A SEMINAR ON

FLUID VOLUME IMBALANCES

SUBMITTED TO SUBMITTED BY

Mrs. Suja Salman Habeeb

Assistant professor 1st year M.Sc nursing

Govt college of nursing Govt college of nursing

Alappuzha Alappuzha

FLUID VOLUME IMBALANCES

INTRODUCTION

Fluid and electrolyte imbalances occur to some degree in most patients with a major illness and injury because illness disrupts the normal homeostatic mechanism. Some imbalances occur due to the direct effect of the illness of injury. e.g. burns. At other times therapeutic measures such as fluid replacement; diuretics can cause or contribute to fluid and electrolyte imbalance.

The imbalances are commonly classified as deficits or excesses. In actual clinical situations, more than one imbalance occurring in the same patient is common. For example, a patient with prolonged nasogastric suction will lose Na+, K+, H+, and Cl- . These imbalances may result in a deficiency of both Na+ and K+ , as well as metabolic alkalosis and fluid volume deficit.

AMOUNT AND COMPOSITION OF BODY FLUIDS

Approximately 60% of the weight of a typical adult consists of fluid. Factors that influence the amount of body fluid are age, gender, and body fat. In general, younger people have a higher percentage of body fluid than older people, and men have proportionately more body fluid than women. Body fluid is located in two fluid compartments: the intracellular space (fluid in the cells) and the extracellular space (fluid outside the cells). Approximately two thirds of body fluid is in the intracellular fluid compartment and is located primarily in the skeletal muscle mass. Approximately one third in the extra cellular fluid compartmented.

The ECF compartment is further divided into the intravascular, interstitial, and transcellular fluid spaces. The intravascular space ( the fluid within the blood vessels) contains plasma, the effective circulating volume. Approximately 3 L of the average 6 L of blood volume is made up of plasma. The interstitial space contains the fluid that surrounds the cell and totals about 11 to 12 L in an adult. Lymph is an interstitial fluid. The transcellular space is the smallest division of the ECF compartment and contains approximately 1 L. Examples include CSF, pericardial, synovial etc.

Body fluid normally shifts between the two major compartments or spaces in an effort to maintain equilibrium between the spaces. Loss of fluid from the body can disrupt this equilibrium. Sometimes fluid is not lost from the body but is unavailable for use by either the ICF or ECF. Loss of ECF into a space that does not contribute to equilibrium between the ICF and the ECF is referred to as a third-space fluid shift, or “third spacing” Third spacing is the unusual accumulation of fluid in a transcellular

space.  . Early evidence of a third-space fluid shift is a decrease in urine output despite adequate fluid intake. Other signs and symptoms of third spacing that indicate an intravascular fluid volume deficit include increased heart rate, decreased blood pressure, edema, increased body weight, and imbalances in fluid intake and output (I & O). third space occur in patients who have hypocalcemia, severe liver diseases, alcoholism etc.

REGULATION OF BODY FLUID COMPARTMENTS

OSMOSIS AND OSMOLALITY

When two different solutions are separated by a membrane that is impermeable to the dissolved substances, fluid shifts through the membrane from the region of low solute concentration to the region of high solute concentration until the solutions are of equal concentration. This diffusion of water caused by a fluid concentration gradient is known as osmosis. OSMOLALITY the concentration of a solution in terms of osmoles of solute per kilogram of solvent The number of dissolved particles contained in a unit of fluid determines the osmolality of a solution, which influences the movement of fluid between the fluid compartments. Normal values range from 275 to 295 milliosmoles per kilogram. Tonicity is the ability of all solutes to cause an osmotic driving force that promotes water movement from one compartment to another. The control of tonicity determines the normal state of cellular hydration and cell size. Three other terms are associated with osmosis: osmotic pressure, oncotic pressure, osmotic dieresis.

Osmotic pressure is the amount of hydrostatic pressure needed to stop the flow of water by osmosis. It is primarily determined by the concentration of solutes.

Oncotic pressure is the osmotic pressure exerted by proteins (eg albumin)

Osmotic dieresis is the increase in urine output caused by the excretion of substances such as glucose, mannitol, or contrast agents in the urine.

DIFFUSION

Diffusion is the natural tendency of a substance to move from an area of higher concentration to one of lower concentration. It occurs through the random movement of ions and molecules. Example of diffusion is the tendency of sodium to move from the ECF compartment, where the sodium concentration is high, to the ICF, where its concentration is low.

FIILTRATION

Hydrostatic pressure in the capillaries tends to filter fluid out of the intravascular compartment to the interstitial fluid. Movement of water and solutes occurs from an area of high hydrostatic pressure to an area of low hydrostatic pressure. The kidneys filter

approximately 180 L of plasma per day. Another example of filtration is the passage of water and electrolytes from the arterial capillary bed to the interstitial fluid.

SODIUM-POTASSIUM PUMP

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

SYSTEMIC ROUTES OF GAINS AND LOSSES

Water and electrolytes are gained in various ways. Healthy people gain fluids by drinking and eating, and their daily average intake and output of water are approximately equal.

Kidneys

The usual daily urine volume in the adult is 1 to 2 L. A general rule is that the output is approximately 1 mL of urine per kilogram of body weight per hour (1 ml/kg/h) in all age groups.

Skin

Sensible perspiration refers to visible water and electrolyte loss through the skin (sweating). The chief solutes in sweat are sodium, chloride and potassium. Actual sweat losses can vary from 0 to 1000ml or more every hour, depending on factors such as the environmental temperature. Continuous water loss by evaporation (approximately 600 mL/day) occurs through the skin as insensible perspiration, a nonvisible form of water loss.

Lungs

The lungs normally eliminate water vapor (insensible loss) at a rate of approximately 300 mL every day. The loss is much greater with increased respiratory rate or depth, or in a dry climate.

Gastrointestinal tract

The usual loss through the GI tract is 100 to 200 mL daily, even though approximately 8 L of fluid circulates through the GI system every 24 hours. Because the

bulk of fluid is normally reabsorbed in the small intestine, diarrhea and fistulas cause large losses.

AVERAGE DAILY INTAKE AND OUTPUT IN AN ADULT

Intake (ml) output (ml)

Oral fluids 1300 urine 1500

Water in food 1000 Stool 200

Water produced

in metabolism 300 Insensible

Lungs 300

Skin 600

Total gain 2600 Total loss 2600

HOMEOSTATIC MECHANISMS

The body is equipped with remarkable homeostatic mechanisms to keep the composition and volume of body fluid within narrow limits of normal. Organs involved in homeostasis include :

Kidney functions

Vital to the regulation of fluid and electrolyte balance, the kidneys normally filter 180 L of plasma every day in the adult and excrete 1 to 2 L of urine. They act both autonomously and in response to blood borne messengers, such as aldosterone and antidiuretic hormone (ADH) . major functions of the kidneys in maintaining normal fluid balance include the following:

Regulation of ECF volume and osmolality by selective retention and excretion of body fluids.

Regulation of normal electrolyte levels in the ECF by selective electrolyte retention and excretion.

Regulation of pH of the ECF by retention of hydrogen ions.

Excretion of metabolic wastes and toxic substances..

HYPOTHALAMIC REGULATION

A body fluid increase or decrease in plasma osmaolality is sensed by osmoreceptors Located on the surface of hypothalamus, osmoreceptos sense changes in sodium concentration. As osmotic pressure increases, the neurons become dehydrated stimulates thirst and quickly release impulses to the posterior pituitary, which increases the release of ADH, which then travels in the blood to the kidneys, where it alters permeability to water, causing increased reabsorption of water and decreased urine output. The retained water dilutes the ECF and returns its concentration to normal. Restoration of normal osmotic pressure provides feedback to the osmoreceptors to inhibit further ADH release.

ADH and the thirst mechanism have important roles in maintaining sodium concentration and oral intake of fluids. Oral intake is controlled by the thirst centre located in the hypothalamus. As serum concentration or osmolality increases or blood volume decreases, neurons in the hypothalamus are stimulated by intracellular dehydration; thirst then occurs, and the person increases his or her intake of oral fluids. The presence or absence of ADH is the most significant factor in determining whether the urine that is excreted is concentrated or dilute.

Pituitary functions

The hypothalamus manufactures ADH, which is stored in posterior pituitary gland and released as needed to conserve water. Functions of ADH include maintaining the osmotic pressure of the cells by controlling the retention or excretion of water by the kidneys and by regulating blood volume.

Adrenal functions

Aldosterone, a mineralocorticoid secreted by the zona glomerulosa (outer zone) of the adrenal cortex, has a profound effect on fluid balance. Increased secretion of aldosterone causes sodium retention, and potassium loss. Conversely decreased secretion of aldosterone causes sodium and water loss and potassium retention.

Heart and blood vessel functions

The pumping action of the heart circulates blood through the kidneys under sufficient pressure to allow for urine formation. Failure of this pumping action interferes with renal perfusion and thus with water and electrolyte regulation

Release of Natriuretic Peptide

Atrial natriuretic peptide (ANP) also called atrial natriuretic factor, is a peptide that is synthesized, stored, and released by muscle cells of the atria of the heart in response to several factors. These factors include increased atrial pressure, angiotensin11 stimulation, and sympathetic stimulation. The action of ANP is the direct opposite of the rennin-angiotensin-aldosterone system; ANP decreases blood pressure and volume. The ANP released in plasma is normally 20 to 77 ng/ml

Parathyroid function

The parathyroid gland regulate calcium and phosphate balance by means of parathyroid hormone(PTH). PTH influences bone resorption, calcium absorption from the intestines and calcium reabsorption from the renal tubules.

Lung functions

The lungs are also vital in maintaining homeostasis. Through exhalation lungs remove approximately 300 mL of water daily in the normal adult. Abnormal conditions such as, hyperpnea (abnormally deep respiration) or continuous coughing, increase this loss; mechanical ventilation with excessive moisture decreases it.

Other mechanisms

Rennin-Angiotensin-Aldosterone System

Rennin is an enzyme that converts angiotensinogen, a substance formed by the liver, into angiotensin 1. Rennin is released by the juxteglomerular cells of kidneys in response to decreased renal perfusion. Angiotensin-converting enzyme(ACE) converts angiotensin 1 to angiotensin 11. Angiotensin 11 with its vasoconstrictor properties increases arterial perfusion pressure and stimulates thirst. As the sympathetic nervous system is stimulated, aldosterone is released in response to an increased release of rennin. Aldosterone is a volume regulator and is also released as serum potassium increase, serum sodium decreases, or adrenocorticotropic hormone (ACTH) increases.

Baroreceptors

The baroreceptors are located in the left atrium and carotid and aortic arches. These receptors respond to changes in the circulating blood volume and regulate sympathetic and parasympathetic neural activity as well as endocrine activities. As arterial pressure decreases, baroreceptors transmit fewer impulses from the carotid and aortic arches to the vasomotor centre. A decrease in impulses stimulate the sympathetic nervous system and inhibits the parasympathetic nervous system. The outcome is an increase in cardiac rate, conduction and contractility and an increasing circulating blood volume. Sympathetic stimulation constricts renal arterioles, this increases the release of aldosterone, decreases glomerular filtration, and increases sodium and water reabsorption.

FLUID VOLUME IMBALANCES

Iso-osmotic volume expansion

Iso-osmotic volume contraction

Hyperosmotic volume contraction

Hypo-osmotic volume expansion

Hypo-osmotic volume contraction

Iso-osmotic volume expansion

Causes of iso osmotic volume expansion include

Infusion of isotonic fluids eg; .9% Nacl solution.

Extracellular fluid volume increases

Extracellular fluid osmolality does not change .so water does not shift between the ECF and icf

plasma protien concentration decreases because of dilutional effect of additional fluid ,resulting in decresed plasma colloid osmotic pressure ,water moves out of blood vessel and disturbed in the interstitial compartment.

Haematocrit decreases because of addition of fluid to ECF dilutes RBC. Because ECF osmolality is unchanged the RBC neither shrink or swell

Arterial blood pressure increases because ECF volume increases

corrective response

Change in plasma volume is sensed by vascular volume receptors and brings about excretion of large volume of hypotonic urine(water dieresis) which gradually restores the plasma volume and osmolality to normal

ISO-OSMOTIC VOLUME CONTRACTION

Causes

Iso-osmotic volume contraction occurs because of loss of isotonic fluid in following conditions :

Diarrhoea, vomiting

Haemorrhage

Ascitis and burns

consequences

ECF volume decresed

ECF osmolality does not change ,so water does not shift between the ECF and ICF compartments

Plasma protein concentration is increased because of loss of ECF concentrates .Due to presence of plasm protein ,the plasma volume is less reduced as compared to interstitial fluid.

Haematocrit is increased because of loss of ECF concentrates the RBCs.because ECF osmolality is unchanged ,the RBC will neither shrink nor swell

Arterial blood pressure is decresded because of decreased in ECF volume.

corrective response

Decreased plasma volume inhibits the vascular volume sensors and reflexly restores the plasma volume by decreasing Na+ and water excretion .it is important to note that the

thirst produced by volume receptors is quenched with isotonic salt solution instead of plain water.

HYPEROSMOTIC VOLUME EXPANSION

Causes .

Hyperosmotic volume expansion results when excessive amount of hypertonic saline is administered.

consequences

ECF osmolality is increased ,because osmoles (nacl) have been added to ECF

Water shifts from ICF to ECF ,as a result of this shift ICF osmolaity increases until it equals that of ECF

ECF volume increases because of addition of fluid as well as shift from ICF to ECF ( volume expansion)

ICF volume is decreased due to fluid shift

Plasma protein concentration decreases becauses of the increases in ECF volume

Haematocrit decreases because of increase in ECF VOLUME .RBC shrink and ECF osmolality is increased .

Arterial blood pressure is increased because of increase in ECF volume

corrective response

Increased plasma osmolality promotes water retention while increase in plasma volume inhibits the same .under such circumstances volume oversides tonicity .Therefore ,the increased plasma volume would suppress thirst and ADH leading to excretion of large volume of hypotonic urine which bring down the plasma volume. The natriuretic hormones ,which is secreted only ,in response to osmolality and not to volume changes,promotes na+ excretion and corrects osmolality.

HYPEROSMOTIC VOLUME CONTRACTION

CAUSES :

hyperosmotic volume contration occurs due to loss of water In following conditions

Decresed water intake

Diabetes mellitus

Diabetes insipidus

Excessive sweating in a desert

Alcoholism

In tracheostomy patients ,insensible loss of water upto 500ml occurs from lungs

CONSEQUENCES

ECF volume is reduced because of loss of water

ECF osmolality increases because more water is lost

Water shifts from ICF ti ECF ,as a result of this shift ,ICF osmolality increases until it equals that of ECF

ICF volume decreases because of shift of water

Plasma protein concentration increases becauses of the decrease in ECF volume

Haematocrit is also expected to increase ,but it remains unchanged because water shifts out of RBC s decreasing their volume and offsetting the concentrating effects of the decreased ECF volume

CORRECTIVE RESPONSE

Increased ECF osmolality stimulates the osmoreceptors ,while reduced plasma volume inhibits the volume receptors .Either of them would relexly restore the plasma osmolality to normal level.

HYPO-OSMOTIC VOLUME EXPANSION

CAUSES .

Hypo-osmotic volume expansion occurs due to gain of water in following conditions

Syndrome of inappropriate anti diuretic hormone secretion

Ingestion of large volume of water

Rectocolonic washouts with plain water

CONSEQUENCES

ECF osmolality decreses because of the excess water retention

ECF volume increases because of excess water retention

Water shift from ECF to ICF increasing the volume of ICF

ICF osmolality decreses until it equals ECF osmolality

Plasma proteins concentration decrease because of increase in the ECF volume

corrective response

The Vascular volume receptors and osmoreceptors sense the changes in plasma volume and osmolality ,respectively .the signals from either of them lead to excretion of large volume of hypotonic water which gradually restores the blood volume and osmolality to normal

HYPO –OSMOTIC VOLUME CONTRACTION

Causes

Causes hypo-osmotic volume contraction results from loss of Nacl or hypotonic fluid from the body in following conditions

Adrenocotical insufficiency is associated with renal loss of nacl

Vomiting or aspiration of gastric secretions is associated with hypertonic fluid loss from the body

CONSEQUENCES

ECF osmolality is decreased because of loss of NaCl or other solutes

Water shifts from ECF to ICF ,increasing the volume of ICF and decreasing the ECF volume

ICF osmollity decreases until it equals ECF osmolality

Plasma volume and osmolality changes tend to parallel those ECF .However a decrease in plasma protein concentration .due to raised colloid oncotic pressure the shift of fluid from the plasma to interstitial fluid is decreased .because of this plasma volume is better preserved than is the volume of interstitial fluid .However in severe cases ,the plasma volume reduces sufficiently to produce a shock like state with signs of renal failure but unlike in shock there is no sensation of thirst

Haematocrit increases because of the decrease in ECF volume and because the RBC s well as result of water entry

Arterial blood pressure decreases because of decrease in ECF volume

CORRECTIVE RESPONSES

The ECF volume is decreased but thirst is absent : this seems to be nature”s defence mechanisms ,since any water ingested would promptly leave the ECF and expand the ICF further .Therefore ,salt craving or salt apittite which stimulate the individual to consume a large amount of Nacl is useful in restoring ECF osmolality . normalization of ECF osmolality shifts water from ICF to ECF shrinks the cells of thirst centre and restore the thirst.consequently ,drinking of water restores the remaining deficits in ECF volume

HYPOVOLEMIA

Fluid volume deficit (FVD) or hypovolemia, occurs when loss of ECF volume exceeds the intake of fluid. It occurs when water and electrolytes are lost in the same proportion as they exist in normal body fluids, so that the ratio of serum electrolytes to water remains the same. FVD may occur alone or in combination with other imbalances.

PATHOPHYSIOLOGY

FVD results from loss of body fluids and occurs more rapidly when coupled with decreased fluid intake. FVD can develop from inadequate intake alone if the decreased intake is prolonged.

ETIOLOGY AND RISK FACTORS

Vomiting, Diarrhea ,GI suctioning, Sweating, Decreased intake as in nausea or inability to gain access to fluids., Diabetes insipidus,Adrenal insufficiency,Osmotic dieresis,Hemorrhage,Coma, Third-space fluid shifts or the movement of fluid from the vascular system to other body spaces (eg. With edema formation in burns, ascites with liver dysfunction also cause FVD.

CLINICAL MANIFESTATIONS

FVD can develop rapidly and can be mild, moderate, or severe depending on the degree of fluid loss. Clinical signs and symptoms include

o Acute weight loss, Decreased skin turgor, Oliguria, Concentrated urine, Postural hypotension, A weak, rapid heart rate, Flattened neck veins, Increased temperature, Decreased central venous pressure

o Cool, clammy skin related to peripheral vasoconstriction.

o Thirst,Anorexia, Nausea, Lassitude, Muscle weakness, Cramps.

DIAGNOSTIC FINDINGS

BUN and its relation to serum creatinine concentration: a volume depleted patient has a BUN elevated out of proportion to the serum creatinine (ratiogreater than 20:1). The BUN can be elevated because of dehydration or decreased renal perfusion and function.

Health history and physical examination

Hematocrit value: hematocrit value is greater than normal because there is decreased plasma volume.

Hypokalemia occurs with GI and renal losses.

Hyperkalemia occurs with adrenal insufficiency.

Hyponatremia occurs with increased thirst and ADH release

Hypernatremia results from increased insensible losses and diabetes insipidus.

Serum electrolytes: potassium or sodium level can be reduced or elevated.

Urine specific gravity: increased in relation to the kidneys’ attempt to conserve water.

Urine osmolality is greater than 450mOsm/kg, because the kidneys try to compensate by conserving water.

MANAGEMENT

MEDICAL MANAGEMENT

The seriousness of a client’s manifestations and the aggressiveness of treatment are related to both the amount and acuteness of fluid loss, and the client’s state of health at the time of loss. Sudden loss of fluid does not give the compensatory mechanisms time to adapt; severe loss is often beyond the potential of compensatory mechanisms to adapt, resulting in vascular collapse or shock. A thorough history and physical examination, including collection of such demographic variables such as age , gender, culture, presence of chronic diseases and socioeconomic status, are critical to identifying realistic and measurable outcomes.

Medical treatment of fluid volume deficit depends on the acuteness and severity of the fluid deficit. The goals of treatment are to restore normal fluid volumes by using fluids similar in composition to those lost, to replace ongoing losses, and to correct the underlying problem (such as vomiting or diarrhea).

FLUID RESTORATION

Oral rehydration. If the fluid loss is mild, the thirst mechanism is intact and the client can drink fluid, replace the fluid orally. Oral glucose replacement solutions are palatable, inexpensive, and a good source of fluid, glucose and electrolytes. These solutions are quickly absorbed when the client has diarrhea or is vomiting. Cola drinks should be avoided because they do not contain adequate electrolyte replacement, the sugar content may lead to osmotic dieresis , and the caffeine may lead to diuresis.

Intravenous rehydration. When the fluid loss is severe or life threatening, intravenous fluids are used for replacement. The volume of fluid is calculated on the basis of the client’s weight and the presence of any other co- morbidities such as cardiac, renal, liver or pulmonary disorders that would decrease the ability of the body to rid excess fluids. The type of solution used is based on on the type of fluid lost from the body. Isotonic solutions (eg. Lactated Ringer’s solution, 0.9% sodium chloride) are frequently used to treat the hypotensive patient with FVD they expand plasma volume. As soon as the patient becomes normotensive, a hypotonic electrolyte solution ( eg. 0.45% sodium chloride) is often used to provide both electrolytes and water for renal excretion of metabolic wastes.

Monitoring for complications of fluid restoration. Accurate and frequent assessment of I&O, weight, vital signs, central venous pressure, level of consciousness, breath

sounds, and skin color should be performed to determine when therapy should be slowed to avoid volume overload. The rate of fluid administration is based on the severity of loss and the patient’s hemodynamic response to volume replacement. A client with severe FVD accompanied by severe heart, kidney, pulmonary or liver disease cannot tolerate large volumes of fluid or sodium without the risk for development of heart failure. For unstable clients, monitors are used to detect increasing pressures from fluids (eg. Measurement of right atrial and pulmonary artery pressure). Urine output, body weight, and laboratory values of sodium, osmolality, urea/nitrogen(BUN), and potassium are monitored closely.

Fluid challenge test. If the patient with severe FVD is not excreting enough urine and is therefore oliguric, the primary health care provider needs to determine whether the depressed renal function is caused by reduced renal blood flow secondary to FVD or more seriously by acute tubular necrosis from prolonged FVD. The test used in this situation is referred to as a fluid challenge test. During a fluid challenge test, volumes of fluids are administered at specific rates and intervals while the patient’s hemodynamic response to this treatment is monitored( ie, vital signs, breath sounds, sensorium, urine output, CVP).

A typical example of fluid challenge involves administering 100 to 200 ml of normal saline solution over 15 minutes. The goal is to provide fluids rapidly enough to attain adequate tissue perfusion without compromising the cardiovascular system. The response by a patient with FVD but normal renal function is increased urine output and an increase in blood pressure and central venous pressure.

Correction of the underlying problem. Antiemetic and antidiarrheal drugs may be prescribed to correct problems with nausea and vomiting or diarrhea. Antibiotics may be used in clients with infectious diarrhea. Antipyretic agents may be used to reduce body temperature.

NURSING MANAGEMENT

T o assess for FVD, the nurse monitors and measures fluid I&O, at least every 8 hours, and sometimes hourly. As FVD develops, body fluid losses exceed fluid intake through excessive urination, diarrhea, vomiting or other mechanisms. Be certain that all sourcesof intake( including liquids with meals and between meals, with medications, in IV lines, in tube feedings) and all sources of output (urine, diarrhea, diaphoresis and hyperventilation) be recorded accurately. Absence of adequate renal perfusion for several hours may result in permanent renal damage. Whenever the output decreases to less than 0.5 ml/ kg/hr for two consecutive hours, urine output must be assessed hourly.

Monitor plasma sodium, urea/nitrogen, glucose and hematocrit values to determine plasma osmolality.

Determine a history of chronic illnesses that may impair the ability to tolerate fluids at rapid speeds. Lung, heart, and renal disease reduce the body’s ability to move fluids through the vascular system. Record the client’s lung sounds on admission to serve as a baseline for later comparison.

Daily body weights are monitored, an acute loss of 0.5 kg represents a fluid loss of approximately 500 ml ( 1 litre of fluid weighs approximately 1 kg).

Vital signs are closely monitored. The nurse observes for a weak, rapid pulse and orthostatic hypotension. A decrease in body temperature often accompanies FVD, unless there is a concurrent infection.

Skin and tongue turgor are monitored on a regular basis. In a healthy person pinched skin immediately returns toits normal position when released. In a person with severe FVD the skin may remain elevated for many seconds. Tissue turgor is best measured by pinching the skin over the sternum, inner aspects of thighs, or forehead. Tongue turgor is not affected by age and is more valid than evaluating skin turgor. In a normal person tongue has one longitudinal furrow. In the person with FVD, there are additional longitudinal furrows, and the tongue is smaller, because of fluid loss.

The degree of oral mucous membrane is also assessed ; a dry mouth may indicate either FVD or mouth breathing.

Urine concentration is monitored by measuring the urine specific gravity. In a volume depleted patient, the urine specific gravity should be greater than 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 Hypovolemia:

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

Correcting Hypovolemia:

When possible, oral fluids are administered to help correct FVD, with consideration given to the patient’s likes and dislikes. If the patient is reluctant to drink

because of oral discomfort, the nurse assists with frequent mouth care and provides non irritating fluids. The patient may be offered small volumes of oral rehydration solutions. These solutions provide fluid, glucose, and electrolytes in concentrations that are easily absorbed. If nausea is present, antiemetics may be needed before oral fluid replacement can be tolerated.

If the deficit cannot be corrected by oral fluids, therapy may need to be initiated by an alternative route (enteral or parenteral) until adequate circulating blood volume and renal perfusion are achieved. Isotonic fluids are prescribed to increase ECF volume.

NURSING DIAGNOSES

Deficient fluid volume related to insufficient fluid intake, vomiting, diarrhea or third space fluid loss such as ascites or burns.

Outcomes. The desired outcome is return of normal level of body fluids.

Interventions:

Restore oral fluid intake

Give small amounts of fluids ‘of choice’ hourly.

Keep fluids fresh and within reach.

If a client’s lips are dry, wet the lips and mouth first to facilitate sucking.

Give antiemetics as needed to control nausea before drinking.

When appropriate begin with clear liquids, progress to full liquids and then to solid foods, if tolerated without vomiting or aspiration.

Encourage family members to participate in feeding.

Restore Fluids by Intravenous Routes

Administer IV fluids cautiously to clients with FVD. Ideally a large IV gauge (18 to 20 gauge) should be used; however most clients have venous collapse, and it is difficult to find a vein. A small IV site may be used initially; once fluids are reestablished, a larger needle can be inserted if fluids or an IV access is still needed.

Use an IV pump to regulate IV infusion and to decrease the decrease the risk of too rapid an infusion.

Monitor IV solutions, IV sites, and client outcomes hourly.

Control the Underlying Problems

Give prescribed antiemetics for nausea, antipyretics for fever, and antibiotics for infection.

Avoid fatty or fried foods also decreases diarrhea and enhances digestion.

If lactose intolerance is the cause for diarrhea encourage the client to avoid milk based products.

Monitor for Complications

When fluid balance is compromised, a person is at risk for tissue breakdown. Apply a moisturizer or skin barrier to protect the skin from the irritants, enzymes, and microorganisms found in urine and feces.

Continue to assess lung sounds for manifestations of fluid overload (crackles) from overcorrection.

Impaired oral mucus membrane related to lack of oral intake or other causes.

Outcomes. The client’s tongue, gums, and lips should become moist and the mouth, gums, and teeth should be clean and free of accumulations and dried mucus.

Interventions:

Give oral care with a regular toothbrush or a foam toothbrush every 2 to 4 hours, and apply lip moisturizer.

Rinse the client’s mouth every 1 to 2 hours.

Examine the client’s mouth with a penlight to make it sure that it remains free of debris.

Avoid mouthwashes with alcohol base, which can dry the mucus membranes.

Artificial saliva can also be used for the client with a very dry and fissured mouth.

Risk for injury related to orthostatic hypotension.

Outcomes. The client will remain free of injury as evidenced by no manifestations of falls or reported episodes of falls.

Interventions

Provide safety through step-progression position changes. Step-progression gives the client’s body to adapt to changes in position. First raise the head of the bed. Next, assist to sit at the edge of the bed in a dangling position until the dizziness has subsided. Have the client stand stand, and assist the client to a chair.

Restraints may be needed if all other measures to control behavior do not work.

HYPERVOLEMIA

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

ETIOLOGY

Compromised regulation of fluid movement and excretion

Cirrhosis of the liver, decreased plasma protein, heart failure, hypothyroidism, lymphatic or venous obstruction, renal disorders.

Excessive ingestion of fluids or foods containing sodium

Excessive amounts of saline intravenous fluids, Ingestion of high-sodium foods, Excessive use of enemas with sodium or medications with sodium

Increased antidiuretic hormone (ADH) and aldosterone

Certain barbiturates and narcotics (eg. Morphine), Cushing’s syndrome, general anesthesia, glucocorticoid use, hyperaldosteronism, Syndrome of inappropriate ADH (secretion).

PATHOPHYSIOLOGY

With a fluid volume excess, the hydrostatic pressure of the fluid is higher than usual at the arterial end of the capillary, pushing excess fluids into the interstitial spaces. The fluid is not absorbed at the venous end of the capillary because the oncotic pressure is too low to pull the fluids back across the capillary membrane. Usually the residual fluids are removed by the lymphatics, but in the case of edema, the fluid volume overloads the lymph system and stays in the interstitial space, leading to peripheral edema.

CLINICAL MANIFESTATIONS

Clinical manifestations of FVE result from expansion of the ECF and include:

o Edema, Distended neck veins, Coughing, dyspnea,crackles (abnormal lung sounds), Tachycardia, Increased blood pressure, Increased pulse pressure, Increased CVP, Increased weight, Increased urine output, Shortness of breath and wheezing.

ASSESSMENT AND DIAGNOSTIC FINDINGS

BUN and Hematocrit values. Both of these values may be decreased because of plasma dilution. Other causes include low protein intake and anemia.

In chronic renal failure , both serum osmolality and sodium level are decreased due to excessive retention of water.

The urine sodium level is increased if the kidneys are attempting to excrete excess volume.

A chest X-ray may reveal pulmonary congestion.

Hypervolemia occurs when aldosterone is chronically stimulated (ie, cirrhosis, heart failure, and nephritic syndrome). Therefore , the urine sodium level does not increase in these conditions.

MEDICAL MANAGEMENT

Management of FVE is directed at the causes, and if related to excessive administration of sodium-containing fluids, discontinuing the infusion may be all that is needed. Symptomatic treatment consists of administering diuretics and restricting fluids and sodium.

Pharmacologic Therapy

Diuretics are prescribed when dietary restriction of sodium alone is insufficient to reduce edema by inhibiting the reabsorption of sodium and water by the kidneys. The choice of diuretic is based on the severity of the hypervolemic state, the degree of impairment of renal function, and the potency of the diuretic. Thiazide diuretics block sodium reabsorption in the distal tubule, where only 5% to 10% of filtered sodium is reabsorbed. Loop diuretics such as furosemide (lasix) or torsemide can cause a greater loss of both sodium and water because they block sodium reabsorption in the ascending limb of the loop of Henle, where 20% to 30% of filtered sodium is normally reabsorbed. Generally, thiazide diuretics, such as hydrochlorothiazide (HydroDIURIL) or metalazone are prescribed for mild to moderate hypervolemia and loop diuretics for severe hypervolemia.

Electrolyte imbalances may result from the effect of the diuretic. Hypokalemia can occur with all diuretics except those that work in the last distal tubule of the nephrons.

Potassium supplements can be prescribed to avoid this complication. Hyperkalemia can occur with diuretics that work in the last distal tubule (spironolactone) especially in patients with decresed renal function. Decreased magnesium levels occur with administration of loop and thiazide diuretics due to decreased reabsorption and increased excretion of magnesium by the kidney.

Dialysis

If renal function is so severely impaired that pharmacologic agents cannot act efficiently, other modalities are considered to remove sodium and fluid from the body. Hemodialysis or peritoneal dialysis may be used to remove nitrogenous wastes and control potassium and acid-base balance, and to remove sodium and fluid. Continuous renal replacement therapy may also be required.

Nutritional Therapy

Treatment of FVE usually involves dietary restriction of sodium. An average daily diet not restricted in sodium contains 6 to 15 g of salt, whereas low sodium diets can range from a mild restriction to as little as 250 mg of sodium per day, depending on the patient’s needs. It is the sodium salt, sodium chloride rather than sodium itself that contributes to edema. Therefore, patients are instructed to read food labels carefully to determine salt content. A mildly restricted sodium diet contains 4 to 5 g of sodium, a moderately restricted diet contains 2 g of sodium, and a severely restricted diet contains 0.5 g of sodium.

NURSING MANAGEMENT

Assessment

Monitor the client”s vital signs for a bounding pulse, elevated blood pressure or both every 4 to 8 hours.

Assess the apical pulse if the radial pulse is irregular or if the client is taking cardiac medication.

Assess the breath sounds every 4 to 8 hours for crackles especially in the bases of the lung, rhonchi, or wheezes. Assess for changes in respiratory effort with activity and rest.

Each morning , palpate the sacrum and legs for pitting edema and observe the client for hand and bilateral neck vein engorgement. Jugular vein distention at or above a 45-degree headrest suggests FVE. Hand veins that do not flatten within 3 to 5 seconds when the hand is raised above the heart level suggests fluid overload.

Assess the condition of skin on the legs. Edematous skin is fragile and is at risk for injury and decreased perfusion, which may lead to pressure sores.

Compare I&O every 4 to 8 hours. Weigh the client daily. Determine whether the client has had expected weight loss or unexpected weight gain.

Monitor plasma osmolality, sodium level, hematocrit, and urine specific gravity. Observe for changes in level of consciousness, which may indicate the more serious complication of ICF shifting.

Preventing hypervolemia

Most patients require sodium restricted diets in some form, and adherence to the prescribed diet is encouraged.

Patients are instructed to avoid over-the-counter medications without first checking with a health care provider, because these substances may contain sodium.

Detecting and Controlling Hypervolemia

Regular rest periods may be beneficial, because bed rest favors diuresis of edema fluid. The mechanism is probably related to diminished venous pooling and the subsequent increase in effective circulating blood volume and renal perfusion.

Sodium and fluid restriction should be instituted as indicated.

Monitor the patient’s response to diuretics.

The rate of parenteral fluids and the patient’s response to these fluids are also closely monitored.

If dyspnea or orthopnea present, the patient is placed in a semi-Fowler’s position to promote lung expansion.

The patient is turned and repositioned at regular intervals because edematous tissue is more to skin breakdown than normal tissue.

Taught patients to monitor their response to therapy by documenting fluid I&O and body weight changes.

Teaching Patients About Edema

Because edema is a common manifestations of FVE, patients need to recognize its symptoms and understand its importance. The nurse gives special attention to edema when teaching the patient with FVE. Edema can occur as a

result of increased capillary fluid pressure, decreased capillary oncotic pressure, or increased interstitial oncotic pressure, causing expansion of the interstitial fluid compartment. Edema can be localized (eg. In the ankle, as in rheumatoid arthritis) or generalized (as in cardiac and renal failure). Severe generalized edema is called anasarca.

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 the increased ECF volume. Obstruction to lymphatic outflow, a plasma albumin level less than 1.5 to 2 g/dl, or a decrease in plasma oncotic pressure contributes to increased interstitial fluid volume. A thorough medication history is necessary to identify any medications that could cause edema, such as NSAIDs, estrogens, corticosteroids, and antihypertensive agents.

Ascites is a form of edema in which fluid accumulates in the peritoneal cavity, it results from nephritic syndrome, cirrhosis and some malignant tumors. The patient commonly reports shortness of breath and a sense of pressure because of pressure on the diaphragm.

The goal of treatment is to preserve or restore the circulating intravascular fluid volume. Thus, in addition to treating the cause of the edema, other treatments may include diuretic therapy, restriction of fluids and sodium, elevation of the extremities, application of anti-embolism stockings, paracentesis, dialysis, and continuous renal replacement therapy in cases of renal failure or life-threatening fluid volume overload.

NURSING DIAGNOSIS

Excess fluid volume related to specific cause such as heart, renal or liver failure.

Outcomes: The desired outcome is return of normal levels of body fluids.

Interventions

Strict I&O may be crucial. Include fluids on meal trays and those given with medications as part of the total fluid intake.

Give the client ice chips, if allowed and provide frequent oral care to decrease the thirst sensation.

Teach the client to hold the water in their mouth for a while to rehydrate the tongue, rather than swallowing it quickly.

Instruct client about the rationale for fluid and sodium restrictions.

Use IV pump to control IV fluid intake. Use only isotonic saline for bladder and nasogastric tube irrigations.

Suggest alternatives for seasoning , such as lemon, garlic or pepper to enhance the taste of foods and increase dietary compliance.

Instruct the client who has dependent leg edema to avoid long periods of standing and to sit with legs elevated.

Elevate the head of the bed 30 to 45 degree to decrease venous return, which decreases cardiac workload and allows for improved diaphragmatic excursion both of which improve oxygenation.

If the client is taking digitalis and diuretics, monitor plasma electrolytes and anticipate digitalis toxic effects resulting from hypokalemia. Report the abnormal levels of plasma electrolytes, especially potassium levels.

When peripheral tissue perfusion is altered because of edema or vascular disease, provide frequent skin care, turn the client often, control moisture, and prevent friction and shear.

CONCLUSION

Fluid volume imbalances make emergency when they are not corrected Adequetly the nurse can assess,prevent the fluid volume imbalances by keen observation and assessment

ELECTROLYTE IMBALANCE

ELECTROLYTES

Electrolytes are substances whose molecules dissociate or split into ions when placed in water. Ions are electrically charged particles. Cations are positively charged particles. Examples include sodium, potassium, calcium and magnesium. Anions are negatively charged ions. Examples include bicarbonate, chloride and phosphate ions. Electrolytes are important because they are what cells (especially nerve, heart, muscle) use to maintain voltages across cell membranes and to carry electrical impulses (nerve impulses, muscle contractions) across themselves and to other cells. The kidneys work to keep the electrolyte concentrations in the blood constant despite changes in the body.

Electrolyte concentrations in the ICF differ from those in the ECF. Sodium ions, which are positively far outnumber the other cations in the ECF. Because sodium concentration affects the overall concentration of the ECF, sodium is important regulating the volume of body fluid. Retention of sodium is associated with fluid retention, and excessive loss of sodium is usually associated with decreased volume of body fluid. The major electrolytes in the ICF are potassium and phosphate. The ECF ha a low concentration of potassium and can tolerate only small changes in potassium.concentrations.therefore the release of large stores of intracellular potassium, typically caused by trauma to the cells and tissues can be extremely dangerous.

Electrolyte imbalances are common, so to help clients achieve the most positive health outcomes, you must understand the underlying causative disorders and conditions as well as the risk factors for electrolyte imbalance and become an active participant in health promotion, health maintenance, and health restoration interventions.

ETIOLOGY AND RISK FACTORS

Anyone who has decreased intake, decreased availability, or increased loss of electrolytes is at risk for electrolyte deficit. When body fluids are lost, the electrolytes in them are also lost. For exam[le. The loss of gastric juice through vomiting may lead to the loss of several electrolytes. Conversely, increased intake or increased retention of an electrolyte or decreased ability to excrete certain electrolytes may increase the risk for

electrolyte excess. For example, ingestion of excess sodium bicarbonate for indigestion can alter both sodium level and acid-base balance.

PATHOPHYSIOLOGY

Physiology of Action Potential

Conduction of electrical current depends on normal membrane permeability, transportation of electrolytes, and ion concentration. Common problems that alter the conduction of electrical current include problems with membrane permeability, ionic gradients, and concentrations. Cells are quickly damaged by lack of blood flow or oxygen. Cardiac, nerve and muscle cells can be damaged by lack of blood flow, altered by toxins (as from various medications), or directly injured (as in crush or stab injuries). Such damage typically increases the permeability of the cell membranes and increases its tendency to “fire”. This phenomenon can be seen in cardiac cells after ischemia.

Potassium levels can significantly influence the resting membrane potential. When potassium levels are lower than normal, the resting membrane potential becomes more positive. It requires less stimulus to make it fire. Cells so affected are called hypopolarised and respond to a weaker stimulus. Conversely, when potassium levels are higher, the resting membrane potential decreases and the cell is less excitable. Such cells are called hyperpolarized and require a stronger-than normal stimulus to reach threshold potential and to generate an action potential. Sodium and calcium also alter resting membrane potential.

SODIUM IMBALANCES

Sodium is the most abundant electrolyte in the ECF. Sodium plays a major role in maintaining the concentration and volume of the ECF. Sodium is important in the generation and transmission of nerve impulses and the regulation of acid-base balance. Serum sodium is measured in milliequivalents per litre or millimoles per litre. The GI tract absorbs sodium from foods. Sodium leaves the body through urine, sweat, and feces. The kidneys are the primary regulator of sodium balance. Sodium deficit is known as hyponatremia. Sodium excess is known as hypernatremia.

HYPONATREMIA

A serum sodium level of less than 135mEq/L is considered hyponatremia. This condition occurs with an actual decrease in the amount of extracellular sodium or an increase in the extracellular fluid volume, resulting in dilutional hyponatremia. Sodium loss can be caused by diuretic use, vomiting, severe burns, lack of dietary sodium, and intracellular sodium shifts. Conditions causing extracellular fluid accumulation include heart failure, hepatic failure, excess ADH secretion, and hyperglycemia. The four types of hyponatremic states are as follows:

Hypovolemic hyponatremia Euvolemic hyponatremia Hypervolemic hyponatremia Redistributive hyponatremia

When sodium loss is greater than water loss, hypovolemic hyponatremia occurs. Euvolemic hyponatremia results when the total body water(TBW) is moderately increased and the total body sodium remains at a normal level. Hypervolemic hyponatremia results when a greater increase occurs in TBW than in total body sodium. In redistributive hyponatremia, no change occurs in TBW or total body sodium; water merely shifts between the intracellular and extracellular compartments relative to the sodium concentration.

CLINICAL CONDITIONS AND DISORDERS THAT MAY CAUSE HYPONATREMIA

Type of Hyponatremia clinical conditions and disorders

Hypovolemic hypo natremia renal loss of sodium from diuretic use, diabetic glycosuria, aldosterone deficiency, intrinsic renal disease. External loss of sodium from vomiting, diarrhea, increased sweating, burns, high volume ileostomy.

Euvolemic hyponatremia sodium deficit resulting from SIADH or the increased secretion of ADH due to pain, emotion, medications, some cancers and CNS disorders.

Hypervolemic hyponatremia edematous disorders resulting in sodium deficits, congestive heart failure, cirrhosis of the liver, nephritic syndrome, acute and chronic renal failure.

Redistributive hyponatremia pseudohyponatremia,hyperglycemia, hyperlipidemia

PATHOPHYSIOLOGY

Most pathophysiologic changes caused by hyponatremia results from the decreased excitability of the membranes from a loss of sodium and changes in water volume. Most of the sodium is outside the cell. Less sodium is available to move across the excitable membrane, resulting in delayed membrane depolarization. Excitable tissues vary in their response to decreased sodium. The cells most sensitive to change are the central nervous system (CNS) cells.

As the concentration of sodium decrease in the ECF, the difference in the gradient between the ECF and ICF compartment also decreases. When the extracellular sodium level decreases, the ECF becomes hypo-osmolar. This osmotic shift can lead to intracellular edema. Water moves into the cell to the area of greater concentration to rebalance the water concentration.

CLINICAL MANIFESTATIONS

Clinical manifestations of hyponatremia depend on the cause, magnitude, and speed with which the deficit occurs.

Poor skin turgor, dryness of the skin, dry mucosa, headache, decreased saliva production.

Neurological changes including altered mental status, status epilepticus, and coma are probably related to the cellular swelling and cerebral edema associated with hyponatremia.

Acute decreases in sodium, developing in less than 48 hours may be associated with brain herniation and compression of mid brain structures. Chronic decreases in sodium, developing over 48 hours or more can occur in status epilepticus and cerebral pontine myelinolysis.

Features of hyponatremia associated with sodium loss and water gain include anorexia, muscle cramps, and a feeling of exhaustion. When the serum sodium level decreases to less than 115mEq/L signs of increasing intracranial pressure such as lethargy, confusion, muscle twitching, focal weakness, hemiparesis, papilledema, seizures, and death may occur.

Cardiovascular manifestations- such as decrease in systolic and diastolic blood pressures, orthostatic hypotension , and a weak thready pulse. Tachycardia is a compensatory response that is the direct result of triggering of the release of sympathetic catecholamines by the baroreceptor reflex.

In severe hypovolemic hyponatremia, a shock like state occurs with blood pressures of 60 mmof Hg and below. An exception is hypervolemic

hyponatremiain which the excess volume causes elevated blood pressure and a full rapid pulse.

Crackles in the lungs are from fluid shifting into the pulmonary alveoli secondary to increasing fluid pressures in the pulmonary capillaries. The changes in respiratory rate and difficulty breathing such as tachypnea, dyspnea, orthopnea and feeling of short of breath are from presence of fluid in the alveoli.

Hyponatremia causes GI manifestations such as nausea, vomiting, hyperactive bowel sounds, abdominal cramping and diarrhea.

Patient with SIADH retains water abnormally and therefore gains body weight, there is no peripheral edema; instead fluid accumulates inside the cells. This phenomenon sometimes manifests as pitting edema.

DIAGNOSTIC FINDINGS

History and physical examination, including a focused neurologic examination.

Serum sodium less than 135mEq/L, SIADH less than 100mEq/L, serum osmolality is also decreased, urinary sodium content less than 20mEq/L, urine specific gravity is low (1.002 to 1.004).

MEDICAL MANAGEMENT

The key to treating hyponatremia is assessment including identifying patients who are at risk and recognizing that the rapidity of onset of hyponatremia is of primary importance.

Sodium Replacement

The most common treatment for hyponatremia is careful administration of sodium by mouth, nasogastric tube, or a parenteral route. Intake of balanced diet is usually adequate therapy for mild hyponatremia, with sodium levels of 126 to 135 mEq/L.

If the plasma sodium level declines below 125mEq/L, sodium replacement is needed. For sodium levels of 125mEq/L or less intravenous therapy is the treatment of choice. Dietary supplementation may still be appropriate for a client who can ingest oral fluids or food.

For moderate hyponatremia, with sodium levels of of 125mEq/L, IV normal saline solution (0.9% NaCl) or lactated Ringer’s solution may be ordered if the client is symptomatic.

When the plasma sodium level is 115mEq/L, or less a concentrated saline solution such as 3% NaCl may be indicated until the plasma sodium reaches 125mEq/L.

Rapid elevation of plasma sodium concentrations to more than 125mEq/L increases intravascular fluid volume and may result in hypernatremia and CNS damage. Recommendations for IV replacement therapy include an infusion rate of 0.5 mEq/L if the loss is chronic, not to exceed a total of 12 mEq of sodium in 48 hours, or of 1 mEq/L if the loss is acute, not to exceed 25 mEq in 48 hours.

To prevent fluid shifts and exacerbation of vasospasm in persons with subarachnoid hemorrhage, normal saline is usually the IV solution of choice.

Water Restriction

In a patient with normal or excess fluid volume, hyponatremia is treated by restricting fluid to a total of 800 ml in 24 hours. This is far safer than sodium administration and is usually an effective treatment. If neurologic symptoms are severe as well as in traumatic brain injury, it may be necessary to administer small volumes of a hypertonic sodium solution. If edema exists alone, sodium is restricted; if edema and hyponatremia occur together, both sodium and water are restricted.

Pharmacologic Therapy

A diuretic such as furosemide is often given intravenously to prevent pulmonary fluid overload. Demeclocycline, an agent that antagonizes ADH is the preferred agent for treatment of hyponatremia resulting from syndrome of inappropriate antidiuretic hormone (SIADH).

NURSING MANAGEMENT

Take a complete history of risk factors and presenting manifestations. Collect complete and detailed information on the client’s diet and medications, including over-the-counter and herbal medications.

Measure the client’s body weight, because the stated weight may not be accurate. Compare the client’s height and weight to the body mass index (BMI) chart. Assess intake and output, peripheral vein filling time, and vital signs every 4 to 8 hours. Monitor plasma sodium levels and estimate the plasma osmolality. It is important to remember that in hyonatremic conditions, such as hypervolemic hyponatremia, plasma sodium level may appear to be normal to low.

NURSING DIAGNOSIS

Hyponatremia related to unreplaced loss or limited intake.

Outcome: the desired outcome is normal level of serum sodium.

Interventions

For a patient with abnormal losses of sodium who can consume a general diet, the nurse encourages foods and fluids with high sodium content.

If the primary problem is water retention it is safer to restrict fluid intake than to administer sodium. In severe hyponatremia the aim of therapy is to elevate the serum sodium level only enough to alleviate neurologic signs and symptoms.

Encourage the intake of a well-balanced diet. If the client is receiving nutrition only through tube feedings, it is sometimes necessary to add extra salt to the feeding to achieve the desired sodium level.

To decrease the thirst that accompanies fluid restriction , offer ice chips, cold fluids and frequent oral care.

When plasma sodium levels are 125 mEq/L or less and the client is symptomatic, notify the physician immediately. Administration of hypertonic IV saline (3% saline) is the most commonly prescribed therapy. Hypertonic saline must be given very slowly by IV piggyback infusion in a large vein to decrease the risk of hypernatremia, pulmonary overload, and phlebitis. If the client is confused or agitated , also initiate safety and seizure precautions.

For the patient taking lithium, the nurse observes for lithium toxicity, particularly when sodium is lost by an abnormal route. Because diuretics promote sodium loss, the patient taking lithium is instructed not to use diuretics without close 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 (as in SIADH).

Actual fluid needs are determined by evaluating fluid I&O, urine specific gravity, and serum sodium levels.

HYPERNATREMIA

Hypernatremia is defined as a plasma sodium level greater than 145mEq/L.it can be caused by a gain of sodium in excess of water or by a loss of water in excess of

sodium. It can occur in patients with normal fluid volume or in those with FVE or FVD. With a water loss, the patient loses more water than sodium; as a result the serum sodium concentration increases and the increased concentration pulls fluid out of the cell.

ETIOLOGY AND RISK FACTORS

A common cause of hypernatremia is fluid deprivation in unconscious patients who cannot perceive, respond to, or communicate their taste. Most often affected are very old, very young and cognitively impaired patients.

o Increased sodium intake, such as with IV administration of hypertonic saline or hypertonic tube feedings.

o Retention of sodium occurs with heart, renal and liver disease.

o Cushing’s syndrome, hyperaldosteronism, corticosteroid therapy, uncontrolled diabetes mellitus and diabetes insipidus

o Less common causes include heat stroke, near drowning in sea water (which contains a sodium concentration of approximately 500 mEq/L), and malfunction of hemodialysis or peritoneal dialysis systems.

o IV administration of hypertonic saline or excessive use of sodium bicarbonate also causes hypernatremia.

PATHOPHYSIOLOGY

When sodium level increase,water moves to maintain balance. The osmotic shift of water from the cells to the ECF in an attempt to dilute hyperosmolar state only creates another problem; cellular dehydration. If the hypernatremia evolves slowly slowly or is chronic, the brain brain develops its own osmoles, to prevent fluid shifts into and out of the brain cells.

The body responds to increased sodium levels by suppressing the effects of aldosterone and ADH. These two substances normally act to increase renal blood flow and cause excretion of sodium and water. In hypernatremia the magnitude of the problem overwhelms the ability of these adaptive mechanisms to compensate.

CLINICAL MANIFESTATIONS

Early manifestations include polyuria followed by oliguria, anorexia, nausea, vomiting, weakness, and restlessness.

Early neurologic manifestations include restlessness, agitation, irritability, and muscle weakness are related to the sensitivity of brain cells to fluid shifting.

As fluid level decrease in the interstitial compartments, the skin becomes dry and flushed, the mucous membrane become dry and sticky, and tongue furrows develop. The person experiences increased thirst and fever.

Cardiovascular manifestations are a hypertensive blood pressure, jugular venous distention, prolonged peripheral vein emptying, S3 gallop, and generalized weight gain and edema .

Pulmonary manifestations are crackles, dyspnea, and pleural effusion.

When sodium level reaches 155mEq/L or more cells (especially brain cells) shrink because of the increased ECF osmolality. More severe neurologic changes occur manifested as confusion, seizures, or coma , in some cases with irreversible brain damage. Altered neuromuscular contractility and irritability lead to muscle twitching, tremor, hyperreflexia, and seizures. The development of rigid paralysis is a grave sign.

DIAGNOSTIC FINDINGS

Serum sodium

Serum osmolality – exceeds 300 mmol/L

Urine specific gravity and urine osmolality.

MEDICAL MANAGEMENT

Medical management is determined by the type of hypernatremia. The goal of medical intervention is correction of the body water osmolality, with restoration of cell volume, by decreasing the ratio of sodium to water in the ECF.

To decrease total boody sodium and replace fluid loss, eithet a hypo-osmolar electrolyte solution (0.2% or 0.45% NaCl) or 5% dextrose in water (D5W)is administered. If the plasma sodium level is lowered too rapidly , fluid shifts from the vascular fluid into the cerebral cells,causing cerebral edema. Slow administration of IV fluids with a goal of reducing plasma sodium levels, at a rate of not more than 2mEq/L for the first 48 hours, decreases this risk.

Hypernatremia caused by sodium excess may be treated with administration of D5W and a diuretic, such as furosemide. When hypernatremia results from diabetes insipidus, desmopressin acetate, in the form of a nasal spray, is commonly ordered to slow the rate of diuresis.

Although dietary sodium restriction is useful in preventing hypernatremia in high risk clients, it cannot bring a high level down to normal. People with renal disease may

need sodium intake restricted to 500 to 2000 mg/day. Clients with diabetes insipidus who are receiving antidiuretic medications must be taught to avoid excessive water intake. Drinking excess water defeats the purpose of the medication.

NURSING MANAGEMENT

ASSESSMENT

Assess for the usual clinical manifestations, especially in head-injured and high risk clients. Obtain a thorough diet and medication history, including the use of corticosteroids and over the counter medications, such as cough medicine, herbals, food flavorings and spices.

Assess vital signs and peripheral vein filling time every 4 to 8 hours, measure intake and output every 8 hours, and monitor body weight daily.

Report early signs of altered mental status, such as agitation, irritability, or confusion that may indicate progression of hypernatremia or hyponatremia.

Monitor lung sounds every 2 to 4 hours, and notify the physician of increasing pulmonary overload.

NURSING DIAGNOSES

Hypernatremia related to decreased thirst, excessive administration of salt solutions or impaired excretion of sodium and water.

Outcomes: the nurse will maintain a high index of suspicion for high risk clients and will monitor plasma sodium and chloride levels and clinical manifestations of hyper natremia.

Interventions

Monitor the client for response to IV fluid replacement of hypo-osmolar electrolyte solutions, absence of clinical manifestations, and to return to normal sodium levels.

Initiate safety and seizure precautions if the client manifests weakness or cerebral changes.

Offer water and fluids hourly to clients with hypovolemic or euvolemic hypernatremia.

Teach the client and family members the food items that should be restricted as well as the rationale for these restrictions

Consult the physician for manifestations that indicate worsening of the hypernatremia or fluid overload, such as increasing weight gain or pulmonary, cardiovascular, or neurologic manifestations.

Impaired oral mucous membrane related to lack of body water secondary to hypernatremia

Provide oral care every 2 hours with a nonalcoholic mouthwash.

Dilute saline and nonalcoholic rinses have been found to be effective.

Use a soft tooth brush to prevent injury to mucosa.

Offer cool non acidic fluids such as apple juice. Limited ice chips may also decrease the discomfort from dry mucous membrane.

Assess the mouth before and after mouthcare and be aggressive in cleaning the mouth.

POTASSIUM IMBALANCES

HYPOKALEMIA

Hypokalemia refers to the condition in which the concentration of potassium (K+) in the blood is low. Normal serum potassium levels are between 3.5 to 5.0 mEq/L.At least 95% of the body's potassium is found inside cells, with the remainder in the blood. This concentration gradient is maintained principally by the Na+/K+ pump.

ETIOLOGY AND RISK FACTORS

Hypokalemia can result from one or more of the following medical conditions:

Inadequate potassium intake

Perhaps the most obvious cause is insufficient consumption of potassium (that is, a low-potassium diet) or starvation. However, without excessive potassium loss from the body, this is a rare cause of hypokalemia.

Gastrointestinal/integument loss

A more common cause is excessive loss of potassium, often associated with heavy fluid losses that "flush" potassium out of the body. Typically, this is a consequence of diarrhea, excessive perspiration, or losses associated with surgical procedures. Vomiting can also cause hypokalemia, although not much potassium is lost from

the vomitus. Rather, there are heavy urinary losses of K+ in the setting of post-emetic bicarbonaturia that force urinary potassium excretion.Other GI causes include pancreatic fistulae and the presence of adenoma.

Urinary loss

Certain medications can cause excess potassium loss in the urine. Diuretics, including thiazide diuretics (e.g. hydrochlorothiazide) and loop diuretics (e.g. furosemide) are a common cause of hypokalemia. Other medications such as the antifungal, amphotericin B, or the cancer drug, cisplatin, can also cause long-term hypokalemia.

A special case of potassium loss occurs with diabetic ketoacidosis. In addition to urinary losses from polyuria and volume contraction, there is also obligate loss of potassium from kidney tubules as a cationic partner to the negatively charged ketone, β-hydroxybutyrate.

Hypomagnesemia can cause hypokalemia. Magnesium is required for adequate processing of potassium. This may become evident when hypokalemia persists despite potassium supplementation. Other electrolyte abnormalities may also be present.

Alkalosis can cause transient hypokalemia by two mechanisms. First, the alkalosis causes a shift of potassium from the plasma and interstitial fluids into cells; perhaps mediated by stimulation of Na+-H+ exchange and a subsequent activation of Na+/K+-ATPase activity.Second, an acute rise of plasma HCO3

- concentration (caused by vomiting, for example) will exceed the capacity of the renal proximal tubule to reabsorb this anion, and potassium will be excreted as an obligate cation partner to the bicarbonate. Metabolic alkalosis is often present in states of volume depletion, so potassium is also lost via aldosterone-mediated mechanisms.

Disease states that lead to abnormally high aldosterone levels can cause hypertension and excessive urinary losses of potassium. These include renal artery stenosis and tumors (generally non-malignant) of the adrenal glands, e.g., Conn's syndrome (primary hyperaldosteronism). Cushing's syndrome can also lead to hypokalaemia due to excess cortisol binding the Na+/K+ pump and acting like aldosterone.

Distribution away from ECF

In addition to alkalosis, other factors can cause transient shifting of potassium into cells, presumably by stimulation of the Na-K-ATPase. These hormones and medications include insulin, epinephrine, and other beta agonists (e.g. salbutamol or salmeterol), and xanthines (e.g. Theophylline)

Rare hereditary defects of muscular ion channels and transporters that cause hypokalemic periodic paralysis can precipitate occasional attacks of severe hypokalemia and muscle weakness. These defects cause a heightened sensitivity to the normal changes in potassium produced by catechols and/or insulin and/or thyroid hormone, which lead to movement of potassium from the extracellular fluid into the muscle cells.

Pseudohypokalemia

Pseudohypokalemia is a decrease in the amount of potassium that occurs due to excessive uptake of potassium by metabolically active cells after blood has been drawn. It is a laboratory artifact that may occur when blood samples remain in warm conditions for several hours before processing.

Other factors associated with an increased risk of hypokalemia include Cushing’s syndrome, the diuretic phase of renal failure, hypoaldosteronism, liver disease, cancer, wounds, and Bartter’s syndrome, a chronic electrolyte wasting syndrome.

PATHOPHYSIOLOGY

Potassium is essential for many body functions, including muscle and nerve activity. The electrochemical gradient of potassium between the intracellular and extracellular space is essential for nerve function; in particular, potassium is needed to repolarize the cell membrane to a resting state after an action potential has passed. Decreased potassium levels in the extracellular space will cause hyperpolarization of the resting membrane potential. This hyperpolarization is caused by the effect of the altered potassium gradient on resting membrane potential as defined by the Goldman equation. As a result, a greater than normal stimulus is required for depolarization of the membrane in order to initiate an action potential.

In certain conditions, this will make cells less excitable. However, in the heart, it causes myocytes to become hyperexcitable. Lower membrane potentials in the atrium may cause arrhythmias because of more complete recovery from sodium-channel inactivation, making the triggering of an action potential more likely. In addition, the reduced extracellular potassium (paradoxically) inhibits the activity of the IKr potassium current and delays ventricular repolarization. This delayed repolarization may promote reentrant arrythmias

CLINICAL MANIFESTATIONS

Mild hypokalemia is often without symptoms, although it may cause a small elevation of blood pressure, and can occasionally provoke cardiac arrhythmias. Moderate hypokalemia, with serum potassium concentrations of 2.5-3 mEq/L (Nl: 3.5-5.0 mEq/L), may cause muscular weakness, myalgia, and muscle cramps (owing to disturbed function

of the skeletal muscles), and constipation (from disturbed function of smooth muscles). With more severe hypokalemia, flaccid paralysis and hyporeflexia may result. There are reports of rhabdomyolysis occurring with profound hypokalemia with serum potassium levels less than 2 mEq/L. Respiratory depression from severe impairment of skeletal muscle function is found in many patients.

Some electrocardiographic (ECG) findings associated with hypokalemia include flattened or inverted T waves, a U wave, ST depression and a wide PR interval. Due to prolonged repolarization of ventricular Purkinje fibers, a prominent U wave occurs, that is frequently superimposed upon the T wave and therefore produces the appearance of a prolonged QT interval. Potassium level less than 2.5 mEq/L increase the risk of ventricular fibrillation and cardiac arrest.

Pulmonary manifestations of shallow respirations, shortness of breath and apnea. The progressive neurologic consequences of altered nerve conduction are manifested as dysphasia, confusion, depression, convulsions, areflexia, and coma. Extreme smooth muscle slowing leads to vomiting and anileus as well as urinary retention.

DIAGNOSTIC FINDINGS

Serum potassium ECG

An ECG in a person with a potassium level of 1.1 showing the classical ECG changes of ST

segment depression, inverted T waves, large U waves, and a slightly prolonged PR interval.

24-hour urinary potassium excretion test

MEDICAL MANAGEMENT

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. As this is often part of a poor nutritional intake, potassium-containing 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 (IV) supplementation. Typically, a saline solution is used, with 20-40 mEq KCl per liter over 3–4 hours. Giving IV 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. Even in severe hypokalemia, oral supplementation is preferred given its safety profile. Sustained release formulations should be avoided in acute settings.

Difficult or resistant cases of hypokalemia may be amenable to a potassium-sparing diuretic,such as amiloride, triamterene ,or spironolactone. Concomittant hypomagnesiumemia will inhibit potassium replacement as magnesium is a cofactor for potassium uptake.

When replacing potassium intravenously, infusion via a 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. The practice of adding lidocaine, however, raises the likelihood of serious medical errors.

NURSING MANAGEMENT

ASSESSMENT

Assessment focuses on identifying risk factors for hypokalemia through history taking and a thorough physical examination. Obtain a history that focuses on dietary intake, conditions promoting potassium loss, and use of diuretics, cortisone, over the counter medications, and herbals.

Review lab results of potassium levels. Report even borderline plasma potassium levels to the physician, especially in high risk clients, particularly those about to undergo surgery. Consult the physician about the need for potassium supplementation in anyone who has been on NPO status

or who has an obvious cause of potassium loss or marked decrease in potassium intake.

Assess cardiac function, including apical pulses, and renal function every hour in the client with severe hypokalemia. Assess neuromuscular and bowel function every 4 to 8 hours. A urine output of 0.5 ml/kg/hr is necessary to prevent rebound hyperkalemia.

Hypokalemia increases the risk of digitalis toxicity, if the client receives digitalis monitor for nausea, anorexia, vomiting, diarrhea, marked change in cardiac rate and rhythm.

NURSING DIAGNOSES

Hypokalemia related to vomiting, diarrhea, Cushing’s disease, prolonged or intensive diuretic use, cortisone therapy, decreased intake, NPO status.

Outcomes: the client’s potassium level will be 3.5 to 5 mEq/L.

INTERVENTIONS

Give oral or IV potassium as prescribed, ensuring that it is diluted in IV fluids; it cannot be given as an IV push.

Monitir IV sites hourly for phlebitis, infiltration, and rate of infusion. Change IV sites every 72 hours or sooner if the vein becomes tender to palpation.

Notify the physician if signs of hypokalemia persist or worsen, such as dysrhythmias of increasing severity, or if signs of over correction occur, such as manifestations of hyperkalemia.

During administration of IV potassium, consult the physician if the clients urine output is less than 0.5 ml/kg/hr for 2 consecutive hours, or if the pulse deficit is greater than 20 beats/min, or if signs of impaired peripheral tissue peerfusion are present.

Anticipate the need for additional potassium with increased IV glucose, such as in total parenteral nutrition (TPN); increased insulin levels result in shifting of potassium into the cell.

Risk for injury related to muscle weakness and hypotension or seizures secondary to hypokalemia.

Outcomes: the client will be at reduced risk of injury, as evidenced by an absence of falls, near falls, bruises, contusions, seizures.

INTERVENTIONS

Employ safety and seizure precautions to reduce the risk of injury. Keep the bed in a low position with padded side rails up.

Before the client walks, clear the path of obstacles and place nonslippery shoes and a gait belt on the client.

Use restraints only after all other alternatives to prevent inadvertent harm to self or others have been tired.

Imbalanced nutrition: less than body requirements related to insufficient intake of foods rich in potassium.

Outcomes: the client will demonstrate improved nutrition, as evidenced by consumption of adequate amounts of food and fluid to maintain a normal potassium level.

INTERVENTIONS

Instruct the client to choose and consume foods rich in potassium . Instruct the client to take potassium supplements with a glass or more of

water or juice and food to decrease GI irritation.

HYPERKALEMIA

Hyperkalemia refers to the condition in which the concentration of the electrolyte potassium (K+) in the blood is elevated. Extreme hyperkalemia is a medical emergency due to the risk of potentially fatal abnormal heart rhythms (arrhythmia).

Normal serum potassium levels are between 3.5 and 5.0 mEq/L; at least 95% of the body's potassium is found inside cells, with the remainder in the blood. This concentration gradient is maintained principally by the Na+/K+ pump.

ETIOLOGY AND RISK FACTORS

Ineffective elimination

Renal insufficiency Medication that interferes with urinary excretion:

o ACE inhibitors and angiotensin receptor blockers

o Potassium-sparing diuretics (e.g. amiloride and spironolactone)

o NSAIDs such as ibuprofen, naproxen, or celecoxib

o The calcineurin inhibitor immunosuppressants ciclosporin and tacrolimus

o The antibiotic trimethoprim

o The antiparasitic drug pentamidine

Mineralocorticoid deficiency or resistance, such as:

o Addison's disease

o Aldosterone deficiency

o Some forms of congenital adrenal hyperplasia

o Type IV renal tubular acidosis (resistance of renal tubules to aldosterone)

Gordon's syndrome (“familial hypertension with hyperkalemia”), a rare genetic disorder caused by defective modulators of salt transporters, including the thiazide-sensitive Na-Cl cotransporter.

Excessive release from cells

Rhabdomyolysis, burns or any cause of rapid tissue necrosis, including tumor lysis syndrome

Massive blood transfusion or massive hemolysis

Shifts/transport out of cells caused by acidosis, low insulin levels, beta-blocker therapy, digoxin overdose, or the paralyzing agent succinylcholine

Excessive intake

Excess intake with salt-substitute, potassium-containing dietary supplements, or potassium chloride (KCl) infusion. Note that for a person with normal kidney function and nothing interfering with normal elimination (see above), hyperkalemia by potassium intake would be seen only with large infusions of KCl or oral doses of several hundred milliequivalents of KCl.

Pseudohyperkalemia

Pseudohyperkalemia is a rise in the amount of potassium that occurs due to excessive leakage of potassium from cells, during or after blood is drawn. It is a laboratory artifact

rather than a biological abnormality and can be misleading to caregivers. Pseudohyperkalemia is typically caused by hemolysis during venipuncture (by either excessive vacuum of the blood draw or by a collection needle that is of too fine a gauge); excessive tourniquet time or fist clenching during phlebotomy (which presumably leads to efflux of potassium from the muscle cells into the bloodstream); or by a delay in the processing of the blood specimen. It can also occur in specimens from patients with abnormally high numbers of platelets (>500,000/mm³), leukocytes (> 70 000/mm³), or erythrocytes (hematocrit > 55%). People with "leakier" cell membranes have been found, whose blood must be separated immediately to avoid pseudohyperkalemia.

PATHOPHYSIOLOGY

Potassium is the most abundant intracellular cation. It is critically important for many physiological processes, including maintenance of cellular membrane potential, homeostasis of cell volume, and transmission of action potentials in nerve cells. Its main dietary sources are vegetables (tomato and potato), fruits (orange and banana) and meat. Elimination is through the gastrointestinal tract and the kidney.

The renal elimination of potassium is passive (through the glomeruli), and reabsorption is active in the proximal tubule and the ascending limb of the loop of Henle. There is active excretion of potassium in the distal tubule and the collecting duct; both are controlled by aldosterone.

Hyperkalemia develops when there is excessive production (oral intake, tissue breakdown) or ineffective elimination of potassium. Ineffective elimination can be hormonal (in aldosterone deficiency) or due to causes in the renal parenchyma that impair excretion.

Increased extracellular potassium levels result in depolarization of the membrane potentials of cells. This depolarization opens some voltage-gated sodium channels, but not enough to generate an action potential. After a short while, the open sodium channels inactivate and become refractory, increasing the threshold needed to generate an action potential. This leads to the impairment of neuromuscular, cardiac, and gastrointestinal organ systems. Of most concern is the impairment of cardiac conduction which can result in ventricular fibrillation or asystole.

During extreme exercise, potassium is released from active muscle and the serum potassium rises to a point that would be dangerous at rest. For unclear reasons, it appears as if the high levels of adrenaline and noradrenaline have a protective effect on the cardiac electrophysiology.

Patients with the rare hereditary condition of hyperkalemic periodic paralysis appear to have a heightened sensitivity of muscular symptoms that are associated with transient

elevation of potassium levels. Episodes of muscle weakness and spasms can be precipitated by exercise or fasting in these subjects

CLINICAL MANIFESTATIONS

Symptoms are fairly nonspecific and generally include malaise, palpitations and muscle weakness; mild hyperventilation may indicate a compensatory response to metabolic acidosis, which is one of the possible causes of hyperkalemia. Often, however, the problem is detected during screening blood tests for a medical disorder, or it only comes to medical attention after complications have developed, such as cardiac arrhythmia or sudden death.

As the plasma potassium level rises, disturbance in cardiac conduction occur. The earliest changes, often occuring at a serum potassium level greater than 6 mEq/L, are peaked, narrow T waves; ST segment depression; and a shortened QT interval. The serum potassium level continues to increase, the PR interval become prolonged and is followed by disappearance of the P waves. Finally, there is decomposition and widening of the QRS complex. Ventricular dysrhythmias and cardiac arres may occur at any point in the progression.

Rapidly ascending muscular weakness leading to flaccid quadriplegia has been reported in patients with very high serum potassium levels. Paralysis of respiratory and speech muscles can also occur. In addition, GI manifestations, such as nausea, intermittent intestinal colic and diarrhea may be evident.

Electrocardiography ishowing precordial leads in hyperkalemia.

DIAGNOSTIC FINDINGS

Serum potassium levels ECG changes

With mild to moderate hyperkalemia, there is reduction of the size of the P wave and development of peaked T waves. Severe hyperkalemia results in a widening of the QRS complex, and the EKG complex can evolve to a sinusoidal shape. There appears to be a direct effect of elevated potassium on some of the potassium channels that increases their activity and speeds membrane repolarization. Also, hyperkalemia causes an overall membrane depolarization that inactivates many sodium channels. The faster repolarization of the cardiac action potential causes the tenting of the T waves, and the inactivation of sodium channels causes a sluggish conduction of the electrical wave around the heart, which leads to smaller P waves and widening of the QRS complex.

The serum K+ concentration at which electrocardiographic changes develop is somewhat variable. Although the factors influencing the effect of serum potassium levels on cardiac electrophysiology are not entirely understood, the concentrations of other electrolytes, as well as levels of catecholamines, play a major role.

MEDICAL MANAGEMENT

When arrhythmias occur, or when potassium levels exceed 6.5 mmol/l, emergency lowering of potassium levels is mandated. Several agents are used to transiently lower K+

levels. Choice depends on the degree and cause of the hyperkalemia, and other aspects of the patient's condition.

Myocardial excitability

Calcium (Calcium chloride or calcium gluconate) increases threshold potential through a mechanism that is still unclear, thus restoring normal gradient between threshold potential and resting membrane potential, which is elevated abnormally in hyperkalemia. One ampule of Calcium chloride has approximately 3 times more calcium than calcium gluconate. Onset of action is <5 min and lasts about 30-60 min. Doses should be titrated with constant monitoring of ECG changes during administration and the dose should be repeated if ECG changes do not normalize within 3 to 5 min.

Lowering K+ temporarily

Several medical treatments shift potassium ions from the bloodstream into the cellular compartment, thereby reducing the risk of complications. The effect of these measures tends to be short-lived, but may temporize the problem until potassium can be removed from the body.

Insulin (e.g. intravenous injection of 10-15 units 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. Its effects last a few hours, so it sometimes needs to be repeated while other measures are taken to suppress potassium levels more permanently.

Bicarbonate therapy (e.g. 1 ampule (50mEq) infused over 5 minutes) is effective in shifting potassium into the cell. The bicarbonate ion will stimulate an exchange of cellular H+ for Na+, thus leading to stimulation of the sodium-potassium ATPase.

Salbutamol (albuterol, Ventolin) is a β2-selective catecholamine that is administered by nebulizer (e.g. 10–20 mg). This drug also lowers blood levels of K+ by promoting its movement into cells.

Increasing elimination

Severe cases require hemodialysis or hemofiltration, which are the most rapid methods of removing potassium from the body. These are typically used if the underlying cause cannot be corrected swiftly while temporizing measures are instituted or there is no response to these measures.

Sodium polystyrene sulfonate with sorbitol (Kayexalate) either orally or rectally is widely used with the goal to lower potassium over several hours. Removal of potassium is assumed to require defecation. However, careful clinical trials to demonstrate the effectiveness of Kayexalate are lacking, and there are small risks of necrosis of the colon.

Furosemide may also be used to promote excretion of potassium in the urine.

Long-term prevention

Preventing recurrence of hyperkalemia typically involves reduction of dietary potassium, removal of an offending medication, and/or the addition of oral bicarbonate or a diuretic (such as furosemide or hydrochlorothiazide). Sodium polystyrene sulfonate and sorbital (Kayexalate) is occasionally used on an ongoing basis to maintain lower serum levels of potassium. Concerns regarding its use are noted in the previous section.

NURSING MANAGEMENT

ASSESSMENT

Assessment focuses on identifying risk factors for hyperkalemia through history taking and a thorough physical examination. Review lab reports.

Ongoing assessments include checking vital signs, bowel function, urine output, lung sounds (crackles), and peripheral edema every 4 to 8 hours.

Monitor plasma levels of potassium, and creatinine and BUN.

ECG changes should be monitored continuously.

Monitor urine output hourly if severe hyperkalemia or renal insufficiency exists.

Monitor for signs of overcorrection also.

NURSING DIAGNOSIS

Hyperkalemia related to renal dysfunction, shock from traumatic injuries, or burns.

Outcomes:the nurse will monitor potassium levels and report abnormal findings or manifestations of hyperkalemia to the physician.

Interventions

Administer fluids as ordered to promote renal excretion of potassium. Report manifestations indicating the development of hypokalemia and urine output less than 0.5 ml/kg/hr for 2 consecutive hours.

If the client is to receive a blood transfusion and is at risk for hyperkalemia, notify the blood bank so that old blood (more than 2 wks) is not supplied.

High potassium levels have the potential to induce life threatening dysrhythmias. Treat them according to protocol, and report ECG changes.

Set cardiac monitor alarms with narrow limits to to ensure early detection of lethal dysrhythmias.

CALCIUM IMBALANCES

HYPOCALCEMIA

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 of less than 1.1 mmol/L or 4.5 mg/dL. In the blood, about half of all calcium is bound to proteins such as serum albumin, but it is the unbound, or ionized, calcium that the body regulates. If a person has abnormal levels of blood proteins, then the plasma calcium may be inaccurate.

ETIOLOGY AND RISK FACTORS

It manifests as a symptom of a parathyroid hormone [PTH] deficiency/malfunction, a Vitamin D deficiency, or unusually high magnesium levels hypermagnesaemia, or low magnesium levels hypomagnesaemia.

More specifically, hypocalcaemia may be associated with low PTH levels as seen in hereditary hypoparathyroidism, acquired hypoparathyroidism (surgical removal MCC of hypoparathyroidism), and hypomagnesaemia. Hypocalcaemia may be associated with high PTH levels when the parathyroid hormone is ineffective; in chronic renal failure, the hydroxylation of vitamin D is ineffective, calcium levels in the blood fall, and high PTH levels are produced in response to the low calcium, but fail to return calcium levels to normal.

Eating disorders Exposure to mercury, including infantile acrodynia

Excessive dietary magnesium, as with supplementation.

Prolonged use of medications/laxatives containing magnesium

Chelation Therapy for metal exposure, particularly EDTA

Absent parathyroid hormone (PTH)

o Hereditary hypoparathyroidism

o Acquired hypoparathyroidism

o Hypomagnesaemia

o Following parathyroidectomy, "Hungry Bone Syndrome"

o Following thyroidectomy, the parathyroid glands are located very close to the thyroid and are easily injured or even accidentally removed during thyroidectomy

o In DiGeorge Syndrome, a disease characterized by the failure of the third and fourth pharyngeal pouches to develop, the parathyroid glands do not form and there is thus a lack of PTH.

Ineffective PTH

o Chronic renal failure

o Absent active vitamin D

Decreased dietary intake

Decreased sun exposure

Defective Vitamin D metabolism

Anticonvulsant therapy

Vitamin-D dependent rickets, type I

o Ineffective active vitamin D

Intestinal malabsorption

Vitamin-D dependent rickets, type II

o Pseudohypoparathyroidism

Deficient PTH

o Severe acute hyperphosphataemia

Tumour lysis syndrome

Acute renal failure

Rhabdomyolysis (initial stage)

Exposure to hydrofluoric acid

As a complication of pancreatitis

As a result of hyperventilation

Alkalosis, often caused by hyperventilation

Chelation Therapy

Neonatal hypocalcaemia

o Very low birth weight (less than 1500 grams)

o Gestational age less than 32 weeks

CLINICAL MANIFESTATIONS

Petechia which appear as on-off spots, then later become confluent, and appear as purpura (larger bruised areas, usually in dependent regions of the body).

Oral, perioral and acral paresthesias, tingling or 'pins and needles' sensation in and around the mouth and lips, and in the extremities of the hands and feet. This is often the earliest symptom of hypocalcaemia.

Carpopedal and generalized tetany (medical sign), (unrelieved and strong contractions of the hands, and in the large muscles of the rest of the body) are seen.

Latent tetany

o Trousseau sign of latent tetany (eliciting carpal spasm by inflating the blood pressure cuff and maintaining the cuff pressure above systolic)

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

Tendon reflexes are hyperactive

Life threatening complications

o Laryngospasm

o Cardiac arrhythmias

ECG changes include:

o Intermittent QT prolongation, or intermittent prolongation of the QTc (corrected QT interval) on the EKG (electrocardiogram) is noted. The implications of intermittent QTc prolongation predisposes to life-

threatening cardiac electrical instability (and this is therefore a more critical condition than constant QTc prolongation). This type of electrical instability puts the patient at high risk of torsades de pointes, a specific type of ventricular fibrillation which appears on an EKG (or ECG) as something which looks a bit like a sine wave with a regularly increasing and decreasing amplitude. (Torsades de pointes, as with any type of ventricular fibrillation, causes death, unless the patient can be electrically cardioverted, and returned to a normal cardiac rhythm.)

DIAGNOSTIC FINDINGS

Serum calcium, serum albumin, arterial pH.

MEDICAL MANAGEMENT

Two ampoules of intravenous calcium gluconate 10% is given slowly in a period of 10 minutes, or if the hypocalcaemia is severe, calcium chloride is given instead. This is only appropriate if the hypocalcemia is acute and has occurred over a relatively short time frame. But if the hypocalcemia has been severe and chronic, then this regimen can be fatal, because there is a degree of acclimatization that occurs. The neuromuscular excitability, cardiac electrical instability, and associated symptoms are then not cured or relieved by prompt administration of corrective doses of calcium, but rather exacerbated. Such rapid administration of calcium would result in effective over correction - symptoms of hypercalcemia would follow.

However, in either circumstance, maintenance doses of both calcium and vitamin-D (often as 1,25-(OH)2-D3, i.e. calcitriol) are often necessary to prevent further decline.

Parenteral calcium salts include calcium gluconate, calcium chloride, and calcium gluceptate. Too rapid IV administration of calcium can cause cardiac arrest preceded by bradycardia. Therefore it should be diluted in D5W and given as a slow IV bolus or a slow IV infusion.

Aluminium hydroxide, calcium acetate,or calcium carbonate antacids may be prescribed to decrease elevated phosphorouslevels before treating hypocalcemia in the patient with chronic renal failure.

Increasing the dietary intake of calcium to atleast 1000 to 1500 mg/day in the adult is recommended.

NURSING MANAGEMENT

A thorough history of the client’s current and chronic illnesses, diet intake, and medications, including over the counter medications and herbals.

Check for Trousseau’s and Chvosetk’s signs in high risk clients. Trousseau’s sign is the occurrence of carpal spasm or contraction of the fingers and hand, when a blood pressure cuff is kept inflated on the upper arm for 5 mts at diastolic pressure. Chvostek’s sign is the occurrence of spasm of the muscles innervated by the facial nerve when the client’s face is tapped below the temple.

Assess for paresthesias (finger, toes, circumoral).

Assess the client’s cardiac status by monitoring the ECG and vital signs. Assess color, warmth, motion, and sensation(CWMS) and peripheral pulses.

Monitor also for bleeding in the gums and petechiae or ecchymosis in the skin. Assess for changes in the clarity of urine and also note black or blood streaked stool which may signify occult bleeding.

Monitor IV sites for infiltration or phlebitis when IV calcium is being infused. Avoid giving calcium and bicarbonate in the same IV solution, because a precipitate will form.

To prevent pathologic fractures ,use caution by obtaining help to turn or move the client.

Instruct the client about foods that are rich in calcium such as milk, cheese etc. encourage calcium supplements with meals and vitamin D milk for better absorption.

HYPERCALCEMIA

Hypercalcaemia 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 diseases, a workup should be undertaken if it persists. It can be due to excessive skeletal calcium release, increased intestinal calcium absorption, or decreased renal calcium excretion.

ETIOLOGY AND RISK FACTORS

Primary hyperparathyroidism and malignancy account for about 90% of cases of hypercalcaemia.

Abnormal parathyroid gland function

primary hyperparathyroidismo solitary parathyroid adenoma

o primary parathyroid hyperplasia

o parathyroid carcinoma

o multiple endocrine neoplasia (MEN)

o familial isolated hyperparathyroidism

lithium use

familial hypocalciuric hypercalcaemia/familial benign hypercalcaemia

Malignancy

solid tumour with metastasis (e.g. breast cancer or classically squamous cell carcinoma, which can be PTHrP-mediated)

solid tumour with humoral mediation of hypercalcaemia (e.g. lung cancer [most commonly non-small cell lung cancer] or kidney cancer, phaeochromocytoma)

haematologic malignancy (multiple myeloma, lymphoma, leukaemia)

Vitamin-D metabolic disorders

hypervitaminosis D (vitamin D intoxication) elevated 1,25(OH)2D ( calcitriol under Vitamin D) levels (e.g. sarcoidosis and

other granulomatous diseases)

idiopathic hypercalcaemia of infancy

rebound hypercalcaemia after rhabdomyolysis

Disorders related to high bone-turnover rates

hyperthyroidism prolonged immobilization

thiazide use

vitamin A intoxication

Paget's disease of the bone

multiple myeloma

Renal failure

severe secondary hyperparathyroidism aluminium intoxication

milk-alkali syndrome

PATHOPHYSIOLOGY

Destruction of bone tissue results in an increased release of calcium into the vascular spaces. Excessive PTH production promotes calcium retention, which leads to hypophosphatemia. This compounds the problem by promoting more calcium retention.

When excess calcium presents the cell membrane threshold potential becomes more positive, which results in membranes that are refractory to depolarization. This decreased cell membrane excitability requires a stronger stimulus for a response to occur.

CLINICAL MANIFESTATIONS

There is a general mnemonic for remembering the effects of hypercalcaemia: "groans (constipation), moans (psychiatric symptoms (e.g., fatigue, lethargy, depression, confusion)), bones (bone pain, especially if PTH is elevated), and stones (kidney stones)."

Other symptoms can include fatigue, anorexia, nausea, vomiting, pancreatitis and increased urination.

Abnormal heart rhythms can result, and ECG findings of a short QT interval and a widened T wave suggest hypercalcaemia. Significant hypercalcaemia can cause ECG changes mimicking an acute myocardial infarction.

Hypercalcemia can increase gastrin production, leading to increased acidity so Peptic ulcers may also occur.

Symptoms are more common at high calcium blood values (12.0 mg/dL or 3 mmol/l). Severe hypercalcaemia (above 15–16 mg/dL or 3.75–4 mmol/l) is considered a medical emergency: at these levels, coma and cardiac arrest can result.

MEDICAL MANAGEMENT

The goal of therapy is to treat the hypercalcaemia first and subsequently effort is directed to treat the underlying cause.

Initial therapy: fluids and diuretics

hydration, increasing salt intake, and forced diuresis. o hydration is needed because many patients are dehydrated due to vomiting

or renal defects in concentrating urine.

o increased salt intake also can increase body fluid volume as well as increasing urine sodium excretion, which further increases urinary calcium excretion (In other words, calcium and sodium (salt) are handled in a similar way by the kidney. Anything that causes increased sodium (salt) excretion by the kidney will, en passant, cause increased calcium excretion by the kidney)

o after rehydration, a loop diuretic such as furosemide can be given to permit continued large volume intravenous salt and water replacement while minimizing the risk of blood volume overload and pulmonary oedema. In addition, loop diuretics tend to depress renal calcium reabsorption thereby helping to lower blood calcium levels

o can usually decrease serum calcium by 1–3 mg/dL within 24 h

o caution must be taken to prevent potassium or magnesium depletion

Additional therapy: bisphosphonates and calcitonin

bisphosphonates are pyrophosphate analogues with high affinity for bone, especially areas of high bone-turnover.

o they are taken up by osteoclasts and inhibit osteoclastic bone resorption

o current available drugs include (in order of potency): (1st gen) etidronate, (2nd gen) tiludronate, IV pamidronate, alendronate (3rd gen) zoledronate and risedronate

o all patients with cancer-associated hypercalcaemia should receive treatment with bisphosphonates since the 'first line' therapy (above) cannot be continued indefinitely nor is it without risk. Further, even if the 'first line' therapy has been effective, it is a virtual certainty that the hypercalcaemia will recur in the patient with hypercalcaemia of malignancy. Use of bisphosphonates in such circumstances, then, becomes both therapeutic and preventative

o patients in renal failure and hypercalcaemia should have a risk-benefit analysis before being given bisphosphonates, since they are relatively contraindicated in renal failure.

Calcitonin blocks bone resorption and also increases urinary calcium excretion by inhibiting renal calcium reabsorption

o Usually used in life-threatening hypercalcaemia along with rehydration, diuresis, and bisphosphonates

o Helps prevent recurrence of hypercalcaemia

o Dose is 4 Units per kg via subcutaneous or intramuscular route every 12 hours, usually not continued indefinitely

Other therapies

rarely used, or used in special circumstances o plicamycin inhibits bone resorption (rarely used)

o gallium nitrate inhibits bone resorption and changes structure of bone crystals (rarely used)

o glucocorticoids increase urinary calcium excretion and decrease intestinal calcium absorption

no effect on calcium level in normal or primary hyperparathyroidism

effective in hypercalcaemia due to osteolytic malignancies (multiple myeloma, leukaemia, Hodgkin's lymphoma, carcinoma of the breast) due to antitumor properties

also effective in hypervitaminosis D and sarcoidosis

o dialysis usually used in severe hypercalcaemia complicated by renal failure. Supplemental phosphate should be monitored and added if necessary

o phosphate therapy can correct the hypophosphataemia in the face of hypercalcaemia and lower serum calcium

Hypercalcaemic crisis

A hypercalcaemic crisis is an emergency situation with a severe hypercalcaemia, generally above approximately 14 mg/dL (or 3.5 mmol/l).

The main symptoms of a hypercalcaemic crisis are oliguria or anuria, as well as somnolence or coma. After recognition, primary hyperparathyroidism should be proved or excluded.

In extreme cases of primary hyperparathyroidism, removal of the parathyroid gland after surgical neck exploration is the only way to avoid death. The diagnostic program should be performed within hours, in parallel with measures to lower serum calcium.Treatment of choice for acutely lowering calcium is extensive hydration and calcitonin, as well as bisphosphonates (which have effect on calcium levels after one or two days).

NURSING MANAGEMENT

Screening assessment include obtaining a thorough history.

Assess vital signs,apical pulses and ECG everu 1 to 8 hours. Bowel sounds , renal function,and hydration status should be assessed every 8 hours. Monitor for fluid volume depletion secondary to Hypercalcemia.

Early treatment may prevent hypercalcemic crisis. If flank pain or renal colic is present, strain all urine to capture renal calculi for analysis. Report any manifestations such as an increase in severity of dysrhythmias, a decrease in sensorium or signs of overcorrection.

Instruct the client to avoid calcium supplements. Sodium intake is increased unless contraindicated to promote calcium loss through the kidneys. Consumption of high fibre foods and fluids should be increased to prevent constipation.

If the client has confusion, lethargy, or coma institute precautions including low bed position. To prevent injury turn and move the client with extreme caution. Gait belts, back braces, tripod canes may be used to facilitate safer ambulation. Assist with resistive ROM and weight bearing activities to decrease calcium loss from the bone.

PHOSPHATE IMBALANCES

HYPOPHOSPHATEMIA

Hypophosphatemia is an electrolyte disturbance in which there is an abnormally low level of phosphate in the blood. The condition has many causes, but is most commonly seen when malnourished patients (especially chronic alcoholics) are given large amounts of carbohydrates, which creates a high phosphorus demand by cells, removing phosphate from the blood (refeeding syndrome).

Because a decrease in phosphate in the blood is sometimes associated with an increase in phosphate in the urine, the terms hypophosphatemia and "phosphaturia" are occasionally used interchangeably; however, this is improper since there exist many causes of

hypophosphatemia besides overexcretion and phosphaturia, and in fact the most common causes of hypophosphatemia are not associated with phosphaturia.

ETIOLOGY AND RISK FACTORS

Refeeding syndrome This causes a demand for phosphate in cells due to the action of phosphofructokinase, an enzyme that attaches phosphate to glucose to begin metabolism of this. Also, production of ATP when cells are fed and recharge their energy supplies, requires phosphate.

Respiratory alkalosis Any alkalemic condition moves phosphate out of the blood into cells. This includes most common respiratory alkalemia (a higher than normal blood pH from low carbon dioxide levels in the blood), which in turn is caused by any hyperventilation (such as may result from sepsis, fever, pain, anxiety, drug withdrawal, and many other causes). This phenomenon is seen because in respiratory alkalosis carbon dioxide (CO2) decreases in the extracellular space, causing intracellular CO2 to freely diffuse out of the cell. This drop in intracellular CO2 causes a rise in cellular pH which has a stimulating effect on glycolysis. Since the process of glycolysis requires phosphate (the end product is adenosine triphosphate), the result is a massive uptake of phosphate into metabolically active tissue (such as muscle) from the serum. It is interesting to note, however, that this effect is not seen in metabolic alkalosis, for in such cases the cause of the alkalosis is increased bicarbonate rather than decreased CO2. Bicarbonate, unlike CO2, has poor diffusion across the cellular membrane and therefore there is little change in intracellular pH.

Alcohol abuse Alcohol impairs phosphate absorption. Alcoholics are usually also malnourished with regard to minerals. In addition, alcohol treatment is associated with refeeding, and the stress of alcohol withdrawal may create respiratory alkalosis, which exacerbates hypophosphatemia (see above).

Malabsorption This includes GI damage, and also failure to absorb phosphate due to lack of vitamin D, or chronic use of phosphate binders such as sucralfate, aluminum-containing antacids, and (more rarely) calcium-containing antacids.

Primary hypophosphatemia is the most common cause of nonnutritional rickets. Laboratory findings include low-normal serum calcium, moderately low serum phosphate, elevated serum alkaline phosphatase, and low serum 1,25 dihydroxy-vitamin D levels, hyperphosphaturia, and no evidence of hyperparathyroidism.

Other rarer causes include

Certain blood cancers such as lymphoma or leukemia hereditary causes

hepatic failure

Tumor-induced osteomalacia

PATHOPHYSIOLOGY

Hypophosphatemia is caused by the following three mechanisms:

Inadequate intake (often unmasked in refeeding after long-term low phosphate intake)

Increased excretion (e.g. in hyperparathyroidism, hypophosphatemic rickets)

Shift from extracellular to intracellular space (seen in treatment of diabetic ketoacidosis, refeeding, short-term increases in cellular demand (e.g., hungry bones syndrome) and acute respiratory alkalosis)

CLINICAL MANIFESTATIONS

Muscle dysfunction and weakness. This occurs in major muscles, but also may manifest as: diplopia, low cardiac output, dysphagia, and respiratory depression due to respiratory muscle weakness.

Mental status changes. This may range from irritability to gross confusion, delirium, and coma.

White cell dysfunction, causing worsening of infections.

Instability of cell membranes due to low ATP levels: this may cause rhabdomyolysis with increased CPK, and also hemolytic anemia.

MEDICAL MANAGEMENT

Standard intravenous preparations of potassium phosphate are available and are routinely used in malnourished patients and alcoholics. Oral supplementation also is useful where no intravenous treatment is available. Aadequate amount of phosphorous should be added to parenteral solutions.

Possible dangers of IV administration of phosphorous include tetany from hypocalcemia and calcifications in tissues from hyperphsphatemia. IV preparations of phosphorous are available as sodium or potassium phosphate. The rate of phosphorous administration should not exceed 10mEq/h and the site should be carefully monitored because tissue sloughing and necrosis can occur with infiltration.

NURSING MANAGEMENT

Identify the patients who are at risk for hypophosphatemia and monitors them. Careful attention is given to preventing infection.

Nurse frequently monitors serum phosphorous levels and documents and report early signs of hypophosphatemia.

If the patient experiences mild hypophosphotemia foods such as milk and milk products, organ meats, nuts, fish etc should be encouraged.

With moderate hypophosphatemia supplements such as Neutra-phos capsules(250 mg phosphorous/capsule), K-Phos may be prescribed.

HYPER PHOSPHATEMIA

Hyperphosphatemia is an electrolyte disturbance in which there is an abnormally elevated level of phosphate in the blood.Often, calcium levels are lowered (hypocalcemia) due to precipitation of phosphate with the calcium in tissues.

ETIOLOGY AND RISK FACTORS

Hypoparathyroidism In this situation, there are low levels of Parathyroid hormone (PTH). PTH normally inhibits renal reabsorption of phosphate, and so without enough PTH there is more reabsorption of the phosphate.

Chronic renal failure: When the kidneys aren't working well, there will be increased phosphate retention.

Osteomalacia, which may be caused by the insufficient content of vitamin D in the diet, the lack of sunlight, malabsorption or renal disorders.

Drugs: hyperphosphatemia can also be caused by taking oral sodium phosphate solutions prescribed for bowel preparation for colonoscopy in children

CLINICAL MANIFESTATIONS

Signs and symptoms include ectopic calcification, secondary hyperparathyroidism, and renal osteodystrophy.

Tetany,anorexia, nausea, vomiting, bone and joint pain, muscle weakness, hyper reflexia, and tachycardia may occur. High serum levels of inorganic phosphorous promote precipitation of calcium phosphate in nonosseous sites, decreasing urine output, impairing vision, and producing palpitations.

DIAGNOSTIC MEASURES

S.Phosphorous, S.Calcium, X-Ray S.PTH

BUN and creatinine.

MEDICAL MANAGEMENT

High phosphate levels can be avoided with phosphate binders and dietary restriction of phosphate.

When possible treatment is directed at the underlying disorder. Measure to decrease the serum phosphate level and bind bind phosphorous in the GI tract of these patient include vitamin D preparations such as calcitriol (oral) and calcijex (parenteral). Administration of amphojel with meals is effective but can cause bone and central nervous system toxicity with long term use. Restriction of dietary phosphate, forced diuresis with a loop diuretic, volume replacement with saline and dialysis may also lower phosphorous. Surgery may be indicated for removal of large calcium and phosphorous deposits.

NURSING MANAGEMENT

Monitor for patients at risk for hyperphosphatemia. If a low phpsphorous diet is prescribed the patient is instructed to avoid phosphorous rich foods such as hard cheeses,nuts , meats, sardines etc.

Instruct the patient to to avoid phosphate containing substances such as laxatives and enemas.

Teaches the client to recognise the signs of impending hypocalcemia and to monitor for changes in urine output.

CHLORIDE IMBALANCES

HYPERCHLOREMIA

Hyperchloremia is an electrolyte disturbance in which there is an abnormally elevated level of the chloride ion in the blood. The normal serum range for chloride is 97 to 107 mEq/L. Hyperchloremia is defined as a chloride concentration exceeding this level. Hyperchloremia can affect oxygen transport.

ETIOLGY AND RISK FACTORS

Elevations in chloride may be associated with diarrhea, certain kidney diseases as Lightwood syndrome, and overactivity of the parathyroid glands. Hyperchloremia is often comorbid with diabetes or hyponatremia. Certain drugs, especially diuretics such as carbonic anhydrase inhibitors, hormonal treatments, and polypharmacy, may contribute to this disorder.

Administration of chloride deficient IV fluids, low sodium intake, metabolic alkalosis, massive blood transfusions, diuretic therapy, burns, fever, administration of aldosterone, ACTH, corticosteroids, or laxatives which decreases chloride level.

CLINICAL MANIFESTATIONS

Often hyperchloremia does not produce any symptoms. However, hyperchloremia is sometimes associated with excess fluid loss such as vomiting and diarrhea. If the sufferer were to be a diabetic, hyperchloremia could lead to poor control of blood sugar concentration, which could cause it to become elevated. Hyperchloremia can be symptomatic with signs of Kussmaul's breathing, weakness, and intense thirst.

MEDICAL MANAGEMENT

As with most types of electrolyte imbalance, the treatment of high blood chloride levels is based on correcting the underlying cause.

If the patient is dehydrated, therapy consists of establishing and maintaining adequate hydration.

If the condition is caused or exacerbated by medications or treatments, these may be altered or discontinued, if deemed prudent.

If there is underlying kidney disease (which is likely if there are other electrolyte disturbances), then the patient will be referred to a nephrologist for further care.

If there is an underlying dysfunction of the endocrine or hormone system, the patient will likely be referred to an endocrinologist for further assessment.

Normal saline 0.9% or half strength saline 0.45% is administered to to replace the chloride.

If the patient is receiving a diuretic, it may be discontinued or another may be prescribed.

Ammonium chloride an acidifying agent may be prescribed to treat metabolic alkalosis. Its use should be avoided in patients with impaired renal or liver function.

NURSING MANAGEMENT

Monitor I&O, ABG values, and serum electrolyte levels. Changes in the patients LOC and muscle strength and movement are reported to the physician promptly.

Vital signs are monitored and respiratory assessment is carried out frequently.

The nurse provides and teaches the patient about food with high chloride content include tomato juice, canned vegetables etc.

HYPOCHLOREMIA

CHLORIDE DEFICIT (HYPOCHLOREMIA)

Chloride control depends on the intake of chloride and the excretionand reabsorption of its ions in the kidneys. Chloride isproduced in the stomach as hydrochloric acid; a small amount ofchloride is lost in the feces. Chloride-deficient formulas, saltrestricteddiets, GI tube drainage, and severe vomiting and diarrheaare risk factors for hypochloremia. As chloride decreases(usually because of volume depletion), sodium and bicarbonateions are retained by the kidney to balance the loss. Bicarbonateaccumulates in the ECF, which raises the pH and leads to hypochloremicmetabolic alkalosis.

Clinical Manifestations

The signs and symptoms of hypochloremia are those of acid–baseand electrolyte imbalances. The signs and symptoms of hyponatremia,hypokalemia, and metabolic alkalosis may also be noted.Metabolic alkalosis is a disorder that results in a high pH and ahigh serum bicarbonate level as a result of excess alkali intake orloss of hydrogen ions. With compensation, the PaCO2 increasesto 50 mm Hg. Hyperexcitability of muscles, tetany, hyperactivedeep tendon reflexes, weakness, twitching, and muscle crampsmay result. Hypokalemia can cause hypochloremia, resulting incardiac dysrhythmias. In addition, because low chloride levelsparallel low sodium levels, a water excess may occur. Hyponatremia

can cause seizures and coma.

Assessment and Diagnostic Findings

The normal serum chloride level is 96 to 106 mEq/L (96–106mmol/L). Inside the cell, the chloride level is 4 mEq/L. In additionto the chloride level, sodium and potassium levels are alsoevaluated because these electrolytes are lost along with chloride.Arterial blood gas analysis identifies the acid–base imbalance,which is usually metabolic alkalosis. The urine chloride level, whichis also measured, decreases in hypochloremia.

Medical Management

Treatment involves correcting the cause of hypochloremia andcontributing electrolyte and acid–base imbalances. Normal saline(0.9% sodium chloride) or half-strength saline (0.45% sodiumchloride) solution is administered IV to replace the chloride. Thephysician may reevaluate whether patients receiving diuretics(loop, osmotic, or thiazide) should discontinue these medicationsor change to another diuretic.Foods high in chloride are provided; these include tomatojuice, salty broth, canned vegetables, processed meats, and fruits.A patient who drinks free water (water without electrolytes) orbottled water will excrete large amounts of chloride; therefore,this kind of water should be avoided. Ammonium chloride, anacidifying agent, may be prescribed to treat metabolic alkalosis;the dosage depends on the patient’s weight and serum chloridelevel. This agent is metabolized by the liver, and its effects last forabout 3 days.

Nursing Management

The nurse monitors intake and output, arterial blood gas values,and serum electrolyte levels, as well as the patient’s level of consciousnessand muscle strength and movement. Changes are reportedto the physician promptly. Vital signs are monitored andrespiratory assessment is carried out frequently. The nurse teachesthe patient about foods with high chloride content.

MAGNESIUM IMBALANCES

HYPOMAGNESEMIA

Hypomagnesemia (or hypomagnesaemia) 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.

Hypomagnesemia is not equal to magnesium deficiency. Hypomagnesemia can be present without magnesium deficiency and vice versa. Note, however, that hypomagnesemia is usually indicative of a systemic magnesium deficit.

Hypomagnesemia may result from a number of conditions including inadequate intake of magnesium, chronic diarrhea, malabsorption, alcoholism, chronic stress, and medications such as diuretics use among others.

ETIOLOGY AND RISK FACTORS

Magnesium deficiency is not uncommon in hospitalized patients. Elevated levels of magnesium (hypermagnesemia), however, are nearly always iatrogenic. Ten to twenty percent of all hospital patients and 60–65% of patient in the intensive care unit (ICU) have hypomagnesemia. Hypomagnesemia is underdiagnosed, as testing for serum magnesium levels is not routine.

Low levels of magnesium in blood may mean that there is not enough magnesium in the diet, the intestines are not absorbing enough magnesium, or the kidneys are excreting too much magnesium. Deficiencies may be due to the following conditions:

Drugs

Alcoholism. Hypomagnesemia occurs in 30% of alcohol abuse and 85% in delirium tremens, due to malnutrition and chronic diarrhea. Alcohol stimulates renal excretion of magnesium, which is also increased because of alcoholic and diabetic ketoacidosis, hypophosphatemia and hyperaldosteronism resulting from liver disease. Also, hypomagnesemia is related to thiamine deficiency because magnesium is needed for transforming thiamine into thiamine pyrophosphate.

Medications

Loop and thiazide diuretic use (the most common cause of hypomagnesemia) Antibiotics (i.e. aminoglycoside, amphotericin, pentamidine, gentamicin,

tobramycin, viomycin) block resorption in the loop of Henle. 30% of patients using these antibiotics have hypomagnesemia,

Long term use of proton pump inhibitors such as omeprazole.

Other drugs.

o Digitalis, displaces magnesium into the cell. Digitalis causes an increased intracellular concentration of sodium, which in turn increases intracellular calcium by passively decreasing the action of the sodium-calcium exchanger in the sarcolemma. The increased intracellular calcium gives a positive inotropic effect.

o Adrenergics, displace magnesium into the cell

o Cisplatin, stimulates renal excretion

o Ciclosporin, stimulates renal excretion

o Mycophenolate mofetil

o Proton Pump Inhibitors (PPIs) such as Nexium, Prilosec, Protonix, Zegrid, etc.

Excess calcium

Excess saturated fats

Excess coffee or tea intake

Excess phosphoric or carbonic acids (soda pop)

Insufficient water consumption

Excess salt or sugar intake

Insufficient selenium, vitamin D, sunlight exposure or vitamin B6

Increased levels of stress

Gastrointestinal causes: the distal tractus digestivus secretes high levels of magnesium. Therefore, secretory diarrhea can cause hypomagnesemia. Thus, Crohn's disease, ulcerative colitis, Whipple's disease and celiac sprue can all cause hypomagnesemia.

Renal magnesium loss in Bartter's syndrome, postobstructive diuresis, diuretic phase of acute tubular necrosis (ATN) and kidney transplant

Diabetes Mellitus: 38% of diabetic outpatient clinic visits involve hypomagnesemia, probably through renal loss because of glycosuria or ketoaciduria.

Acute myocardial infarction: within the first 48 hours after a heart attack, 80% of patients have hypomagnesemia. This could be the result of an intracellular shift because of an increase in catecholamines.

Malabsorption

Milk diet in infants

Acute pancreatitis

Hydrogen fluoride poisoning

Gitelman/Bartter Syndromes

Massive transfusion (MT) is a lifesaving treatment of hemorrhagic shock, but can be associated with significant complications.

PATHOPHYSIOLOGY

Homeostasis

The body contains 21–28 grams of magnesium (0.864–1.152 mol). Of this, 53% is located in bone, 19% in non-muscular tissue, and 1% in extracellular fluid. For this reason, blood levels of magnesium are not an adequate means of establishing the total amount of available magnesium. Most of the serum magnesium is bound to chelators, (i.e. ATP, ADP, proteins and citrate). Roughly 33% is bound to proteins, and 5–10% is not bound. This "free" magnesium is essential in regulating intracellular magnesium. Normal plasma Mg is 1.7–2.3 mg/dl (0.69–0.94 mmol/l). Of this 60% is free, 33% is bound to proteins, and less than 7% is bound to citrate, bicarbonate and phosphate.

Magnesium is abundant in nature. It can be found in green vegetables, chlorophyll, cocoa derivatives, nuts, wheat, seafood, and meat. It is absorbed primarily in the duodenum of the small intestine. The rectum and sigmoid colon can absorb magnesium. Hypermagnesemia has been reported after enemas containing magnesium. Forty percent of dietary magnesium is absorbed. Hypomagnesemia stimulates and hypermagnesemia inhibits this absorption.

The kidneys regulate the serum magnesium. About 2400 mg of magnesium passes through the kidneys, of which 5% (120 mg) is excreted through urine. The loop of Henle is the major site for magnesium homeostasis, and 60% is resorbed.

Magnesium homeostasis comprises three systems: kidney, small intestine, and bone. In the acute phase of magnesium deficiency there is an increase in absorption in the distal small intestine and tubular resorption in the kidneys. When this condition persists,

serum magnesium drops and is corrected with magnesium from bone tissue. The level of intracellular magnesium is controlled through the reservoir in bone tissue.

CLINICAL MANIFESTATIONS

Deficiency of magnesium causes weakness, muscle cramps, cardiac arrhythmia, increased irritability of the nervous system with tremors, athetosis, jerking, nystagmus and an extensor plantar reflex. In addition, there may be confusion, disorientation, hallucinations, depression, epileptic fits, hypertension, tachycardia and tetany.

DIAGNOSTIC INVESTIGATIONS

The diagnosis can be made by finding a plasma magnesium concentration of less than 0.7 mmol/l. Since most magnesium is intracellular, a body deficit can be present with a normal plasma concentration. In addition to hypomagnesemia, up to 40% cases will also have hypocalcemia while in up to 60% of cases, hypokalemia will also be present. The ECG shows a prolonged QT interval.

MANAGEMENT

Treatment of hypomagnesemia depends on the degree of deficiency and the clinical effects. Oral replacement is appropriate for patients with mild symptoms, while intravenous replacement is indicated for patients with severe clinical effects.

Numerous magnesium dietary supplements are available. Magnesium oxide, one of the most common because it has high magnesium content per weight, has been reported to be the least bioavailable. Magnesium citrate has been reported as more bioavailable than oxide or amino-acid chelate (glycinate) forms.

Intravenous magnesium sulfate (MgSO4) can be given in the following conditions:

Arrhythmia

Magnesium is needed for the adequate function of the Na+/K+-ATPase pumps in the cells of the heart. A lack of it depolarizes and results in tachyarrhythmia. Magnesium inhibits release of potassium, a lack of magnesium increases loss of potassium. Intracellular levels of potassium decrease and the cells depolarize. Digoxin increases this effect. Both digoxin and hypomagnesemia inhibit the Na-K pump resulting in decreased intracellular potassium.

Magnesium intravenously helps in refractory arrhythmia, most notably torsade de pointes. Others are ventricular tachycardia, supraventricular tachycardia and atrial fibrillation.

The effect is based upon decreased excitability by depolarization and the slowing down of electric signals in the AV-node. Magnesium is a negative inotrope as a result of decrease calcium influx and calcium release from intracellular storage. It is just as effective as verapamil. In myocardial infarction there is a functional lack of magnesium, supplementation will decrease mortality.

Obstetric

Most importantly pre-eclampsia. It has an indirect antithrombotic effect upon thrombocytes and the endothelial functions (increase in prostaglandin, decrease in thromboxane, decrease in angiotensin II), microvascular leakage and vasospasm through its function similar to calcium channel blockers.

Convulsions are the result of cerebral vasospasm. The vasodilatatory effect of magnesium seems to be the major mechanism.

Electrolyte disturbances

Hypokalemia: 42% of patients with hypokalemia also have hypomagnesemia, which is why they may not be responding to potassium supplementation. Magnesium is needed for the ATPase, Na-K-pump.

Hypomagnesemia is present in 33% of patients in the intensive care unit not responding to calcium supplementation. This is because of decreased function of the calcium pump, but also because of a decreased release of calcium by inhibition of parathyroid hormone release.

Pulmonary

Acute asthma: here there is a bronchodilatatory effect, probably by antagonizing a calcium-mediated constriction. Also, adrenergic stimulation, i.e. sympatheticomimetics used for treatment of asthma, might lower serum levels of magnesium, which must therefore be supplemented.

HYPERMAGNESEMIA

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.

ETIOLOGY AND RISKFACTORS

Since magnesium is excreted through the kidneys, renal failure (as a result of hypermagnesemia) most often occurs due to prolonged over supplementation or long term use of magnesium containing medications or laxatives.

Predisposing conditions

Hemolysis, magnesium concentration in erythrocytes is approximately three times greater than in serum, therefore hemolysis can increase plasma magnesium. Hypermagnesemia is expected only in massive hemolysis.

Renal insufficiency, excretion of magnesium becomes impaired when creatinine clearance falls below 30 ml/min. However, hypermagnesemia is not a prominent feature of renal insufficiency unless magnesium intake is increased.

Other conditions that can predispose to mild hypermagnesemia are diabetic ketoacidosis, adrenal insufficiency, hyperparathyroidism and lithium intoxication.

CLINICAL MANIFESTATIONS

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.

Clinical consequences related to serum concentration:

4.0 mEq/l hyporeflexia >5.0 mEq/l Prolonged atrioventricular conduction

>10.0 mEq/l Complete heart block

>13.0 mEq/l Cardiac arrest

Note that the therapeutic range for the prevention of the pre-eclampsic uterine contractions is: 4.0-7.0 mEq/L.[2] As per Lu and Nightingale,[3] serum Mg2+ concentrations

associated with maternal toxicity (also neonate depression - hypotonia and low Apgar scores) are:

7.0-10.0 mEq/L - loss of patellar reflex 10.0-13.0 mEq/L - respiratory depression

15.0-25.0 mEq/L - altered atrioventricular conduction and (further) complete heart block

>25.0 mEq/L - cardiac arrest

MANAGEMENT

Prevention of hypermagnesemia usually is possible. In mild cases, withdrawing magnesium supplementation is often sufficient. In more severe cases the following treatments are used:

Intravenous calcium gluconate, because the actions of magnesium in neuromuscular and cardiac function are antagonized by calcium.

Definitive treatment of hypermagnesemia requires increasing renal magnesium excretion through:

Intravenous diuretics, in the presence of normal renal function Dialysis, when kidney function is impaired and the patient is symptomatic

CONCLUSION

Electrolyte imbalances are found in all age groups in every type of health care setting. It is rare for a person to have only one electrolyte imbalance, more commonly, multiple electrolyte and fluid imbalances are present, especially in high-risk populations such as the very young, older adults, and people with chronic illnesses.