of foods in cooking & at the table, & no addition of salt to commercially prepared foods that are already seasoned. Therefore, patients need to read food labels carefully to determine salt content. Lemon juice, onion & garlic are excellent substitute flavoring, although some patients prefer salt substitutes. Most salt substitutes contain potassium & must therefore be used cautiously by patients taking potassium sparing diuretics. Also patients on sodium restricted diet should be cautioned to avoid water softeners that add sodium to water in exchange for other ions, such as calcium. Nursing Management:

To assess for FVE, the nurse measures intake & output at regular intervals to identify excessive fluid retention. The patient is weighed daily & acute weight gain is noted. An acute weight gain of 0.9kg represents a gain of approximately 1L of fluid. The nurse also needs to assess breath sounds at regular intervals in at-risk patients, particularly when parenteral fluids are being administered. The nurse monitors the degree of edema in the most dependent parts of the body, such as feet & ankles in ambulatory patients & sacral region in bedridden patients.  Preventing FVE: Specific interventions vary somewhat with the underlying conditions & the degree of FVE. Most patients, however, require sodium-restricted diets in some form, & adherence to the prescribed diet is encouraged. The patient is instructed to avoid over-the-counter medications without the first checking with a health care provider because these substances may contain sodium.  Detecting & controlling FVE: Detecting FVE is of primary importance before the condition becomes critical. Interventions include promoting rest, restricting sodium intake, monitoring parenteral therapy & administering appropriate medications. Some patients’ benefits from regular rest periods, as bed rest favors diuresis of edema fluid. The mechanism is probably related to diminish venous pooling & the subsequent increase in effective circulating blood volume & renal perfusion. The rate of parenteral fluids & patient’s response to these fluids are also closely monitored. If dyspnea or orthopnea is present, the patient is placed in semi-fowlers position to promote lung expansion.  Teaching Patient About Edema: The nurse gives special attention to edema when teaching the patients with FVE. Edema can occur from increased capillary pressure, decreased capillary oncotic pressure, or increased interstitial oncotic pressure, thus expanding the interstitial fluid compartment. Edema can be local or generalized. Edema occurs when there is a change in the capillary membrane increasing the formation of interstitial fluid or decreasing the removal of interstitial fluid. Sodium retention is a frequent cause of increased ICF volume. Burns & infections are examples of conditions associated with increased interstitial fluid volume. A thorough medication history is necessary to identify any medications that may cause edema, such as NSAIDS, estrogens, corticosteroids, or hypertensives. Ascites is a form of edema in which the fluid accumulates in the peritoneal cavity; it results from nephritic syndrome or cirrhosis. Patients commonly report shortness of breath & sense of pressure on the diaphragm. Edema usually affects dependent areas. It can be seen in the ankles, sacrum, scrotum, or the periorbital region of the face. Pitting edema is so named because pit forms after a finger is pressed into edematous tissue. In pulmonary edema the amount of fluid in the pulmonary interstitium & the alveoli increases. Manifestations include shortness of breath, increased respiratory rate, diaphoresis, crackles & wheezing on auscultation of the lungs. The goal of the treatment is to preserve or restore the circulating intravascular fluid volume.


Disturbances in electrolyte balance occur in clinical practice & must be corrected for the patient’s health & safety. Significance of Sodium: Sodium is the most abundant electrolyte in the ECF; its concentration ranges from 135 to 145mEq/L. Consequently sodium is the primary determinant of ECF osmolality Decrease sodium is associated with parallel changes in osmolality. It accounts for its primary role in controlling water distribution throughout the body. Sodium also functions in establishing the electrolyte state necessary for muscle contraction & transmission of nerve impulses. Sodium imbalances occur frequently in clinical practice & can develop under simple & complex circumstances. Sodium deficit & excess are the two common sodium imbalances. •

SODIUMM DEFICIT (Hyponatremia):
Hyponatremia refers to a serum level below normal(less than 135mEq/L. Plasma sodium concentration represents the ratio of total body sodium to total body water. A decrease in this ratio can occur from a low quantity of total body sodium with a lesser reduction in total body water, normal total body sodium content with excess total body water, & an excess of total body sodium with an even greater excess of total body water. Contributing factors:
 Loss of water & electrolytes as in o Vomiting o Diarrhea o Fistulas o Fever o Excessive sweating o Burns o Blood loss o Gastrointestinal suctioning  Decreased intake o Anorexia o Nausea o Inability to gain access to fluid

Clinical Manifestations: Clinical manifestations depend on the cause, magnitude & speed with which the deficits occur. Poor skin turgor, dry mucosa, decreased salivation production, orthostatic fall in BP, nausea & abdominal cramps occur. Neurologic changes including altered mental status related to the cellular swelling & cerebral edema associated with the Hyponatremia. As the extracellular sodium level decreases, the cellular fluid becomes relatively more concentrated & pulls water into the cells. Features of Hyponatremia associated with sodium loss & water gain includes anorexia, muscle cramps & a feeling of exhaustion. When the sodium level falls below 115m/Eq/L signs of increasing intracranial pressure, such as lethargy, confusion, muscle twitching, hemiparesis, seizures may occur. Diagnostic findings:

When Hyponatremia is primarily due to sodium loss, the urinary sodium content is less than 20mEq/L, suggesting increased reabsorption of sodium secondary to ECF volume depletion; the specific gravity is low(1.002-1.004). Medical Management: The key to treating Hyponatremia is assessment; this includes the speed with which Hyponatremia occurred rather than relying only on the patient’s actual serum sodium value (Fall, 2000) • Sodium Replacement: The obvious treatment for Hyponatremia is careful administration of sodium by mouth, nasogastric tube, or the parenteral route. For patients who can eat and drink, sodium is easily replaced because sodium is consumed abundantly in a normal diet. For those who cannot consume sodium, lactated Ringer’s solution or isotonic solution may be prescribed. Serum sodium must not be increased greater than 12mEq/L in 24 hours, to avoid Neurologic damage due to osmotic demyelination. • Water Restriction: In a patient with normal or excess fluid volume, Hyponatremia is treated by restricting fluid to a total of 800mL in 24 hours. This is far safer than sodium administration & is usually effective. When Neurologic symptoms are present, however it may be necessary to administer small volumes of a hypertonic sodium solution, 3% or 5% sodium chloride. Nursing Management: The nurse needs to identify patients at risk for Hyponatremia so that they can be monitored. Early detection & treatment of this disorder are necessary to prevent serious consequences. For patient at risk, the nurse monitors fluid intake & output as well as daily body weights. Abnormal losses of sodium or gains of water are noted. GI manifestations, such as anorexia, nausea, vomiting, & abdominal cramping are also noted. The nurse must particularly alert for central nervous system changes, such as lethargy, confusion, muscle twitching, & seizures. • Detecting & controlling Hyponatremia: For patients experiencing abnormal losses of sodium who can consume a general diet, the nurse encourages foods & fluids with high sodium content. For patients taking lithium, the nurse observes for lithium toxicity, particularly when sodium is lost by an abnormal route. In such instances, supplementary salt & fluids are administered. Because diuresis promotes sodium loss, patients taking lithium are instructed not to use diuretics without medical supervision. Excess water supplements are avoided in patients receiving isotonic or hypotonic enteral feedings, particularly if abnormal sodium loss occurs or water is being abnormally retained. • Returning sodium level to normal: When the primary problem is water retention, it is safer to restrict fluid intake than to administer sodium. Administering sodium to a patient with normovolemia or Hypervolemia predisposes the patient to fluid volume overload. The nurse must closely monitor patient with cardiovascular disease very closely. In severe Hyponatremia, the aim of therapy is to elevate the serum sodium level only enough to alleviate Neurologic signs & symptoms. •

SODIUM EXCESS (Hypernatremia)

Hypernatremia is serum Na concentration > 145 mEq/L. It implies a deficit of total body water relative to total body Na, caused by water intake being less than water losses.
Common causes of hypernatremia include:


 Inadequate intake of water, typically in elderly or otherwise disabled patients who are unable to take in water as their thirst dictates. This is the most common cause of hypernatremia.

 Excessive losses of water from the urinary tract, which may be caused by glycosuria, or other
osmotic diuretics.  Water losses associated with extreme sweating.  Severe watery diarrhea


 Excessive excretion of water from the kidneys caused by diabetes insipidus, which involves
either inadequate production of the hormone, vasopressin, from the pituitary gland or impaired responsiveness of the kidneys to vasopressin.


 Intake of a hypertonic fluid (a fluid with a higher concentration of solutes than the remainder of
the body). This is relatively uncommon, though it can occur after a vigorous resuscitation where a patient receives a large volume of a concentrated sodium bicarbonate solution. Ingesting seawater also causes hypernatremia because seawater is hypertonic.

 Mineralcorticoid excess due to a disease state such as Conn's syndrome or Cushing's Disease

Symptoms and Signs
The major symptom of hypernatremia is thirst. The absence of thirst in conscious patients with hypernatremia suggests an impaired thirst mechanism. Patients with difficulty communicating may be unable to express thirst or obtain access to water. The major signs of hypernatremia result from CNS dysfunction due to brain cell shrinkage. Confusion, neuromuscular excitability, hyperreflexia, seizures, or coma may result; cerebrovascular damage with subcortical or subarachnoid hemorrhage and venous thromboses are common in patients who died from severe hypernatremia.

In chronic hypernatremia, osmotically active substances occur in CNS cells (idiogenic osmoles) and increase intracellular osmolality. Therefore, the degree of brain cell dehydration and resultant CNS symptoms are less severe in chronic than in acute hypernatremia. When hypernatremia occurs with abnormal total body Na, the typical symptoms of volume depletion or overload are present. A large volume of hypotonic urine is characteristically excreted in patients with renal concentrating defects. When losses are extrarenal, the route of water loss is often evident (eg, vomiting, diarrhea, excessive sweating), and the urinary Na concentration is low.

Assessment & Diagnostic Findings: In hypernatremia, the serum sodium level exceeds 145mEq/L & the serum osmolality exceeds 295mOsm/kg. The urine specific gravity & urine osmolality are increased as the kidneys attempt to conserve water (Fall, 2000). Medical Management:
Replacement of intravascular volume and of free water is the main goal of treatment. Oral hydration is effective in conscious patients without significant GI dysfunction. In severe hypernatremia or in patients unable to drink because of continued vomiting or mental status changes, IV hydration is preferred. Hypernatremia that lasts < 24 h should be corrected within 24 h. However, hypernatremia that is chronic or of unknown duration should be corrected over 48 h, and the serum osmolality should be lowered at a rate of no faster than 2 mOsm/L/h to avoid cerebral edema caused by excess brain solute. The amount of water (in liters) necessary to replace existing deficits may be estimated by the following formula: Free water deficit = TBW × [(serum Na/140) − 1] where TBW is in liters and is estimated by multiplying weight in kilograms by 0.6; serum Na is in mEq/L. This formula assumes constant total body Na content. In patients with hypernatremia and depletion of total body Na content (ie, who have volume depletion), the free water deficit is greater than that estimated by the formula. In patients with hypernatremia and ECF volume overload (excess total body Na content), the free water deficit can be replaced with 5% D/W, which can be supplemented with a loop diuretic. However, toorapid infusion of 5% D/W may produce glycosuria, thereby increasing salt-free water excretion and hypertonicity, especially in patients with diabetes mellitus. Other electrolytes, including serum K, should be monitored and should be replaced as needed.

Nursing Management: The nurse should assess for abnormal losses of water or low water intake & for large gains of sodium, as might occur with the ingestion of over-the-counter medications with high sodium content. It is important to obtain a medication history because some prescription medications have a high sodium content. The nurse monitors for changes in behavior, such as restlessness, disorientation & lethargy.  Preventing Hypernatremia: The nurse attempts to prevent hypernatremia by offering fluids at regular intervals, particularly in debilitated patients unable to perceive or respond to thirst. If fluid intake remains inadequate, the nurse consults with the physician to plan an alternate route for intake either by enteral feeding or by the parenteral route. If enteral feedings are used, sufficient water should be administered to keep the serum sodium & BUN within normal limits. For patients with diabetes insipidus, adequate water intake must be ensured. If the patient has a decreased level of consciousness or other disability interfering with adequate fluid intake, parenteral fluid replacement may be prescribed.  Correcting Hypernatremia: When parenteral fluids are necessary for managing hypernatremia, the nurse monitors the patient’s response to the fluids by reviewing serum sodium levels & by observing for the changes in Neurologic signs. With a gradual decrease in the serum sodium level, the Neurologic signs should improve.

Significance of Potassium:
Potassium is the major intracellular electrolyte; in fact 98% of the body’s potassium is inside the cells. The remaining 2% is in the ECF, & it is this 2% that is important in neuromuscular functioning. Potassium influences both skeletal & cardiac muscle activity. The normal serum potassium ranges from 3.5-5.5mEq/L. Potassium imbalances are commonly associated with various diseases, injuries, medications, & special treatments, such as parenteral nutrition & chemotherapy.

Hypokalemia is defined as a potassium level less than 3.5 mEq/L. Moderate hypokalemia is a serum level of 2.5-3 mEq/L. Severe hypokalemia is defined as a level less than 2.5 mEq/L. Causes

Renal losses o Renal tubular acidosis o Hyperaldosteronism

Magnesium depletion Leukemia (mechanism uncertain) GI losses o Vomiting or nasogastric suctioning o Diarrhea o Enemas or laxative use o Ileal loop Medication effects o Diuretics (most common cause) o Beta-adrenergic agonists o Steroids o Theophylline Transcellular shift o Insulin o Alkalosis Malnutrition or decreased dietary intake, parenteral nutrition
o o

Symptoms: Common symptoms include the following:
• • • • • • • • •

Palpitations Skeletal muscle weakness or cramping Paralysis, paresthesias Constipation Nausea or vomiting Abdominal cramping Polyuria, nocturia, or polydipsia Psychosis, delirium, or hallucinations Depression

Diagnostic Findings
• • • •

Serum potassium level <3.5 mEq/L (3.5 mmol/L) BUN and creatinine level Glucose, calcium, and/or phosphorus level if coexistent electrolyte disturbances are suspected.. Consider arterial blood gas (ABG): Alkalosis can cause potassium to shift from extracellular to intracellular. Electrocardiography o T-wave flattening or inverted T wave Prominent U wave that appears as QT prolongation
o o

ST-segment depression Ventricular arrhythmias (eg, premature ventricular contractions [PVCs], ventricular fibrillation)5

Atrial arrhythmias (eg, premature atrial contractions [PACs], atrial fibrillation) Thyroid screening studies - Thyroid-stimulating hormone (TSH), free T3, and free T4 in patients with tachycardia, especially Asian patients

The most important treatment in severe hypokalemia is addressing the cause, such as improving the diet, treating diarrhea or stopping an offending medication. Patients without a significant source of potassium loss and who show no symptoms of hypokalemia may not require treatment.

Mild hypokalemia (>3.0 mEq/L) may be treated with oral potassium chloride supplements (Klor-Con, Sando-K, Slow-K). As this is often part of a poor nutritional intake, potassiumcontaining foods may be recommended, such as leafy green vegetables, tomatoes, citrus fruits, oranges or bananas. Both dietary and pharmaceutical supplements are used for people taking diuretic medications .Severe hypokalemia (<3.0 mEq/L) may require intravenous supplementation. Typically, saline is used, with 20-40 mEq KCl per liter over 3-4 hours. Giving intravenous potassium at faster rates (20-25 mEq/hr) may predispose to ventricular tachycardias and requires intensive monitoring. A generally safe rate is 10 mEq/hr. When replacing potassium intravenously, infusion via central line is encouraged to avoid the frequent occurrence of a burning sensation at the site of a peripheral IV, or the rare occurrence of damage to the vein. When peripheral infusions are necessary, the burning can be reduced by diluting the potassium in larger amounts of IV fluid, or mixing 3 ml of 1% lidocaine to each 10 mEq of kcl per 50 ml of IV fluid Nursing Management: As hypokalemia is life threatening, the nurse needs to monitor for its early presence in patients at risk. When available, ECG may provide useful information. E.g. patients receiving digitalis who are at risk for potassium deficiency should be monitored for closely for the signs of digitalis toxicity, because hypokalemia potentiates the action of digitalis. • Preventing Hypokalemia:

Prevention may involve encouraging the patients at risk to eat foods rich in potassium. Sources of potassium includes: Fruits, fruit juices (banana, melon, and citrus fruits), fresh & frozen vegetables, fresh meat, & processed foods. When hypokalemia is due to abuse of laxatives or diuretics, patient education may alleviate the problem. Careful monitoring of fluid intake & output is necessary because 40mEq of potassium is lost for every liter of urine output. • Correcting hypokalemia:

Great care should be exercised when administering potassium, particularly in older adults, who have lower lean body mass & total body potassium levels & therefore lower potassium requirements. Additionally with the physiologic loss of renal function with advancing years, potassium may be retained more readily in older than in younger people. • Administering potassium:

Potassium should be administered only after adequate urine flow has been established. A decrease in urine volume less than 20mL/h for 2 consecutive hours is an indication to stop the potassium infusion until the situation is evaluated.

IV potassium should not be administered faster than 20mEq/ZL unless hypokalemia is severe because this can cause life threatening dysrhythmias. When prepared for IV infusions the fluid should be agitated well to prevent bolus doses that can result when the potassium concentration concentrates at the bottom of the IV container. •

5.5-6.0 mEq/L - Mild 6.1-7.0 mEq/L - Moderate 7.0 mEq/L and greater - Severe

Hyperkalemia is defined as a potassium level greater than 5.5 mEq/L. Ranges are as follows:
• • •

Causes include: Ineffective elimination from the body
 

Renal insufficiency Medication that interferes with urinary excretion:
 ACE inhibitors and angiotensin receptor blockers  Potassium-sparing diuretics (e.g. amiloride and spironolactone)  NSAIDs such as ibuprofen, naproxen, or celecoxib  The antibiotic trimethoprim  The antiparasitic drug pentamidine

Mineralocorticoid deficiency or resistance, such as:
 Addison's disease  Aldosterone deficiency, including reduced levels due to the blood thinner, heparin

 Some forms of congenital adrenal hyperplasia  Type IV renal tubular acidosis (resistance of renal tubules to aldosterone)

Excessive intake  Intoxication with salt-substitute, potassium-containing dietary supplements,
or potassium chloride (KCl) infusion.

Lethal injection

Hyperkalemia is intentionally brought about in an execution by lethal injection, with potassium chloride being the third and last of the three drugs administered to cause death.

Signs & Symptoms:

Patients may be asymptomatic or report the following: o Generalized fatigue o Muscle Weakness o Paresthesias o Paralysis o Palpitations o Nausea, intestinal colic, diarrhea

Diagnostic findings: . The normal serum level of potassium is 3.5 to 5 mEq/L. Generally, blood tests for renal function (creatinine, blood urea nitrogen), glucose and occasionally creatine kinase and cortisol will be performed. Calculating the trans-tubular potassium gradient can sometimes help in distinguishing the cause of the hyperkalemia. In many cases, renal ultrasound will be performed, since hyperkalemia is highly suggestive of renal failure. Also, electrocardiography (EKG/ECG) may be performed to determine if there is a significant risk of cardiac arrhythmias

• • •

Reduction of the size of the P wave Development of peaked T waves. Severe hyperkalemia results in a widening of the QRS complex

Medical management:

Acute: When arrhythmias occur, or when potassium levels exceed 6.5 mmol/l, emergency lowering of

potassium levels is mandated. Several agents are used to lower K levels. Choice depends on the degree and cause of the hyperkalemia, and other aspects of the patient's condition.

Calcium supplementation, preferably through a central venous catheter as the calcium may

cause phlebitis) does not lower potassium but decreases myocardial excitability, protecting against life threatening arrhythmias.

Insulin (e.g. intravenous injection of 10-15u of regular insulin {along with 50ml of 50%

dextrose to prevent hypoglycemia}) will lead to a shift of potassium ions into cells, secondary to increased activity of the sodium-potassium ATPase.

Bicarbonate therapy (e.g. 1 ampoule (45mEq) infused over 5 minutes) is effective in cases of

metabolic acidosis. The bicarbonate ion will stimulate an exchange of cellular H+ for Na+, thus leading to stimulation of the sodium-potassium ATPase In non-acute conditions: Restrictions of dietary potassium & potassium containing medications may suffice. E.g. eliminating the use of potassium containing salt substitutes in the patient taking a potassium conserving diuretic may be all needed to deal with mild hyperkalemia. Nursing Management: Patients at risk for potassium excess should be identified so that they can be monitored closely for signs of hyperkalemia. The nurse observes for the signs of muscle weakness & dysrhythmias. The presence of paresthesias is noted, as are GI symptoms such as nausea & intestinal colic. For patients at risk, serum potassium levels are monitored periodically.

Preventing hyperkalemia: Measures are taken to prevent hyperkalemia in patients at risk, when possible, by encouraging the patient to adhere to the prescribed potassium restriction. Potassium rich foods to be avoided include coffee, cocoa, tea, dried fruits, dried beans, & whole grain bread. Milk & egg also contain substantial amount of potassium. Foods with lower potassium content include butter, cranberry juice, ginger, hard candy, beer, sugar & honey.

Correcting Hyperkalemia: Great care should be taken to monitor potassium solutions closely, paying close attention to the solutions concentration & rate of administration. When potassium is added to parenteral solutions, the potassium is mixed the fluid by inverting the bottle several times. Potassium chloride should never be added to a hanging bottle because the potassium might be administered as a bolus.


More than 99% of the body’s calcium is located in the skeletal system; it is a major component of bones & teeth. About 1% of skeletal calcium is rapidly exchangeable with blood calcium; the rest is more stable & only slowly exchanged. The small amount of calcium located outside the bones circulates in the serum. Calcium plays a major role in transmitting nerve impulses & helps to regulate muscle contraction & relaxation, including cardiac muscle. Calcium is instrumental in activating enzymes that stimulate many essential chemical reactions in the body, & it also play a role in blood coagulation. The

normal calcium level is 8.5-10.5mg/dL.
Parathyroid hormone (PTH) and vitamin D regulate calcium balance in the body. PTH is produced by the parathyroid glands -- four small glands located in the neck behind the thyroid gland. Vitamin D is obtained when the skin is exposed to sunlight, and from dietary sources such as:
• • • •

Egg yolks Fish Fortified cereals Fortified dairy products

Hypocalcemia is the presence of low serum calcium levels in the blood, usually taken as less than 2.1
mmol/L or 9 mg/dl or an ionized calcium level mm of less than 1.1 mmol/L (4.5 mg/dL).

The causes of hypocalcemia include hypoalbuminemia, hypomagnesemia, hyperphosphatemia, multifactorial enhanced protein binding and anion chelation, medication effects, surgical effects, PTH deficiency or resistance, and vitamin D deficiency or resistance.

Hypoalbuminemia is the most common cause of hypocalcemia and is due to cirrhosis, nephrosis, malnutrition, burns, chronic illness, and sepsis.

• •

Hypomagnesemia causes end-organ resistance to PTH and inhibits the hypocalcemic feedback loop through uncertain mechanisms. Causes of hypomagnesemia include pancreatitis, aminoglycoside treatment, amphotericin B, loop diuretics, alcoholism, and malnutrition. Hyperphosphatemia may be seen in critical illness and in patients who have ingested phosphate-containing enemas. Phosphate binds calcium avidly, causing acute hypocalcemia. Multifactorial causes are probably the most clinically relevant hypocalcemic emergencies in the ED and include the following: o Acute pancreatitis: Free fatty acids chelate calcium, causing saponification in the retroperitoneum. o Sepsis can cause hypocalcemia through many mechanisms. o Toxic shock syndrome can cause hypocalcemia. o High calcitonin levels cause low calcium.

o o o o o     

Malignancy: Osteoblastic metastases (eg, breast cancer, prostate cancer) and tumor lysis syndrome may cause hypocalcemia (by differing mechanisms). Hepatic or renal insufficiency: Calciuresis, hypomagnesemia, hypoalbuminemia, and low active vitamin D levels may contribute to poor calcium homeostasis. Infiltrative disease: Sarcoidosis, tuberculosis, and hemochromatosis may infiltrate the parathyroids, causing dysfunction. Toxicologic causes include hydrofluoric acid burn or ingestion. Medication effects Proton pump inhibitors (PPIs) reduce gastric acid production resulting in reduced calcium absorption. Selective serotonin inhibitors can have a calcium antagonistic effect on smooth muscle, particularly vascular endothelium. Phenobarbital and phenytoin enhance vitamin D catabolism and decrease calcium resorption in the gut. Cimetidine decreases gastric pH, slowing fat breakdown, which is necessary to complex calcium for gut absorption. Aluminum and alcohol suppress PTH.

 

Petechia which appear as one-off spots, then later become rashes. Perioral tingling and parasthesia, 'pins and needles' sensation over the extremities of hands and Tetany, carpopedal spasm are seen. Latent tetany

feet. This is the earliest symptom of hypocalcemia.
 

Trousseau sign of latent tetany (eliciting carpal spasm by inflating the blood pressure cuff and maintaining the cuff pressure above systolic within 2-5min carpopedal (an adducted thumb, flexed wrist & metacarpophalangeal joint, extended interphalangeal joints with fingers together )spasm occur.)

Chvostek's sign (tapping of the inferior portion of the zygoma will produce facial spasms)

 

Tendon reflexes are hyperactive Life threatening complications
 

Laryngospasm Cardiac arrhythmias

Laboratory Findings:

 Elevated BUN and creatinine levels may indicate renal dysfunction  A serum calcium level less than 9 mg/dL or an ionized calcium level less than 1.1mmol/L is considered hypocalcemia  Magnesium & phosphorous levels need to be assessed to identify possible causes of decreased calcium.
 ECG and electrocardiographic monitoring should be obtained to rule out dysrhythmias and a prolonged QT interval.

Medical Management: Acute symptomatic hypocalcemia is life threatening & requires prompt treatment with IV administration of calcium (Marx, 2000). Parenteral calcium salts include calcium gluconate, calcium chloride, & calcium gluceptate. Too rapid IV administration of calcium can cause cardiac arrest, preceded by bradycardia. IV calcium should be diluted in D5W & gives as a slow IV bolus or slow IV infusion using a volumetric infusion pump. A 0.9% sodium chloride should not be used with calcium because it will increase calcium loss. Solutions containing phosphorous or bicarbonate should not be used with calcium because they will cause precipitation when calcium is added. Vitamin D therapy may be instituted to increase calcium absorption from the GI tract. Aluminum hydroxide, calcium acetate, or calcium carbonate antacids may be prescribed to decrease elevated phosphorous levels before treating hypocalcaemia for patients with chronic renal failure. Increasing the dietary intake of calcium to atleast 1000-1500mg/day in the adult is recommended (e.g. milk products, green, leafy vegetables, canned salmon, fresh oysters) Nursing Management: It is important to observe for hypocalcaemia in patients at risk. Seizure precautions are initiated when hypocalcemia is severe. The status of the airway is clearly monitored because laryngeal stridor can occur. Safety precautions are taken, as indicated, if confusion is present. People at risk for osteoporosis are instructed about the need for adequate dietary calcium intake, if not consumed in diet, calcium supplements should be considered. The value of regular weight bearing exercise in decreasing bone loss should be emphasized, as should the effect of medications on calcium balance.e.g. Alcohol & caffeine in high doses exhibit calcium absorption.


It is an elevated calcium level in the blood. (Normal range: 9-10.5 mg/dL or 2.2-2.6 mmol/L). It can be an asymptomatic laboratory finding, but because an elevated calcium level is often indicative of other.

Primary hyperparathyroidism is the most common cause of hypercalcemia and is due to excess

PTH. This excess occurs due to an enlargement of one or more of the parathyroid glands.
Other medical conditions can also lead to hypercalcemia:
• • • • • • • • •

Adrenal gland failure An inherited condition that affects the body's ability to regulate calcium A type of diuretic medication called thiazides Excess vitamin D (hypervitaminosis D) from diet or inflammatory diseases Hyperthyroidism Kidney failure Massive amounts of calcium in diet (milk-alkali syndrome) Not moving for long periods of time

Some cancerous tumors (for example, lung cancers, breast cancer)

Signs & Symptoms:
• • • Symptoms of hypercalcemia depend on the underlying cause of the disease, the time over which it develops (rapid increases in calcium cause more severe symptoms), and the overall physical health of the patient. Mild elevations in calcium levels usually have few or no symptoms. Increased calcium levels may cause the following: o Nausea o Vomiting o Alterations of mental status o Abdominal or flank pain (The workup of patients with a new kidney stone occasionally reveals an elevated calcium level.) o Constipation o Lethargy o Depression o Weakness and vague muscle/joint aches o Polyuria, polydipsia, nocturia o Headache o Confusion Severe elevations in calcium levels may cause coma. Elderly patients are more likely to be symptomatic from moderate elevations of calcium levels. Hypercalcemia of malignancy may lack many of the features commonly associated with hypercalcemia caused by hyperparathyroidism. In addition, the symptoms of elevated calcium level may overlap with the symptoms of the patient's malignancy.

• • •

Hypercalcemia associated with renal calculi, joint complaints, and ulcer disease is more likely to be caused by hyperparathyroidism.

Diagnostic Findings:
• • • • • •

Serum calcium: Changes in serum protein concentrations alter the total serum calcium level but do not affect the unbound fraction. Serum PTH: The measurement of circulating PTH in the serum is the most direct and sensitive measure of parathyroid function. A reference range is 2-6 mol/L. A nonsuppressed PTH level in the presence of hypercalcemia suggests a diagnosis of primary hyperparathyroidism Serum PTHrP: Parathyroid hormone-related peptide (PTHrP) is thought to mediate the hypercalcemia that develops with many malignancies. Urine calcium Vitamin D level Hypercalcemia may produce ECG abnormalities related to altered trans-membrane potentials that affect conduction time. QT interval shortening is common, and, in some cases, the PR interval is prolonged. At very high levels, the QRS interval may lengthen, T waves may flatten or invert and a variable degree of heart block may develop. Digoxin effects are amplified.

Medical management:

The initial step in the care of severely hypercalcemic patients is hydration with saline. Hydration helps decrease the calcium level through dilution. The expansion of extracellular volume also increases the renal calcium clearance. The rate of fluid therapy is based upon the following: o Degree of hypercalcemia o Severity of dehydration o Ability of the patient to tolerate rehydration - Vigilance to prevent volume overload is critical. o Hydration is ineffective in patients with kidney failure because diuresis is impossible. Dialysis is necessary to correct hypercalcemia in patients with renal failure. Loop diuretics o A loop diuretic (e.g., furosemide) may be used with hydration to increase calcium excretion. This may also prevent volume overload during therapy. o In contrast to loop diuretics, avoid thiazide diuretics because they increase the reabsorption of calcium. Bisphosphates - These agents will inhibit osteoclast activity for up to a month.

Treatment is directed at the cause of hypercalcemia whenever possible. In cases of hyperparathyroidism, surgery may be needed to remove the abnormal parathyroid gland and cure the hypercalcemia. Nursing Management: It is important to monitor hypercalcemia in patients at risk. Interventions such as increasing patient mobility & encouraging fluids can help prevent hypercalcemia, or at least minimize its severity. Hospitalized patient at risk for hypercalcemia are encouraged to ambulate as soon as possible; outpatients & those cared for in their homes are informed of the importance of frequent ambulation.

When encouraging oral fluids, the nurse considers the patient’s likes & dislikes. Fluids containing sodium should be administered unless contraindicated by other conditions, because sodium favors calcium excretion. Patients are encouraged to drink 3-4 quarts of fluid daily. Adequate fiber should be provided in diet to offset the tendency for constipation. Safety precautions are taken, as necessary, when mental symptoms of hypercalcemia are present. The patient & family are informed that these mental changes are reversible with treatment.

Magnesium is one of the body's major electrolytes. As the second most common intracellular cation, it plays a vital role in many cellular metabolic pathways. Magnesium is required for deoxyribonucleic acid (DNA) and protein synthesis. It is a necessary cofactor for most enzymes in phosphorylation reactions. It is also important for parathyroid hormone synthesis. The total body content of this central cation is 2000 mEq, or 24 g. The magnesium is distributed in bone (67%), intracellularly (31%), and extracellularly (a mere 1%). The intracellular concentration is 40 mEq/L, while the normal serum concentration is 1.5-2.0 mEq/L. Of this serum component, 25-30% is protein bound, 10-15% is complexed, and the remaining 50-60% is ionized. Magnesium is absorbed in the ileum and excreted in stool and urine. The minimum daily requirement of magnesium is 300-350 mg, or 15 mmol; this amount is easily obtainable with a normal daily intake of fruits, seeds, and vegetables because magnesium is a component of chlorophyll and is present in high concentrations in all green plants. The kidney is the main regulator of magnesium concentrations. Absorption occurs primarily in the proximal tubule and thick ascending limb of the loop of Henle.


Hypomagnesemia is an electrolyte disturbance in which there is an abnormally low level of magnesium in the blood. Usually a serum level less than 0.7 mmol/L is used as reference

The causes of hypomagnesemia are numerous. Most causes are related to renal and GI losses.

GI losses o Malabsorption of magnesium in the ileum results in hypomagnesemia. Situations of decreased absorption include malabsorption syndromes (eg, celiac sprue), radiation injury to the bowel, bowel resection, or small bowel bypass. o GI secretions in large amounts may cause hypomagnesemia. Upper GI secretions contain 1 mEq/L of magnesium, while lower GI secretions contain 15 mEq/L of magnesium. Significant losses of magnesium that result in hypomagnesemia may result from chronic diarrhea, laxative abuse, inflammatory bowel disease, or neoplasm. Malnutrition leads to hypomagnesemia when dietary intake of magnesium is low. Dietary sources include green vegetables, fruits, fish, fresh meat, and cereal. Alcoholics are classically hypomagnesemic in part due to poor nutrition. . Renal losses from primary renal disorders or secondary causes (eg, drugs, hormones, osmotic load) may result in magnesium wasting and subsequent hypomagnesemia.

o o



Primary renal disorders cause hypomagnesemia by decreased tubular reabsorption of magnesium by the damaged kidneys. Drugs may cause magnesium wasting.  Diuretics (e.g., thiazide, loop diuretics) decrease the renal threshold for magnesium reabsorption in addition to wasting of potassium and calcium.  Fluoride poisoning similarly causes hypomagnesemia. Endocrine disorders may cause hypomagnesemia.  Primary aldosteronism decreases magnesium levels by increasing renal flow.  Hypoparathyroidism and hyperthyroidism may cause renal wasting. Osmotic diuresis results in magnesium loss in the kidney.  Diabetic patients, especially those with poor glucose control, develop hypomagnesemia from a glucose-induced osmotic diuresis.  Alcoholics become hypomagnesemic partially by an osmotic diuresis from alcohol. Urinary losses have been reported to be 2-3 times control values.

Clinical features Deficiency of magnesium causes:

Neuromuscular irritability o Hyperactive deep tendon reflexes o Muscle cramps o Muscle fibrillation o Trousseau and Chvostek signs o Dysarthria and dysphagia from esophageal dysmotility CNS hyperexcitability o Irritability and combativeness o Disorientation o Psychosis o Ataxia, vertigo, nystagmus, and seizures (at levels <1 mEq/L) Cardiac arrhythmias that may be caused by hypomagnesemia alone or concomitant hypokalemia result from decreased activity of ATPase. o Paroxysmal atrial and ventricular dysrhythmias o Repolarization alternans Neonates o Apnea o Weakness o Seizures o Jitteriness

Laboratory Studies

Serum magnesium, calcium, potassium, and phosphorus levels o The serum magnesium level is not a reliable way to determine total body magnesium depletion because only a small fraction of magnesium in the body is extracellular. Consider obtaining an ionized magnesium level.<1.5mEq/L or 1.8mg/dL o Hypocalcemia is caused by magnesium depletion, but the reason is not known.

• • •

Some studies link hypomagnesemia to decreased parathyroid hormone levels and end-organ resistance to parathyroid hormone.  Alterations in vitamin D metabolism contribute to hypocalcemia. o Hypophosphatemia has been found in patients with hypomagnesemia. BUN and creatinine levels Blood glucose level

ECG and cardiac monitor o Findings include ST segment depression; tall, peaked T waves; flat T waves; U waves; loss of voltage; PR prolongation; and widened QRS.

Medical Management: Mild magnesium deficiency can be corrected by diet alone. Principal dietary sources of magnesium are green leafy vegetables, nuts, legumes, whole grains & seafood. Magnesium is also plentiful in peanut butter, chocolate. When necessary, magnesium salts can be administered orally to replace continuous excessive losses. Diarrhea is a common complication of excessive ingestion of magnesium. Patients receiving parenteral nutrition require magnesium in the IV solution to prevent hypomagnesemia. IV administration of magnesium sulfate must be given by an infusion pump & at a rate not to exceed 150mg/min. A bolus dose of magnesium sulfate given too rapidly can produce cardiac arrest. Vital signs must be assessed frequently during magnesium administration to detect changes in cardiac rate, rhythm, hypotension & respiratory distress. Monitoring urine output is essential before, during, & after magnesium administration. Nursing Management: The nurse should be aware of patients at risk hypomagnesemia & observe for its sign & symptoms. Patients receiving digitalis are monitored closely because deficit of magnesium can predispose them to digitalis toxicity. When hypomagnesemia is severe, seizure precautions are implemented. Other safety precautions are instituted, if confusion is observed. Because difficulty in swallowing may occur in magnesium-depleted patients, the ability to swallow should be tested with water before oral medications or foods are offered. Dysphagia is probably related to the athetoid or choreiform (rapid, involuntary, irregular jerking) movements associated with magnesium deficit. To determine neuromuscular irritability, the nurse needs to assess & grade deep tendon reflex. Teaching plays an important role in treating magnesium deficit, particularly that resulting from abuse of diuretic or laxative medications. In such cases, nurse can instruct the patient about the need to consume magnesium rich foods.


Hypermagnesemia is an electrolyte disturbance in which there is an abnormally elevated level

of magnesium in the blood. Usually this results in excess of magnesium in the body.

Hypermagnesemia occurs rarely because the kidney is very effective in excreting excess magnesium. It usually develops only in people with kidney failure who are given magnesium salts or who take drugs that contain magnesium (e.g. some antacids and laxatives). It is usually concurrent with hypocalcemia and/or hyperkalemia

Most cases of hypermagnesemia are due to iatrogenic interventions and administration,1 especially errors in calculating appropriate infusions. Additional causes include the following:
• • • • •

• • • • • • •

Ingestion of magnesium-containing substances such as vitamins, antacids, or cathartics by patients with chronic renal failure Acute renal failure (in the absence of dialysis) Excessive intravenous infusions of magnesium in patients being treated for eclampsia, asthma, torsade de pointes, or other cardiac arrhythmias In neonates, treatment of maternal eclampsia with magnesium, which passes through the placental circulation Decreased GI elimination and increased GI absorption of magnesium due to intestinal hypomotility from any cause o GI medications that decrease motility, including narcotics and anticholinergics o Hypomotility disorders such as bowel obstruction and chronic constipation Adrenal insufficiency (secondary hypermagnesemia) Rhabdomyolysis, like tumor lysis syndrome, by releasing significant amounts of intracellular magnesium Hypothyroidism Hypoparathyroidism Neoplasm with skeletal muscle involvement Lithium intoxication Extracellular volume contraction, as in diabetic ketoacidosis

    

Weakness, nausea and vomiting Impaired breathing Hypotension Hypocalcemia Arrhythmia and Asystole

Arrhythmia and asystole are possible cardiac complications of hypermagnesemia. Magnesium acts as physiologic calcium blocker, which results in electrical conduction abnormalities.
Laboratory Studies

Electrolytes, including potassium, magnesium, and calcium levels o A test for ionized magnesium is clinically available. The serum magnesium level is often used as an initial study in the ED.> 2.5mEq/L or 3.0mg/dL

• •

Elevation in magnesium level is usually not found as an isolated electrolyte abnormality. o Hyperkalemia and hypercalcemia are often present concurrently. BUN and creatinine levels o Obtain renal function tests and calculate creatinine clearance to assess the ability of the kidney to excrete magnesium. o Serum magnesium levels rise when creatinine clearance is less than 30 mL/min. Arterial blood gases (ABG) may reveal a respiratory acidosis.

An ECG and cardiac monitor may show prolongation of the PR interval or intraventricular conduction delay, which are nonspecific findings.

Medical Management:
Treatment depends upon the level of magnesium and the presence of symptoms. In patients with mildly increased levels, simply stop the source of magnesium. In patients with higher concentrations or severe symptoms, other treatments are necessary. In patients with severe hypermagnesemia, all parenteral & oral magnesium salts are discontinued. In emergency such as respiratory depression or defective cardiac conduction, ventilatory support & IV calcium are indicated. In addition hemodialysis with a magnesium free dialysate can reduce the serum magnesium to a safe level within hours. should be reserved for patients with life-threatening symptoms, such as arrhythmia or severe respiratory depression. Nursing Management: Patients at risk for hypermagnesemia are identified & assessed. When hypermagnesemia is suspected, the nurse monitors the vital signs, noting hypertension & shallow respirations. The nurse also observes for decreased patellar reflexes & changes in the level of consciousness. Medications that contain magnesium are not given to patients with renal failure or compromised renal function, and patients with renal function are cautioned to check with their health care providers before taking over-the-counter medications. Caution is essential when preparing & administering magnesium containing fluids parenterally because available parenteral magnesium differ in concentration.

 CHLORIDE IMBALANCE • Hypochloremia: It occurs when sodium level falls below 100meq/L.

Causes: 1. Vomiting or prolonged & excessive nasogastric or fistula drainage. 2. Increased chloride secretion due to administration of certain diuretics. 3. Diarrhea in newborn.

Hyperchloremia: It occurs when serum sodium level rises above 106meq/L resulting in decreased bicarbonate value. ACID BASE IMBALANCE

An excess of acid is called acidosis (pH less than 7.35) and an excess in bases is called alkalosis (pH greater than 7.45). The process that causes the imbalance is classified based on the etiology of the disturbance (respiratory or metabolic) and the direction of change in pH (acidosis or alkalosis). This yields the following four basic processes:

Disturbance Respiratory Acidosis Respiratory Alkalosis Metabolic Acidosis Metabolic Alkalosis

Plasma PH

Plasma PCO2

Plasma HCO3

Disturbance of acid based balance RESPIRATORY ACIDOSIS  Increased pCO2 and pH below 7.35 due to

hypoventilation, emphysema etc. Compensation occurs in the kidney through increased H+ excretion and HCO3reabsorption. Bicarbonate/carbonic acid ratio is 10-15:1. RESPIRATORY ALKALOSIS  Hyperventilation due to O2 deficiency, CVA, or anxiety are causes of respiratory alkalosis. Renal compensation occurs by decreasing H+ excretion and HCO3reabsorption.  H+ is reabsorbed. Bicarbonate/carbonic acid ratio is 30-40:1. METABOLIC ACIDOSIS  Due to loss of HCO3- by diarrhea, ketoacidosis, keto acids from a high protein diet, high stomach acidity, anaerobic fermentation, and renal disease. Compensation occurs by an increase in respiration rate. Bicarbonate/carbonic acid ratio is 10-15:1. METABOLIC ALKALOSIS

 Increased intake of antacids, low protein/high vegetable diet, and vomiting/loss of HCl are common causes. Compensation is by hypoventilation. Bicarbonate/carbonic acid ratio is 35:1. Summary:
The main fluid in the body is water. Total body water is 60% of body weight. The water is distributed in three main compartments separated from each other by cell membranes. The intracellular compartment is the area within the cell. The extracellular compartment consists of the interstitial area (between and around cells) and the inside of the blood vessels (plasma).

Electrolytes are minerals in your body that have an electric charge. They are in your blood, urine and body fluids. Maintaining the right balance of electrolytes helps our body's blood chemistry, muscle action and other processes. Sodium, calcium, potassium, chlorine, phosphate and magnesium are all electrolytes.

 Potter & Perry, Fundamentals of nursing, 6th Edition, Elsevier publishers, Pp 1136-1152  Smeltzer et al., Textbook of Medical Surgical Nursing, 10th Edition, Lippincott Williams &
Wilkins publishers, Pp 250-276.

 En .wikipedia.Org  