Interventions for Clients with Fluid, Electrolyte, and Acid-Base Imbalances

Interventions for Clients with Fluid, Electrolyte, and Acid-Base Imbalances

 

HOMEOSTASIS

The human body functions best when certain conditions are kept within a narrow range of normal. One area extremely important for homeostasis is maintenance of the body’s normal fluid volume and composition. Water is the most common substance in the body. It is needed to deliver dissolved nutrients, electrolytes, and other substances to all organs, tissues, and cells. Changes in body fluid in terms of either the amount of water or the concentration of electrolytes can affect the functioning of all cells, tissues, and organs. For proper physiologic function, the volume of all body fluids and the types and amount of dissolved substances must be carefully regulated.

 

Fluid Compartments

         The body’s fluid is contained within three compartments: cells, blood vessels, and the tissue space (space between the cells and blood vessels). To understand this concept, visualize cars on a freeway. The cars represent cells; the lanes represent the blood vessels, and the space between the cars in the lanes represents the tissue space. The freeway itself is the body. Just as traffic is ongoing and continuous, fluids move constantly from one compartment to another to accommodate the cell’s metabolic needs  Specific terms are used in describing compartmentalized body fluid. The prefixes (see the accompanying display) used with the root words for the compartments that contain the body fluid give meaning to the following terms:

• Intracellular fluid: within the cell

• Intra vascular fluid: within blood vessels

• Interstitial fluid: between cells; fluid that surrounds cells

There are two types of body fluid: intracellular (ICF) and extracellular (ECF). Because intravascular and interstitial fluid are outside the cells, these fluids are extracellular. Key terms used in explaining the movement of molecules in body fluids are:

• Solute: Substance dissolved in a solution

• Solvent: Liquid that contains a substance in solution

• Permeability: Capability of a substance, molecule, or ion to diffuse through a membrane (covering of tissue over a surface, organ, or separating spaces)

• Semipermeable: Selectively permeable (All membranes in the body allow some solutes to pass through the membrane without restriction but will prevent the passage of other solutes.)  Cells have permeable membranes that allow fluid and solutes to pass into and out of the cell. Permeability allows the cell to acquire the nutrients it needs from extracellular fluid to carry on metabolism and to eliminate metabolic waste products.

 

FILTRATION  Definition

Filtration is the movement of fluid through a cell or blood vessel membrane because of hydrostatic pressure differences on both sides of the membrane. Basically, filtration depends on differences in water volume exerting pressure against confining walls.

All fluid has weight. The overall weight of a fluid is related to the amount of fluid present in the confined space. Water molecules in a confined space constantly press outward against the confining walls or boundaries. Hydrostatic pressure is the force exerted by water molecules against the con­fining walls of a space. This pressure is caused by the weight of fluid against the walls. Hydrostatic pressure may be thought of as “water-pushing” pressure, because it is a force that moves water outward from a confined space through a membrane.

Physiologic Activity

Water is the largest component of any body fluid. The amount of water in any body fluid compartment is a main factor in determining the hydrostatic pressure of that compartment. The proportion of water present in a fluid is inversely related to the viscosity (thickness) of that fluid. Thus more water and less solute results in decreased viscosity, and less water with more solute results in increased viscosity. Blood, a viscous fluid (more viscous than water), is confined within the blood vessels. Blood has hydrostatic pressure because of its weight and volume and also because the heart is pumping blood into the arterial circulation. The hydrostatic pressures of two fluid compartments can be compared whenever a permeable (porous) membrane sep­arates the two compartments. If the hydrostatic pressure is the same in both fluid compartments, a state of equilibrium exists for hydrostatic pressure. If the hydrostatic pressure is not the same in both compartments, a state of disequilibrium. This means that the two compartments have a gradient, or graded difference, of hydrostatic pressure: one compartment has a higher hydrostatic pressure than the other. Because the human body constantly seeks equilibrium, a gradient across a cell membrane causes forces to rearrange the distribution of substances on both sides of the membrane until an equilibrium is reached. In most instances, substances move or are rearranged from the greater amount of pressure or concentration to the lesser amount. Thus when a hydrostatic pressure gradient exists between two fluid compartments, fluid from the compartment with the higher hydrostatic pressure moves through (filters) the membrane into the compartment with the lower hydro­static pressure. This filtration continues only as long as the hydrostatic pressure gradient exists. An equilibrium is reached when enough fluid leaves one compartment and enters the other compartment to make the hydrostatic pressure in both compartments equal.

When the two compartments are in equilibrium for hydrostatic pressure, a gradient no longer exists between them. Although water molecules may be exchanged evenly back and forth between two compartments in equilibrium, no net filtration of fluid occurs. In equilibrium, neither compartment gains or loses water molecules, and the hydrostatic pressure in both compartments remains the same.

 Clinical Function and Significance

Blood pressure is a hydrostatic filtering force measured in millimeters of mercury (mm Hg). It moves whole blood from the heart to tissue areas where filtration can occur. Filtration is important for the exchange of water, nutrients, and waste products when blood arrives at the tissue capillaries. One fac­tor that determines whether or not fluid leaves the blood vessels and enters the tissue spaces (interstitial fluid) is the difference between the hydrostatic pressure of the fluid in the capillaries and that of the fluid in the interstitial tissue spaces. The lining of the capillaries is only one cell layer thick. Therefore the “wall” that holds blood in the capillaries is thin. Large spaces (pores) between the cells in the capillary membrane help water filter freely through capillary membranes in either direction if a hydrostatic pressure gradient is present

 

Figure   • The process of filtration. (© 1992 M. Linda Workman. All rights reserved.)

 

Compartment A has more water molecules and greater hydrostatic pressure than does compartment B.

Water molecules move down the hydrostatic pressure gradient from compartment A through the permeable membrane into compartment B, which has a lower hydrostatic pressure. Enough water molecules have moved down the hydrostatic pressure gradient from compartment A into compartment В that both sides now have the same amount of water and the same amount of hydrostatic pressure. An equilibrium of hydrostatic pressure now exists between the two compartments, and no further net movement of water will occur.

Edema (tissue swelling) can develop as a result of changes iormal hydrostatic pressure gradients, such as in clients with right-sided congestive heart failure. In this condition, the volume of blood in the right side of the heart increases greatly because the right ventricle is too weak to pump blood efficiently into the pulmonary blood vessels. As blood volume accumulates, blood backs up into the venous system, and venous hydrostatic pressure rises. The increased venous pressure causes capillary hydrostatic pressure to increase until it is higher than the hydrostatic pressure in the interstitial spaces. Excess filtration of fluid from the capillaries into the interstitial tissue spaces occurs, resulting in the formation of visible edema.

DIFFUSION

Diffusion is the free movement of particles (solute) across a permeable membrane down a concentration gradient, that is, from an area of higher concentration to an area of lower concentration. Diffusion controls the movement of particles in solution across various body membranes.

Figure:  The process of diffusion.

    A. A small lump of sugar is placed in a beaker of water, its molecules dissolve and begin to  diffuse outward. B., C. The sugar molecules continue to diffuse through the water from an area of greater concentration to an area of lesser concentration. D. Over a long period of time, the sugar molecules are evenly distributed throughout the water, reaching a state of equilibrium. Example of diffusion in the human body: Oxygen diffuses from an alveolus in a lung, where it is in greater concentration, across the capillary membrane, into a red blood cell, where it is in lesser concentration.

Physiologic Activity

The diffusion of particles into and out of cells and fluid compartments occurs via brownian motion, the kinetic energy of molecular motion. Brownian motion is the vibration of single molecules caused by electrons orbiting at the core of each molecule. Such motion produces totally random movement of molecules, which causes molecules to move and bump into each other within a confined space. These collisions cause a temporary increase in the speed of movement. As a result of the collisions, molecules in a solution spread out evenly through whatever space is available. They move from an area of higher concentration of molecules to an area of lower concentration until equal concentrations are present in all areas. The number of collisions is related to the concentration of molecules in a confined space. Spaces with many molecules have more collisions and faster molecule motion than spaces with fewer molecules.

A concentration gradient exists when two areas have different concentrations of the same type of molecules. Brownian motion of the molecules causes them to move down the concentration gradient. As a result of brownian motion, any membrane that separates two areas is struck repeatedly by molecules. When the molecule strikes a pore in the membrane that is large enough for it to pass through, diffusion occurs. The likelihood of any single molecule colliding with the membrane and going through a pore is much greater on the side of the membrane with a higher molecule concentration. The speed of diffusion is directly related to the degree of concentration difference between the two sides of the membrane. The degree of concentration difference is usually referred to as the steepness of the gradient: The larger the concentration difference between the two sides, the steeper the gradient. Diffusion is more rapid when the concentration gradient is steeper (just as a ball rolls downhill more rapidly when the hill is steep than when the hill is nearly flat). The greater the difference in concentration, the more rapidly diffusion occurs from the area of higher concentration to the area of lower concentration. Diffusion of solute particles continues through the membrane as long as a concentration gradient exists between the two sides of the membrane. When the concentration of solute is the same on both sides of the membrane, an equilibrium exists and an equal exchange (not a net movement) of solute continues.

 Clinical Function and Significance

Diffusion is important in the transport of gases and in the movement of most electrolytes, atoms, and molecules through cell membranes. Unlike capillary membranes, which permit the diffusion of most small-sized substances down a concen­tration gradient, cell membranes are selective. They permit the movement of some substances and inhibit the movement of other substances. Some molecules cannot move across a cell membran.

“downhill” gradient exists, because the membrane is impermeable (not porous) to that molecule. Thus the concentration gradient is maintained permeability and special transport systems cause differ­ences in the concentrations of specific substances from one fluid compartment to another. For example, under normal conditions the fluid outside of the cells, the extracellular fluid (ECF), contains almost ten times more sodium ions than the fluid inside the cell, the intracellular fluid (ICF). This extreme concentra­tion difference results from the relative impermeability of the cell membrane to sodium and from a special “sodium pump” that moves any extra sodium out of the cell “uphill” against its concentration gradient and back into the ECF.

In some instances diffusion cannot occur without assistance, even down steep concentration gradients, because of membrane selectivity. A clinical example is the fact that even though the concentration of glucose is much higher in the ECF than in the ICF (creating a steep gradient for glucose), glucose cannot cross most cell membranes without the help of insulin. When insulin is present in the ECF, it binds to insulin receptor sites on cell membranes, which makes the membranes much more perme­able to glucose. Glucose can then cross the cellular membrane down its concentration gradient until either an equilibrium of glucose concentration is created or insulin binding decreases.

Diffusion across a cell membrane that requires the assistance of a transport system or membrane-altering system (e.g., insulin) is called facilitated diffusion or facilitated transport. Because this type of transport occurs down a con­centration gradient and requires no energy from the cell, it is a form of diffusion.

OSMOSIS Definition

Osmosis is the process by which only water molecules (solvent) move through a selectively permeable membrane. For osmosis to occur, a membrane must separate two fluid com­partments, at least one of which must contain a solute that cannot move through the membrane. (The membrane is therefore impermeable to this solute.) A concentration gradient of this solute must also exist. If the membrane were permeable to this solute, then the solute would diffuse through the membrane down its concentration gradient until the concentrations of solute were equal on both sides of the membrane. Because the membrane is impermeable to the solute, these particles cannot cross the membrane, but water molecules can.

Physiologic Activity

For the fluid compartments to have equal concentrations of solute, the water molecules must move down their concentration gradient from the side with the higher concentration of water molecules (and thus a lower concentration of solute molecules) to the side with the lower concentration of water molecules (and thus a higher concentration of solute molecules). This movement continues until both compartments contain the same proportions of solute to solvent. The more dilute (less concentrated) fluid contains proportionately fewer solute molecules and more water molecules than the more concentrated fluid. Thus water moves by osmosis down its concentration gradient from the area of more dilute solute to the area of more concentrated solute until a new equilibrium is achieved. At this point, the concentrations of solute in the fluid compartments (the proportion of solute to solvent) on both sides of the membrane are equal, even though the total numbers of solute and volume of water may be different. This equilibrium is achieved by the movement of water molecules rather than the movement of solute molecules. Factors that determine whether and how fast osmosis occurs include the overall concentration of particles (solute) in solution, how easily the solute dissolves in water (solubility), and the amount of membrane available for osmosis.

  CONCENTRATION OF SOLUTE

The concentration of particles in body fluids is expressed in milliequivalents per liter (mEq/L), millimoles per liter (mmol/L), and milliosmoles per liter (mOsm/L). Osmoles and milliosmoles are used to describe the total concentration of solute particles (including electrolytes) contained in a solu­tion. The number of milliosmoles present in body fluids can be expressed as either osmolarity or osmolality.

Osmolarity is the number of milliosmoles in a liter of solution; osmolality is the number of milliosmoles in a kilogram of solution. The normal osmolarity value for plasma and other body fluids ranges from 270 to 300 mOsm/L.

The body functions best when the osmolarity of the fluids in all compartments is approximately 300 mOsm/L. Many mechanisms work to keep the solute concentration close to optimum levels. When all body fluids have this solute con­centration, the osmotic pressures (water-pulling) of the vari­ous fluid compartments are essentially equal, and no net water movement occurs. In such a situation, the body fluids are said to be isosmotic to each other. Another term with essen­tially the same meaning is isotonic (sometimes called nor-motonic). Examples of specific intravenous (IV) solutions with overall concentrations of specific substances equaling 270 to 300 mOsm/L include 0.9% sodium chloride in water and Ringer’s lactate in water. Because these solutions are iso­tonic (or isosmotic) to plasma, their addition to plasma does not change the osmolarity or osmotic pressure of the plasma.

Fluids with osmolarities (solute concentrations) greater than 300 mOsm/L are hyperosmotic, or hypertonic, com­pared with isosmotic fluids. Hyperosmotic fluids have a greater osmotic pressure than do isosmotic fluids and tend to pull water from the isosmotic fluid compartment into the hy­perosmotic fluid compartment until an osmotic balance is achieved.  Fluids with osmolarities of less than 270 mOsm/L are hypo-osmotic, or hypotonic, compared with isosmotic fluids. Hypo-osmolar fluids have a lower or smaller osmotic pressure than isosmotic fluids. As a result, water tends to be pulled from the hypo-osmotic fluid compartment into the isosmotic fluid compartment until an osmotic balance is achieved.

 SOLUBILITY OF SOLUTE

Solubility refers to the degree to which a solute dissolves or dissociates completely in water. Solubility is directly related to osmotic pressure: The greater the solubility of the solutes in a fluid, the higher the osmotic pressure of that fluid.

 AMOUNT OF AVAILABLE MEMBRANE

The greater the amount of membrane available for osmosis, the faster the rate of osmosis. More membrane increases the

Side A has more solute molecules than does side B, even though the number of water molecules is the same on both sides. Thus side A has a greater osmotic (water pulling) pressure than does side B.

 

Movement of water occurs by osmosis toward side A because it has greater osmotic pressure. The membrane is not permeable to the solute molecules, so the actual number of solute molecules on side A and side В does not change. Only the water molecules move, because the membrane is not permeable to the solute molecules.Enough water molecules have moved from side В into side A that the actual concentration of solute is now the same on both sides, with a ratio of water to solute of 2:1. An equilibrium of osmotic pressure now exists between the two compartments, and no further net movement of water molecules or solute molecules will occur.

 Clinical Function and Significance

Osmosis and filtration act together in capillary fluid dynam­ics to regulate both extracellular and intracellular fluid volumes. The thirst mechanism is an excellent example of the importance of osmosis in maintaining homeostasis. Thirst re­sults from the activation of cells in the hypothalamus of the brain that respond to changes in extracellular fluid (ECF) os-molarity. These cells are so sensitive to changes in ECF os-molarity that they are called osmoreceptors. When a person loses body water, such as through excessive sweating during prolonged heavy exercise, ECF volume is decreased and os-molarity is increased (hypertonic conditions exist). The cells in the thirst center shrink as water moves from the cells into the hypertonic ECF. The shrinking of these cells stimulates a person’s awareness of thirst and increases the urge to drink. The person will usually drink enough fluid to replace the wa­ter lost through sweating and restore the ECF osmolarity to normal. After the ECF volume and osmolarity return to nor­mal levels, the osmoreceptors return to their normal size and no longer send stimulatory messages.

 ACTIVE TRANSPORT Definition

A cell must use extra energy to move a substance across the cell membrane against a concentration gradient (uphill). This type of movement is called active transport because the cell must make active efforts for net movement to occur. Because of its energy demands and uphill movement, active transport is sometimes called “pumping,” and the mechanisms are known as membrane pumps.

 Physiologic Activity

Active transport systems, or pumps, are usually located in the cell membrane and act as “gatekeepers” to maintain special en­vironments inside cells. Some active transport pumps can carry more than one substance across the membrane at the same time. The sodium-potassium pump is an example of a common ac­tive transport system that simultaneously moves two substances in opposite directions against concentration gradients.

Sodium tends to diffuse slightly down its concentration gradient into the intracellular fluid (ICF) because it has such a high extracellular fluid (ECF) concentration compared with its ICF concentration. Similarly, because potassium has such a high concentration inside the cells compared with its con­centration in ECF, it tends to diffuse slightly down its con­centration gradient into the ECF. The action of the sodium-potassium pump moves the extra sodium out of the cell and returns the lost potassium back into the cell. The sodium-potassium pump requires the use of cellular energy. The energy for this process usually comes from breaking a high-energy bond (~P), which occurs when a phosphate group is split off from an adenosine triphosphate (ATP) molecule. The functioning of active transport pumps depends on the presence of adequate cellular ATP.

         Clinical Function and Significance

Cells use active transport to regulate cell volume and to con­trol the intracellular concentration of many substances. All cells function best when their internal environments are maintained separately from the changes occurring in the extracel­lular fluid (ECF) environment.

A clinical example of what occurs when active transport fails is what results from tissue hypoxia (decreased oxygen supply in the body). Without adequate oxygen, ATP cannot be produced in sufficient amounts. Without ATP, the sodium-potassium pump cannot remove the extra sodium ions that have diffused from the ECF into the cell. The increased sodium concentration inside the cell increases the osmolarity and the osmotic pressure of the fluid inside the cell. Water moves into the cell in response to the increased osmotic pressure, causing the cell to swell and perhaps to lyse (break open) and die if oxygen is not provided.

         CAPILLARY DYNAMICS

The circulatory system delivers nutrients and removes wastes at the tissue level. The important blood vessels for nutrient waste exchange are the thin-walled, porous capillaries. Nutrient delivery and waste removal depend on fluid movement in the capillary. Fluid movement at the capillary level is dynamic not only because it is continuous but also because the homeostasis of plasma and interstitial fluid volumes must be maintained. Opposing processes must occur for nutrients to move into tissue spaces, for wastes to move into circulation, and for the fluid vol­umes of both the vascular and tissue spaces to be maintained.

During these processes, some fluid with nutrients must leave the capillary and enter the interstitial (tissue space) fluid compartment for a short period, which temporarily expands the interstitial fluid volume. The nutrients in the interstitial fluid are taken up by the cells through various membrane transport processes. Water may be exchanged between the intracellular compartment and the interstitial compartment, but under normal circumstances there is no net change in water volume. Metabolic wastes created in the cells are moved into the interstitial fluid. These waste products and any extra fluid in the interstitial space must be returned via the capillary to the systemic circulation. If there were no way to return the fluid originally lost into the interstitial compartment back to the blood, the blood volume would be depleted to the point of circulatory failure, and the interstitial fluid compartment would greatly expand.

 Capillary Forces Influencing Fluid Movement

Forces at the capillary level permit capillary fluid loss to be followed by a return of fluid to the capillary so that a near-equilibrium of fluid distribution is maintained at the capillary tissue level. These forces, known as Starling’s forces, are outlined in Figure 11-6. The near-equilibrium is based on the fact that the forces tending to move fluid out from the capil­lary at the arterial end are nearly equal to the forces tending to move fluid from the interstitial compartment back into the capillary at the venous end.

Blood flowing from the arterial end of the capillary to the venous end is controlled by the following:

* Hydrostatic pressure of the blood

* Dynamic ejection of the blood from the left ventricle of the heart

* Patency or openness of the capillaries

The blood entering the arterial end of the capillary has a blood pressure, or a capillary (plasma) hydrostatic pressure (PHP), of about 32 mm Hg. The capillary membrane is and permeable, and the usual tissue hydrostatic pressure is low. These factors create a natural tendency for filtration of fluid from the blood outward into the tissue spaces. The fluid portion of the blood, along with most of the smaller substances dissolved in the blood, filters through the capillary membrane into the tissue spaces. Through this process, nutri­ents and other essential substances can reach the cells.

If net filtration as a result of plasma hydrostatic pressure were the only force or factor involved at this level, blood vol­ume would be progressively lost from circulation and would appear in the tissues. Fortunately, other mechanisms that fa­vor the reabsorption of tissue fluid into the capillaries are also part of capillary dynamics. These mechanisms are plasma os­motic pressure and tissue hydrostatic pressure.

Osmosis (of water) through the capillary membrane (in either direction) occurs in response to differences in the concentrations of osmotically active substances in the capillary blood and tissue fluid. Tissue osmotic pressure (TOP) tends to draw fluid out of the capillary. Plasma osmotic pressure(POP) in the capillary tends to keep fluid in the capillary and draw fluid from the interstitial space into the capillary. Under normal conditions, osmotic pressure in capillary plasma is greater than osmotic pressure in tissue because there is a higher concentration of proteins in the blood than in the interstitial fluid.

Because the capillary membrane is highly impermeable to proteins, it does not allow blood proteins to pass freely through it into the tissue space. Therefore blood proteins remain in the capillary and add to the osmotic pressure. The specific type of osmotic pressure exerted by plasma proteins is called colloidal oncotic pressure because it is caused by the presence of proteins (colloidal substances) rather than by dissociated ions such as sodium (crystalloid substances). The average colloidal oncotic pressure in capillary blood is about 22 mm Hg.

Blood pressure (hydrostatic pressure) is greater than colloidal oncotic pressure at the arterial end of the capillary. Capillary hydrostatic pressure favors the filtration of fluid fromCapillary blood normally flows from the arterial end to the venous end:

Venous end of capillary

At the arterial end, the forces that tend to move fluid from the capillary into the tissue space are

Plasma hydrostatic pressure 32 mm Hg

Tissue osmotic pressure 10 mm Hg

Total forces moving fluid out = 42 mm Hg

At the arterial end, the forces that tend to move fluid from the tissue spaces into the capillary are

Tissue hydrostatic pressure 4 mm Hg

Plasma colloidal oncotic pressure 22 mm Hg

Total forces moving fluid in = 26 mm Hg

The total forces tending to move fluid out at the arterial end are 16 mm Hg higher than the total forces tending to move fluid in at the arterial end (42 – 26 = 16). Thus, at the arterial end, fluid leaks out of the capillary into the tissue (interstitial) spaces. At the venous end of the same capillary, the forces that tend to move fluid from the capillary into the tissue space are

Plasma hydrostatic pressure 17 mm Hg

Tissue osmotic pressure 6 mm Hg

Total forces moving fluid out = 23 mm Hg

At the venous end of the capillary, the forces that tend to move fluid from the tissue spaces back into the capillary are

Tissue hydrostatic pressure-8 mm Hg

Plasma colloidal oncotic pressure 24 mm Hg

Total forces moving fluid in = 32 mm Hg

The total forces tending to move fluid out at the venous end are 9 mm Hg lower than the total forces tending to move fluid into the capillary at the venous end (32 – 23 = 9). Thus, at the venous end, fluid moves from the tissue spaces back into the capillary.

Because the pressures tending to move fluid out of the capillary at the arterial end (16 mm Hg) are greater than the pressures that tend to move fluid back into the capillary at the venous end (9 mm Hg), more fluid is lost from the capillary than is returned to it. Lymph drainage eventually returns this extra lost fluid to the systemic circulation.

The capillary into the tissue spaces, and colloidal oncotic pressure favors the reabsorption of fluid from the interstitial space into the capillary. The difference between these two capillary pressures at the arterial end of the capillary indicates that the filtering force outward is greater than the reabsorbing force inward.arterial end of the capillary because the water lost from the capillary has diluted the solute concentration of the tissue fluid. As a result, forces favoring the return of water from the tissues into the capillary are greater than the forces favoring filtration, and some water returns from the interstitial space back into the capillary at the venous end.

Tissue Forces Influencing Fluid Movement

Tissue forces also influence the movement of solutions at the capillary level. These forces are tissue hydrostatic pres­sure (THP) and tissue osmotic pressure (TOP), both of which are usually relatively small forces. In some diseases, however, these forces increase greatly and change capillary dynamics.

To determine the direction of fluid movement in any one area of the capillary, the forces that move fluid out from the capillary are compared with the forces that move fluid into the capillary. Two forces at the arterial end that move fluid out from the capillary are the plasma hydrostatic pressure (PHP) (normally about 32 mm Hg) and the TOP (normally about 10 mm Hg). The pressures at the arterial end that return fluid to the capillary are the plasma colloidal oncotic pressure (nor­mally about 22 mm Hg) and the tissue hydrostatic pressure (THP) (normally about 4 mm Hg). Because the outward filtration force is 16 mm Hg higher than the inward reabsorbing force, the overall result at the arterial end of the capillary is the outward filtration of fluid and small solute particles into the tissue spaces.

Plasma hydrostatic pressure (PHP) decreases as blood flows through the length of the capillary. As filtration pro­ceeds along the capillary, water is lost from the capillary, and the PHP gradually decreases. Therefore the pressures that cre­ate the outward filtration force (from the capillary into the in­terstitial fluid) decrease, whereas the pressures that create the inward reabsorption force (from the interstitial fluid into the capillary) remain the same. Eventually, the outward filtration pressures and the inward reabsorption pressures become equal.

 Clinical Function and Significance

Finally, at the venous end of the capillary, the inward reabsorption forces exceed the outward filtration forces. The venous end of the capillary has a much lower hydrostatic pressure than does the arterial end. This decreased hydrostatic pressure has two causes:

• Because much of the water in the blood was filtered out of the capillary at the arterial end, the volume of water remaining in the blood at the venous end of the capillary is diminished.

■ Because the venous portion of the capillary is farther away from the heart than the arterial end, blood pressure is lower in the venous end.

At the venous end of the capillary, the hydrostatic pressure is low and the interstitial fluid (tissue) hydrostatic pressure is high (because water has moved from the arterial end of the capillary into the interstitial space). The colloidal os­motic pressure at the venous end of the capillary exceeds that at the arterial end because water has been lost, which in­creases the concentration of proteins. The tissue osmotic pressure at the venous end of the capillary is lower than at the Lymph

In most cases, not all of the fluid that leaves the capillary at the arterial end and enters the interstitial space is returned to the capillary at the venous end. A small amount remains in the tissues. If this situation is not balanced by another mechanism to return the fluid to the systemic circulation, blood volume would become depleted and the interstitial areas would constantly be edematous. Instead, this extra fluid leaking out from the capillaries is returned to the systemic circulation as lymph.

Lymph fluid is similar to blood plasma (from which it is formed) but contains far less protein. It is returned to the circulation by lymph vessels, or lymphatics. Lymphatics begin as small, thin-walled, vein-like vessels that join to form larger lymphatic vessels. Two large groups of lymphatic vessels connect the entire lymph system with the general circulatory system. The left thoracic lymph duct drains lymph from the abdomen, gastrointestinal tract, pelvis, lower extremities, left side of the thorax, left arm, and left side of the head and neck into the left subclavian vein at the point where it joins the left internal jugular vein. Lymph from the right arm, right side of the thorax, and right side of the head and neck drains into the right subclavian vein through three lymph ducts. Lymph nodes are situated along the lymphatic paths and filter the lymph fluid.

Lymphatics carry lymph fluid in one direction: toward the heart. Lymph flow is slower than blood flow because lymph has no pump and no direct connection between the arterial blood circulation and the lymphatic system. Lymph flow is enhanced by skeletal muscle contractions, intrathoracic pres­sure changes during breathing, and a peristalsis-like motion in the lymph vessels.

Hormonal Regulation of Fluid and Electrolyte Balance

The endocrine system helps to control fluid and electrolyte balance. Three hormones that help control these critical balances are aldosterone, antidiuretic hormone (ADH), and atrial natriuretic peptide (ANP).

 ALDOSTERONE

Aldosterone is a hormone secreted by the adrenal cortex. Al­dosterone secretion is stimulated by either a decreased sodium level in the extracellular fluid (ECF) or an increased sodium level in urine. The secretion and function of aldos­terone, angiotensinogen, and angiotensin are outlined in Fig­ure 11-8. Aldosterone directly influences sodium balance by preventing sodium loss. Because sodium in body fluids exerts osmotic (water-pulling) pressure, water attempts to follow sodium in physiologically proportionate amounts (Guyton & Hall, 2000). As a result of this sodium-water relationship, al­dosterone secretion also indirectly regulates water balance.

In the kidney, blood is supplied to the nephrons via the af­ferent arteriole. Specialized cells (juxtaglomerular cells) inside the afferent arteriole near the nephron glomeralus are sensitive to changes in serum concentrations of sodium. This area of the afferent arteriole comes into direct contact with a specialized area of the distal convoluted tubule (the macula densa). Together, the juxtaglomerular cells and the macula densa form the juxtaglomerular complex. When this com­plex senses that actual serum sodium concentrations are lower thaormal or that the total blood volume is low, the macula densa stimulates juxtaglomerular cells to secrete renin.

Renin acts on an inactive plasma protein called an-giotensinogen, converting it to angiotensin I. Angiotensin I is immediately further degraded into angiotensin II by an en­zyme called angiotensin-converting enzyme (ACE). An­giotensin II causes the constriction of many blood vessels and stimulates an increased secretion of aldosterone from the adrenal cortex. Aldosterone acts on the distal convoluted tubules of the nephrons. When serum osmolarity is too low, aldosterone se­cretion stimulates these areas to reabsorb sodium from the urine back into the circulation (in exchange for potassium); this increases serum osmolarity. Aldosterone secretion in­creases when blood osmolarity or serum sodium levels are low, and its presence is normally required to prevent excessiverenal excretion of sodium. Aldosterone secretion also helps to prevent serum potassium levels from becoming too high. The secretion of aldosterone is inhibited when blood osmolarity or serum sodium levels are greater thaormal.

         ANTIDIURETIC HORMONE

Antidiuretic hormone (ADH), also known as vasopressin, is produced in the brain and stored in the posterior pituitary gland. The release of ADH from the posterior pituitary gland is controlled by the hypothalamus in response to changes in blood osmolarity. The hypothalamus contains specialized cells (osmoreceptors) that are sensitive to changes in blood osmolarity. Increased blood osmolarity, especially an increase in the concentration of plasma sodium, results in a slight shrinkage of these cells and triggers the hypothalamus to stimulate the posterior pituitary to release ADH.

ADH acts directly on kidney tubules and collecting ducts, making them more permeable to water. As a result, more water is reabsorbed by these tubules and returned to the cir­culation, which in turn decreases the osmolarity of the blood by making it more dilute. When blood osmolarity decreases, especially when the plasma sodium concentration is below normal, the osmoreceptors swell slightly and inhibit the re­lease of ADH. Less water is reabsorbed and more is lost from the body in the urine. As a result, the amount of water in the extracellular fluid (ECF) decreases, bringing osmolar­ity to normal.

         ATRIAL NATRIURETIC PEPTIDE

Atrial natriuretic peptide (ANP) is secreted by special cells that line the atria of the heart. It is secreted in response to increased blood volume and blood pressure. ANP binds to receptor sites in the collecting ducts of the nephrons, creat­ing effects opposite those of aldosterone. Kidney reabsorp-tion of sodium is inhibited at the same time that glomerular filtration is increased (Briggs et al., 1996). The outcome is increased output of urine with a high sodium content, which results in decreased circulating blood volume and decreased blood osmolarity.

Body Fluids

Fluids, especially water, make up about 55% to 60% of to­tal adult body weight and can be divided into the extracel­lular fluid (ECF) and intracellular fluid (ICF). The ECF compartment accounts for approximately 15 L (40%) of to­tal body water and includes interstitial fluid, blood plasma, lymph, bone and connective tissue water, and the fluid within special spaces (transcellular fluid), such as cere-brospinal fluid, synovial fluid, peritoneal fluid, and pleural fluid. ICF accounts for the remaining 25 L (60%) of total body water.

A person’s age, gender, and ratio of lean mass to body fat influence the amount and distribution of body fluids. An older adult has less total body water than a younger adult. Because fat cells contain practically no water, an obese per­son has less total body water than a lean person of the same body weight.Decreased serum sodium concentration sensed by cells in afferent arterioleStimulates secretion of renin from juxtaglomerular complexAngiotensin I ReninBlood volume lowAngiotensin II constricts afferent arterioleBlood volume normal or highAngiotensin II constricts efferent arteriole  Allows fluid to be removed, thus increasing the relative concentration of sodium in the blood Increases serum sodium level without further decreasing blood volume

 WOMEN’S HEALTH CONSIDERATIONS

 A woman of any age usually has less total body water than does a man of similar size and age. This difference exists be­cause men generally have more muscle mass than women and because women have a higher percentage of body fat. Differ­ences in muscle mass and percentage of body fat are partly a result of the influence of sex hormones. These differences in fat to lean body weight may be responsible for some of the differ­ences seen in women’s and men’s responses to drugs.

Body fluids allow cell nutrition and transport active mol­ecules (e.g., hormones) that are important to the regulation of normal physiologic functions. Most physiologic processes occur only in a watery environment. Body fluids are constantly renewed, purified, and replaced as fluid bal­ance is maintained through intake and output. The total amount of water within each fluid compartment is stable, but water moves continually among all compartments. Wa­ter is not static in any compartment but is exchanged con­stantly while maintaining a volume equilibrium. summarizes the key points regarding fluid and electrolyte balance.

 SOURCES OF FLUID INTAKE

Fluid intake is regulated through the thirst drive. Fluids enter the body primarily as liquids. Because solid foods contain up to 85% water, some fluid also enters the body as in­gested solid foods. In addition, water is a by-product of cellu­lar metabolism. This metabolic water accounts for about 300 mL of the daily water requirement. A rising plasma osmolarity or a decreasing plasma volume stimulates the sensation of thirst. Sensations such as mouth dryness or the thought that a person has not had a drink recently can trigger the thirst drive. An adult drinks an average of 1500 mL of fluid per day and ob­tains an additional 800 mL of fluid from ingested foods kidney is the most important and the most sensitive. Water loss via the kidney is closely regulated and is adjustable. The volume of urine excreted daily varies depending on the amount of fluid intake and the body’s need to conserve fluids.

The minimum amount of urine per day needed to dissolve and excrete toxic waste products is 400 to 600 mL. This min­imal volume is called the obligatory urine output. If the 24-hour urine output falls below the obligatory output amount, wastes are retained and can cause lethal electrolyte imbal­ances, acidosis, and a toxic build up of nitrogen. This urine is maximally concentrated, with a specific gravity (the weight of the liquid compared with the weight of pure water) of 1.032 or higher and an osmolarity of at least 1200 mOsm/L.

Urine can also become very dilute, with a specific gravity of 1.005 and an osmolarity of 200 mOsm/L. Dilution can result from a large fluid intake and is reflected in a large volume of urine output. The ability of the kidneys to make either con­centrated or very dilute urine helps to maintain fluid and electrolyte balance. With the influence of aldosterone, antidiuretic hormone (ADH), and atrial natriuretic peptide (ANP), the kidney is able to respond when extracellular fluid concentra­tions, volumes, or pressures change.

Other normal water loss occurs through the skin, the lungs, and the gastrointestinal tract. Additional water losses can oc­cur via salivation, drainage from fistulas and drains, and gastrointestinal suction. “Measured by subtracting the amount returned from the amount instilled. Measurement is accurate only when these substances are excreted in liquid form.

Water loss from the skin, lungs, and stool — called insensible water loss because it cannot be controlled—can be significant. In a healthy adult, insensible water loss is about 15 to 20 mL/kg/day. Insensible water loss can increase dramatically in hypermetabolic states such as thyroid crisis, trauma, burns, states of extreme stress, and fever. For every degree Celsius of increase in body temperature, insensible water loss increases by 10%. Insensible water loss also increases when atmospheric conditions are hot and dry. Examples of clients at risk for increased insensible water loss include those undergoing mechanical ventilation and those with rapid respirations (tachypnea). Insensible water loss (not including sweat) is pure water and does not contain electrolytes. Therefore excessive amounts of insensible water loss result in a more hypertonic extracellular fluid (ECF) with a smaller volume. If this loss is not balanced by intake, the hypertonic ECF and ac­companying dehydration can lead to hypernatremia (ele­vated serum sodium level).

Loss by sweating is variable and can reach a maximum rate of about 2 L/hr. Although it contains electrolytes, sweat is slightly hypotonic compared to plasma. The amount of sweating is regulated by the autonomic nervous system, body temperature, and blood flow in the skin. Water loss through stool is normally minimal. However, this loss can increase significantly with severe diarrhea or ex­cessive fistula drainage. Clients with ulcerative colitis can ex­perience a diarrheal fluid loss of several liters per day. Diar-rheal fluid contains water, potassium, sodium, bicarbonate, and chloride. Thus, with diarrhea, hypotonic fluid containing some electrolytes is lost.

Electrolytes

Electrolytes, or ions, are substances in body fluids that carry an electrical charge. Cations are positively charged ions; an-ions are negatively charged ions. Body fluids are electro-chemically neutral, which means that the number of positive ions is balanced by an equal number of negative ions. However, the distribution of ions differs in the extracellular fluid (ECF) and the intracellular fluid (ICF)

Most electrolytes have different concentrations in the ICF and ECF. This concentration difference helps maintain mem­brane excitability and transmit nerve impulses. The ranges of electrolyte concentration in these fluid compartments are ex­tremely narrow. Thus even small changes in these concentra­tions can result in major pathologic alterations.

Maintenance of plasma and interstitial osmolarity. Generation and transmission of action potentials Maintenance of acid-base balance Maintenance of electroneutrality

Regulation of intracellular osmolarity. Maintenance of electrical membrane excitability Maintenance of plasma acid-base balance

Cofactor in blood-clotting cascade Excitable membrane stabilizer Adds strength/density to bones and teeth Essential element in cardiac, skeletal, and smooth muscle contraction

Maintenance of plasma acid-base balance Maintenance of plasma electroneutrality Formation of hydrochloric acid

Excitable membrane stabilizer

Essential element in cardiac, skeletal, and smooth muscle contraction

Cofactor in blood-clotting cascade Cofactor in carbohydrate metabolism Cofactor in DNA and protein synthesis

Activation of B-complex vitamins

Formation of adenosine triphosphate and other high-energy substances Cofactor in carbohydrate, protein, and lipid metabolism.

Electrolyte homeostasis is controlled by balancing the di­etary intake of electrolytes with the renal excretion or reab-sorption of electrolytes. For example, the concentration of plasma potassium is maintained between 3.5 and 5.0 mmol/L. In theory, the potassium in common foods could greatly in­crease the ECF potassium concentration and lead to major problems. Usually, however, the excretion of potassium by the kidney keeps pace with potassium intake and prevents major changes in the concentration of plasma potassium.

 SODIUM

Sodium (Na⁺) is the major cation in the extracellular fluid (ECF) and is the main factor responsible for maintaining ECF osmolarity. The activity of the sodium-potassium pump keeps the sodium concentration of the intracellular fluid (ICF) low (about 14 mmol/L) while maintaining high sodium concen­trations in the plasma and other extracellular fluids. Maintaining this difference in sodium concentration is vital for the following physiologic functions:

Initiation of skeletal muscle contraction

•  Initiation of cardiac contractions

•  Transmission of nerve impulses

Maintenance of ECF osmolarity Maintenance of ECF volume

•        Maintenance of the kidney urine-concentrating system
The concentration of sodium in the ECF determines whether water is retained, excreted, or moved from one body compartment to another.

To maintain electrical balance, the concentration of sodium (a cation) within a body fluid must be matched by an equal concentration of anions (negatively charged substances). Each positive charge in the ECF must be balanced by a negative charge so the fluid does not carry either an over­all positive or an overall negative charge. When this balance is present, a state of electroneutrality exists in that fluid. Changes in the concentration of plasma sodium seriously change fluid volume and the distribution of other electrolytes.

The normal concentration of plasma sodium ranges be­tween 136 and 145 mEq/L or mmol/L. Sodium enters the body through the ingestion of many foods and fluids . The average dietary intake of sodium is about 6 to 12 g/day. Sodium is also stored deep within the kidney tissues and can be released to the ECF as needed. De­spite great variations in sodium intake, the concentration of serum sodium usually remains within the normal range. Serum sodium balance is regulated by the kidney under the influences of aldosterone, antidiuretic hormone (ADH), and atrial natriuretic peptide (ANP).

Low serum sodium levels inhibit the secretion of ADH and ANP and stimulate aldosterone secretion. Together these actions increase serum sodium concentration by increasing kidney re-absorption of sodium and enhancing kidney loss of water.

High serum sodium levels inhibit aldosterone secretion and directly stimulate the secretion of ADH and ANP. To­gether these hormones cause an increase in kidney excretion of sodium and kidney reabsorption of water.

 POTASSIUM

In contrast to sodium, potassium (K⁺) is the major cation of the intracellular fluid (ICF). The normal plasma concentration of potassium ranges from 3.5 to 5.0 mEq/L or mmol/L (see Table 11-5). The normal ICF concentration of potassium is about 140 mEq/L (mmol/L). Because of its high concentra­tion inside cells, potassium has some control over intracellu­lar osmolarity and volume. Keeping this large difference in potassium concentration between the ICF and the extracellu­lar fluid (ECF) is critical for excitable tissues to generate ac­tion potentials and transmit impulses. Functions of potassium include the following:

•        Regulation of protein synthesis Regulation of glucose use and storage

•        Maintenance of action potentials in excitable membranes Because potassium levels in the plasma and interstitial fluid are so low, any change in concentration is poorly tolerated by the body and seriously affects physiologic activities. For example, a decrease in plasma potassium of only 1 mEq/L (from 4 mEq/L to 3 mEq/L) is a 25% difference in total ECF potassium con­centration. In contrast, a decrease in plasma sodium of 1 mEq/L (from 140 mEq/L to 139 mEq/L) is, overall, a much smaller change (less than 1%) in total ECF sodium concentration.

Potassium drifts out of cells down its concentration gradi­ent into the ECF. Almost all foods contain potassium. Potassium intake averages approximately 2 to 20 g/day. Despite heavy potassium intake and the drifting of potassium from cellular storage sites into the ECF, the healthy body keeps plasma potassium levels within the narrow range of normal values required for physiologic function.

The primary controller of ECF potassium concentration is the sodium-potassium pump within the membranes of all body cells. This pump removes three sodium ions from the fluid inside the cell for every two potassium ions that it re­turns to the cell. In this way, the levels of both serum sodium and cellular potassium remain high.

Some potassium regulation also occurs through kidney function. The kidney is the excretory route for ridding the body of ECF potassium (80% of potassium removed from the body occurs via the kidney). Unlike sodium, no hormone has been identified that directly controls kidney reabsorption of potas­sium; thus the kidney does not conserve potassium directly.

 CALCIUM

Calcium (Ca²⁺) is a mineral whose presence and functions are closely related to those of phosphorus and magnesium. Cal­cium is a divalent cation (an ion having two positive charges) that exists in the body in two forms: bound and ionized (un­bound or free).

Bound calcium is usually connected to specific serum pro­teins, especially albumin. Ionized calcium is present in the blood and other extracellular fluid (ECF) as free calcium. Free calcium is the active form and must be kept within a nar­row range in the ECF. The body functions best when plasma calcium concentrations are maintained between 9.0 and 10.5 mg/dL, or between 2.25 and 2.75 mmol/L (see Table 11-5). Because the concentration of calcium in the intracellular fluid (ICF) is low, calcium has a steep gradient between ECF and ICF. Calcium functions in many ways and in many special­ized body systems, including the following:

•  Enhances the activity of enzymes or reactions Increases skeletal muscle contraction
Increases cardiac muscle contraction

•  Regulates nerve impulse transmission

•  Assists in blood clotting

•  Provides bone strength and density

Calcium enters the body by dietary intake and absorption through the intestinal tract (Table 11-8). Absorption of dietary calcium requires the active form of vitamin D. Calcium is stored in the bones. When both plasma calcium levels and stored calcium levels are adequate, intestinal absorption of di­etary calcium is inhibited and urine excretion of excess cal­cium increases. When more plasma calcium is needed, parathyroid hormone (PTH) is secreted and released from the parathyroid glands. PTH causes serum cal­cium levels to increase in the following ways:

•  Releasing free calcium from bone storage sites directly into the ECF (resorption)

•  Stimulating vitamin D activation, thus increasing intestinal absorption of dietary calcium

•  Inhibiting kidney excretion of calcium and stimulating kidney reabsorption of calcium

When excess calcium is present in plasma, secretion of PTH is inhibited and the secretion of thyrocalcitonin (TCT), a hor­mone secreted by the thyroid gland, is increased. TCT causes the plasma calcium level to decrease in the following ways:

•  Inhibiting bone resorption of calcium

•  Inhibiting activation of vitamin D, causing decreased gastrointestinal uptake of calcium

•  Increasing kidney excretion of calcium in the urine

 

MAGNESIUM

Magnesium (Mg²⁺) is another mineral that forms a cation when dissolved in water. Adults have an average of 25 g of magnesium, most of which (60%) is stored in bones and car­tilage. Little magnesium is present in the extracellular fluid (ECF). Serum levels of free magnesium range from 1.2 to 2.0 mg/dL, or 0.66 to 1.07 mmol/L (see Table 11-5). Much more magnesium is present in the intracellular fluid (ICF), and Increases bone resorption of calcium (leaching of stored calcium) Increases the absorption of ingested calcium from the gastrointestinal tract into the TABLE 11-11      extracellular fluid Increases the renal reabsorption of calcium at the proximal convoluted tubule  has more functions inside the cells than in the plasma. Mag­nesium is critical for the following intracellular reactions or activities:

•  Stimulating skeletal muscle contraction

•  Participating in carbohydrate metabolism

•  Activating adenosine triphosphate (ATP)

•  Activating B-complex vitamins

•  Enhancing deoxyribonucleic acid (DNA) synthesis

•  Enhancing protein synthesis

Extracellular magnesium regulates blood coagulation and skeletal muscle contractility.

Magnesium is found in many foods, such as nuts, vegetables, fish, and whole grains. The daily magne­sium requirement for adults is approximately 300 mg.

Although magnesium is similar to calcium in many re­spects and its presence in serum must be kept within a narrow range of normal values, little is known about its regulation. Magnesium is absorbed from the intestinal tract at the same place as calcium. The absorption of phosphorus inhibits mag­nesium absorption. Parathyroid hormone (PTH) stimulates the release of magnesium from bone in much the same way that it stimulates the release of calcium.

 CHLORIDE

Chloride (Cl~) is the major anion of the extracellular fluid (ECF) and works with sodium in aintaining ECF osmotic pressure. Chloride is important in the formation of hydrochloric acid in the stomach. The normal plasma concentration of chloride ranges from 90 to 110 mEq/L or mmol/L.

Only a small amount of chloride is present inside the cells because negatively charged particles on the cell membrane repel chloride and prevent it from crossing the membrane. However, extracellular chloride can enter cells when ex­changed for another anion that is leaving the cell. This situa­tion, called a chloride shift, results in decreased concentra­tions of plasma chloride but no net body loss of chloride. Bicarbonate (HCO₃) is the anion most commonly exchanged for chloride. Chloride enters the body through dietary intake. Because chloride (along with sodium, potassium, and many other minerals) is a part of a salt, most diets contain enough chloride to meet the normal needs of the body.

Fluid and Electrolyte Changes Associated with Aging

Only 45% to 50% of the body weight of older adults is water, compared with 55% to 60% in younger adults. This decrease occurs because of a loss of muscle mass and a reduced ratio of lean body weight to total body weight. This decrease in to­tal body water places older adults at greater risk for dehydra­tion. Multiple symptoms point to fluid volume deficit in the older adult.

Skin turgor (the normal resiliency of a pinched fold of skin) is not always an accurate assessment of extracellular fluid (ECF) volume deficit (dehydration) in the older adult because the natural aging process is associated with decreased turgor. Furthermore, the older adult may have a diminished thirst sensation and decreased kidney function, both of which contribute to the risk for dehydration and make assessment more difficult. Wheurses work with older clients, it is extremely important that they accurately record intake and output and weight, because these measurements reflect hydration status more accurately than does skin turgor.

The normal concentration of serum electrolytes also changes with the aging process. Electrolyte balance may be more difficult to maintain in older adults. In particular, small changes in the concentrations of potassium and calcium may produce unexpectedly serious results. Although the ranges of electrolytes in plasma and in-tracellular fluid (ICF) may remaiormal, the balance is frag­ile and more easily disturbed in an older adult. Part of this fragility is related to decreased regulatory functions that occur with aging. Age-related kidney changes include decreased blood flow, decreased filtration, and decreased numbers of functional nephrons. Kidney and capillary changes associated with hypertension are more likely to be present in the older adult.

ASSESSMENT OF FLUID AND ELECTROLYTE BALANCE.

History

One way of organizing history data to assess the client’s fluid and electrolyte status is to use Gordon’s Functional Health Patterns (Gordon, 2000). The patterns that most affect fluid and electrolyte status are the Nutritional-Metabolic The client’s nutritional history can often reveal a problem that affects fluid and electrolyte balance. The nurse obtains this information directly because the client may not under­stand the connection between dietary intake and the onset of fluid and electrolyte imbalances.

The guidelines for obtaining a thorough fluid and elec­trolyte history do not differ from those for assessing any other system; however, the information collected is more specific. For example, exact intake and output volumes are important, as are serial daily weights. The nurse may need to guide the client in accurately reporting the amount of fluid ingested and changes in urine patterns. The nurse also assesses the types of fluids and foods ingested to determine amount and osmolar-ity. Many clients do not consider solid food to contain liquid. Solid foods such as ice cream, gelatin, and ices are liquids at body temperature, and the nurse includes them when calcu­lating fluid intake.

Output fluids include losses not only through urine but also through perspiration, diarrhea, and insensible loss during fevers. The nurse asks specific questions about prescribed and over-the-counter medications and checks the dosage, the length of time taken, and the client’s compliance with the medication regimen.

How much salt do you typically add to your food? Do you use salt substitutes? How is your appetite?

Do you have any difficulty chewing or swallowing? What is your typical daily fluid intake? What types of fluids (water, juices, soft drinks, coffee, tea)? How much? Have you had any recent change in your weight? Weight gain? Weight loss? How much? Have you noticed a change in tightness of your rings or shoes? Tighter? Looser?

Elimination Pattern

What is your usual bowel elimination pattern? Frequency?

Character? Discomfort? Laxatives? What is your usual urinary elimination pattern? Frequency?

Amount? Color? Odor? Control? Have you noticed a change in the amount of urine? Do you have any problem with excessive perspiration? Do you have any other type of drainage?

an imbalance of fluid, potassium, sodium, or hydrogen ions if additional conditions of water loss, such as vomiting or ex­cessive sweating, also occur.

Older adults often use laxatives, which can disturb fluid and electrolyte balance. Misuse and overuse of these drugs can lead to serious imbalances.

Other important areas of the client history include body weight changes, thirst or excessive drinking, exposure to hot environments, and the presence of other disorders, such as kidney or endocrine diseases (e.g., Cushing’s disease, Addi-son’s disease, diabetes mellitus, and diabetes insipidus). The nurse makes a general assessment of the client’s level of consciousness and mental status, because changes in mental sta­tus may support findings of imbalance. In such cases, the nurse may need to check the accuracy of historical data with family members.

Physical Assessment

Hydration is the normal state of fluid balance. A normally hydrated adult is alert and has moist eyes and mucous mem­branes, a urine output nearly the same as the amount of fluid ingested (with a urine specific gravity of approximately 1.015), and good skin turgor.

The nurse assesses skin turgor by pinching a fold of skin. This pinched fold should return immediately to its original shape after release. Decreased turgor, a sign of dehydration, is present when the fold remains in a pinched shape after being released and rebounds slowly (tenting). The nurse can best assess skin turgor in body areas that contain lit­tle fat tissue, such as over the sternum, on the forehead, or on the back of the hand. An older person may have poor skin tur­gor because of the loss of tissue elasticity related to the aging process; thus a true state of hydration may be more difficult to assess in an older adult than in a younger adult. The best areas for assessing turgor in the older adult are over the sternum and on the forehead.

Skin hydration assessment also includes an examination for dryness. The mucous membranes and the conjunctiva are normally moist. An assessment of fluid balance always in­cludes an examination of the eyes, nose, and oral mucous membranes. A dry, sticky, “cottony” mouth; the absence of tearing; weight loss; and decreased urine output all indicate an actual fluid volume deficit. A major criterion used in assessing fluid and electrolyte status is accurate measurement of fluid intake and output. Ac­curate assessment of actual fluid intake and output is the nurse’s responsibility, and volumetric measuring devices must be used.

Behavioral and neurologic assessments are included in fluid assessment because changes in fluid balance can result in an alteration of neurologic function. In hypertonic states, neuronal cell shrinkage may induce serious nervous system excitability and hyperactivity, and convulsions may occur. Another variable to assess is the degree of thirst, but this may be difficult to gauge in a confused older client. The nurse approximates insensible water loss (e.g., sweat) in every client. Special situations also require an as­sessment of fluid loss from other routes, including the following:

•  Fluid losses from wounds

•  Gastric or intestinal drainage

•  Blood loss from hemorrhage

•  Drainage of body secretions, such as bile and pancreatic juices, through fistulas

Electrolytes control the activity of excitable membranes, and electrolyte imbalances are associated with altered func­tion of these membranes. Electrolyte assessment includes a complete neuromuscular assessment of muscle tone and strength, movement, coordination, and tremors. Assessment of other systems, including the cardiac system (heart rate, the strength of contractions, and the presence of dysrhythmias) and gastrointestinal system (peristalsis), may indicate changes of excitable membrane function.

Part of the nurse’s assessment focuses on changes from previous findings (including mental status, physical exami­nation data, and laboratory data). Fluid and electrolyte im­balances can occur quickly; therefore the nurse must be fa­miliar with the client’s baseline assessment data to detect any changes

Psychosocial Assessment

Psychosocial assessment related to fluid and electrolyte sta­tus includes both psychologic and cultural factors that might influence balance. Depressed clients may refuse fluids or for­get to drink adequate fluids. Clients with bulimia or anorexia nervosa (eating disorders) may use laxatives to excess or may induce vomiting, resulting in fluid and electrolyte imbal­ances. The nurse also assesses social practices. For example, excessive alcohol or drug use may lead to fluid or electrolyte imbalance.

Diagnostic Assessment

Laboratory results are important in identifying specific fluid and electrolyte imbalances or disorders that alter fluid and electrolyte status. Other laboratory values that are helpful in assessing fluid and electrolyte status include blood urea nitrogen level (BUN), glucose concentration, creatinine level, pH, bicarbonate level, osmolarity, hemoglobin, and hematocrit.

The urine test results may be helpful in assessing fluid status. If a laboratory report is not available, the nurse can perform various tests using a dipstick to help determine fluid and electrolyte status, including detecting substances that should not be present in the urine, such as glucose, acetone, protein, and blood. Urine measurements such as pH and specific gravity also can be determined in this way.Lormal body functioning requires a proper balance of all body fluids. Many health problems can disrupt fluid intake or output, placing all clients at risk for some degree of fluid im­balance. Although most imbalances of fluid are accompanied by electrolyte imbalances, this chapter focuses only on client problems associated with fluid imbalances.

 OVERVIEW

 

In dehydration, the body’s fluid intake is not sufficient to meet the body’s fluid needs, resulting in a fluid volume deficit. Three basic types of dehydration are possible Isotonic dehydration, in which water and dissolved electrolytes are lost in equal proportions

•  Hypertonic dehydration, in which water loss is greater than electrolyte loss

■ Hypotonic dehydration, in which electrolyte loss is greater than water loss

Dehydration is a clinical state rather than a disease and can be caused by many factors. Dehydration may be an actual de­crease in total body water caused by either too little an intake of fluid or too great a loss of fluid. Dehydration also can oc­cur without an actual decrease in total body water, such as when water shifts from the plasma into the interstitial space. This condition is called relative dehydration.

  Pathophysiology

 ISOTONIC DEHYDRATION

Isotonic dehydration is the most common type of fluid vol­ume deficit. Problems caused by isotonic dehydration result from loss of plasma volume. Isotonic dehydration involves loss of isotonic fluids from the extracellular fluid (ECF) com­partment, including both the plasma and the interstitial space. Because isotonic fluid is lost, plasma osmolarity remains nor­mal. This type of dehydration does not cause a shift of fluids between compartments, so the intracellular fluid (ICF) volume remains normal. Isotonic dehydration decreases circulat­ing blood volume (hypovolemia) and leads to inadequate tis­sue perfusion. Compensatory mechanisms attempt to main­tain adequate tissue perfusion to vital organs in spite of decreased vascular volume

Isotonic dehydration has many causes. These include inadequate intake of fluids and solutes, fluid shifts be­tween compartments, and excessive losses of isotonic body fluids.

 HYPERTONIC DEHYDRATION

 

Hypertonic dehydration is the second most common type of fluid volume deficit. The problems caused by hypertonic de­hydration result from changes in the concentrations of spe­cific electrolytes.

Hypertonic dehydration occurs when water loss from the extracellular fluid (ECF) is greater than electrolyte loss. This water loss increases the osmolarity of the remaining plasma, making it hypertonic or hyperosmolar compared with normal ECF. The hyperosmolar plasma has an in­creased osmotic pressure that causes fluid to move from the intracellular fluid (ICF) into the plasma and interstitial fluid spaces. The fluid shift leads to cellular dehydration and shrinkage. The fluid shift also causes the plasma volume to increase to normal or greater thaormal levels.

Hypertonic dehydration is caused by the loss of any body fluid that is hypotonic (low osmolarity, or decreased concen­tration of solute particles compared with isotonic body fluid) or occurs when water loss is greater than electrolyte loss. Common causes of hypertonic dehydration are conditions such as excessive perspiration, hyperventilation, ketoacido­sis, prolonged fevers, diarrhea, early-stage renal failure, dia­betes insipidus, and ketoacidosis in the diuretic phase

  HYPOTONIC DEHYDRATION

Hypotonic dehydration is the least common type of fluid vol­ume deficit. The problems caused by hypotonic dehydration result from fluid shifts between compartments, causing a de­crease in plasma volume.

Hypotonic dehydration involves excessive loss of sodium and potassium from the ECF. This loss leads to decreased os­molarity of the remaining ECF, making it hypotonic compared with normal ECF. The decreased ECF osmolarity low­ers the osmotic pressure of plasma and interstitial fluids to be­low that of the fluid inside the cells, the ICE As a result of this difference in osmotic pressure, water moves from the plasma and interstitial spaces into the cells, creating a plasma volume deficit and causing the cells to swell. Cell swelling causes widespread problems and symptoms. Because brain cells are more sensitive to swelling than the cells of other tissues, neurologic problems usually occur with hypotonic dehydration. Hypotonic fluid also dilutes the nor­mal electrolyte concentrations and causes sodium and potassium imbalances. Hypotonic dehydration is usually associated with chronic illness. Chronic renal failure, in which the kidneys waste sodium, leads to hypotonic dehydration. Chronic malnutrition and taking in excessive amounts of hypotonic fluids also cause hypotonic dehydration.

OTHER CHANGES. The nurse asks the client about changes in the tightness of clothing, rings, and shoes. A sud­den decrease in tightness may indicate dehydration; an in­crease may reflect edema. Other related findings include the sensation of palpitations or lightheadedness on moving from a lying or a sitting position to a standing position (caused by orthostatic, or postural, hypotension).

The nurse asks about any abnormal or excessive fluid losses, such as perspiration, diarrhea, bleeding, vomiting, uri­nation, salivation, and wound drainage. Other important in­formation to collect includes chronic illnesses, recent acute illnesses, recent surgery, and medications.

The nurse asks specific questions about urine output, in­cluding the frequency and amount of voidings. The nurse also asks about the client’s usual fluid intake and the intake during the previous 24 hours. It is just as important to determine the types of fluids ingested as it is to determine the amount of flu­ids ingested, because fluids vary widely in osmolarity.

ILLNESSES

•  Vomiting    Diarrhea

•  Burns   Large, draining wounds

•  Liver dysfunction     Diabetes mellitus

•  Diabetes insipidus   Renal disease

•  Hemorrhage      Major venous obstruction

•  Prolonged febrile state

Nurse also asks whether the client has recently engaged in strenuous physical activity and, if so, whether the activity took place in hot or dry environmental conditions.

    PHYSICAL ASSESSMENT/CLINICAL MANIFESTATIONS

The clinical manifestations of dehydration depend on which fluid compartments lose fluid, although all body systems are affected to some degree. The most obvious and life-threatening clinical manifestations are seen when dehydration causes a decrease in the plasma volume.

RESPIRATORY MANIFESTATIONS. The respira­tory rate increases directly with the degree of fluid loss from plasma volume. The decreased blood volume is per­ceived by the body as decreased oxygen levels (hypoxia), and increased respiration is an attempt to maintain oxygen delivery.

INTEGUMENTARY MANIFESTATIONS. Changes in skin may be useful indicators of hydration. The nurse assesses for changes in the skin and mucous membranes that may indicate dehydration, including skin color, mois­ture, skin turgor, and edema. In older clients this informa­tion is less reliable because of poor skin turgor resulting from the loss of elastic tissue and the loss of tissue fluids with aging. The nurse assesses skin turgor by noting the following:

•  How easily the skin over the back of the hand and arm can be gently pinched between the thumb and the fore­ finger to form a “tent”

•  How soon the pinched skin resumes its normal position after release

•  Whether depressions (pits) remain in the skin after a fin ger is pressed firmly but gently (over the shin, over the sternum, and over the sacrum)

•  How deep the depression is (in millimeters)

•  How long the depression remains

In generalized dehydration, skin turgor is poor, with the tenting remaining for minutes after pinching the skin, and no skin depressions occur with gentle pressure. The skin appears dry and scaly. The nurse assesses skin turgor in an

Figure Hand veins full and bulging in the dependent po­sition (top). Hand veins collapsed (bottom).

Older adult by pinching the skin over the sternum, the forehead, or the abdomen because these areas more reliably indicate hydration. As a person ages, the skin loses elasticity and tents on extremities even when the person is well hydrated. In dehydration, oral mucous membranes are not moist. They may be covered with a thick, sticky, pastelike coating and may have cracks and fissures. The surface of the tongue may have deep furrows.

NEUROLOGIC MANIFESTATIONS. Dehydration may cause changes in body temperature and mental status as the brain is less perfused. The client with dehydration typi­cally has a low-grade fever. One cause of the fever is the con­striction of blood vessels that occurs as a compensation for hypovolemia. The blood vessel constriction makes heat dissi­pation more difficult.

Fever can also cause dehydration. A client with a tem­perature greater than 102° F (39° C) for longer than 6 hours is especially at risk. Older adults, who normally have a body temperature range of 96° to 98° F (35.4° to 36.6° C), are at greater risk for dehydration during epi­sodes of fever. Mental status changes are also common with dehydration. Chart 12-2 outlines how to assess men­tal status quickly.

RENAL MANIFESTATIONS. The volume and the composition of urine output indicate the hydration status of the renal system. The nurse monitors urine output, comparing total output with total fluid intake and daily weights. Accurate intake and output measurement is a major nursing responsi­bility. Urine output below 500 mL/day for any client without renal disease is cause for concern. A client with fluid imbalance is weighed each day at the same time and on the same scale. When possible, the client wears the same amount and type of clothing for each weigh-in. Metabolic weight loss (even in starvation) usually accounts for only about V₂ pound of weight loss per day. Any weight loss in excess of this amount is considered fluid loss of health and possible treatment regimens. As dehydration worsens, psychosocial activities reflect abnormal functioning of the central nervous system. The client may become anxious, restless, lethargic, and confused. These behavioral changes are more obvious in hypertonic and hypotonic dehydration be­cause of intracellular fluid (ICF) shifts in brain cells, resulting in shrinkage or swelling of the cells. If the conditions causing the dehydration continue, circulation to cerebral tissues be­comes so impaired that delirium and coma can occur.

 LABORATORY ASSESSMENT

No single laboratory test result confirms or rales out dehydra­tion. Instead, a diagnosis of dehydration is based on laboratory findings along with presenting signs and symptoms. Laboratory findings depend on the type of dehydration present (Chart 12-3). Isotonic and hypotonic dehydration states with accompanying plasma volume deficits show hemoconcentration (elevated levels of hemoglobin, hematocrit, serum osmolarity, glucose, protein, blood urea nitrogen, and various electrolytes) because only the water is lost and other substances remain. Hemocon­centration is not present when dehydration is caused by hemor­rhage, because loss of all blood and plasma products occurs. Specific urine laboratory values can help to confirm dehy­dration if the client does not have renal dysfunction. Usually the urine of the client with dehydration is concentrated, with a specific gravity greater than 1.030. Volume is decreased, and osmolarity is greatly increased. Usually the color is dark am­ber and a strong odor is evident.

 Analysis

   COMMON NURSING DIAGNOSES AND COLLABORATIVE PROBLEMS

The following are priority nursing diagnoses for clients with dehydration:

1.   Deficient Fluid Volume related to excessive fluid loss or inadequate fluid intake

2.   Decreased Cardiac Output related to decreased plasma volume

3.   Impaired Oral Mucous Membrane related to inadequate oral secretions

The primary collaborative problem is Potential for Dys-rhythmias.

   ADDITIONAL NURSING DIAGNOSES AND COLLABORATIVE PROBLEMS

In addition to the commoursing diagnoses and collabora­tive problems, clients with dehydration may have one or more of the following:

•  Constipation related to decreased body fluids

•  Risk for Injury (fall) related to orthostatic (postural) hypotension

•  Deficient Knowledge related to medication regimen and preventive measures

•  Risk for Impaired Skin Integrity related to deficiencies of interstitial fluid and inadequate tissue perfusion

•  Ineffective Airway Clearance related to thick, tenacious secretions

•  Potential for Hypovolemic Shock

•  Potential for Electrolyte ImbalancesLABORATORY PROFILE Dehydration

	Values*	Isotonic Dehydration	Hypotonic Dehydration	Hypertonic Dehydration
	BLOOD VALUES
	BUN	Normal or increased	Increased	Increased
	Creatinine	Normal or increased	Increased	Increased
	Sodium	Normal	<120 mEq/L(mmol)	>150 mEq/L (mmol)
	Osmolality	Normal	Decreased	Increased
	Hematocrit	Increased	Increased	Normal or decreased
	Hemoglobin	Increased	Increased	Normal or decreased
	WBCs	Increased	Increased	Normal or decreased
	Protein	Increased	Increased	Increased
	URINE VALUES
	Specific gravity	>1.010	<1.010	>1.030
	Osmolality	Increased	Increased	Increased
	Volume	Decreased	Decreased	Decreased

BUN, Blood urea nitrogen; WBC, white blood cell.

*AII values reflect dehydration states alone and not the underlying pathologic changes or disease states contributing to the dehydration.INTERVENTION ACTIVITIES/or The Client with Fluid Volume Deficit

Fluid Monitoring: Collection and analysis of client data to regulate fluid balance

•  Monitor serum and urine electrolyte values, as appropriate.

•  Monitor BP, heart rate, and respiratory status.

•  Monitor orthostatic blood pressure and change in cardiac rhythm, as appropriate.

•  Monitor weight.

•  Maintain intake and output.

•  Note presence or absence of vertigo on rising.

•  Monitor color, quantity, and specific gravity of urine.

Fluid Management: Promotion of fluid balance and preven­tion of complications resulting from abnormal or undesired fluid levels

•  Administer IV therapy, as prescribed.

•  Give fluids, as appropriate.

•  Promote oral intake (e.g., provide a drinking straw, offer fluid between meals, change ice water routinely), as appropriate.

•  Distribute the fluid intake over 24 hours, as appropriate.

•  Encourage significant other to assist client with feedings, as appropriate.

•  Offer snacks (e.g., frequent drinks and fresh fruit/fruit juice), as appropriate.

Oral Health Restoration: Promotion of healing for a client who has an oral mucosa or dental lesion

•  Encourage frequent rinsing of mouth with any of the following: sodium bicarbonate solution, warm saline, or hydrogen peroxide solution.

•  Monitor lips, tongue, mucous membranes, tonsillar fossae, and gums for moisture, color, texture, presence of debris, and infection, using good lighting and a tongue blade.

•  Instruct client to avoid commercial mouthwashes.

•  Monitor client every shift for dryness of the oral mucosa.

•  Increase mouth care to every 2 hours and twice at night, if stomatitis is not controlled.

•  Avoid use of lemon-glycerin swabs.

•  Increase liquids on the meal tray.

• Planning and Implementation

 DEFICIENT FLUID VOLUME

PLANNING: EXPECTED OUTCOMES. The client with dehydration is expected to have body fluid levels re­stored to normal.

INTERVENTIONS. Management of dehydration aims to prevent further fluid losses and increase fluid compartment volumes to normal ranges.

 FLUID MANAGEMENT. Diet therapy, oral rehydration therapy, and drug therapy are the methods of choice to man­age fluid volume deficit (Chart 12-4).

DIET THERAPY. Mild to moderate dehydration is cor­rected with oral fluid replacement if the client is alert enough to swallow and can tolerate oral fluids. The nurse or assistive nursing personnel encourages and measures fluid intake. The specific type of fluid needed for replacement varies with the type of dehydration.

The client’s compliance in drinking oral replacement flu­ids can be enhanced by using fluids he or she enjoys and by carefully timing the intake schedule. Dividing the total amount of fluids needed by nursing shifts helps to meet fluid needs more evenly with less danger of overhydration. The conscious client is offered small volumes of fluids every hour to increase intake.

ORAL REHYDRATION THERAPY. Oral rehydration ther­apy (ORT) is the most cost-effective way to replace fluids for the client with dehydration. Specifically formulated solutions containing glucose and electrolytes cause water to be ab­sorbed even when the client is vomiting or has diarrhea. Fluid losses from diarrhea are usually 2 to 3 L/day and should be replaced liter for liter, especially in older clients. A typical or­der might be “Resol 1 L every 8 hours.” Table 12-3 lists com­mercially available ORT solutions.

DRUG THERAPY. Drug therapy for dehydration is di­rected at restoring fluid balance and controlling the causes of dehydration. Whenever possible, fluids are replaced by the oral route. When dehydration is severe or life threaten­ing, intravenous (IV) fluid replacement may be necessary. Calculation of how much fluid to replace is based on the client’s weight loss and clinical manifestations. The rate of fluid replacement depends on the degree of dehydration and the presence of pre-existing cardiac, pulmonary, or renal problems.

The type of fluid ordered by the health care provider varies with the type of dehydration and the client’s cardiovascular status. The desired outcomes of therapy are appropriate fluid replacement and normal volumes in all body fluid compart­ments. Usually the client receives IV infusions of water with whatever solutes (especially electrolytes) are determined nec­essary on the basis of laboratory values. Table 12-4 lists the osmolarity, caloric content, and tonicity of common IV fluids. Generally, isotonic dehydration is treated with isotonic fluid solutions, hypertonic dehydration is treated with hypotonic fluid solutions, and hypotonic dehydration is treated with hy­pertonic fluid solutions.

Drug therapy includes the use of medications to correct the cause of the dehydration. Antidiarrheal medications are ordered when excessive diarrhea causes dehydration. Antimicrobial therapy may be used in clients with bacterial diarrhea. Antiemet-ics to control vomiting may be necessary when excessive vom­iting produces dehydration. Antipyretics to reduce body temper­ature are helpful when fever contributes to dehydration.*

DECREASED CARDIAC OUTPUT

PLANNING: EXPECTED OUTCOMES. The client with dehydration is expected to have cardiac output restored to normal levels and to maintain adequate oxygenation to vi­tal organs.

INTERVENTIONS. Interventions of drug and oxygen therapy aim to increase circulating fluid volume, support compensatory mechanisms, and prevent complications.

DRUG THERAPY. Drug therapy to increase body fluid volume and prevent excessive fluid loss is the same as that for the client with fluid volume deficit. Drugs to increase venous return or improve cardiac contractility are used only when a cardiac problem also is present.

OXYGEN THERAPY. Oxygen is usually delivered by mask or nasal cannula to the client with dehydration. The nurse administers water-nebulized oxygen at the rate or amount specified by the health care provider’s order.

 FLUID MONITORING. Monitoring vital signs and level of consciousness is important when caring for clients with dehy­dration (see Chart 12-4). The nurse or assistive nursing per­sonnel monitors the pulse, blood pressure, pulse pressure, central venous pressure, respiratory rate, skin and mucous membrane color, and urine output at least every hour until the fluid imbalance is resolved.

 CRITICAL THINKING CHALLENGE

 When you take the client’s blood pressure in a sitting position and in a standing position, the systolic pressure is 24 mm Hg lower with the client standing compared with the pres­sure taken with the client sitting.

•  Is this finding supportive or nonsupportive of fluid volume deficit?

•  What would you teach this client to avoid complications associated with this problem?

 IMPAIRED ORAL MUCOUS MEMBRANE

PLANNING: EXPECTED OUTCOMES. The client with dehydration is expected to have less discomfort and re­main free of complications.

INTERVENTIONS

ORAL HEALTH RESTORATION. Interventions include drug therapy, fluid replacement, and good oral hygiene, as well as the early diagnosis and prevention of complications (see Chart 12-4).

DRUG THERAPY. Drug therapy to increase fluid volume and prevent fluid loss is the same as that discussed earlier for deficient fluid volume (p. 165). Saliva substitutes, such as Salivart, can reduce the sensation of mouth dryness. To pre­vent aspiration, the nurse does not use such agents in an un­conscious client.

ORAL HYGIENE. Nursing actions to promote oral hy­giene can increase the client’s comfort. The lips are kept clean and moist. The thick, sticky coating on the tongue and mouth during dehydration can be reduced with frequent mouth care. Mouth care includes gentle toothbrushing several times a day and rinsing hourly. The nurse teaches the client to avoid mouthwashes and swabs that contain alcohol or glycerin be­cause these products dry the oral mucosa further and may cause more discomfort by stinging or burning open areas of the mucosa. Rinsing the mouth with dilute solutions of hy­drogen peroxide two or three times per day is a good form of oral hygiene; however, when used more frequently, this treat­ment increases oral dryness. Tap water and normal saline rinses can be used safely as often as the client wishes.

PREVENTION OF COMPLICATIONS. A dry mouth can lead to the development of sores and fissures in the mucosa, providing a portal of entry for many pathogens. The thick, sticky coating also is an excellent breeding ground for mi­croorganisms. A major complication of mouth dryness is a wide variety of oral infections. Chart 12-4 summarizes nurs­ing interventions for mouth care.

 POTENTIAL FOR DYSRHYTHMIAS

PLANNING: EXPECTED OUTCOMES. The client with dehydration is expected to maintain his or her normal cardiac rhythm.

INTERVENTIONS. Interventions are aimed at correct­ing the dehydration and recognizing dysrhythmias so that ap­propriate drug therapy can be initiated.

DRUG THERAPY. Drug therapy to increase body fluid volume and prevent excessive fluid loss is the same as that discussed earlier for deficient fluid volume (p. 165).

Elevated potassium or calcium levels can cause life-threat­ening dysrhythmias. Drug therapy to reduce these electrolytes may be ordered. If potassium levels are elevated, a combina­tion of 20 units of regular insulin in 100 mL of 20% dextrose may be administered to promote movement of potassium from the blood into the intracellular fluid (ICF). Drugs such as etidronate (Didronel) and plicamycin (Mithracin) may be ad­ministered to reduce an elevated serum calcium level.

MONITORING. The nurse monitors the client for signs and symptoms of cardiac dysrhythmias every 15 minutes un­til he or she is fully rehydrated. The rate, rhythm, and quality of the apical pulse are assessed and compared with the client’s baseline measurements. The nurse further assesses for fa­tigue, chest discomfort or pain, and shortness of breath. Hand grasps and deep tendon reflexes are assessed, and changes from baseline are noted. Clients at risk for dysrhythmias are monitored using elec-trocardiography (ECG). The pattern may show tall T waves or a shortened ST segment. Any change from the client’s base­line ECG is reported to the physician immediately.

Community-Based Care

No extensive home care preparations are necessary for clients with mild dehydration or for those with dehydration of sud­den onset. The imbalance is corrected before discharge from the facility and, with minimal precautions, is unlikely to recur. Clients who are most likely to be discharged before the im­balance is completely corrected and who are susceptible to recurrent episodes are those with chronic pathologic condi­tions, such as renal insufficiency, diabetes, malignancy, adre­nal insufficiency, and many endocrine disorders. These clients often require long-term diet and drug therapy. The nurse performs a focused assessment and a mental status check at every home visit to a client at risk for de­hydration. Medications, signs and symptoms of dehydration, and health care resources are reviewed with the client and family. Education is important in the prevention and early detec­tion of dehydration. The nurse teaches the client at risk for de­hydration about diet, drug regimens, and the signs and symptoms of dehydration, explaining the meaning of changes found on assessment.

The nurse stresses the importance of recording accurate daily weights in assessing hydration status. Clients are in­structed to weigh themselves on the same scale daily, close to the same time each day, and with approximately the same amount of clothing on each time. Keeping a chart comparing the recorded weights from one day to the next can help the client recognize early-stage dehydration. Clients are instructed to take medications as prescribed and not increase the use of diuretics. The nurse explains that if a diuretic is not taken one day, the next day’s dose should not be doubled. Clients are taught how and where to assess skin turgor. The nurse teaches them how to measure their own peripheral pulse and obtains a return demonstration. The nurse instructs the family to keep fluids for the client in places that he or she can access. Container modifications, such as opening zip-top cans and covering them with foil, can be made to ensure that the client can easily open container lids. “Sipper” containers not only provide easy access but also are unbreakable and reduce spillage.

Interventions

The focus of therapy is to reduce the client’s body tempera­ture and restore fluid volume. After determining a patent air­way, the first priority is to cool the client. All clothing is re­moved. If possible, the client is taken immediately to an air-conditioned environment and placed in the position for shock with the legs elevated. If no air-conditioning is avail­able, he or she is placed in the shade. Water is sprayed or poured on the client, and all surrounding personnel fan him or her. Ice packs are wrapped in cloth and positioned on the client’s groin, head, and armpits.

Oxygen is administered by mask or nasal cannula. At least one IV line is started with a large-bore needle. When avail­able, cooled normal saline (0.9% sodium chloride) is admin­istered intravenously. Depending on how high the client’s temperature is, cooled sterile saline may be administered by peritoneal lavage. Vital signs, including rectal temperature, are monitored every 15 minutes until the client responds to therapy. An in­dwelling catheter is placed so that output can be monitored accurately. Depending on the severity of the client’s condi­tion, a pulmonary artery catheter may be needed to monitor hydration status. If interventions are started promptly, the client has a good chance for full recovery. Responses usually start to occur within half an hour. If vital signs remain poor in spite of in­tervention, extensive laboratory assessment may be needed to determine possible organ damage.

Overhydration     

Overhydration, also called fluid overload, is an excess of body fluid. It is not an actual disease but rather a clinical sign of a physiologic problem in which fluid intake or retention is greater than the body’s fluid needs. Overhydration may be ei­ther an actual excess of total body fluid or a relative fluid ex­cess in one or more fluid compartments. The three basic types of fluid volume excess are isotonic overhydration, hypotonic overhydration, and hypertonic overhydration . Most problems caused by overhydration are related to fluid volume excess in the vascular space or to dilution of specific electrolytes and blood components. Clinical manifestations vary with the type and degree of overhydration (Chart 12-6). The conditions leading to overhydration (fluid overload) are related to excessive intake or inadequate excretion of fluid.

POTASSIUM IMBALANCE

 Hypokalemia

 OVERVIEW

Because 98% of total body potassium (K⁺) is intracellular, minor changes in extracellular potassium levels cause major changes in cell membrane excitability and in other cellular processes. Hypokalemia is a serum potassium level below 3.5 mEq/L (mmol/L). A relatively common electrolyte imbalance, hypokalemia is potentially life threatening because every body system can be affected.

 Pathophysiology

Decreased serum potassium levels increase the difference in potassium concentration between the fluid inside the cells (in­tracellular fluid [ICF]), and the fluid outside the cells (ex­tracellular fluid (ECF]). This increased difference reduces the excitability of cells. Consequently, the cell membranes of all excitable tissues, such as nerve and muscle, are less re­sponsive to normal stimuli.

The severity of problems caused by hypokalemia is di­rectly related to how rapidly the serum potassium level de­creases. When the loss of extracellular potassium is gradual, cells adjust and intracellular potassium decreases in propor­tion to the ECF potassium level. In this situation, the potas­sium concentration difference between the two fluid compart­ments remains unchanged; symptoms of hypokalemia may not appear until the potassium loss is extreme. Rapid changes in extracellular potassium levels (representing a more rapid loss of potassium) cannot be compensated for quickly and re­sult in dramatic changes in body function.

•   Etiology

Hypokalemia may result either from an actual total body potassium loss or from the movement of potassium from the ECF to the ICF, causing a relative decrease in extracellular potassium level. Table 13-1 summarizes the common causes of hypokalemia.

Actual potassium depletion occurs when potassium loss is excessive or when potassium intake is not sufficient to match normal potassium loss. Relative hypokalemia occurs when total body potassium levels are normal but the potas­sium distribution between fluid compartments is abnormal. Conditions that increase the cellular uptake of potassium, leading to hypokalemia, include metabolic alkalosis and in­sulin administration.

 COLLABORATIVE MANAGEMENT  Assessment

 HISTORY

The nurse collects data from clients at risk as well as from those with actual hypokalemia.

AGE. Age is an important consideration because renal ca­pacity to concentrate urine decreases with aging, which in­creases potassium loss. Moreover, older adults are more likely to use medications that promote potassium loss.

MEDICATION USE. The nurse asks the client about medication use, especially diuretics, corticosteroids, and beta-adrenergic agonists or antagonists. These drugs increase potassium loss through the kidneys. One of the most common causes of hypokalemia is the use and misuse of diuretics. In clients taking digoxin (Lanoxin, Novodigoxin^X hypo­kalemia increases the sensitivity of the myocardium to the drug and may result in digoxin toxicity, even when the dosage is within the therapeutic range.

The nurse asks whether the client is taking a prescribed potassium supplement, such as potassium chloride (KC1). The client may not be taking the potassium chloride as prescribed because of its unpleasant taste.

OTHER FACTORS. Any acute or chronic disease state may lead to hypokalemia. The client is asked about re­cent illnesses and medical or surgical interventions. A thor­ough diet history, including a typical day’s food and bever­age intake, helps the nurse to identify clients at risk for hypokalemia.

  PHYSICAL ASSESSMENT/CLINICAL MANIFESTATIONS

The clinical manifestations of hypokalemia are associated with the altered function of many systems Skele­tal muscles become weak in response to hypokalemia, and a stronger stimulus is needed to begin muscle contraction. A client may be so weak that he or she is unable to stand. Hand-grasps are weak, and hyporeflexia (a decreased response to deep tendon reflex stimulation) may be noted. Severe hy­pokalemia can lead to flaccid paralysis. The nurse assesses the degree of muscle weakness and determines the client’s ability to perform activities of daily living (ADLs).

RESPIRATORY MANIFESTATIONS. The respira­tory system can be seriously affected by hypokalemia through the depression of the nerves and muscles needed for breath­ing. Weakness of the skeletal muscles of respiration results in shallow respirations. The nurse assesses the client’s breath sounds, ease of respiratory effort, color of nail beds and mu­cous membranes, and rate and depth of respiration. Respira­tory status is assessed at least every 2 hours because respira­tory insufficiency often accompanies hypokalemia and is a major cause of death.

CARDIOVASCULAR MANIFESTATIONS. Cardio­vascular changes often accompany hypokalemia. The nurse assesses the cardiovascular system by first palpating the pe­ripheral pulses. In the client with hypokalemia, the pulse is usually thready and weak. Palpation is difficult, and the pulse is easily blocked with light pressure. The pulse rate ranges from excessively slow to excessively rapid, depending on whether a dysrhythmia (irregular heartbeat), especially pre­mature ventricular contraction (PVC), is present. The nurse measures blood pressure with the client in the lying, sitting, and standing positions because orthostatic (postural) hypoten­sion accompanies hypokalemia.

NEUROLOGIC MANIFESTATIONS. The neuro­logic manifestations of hypokalemia include changes in mental status. The client may experience short-term irri­tability and anxiety followed by lethargy that progresses to confusion and coma as hypokalemia worsens. Severe hy­pokalemia decreases sensory awareness. For example, the client may not be able to identify mild sensations of pain, touch, heat, and cold.

GASTROINTESTINAL MANIFESTATIONS. Hypo­kalemia decreases smooth muscle contractions within the gastrointestinal system, which leads to decreased peristalsis. The affected client has hypoactive bowel sounds and may ex­perience nausea, vomiting, constipation, and abdominal dis-tention. The nurse assesses distention by measuring abdomi­nal girth. Bowel sounds are assessed in all four abdominal quadrants to determine the extent of decreased peristalsis. Se­vere hypokalemia can cause paralytic ileus (the absence of peristalsis).

 PSYCHOSOCIAL ASSESSMENT

Behavioral changes caused by hypokalemia usually occur within a short period. Information about the client’s behavior may need to be obtained from close family members or friends, depending on the client’s condition.

The nurse collects data about the onset and duration of be­havioral changes as well as their association with any other physical signs and symptoms. The client may be lethargic and unable to perform simple problem-solving tasks that require concentration, such as counting backward from 100 by threes. As hypokalemia progresses, the client may become increasingly confused, especially to time and place. In severe hy­pokalemia, coma may develop.

 LABORATORY ASSESSMENT

Hypokalemia is confirmed by a serum potassium value below 3.5 mEq/L (mmol/L). However, this value alone does not determine whether potassium loss has occurred or whether potassium has moved from the blood into the cells.

 OTHER DIAGNOSTIC ASSESSMENTS

The health care provider may order a baseline electrocardio­gram (ECG) and continuous cardiac monitoring for a client with severe hypokalemia. Hypokalemia causes electrical con­duction abnormalities in the heart, including ST-segment de­pression, flat or inverted T waves, and increased U waves. Dysrhythmias can result in death, particularly in older adults who are taking digoxin.

 Analysis

 COMMON NURSING DIAGNOSES AND COLLABORATIVE PROBLEMS

The following are priority nursing diagnoses for clients with hypokalemia:

1.  Risk for Injury related to skeletal muscle weakness

2.  Constipation related to smooth muscle atony

The primary collaborative problem is High Risk for Ineffective Breathing Pattern related to neuromuscular impairment.

 ADDITIONAL NURSING DIAGNOSES AND COLLABORATIVE PROBLEMS

In addition to the commoursing diagnoses and collabora­tive problems, clients with hypokalemia may have one or more of the following:

•  Impaired Physical Mobility related to skeletal muscle weakness

INTERVENTION ACTIVITIES/or The Client with Hypokalemia

Electrolyte Management: Hypokalemia: Promotion of potassium balance and prevention of complications resulting from serum potassium levels lower than desired

•  Monitor lab values associated with hypokalemia (e.g., elevated glucose, metabolic alkalosis, reduced urine osmolality, urine potassium, hypochloremia, and hypocalcemia).

•  Administer prescribed supplemental potassium (PO, NG, or IV), per policy.

•  Prevent/reduce irritation from potassium supplement (e.g., administer PO or NG potassium supplements during or after meals to minimize Gl irritation, dilute IV potassium adequately, administer IV supplement slowly, and apply topical anesthetic to IV site), as appropriate.

•  Administer potassium-sparing diuretics (e.g., spirono- lactone [Aldactone] or triamterene [Dyrenium]), as appropriate.

•  Avoid administration of alkaline substances (e.g., IV sodium bicarbonate and PO or NG antacids), as appropriate.

•  Monitor neurologic manifestations of hypokalemia (e.g., muscle weakness, altered level of consciousness, drowsiness, apathy, lethargy, confusion, and depression).

•  Monitor cardiac manifestations of hypokalemia (e.g., hypotension, broad T wave, U wave, ectopy, tachycardia, and weak pulse).

•  Monitor renal manifestations of hypokalemia (e.g., acidic urine, reduced urine osmolality, nocturia, polyuria, and polydipsia).

•  Monitor Gl manifestations of hypokalemia (e.g., anorexia, nausea, cramps, constipation, distension, and paralytic ileus).

•  Monitor pulmonary manifestations of hypokalemia (e.g., hypoventilation and respiratory muscle weakness).

•  Monitor for symptoms of respiratory failure (e.g., low Pao₂ and elevated Paco₂ levels and respiratory muscle fatigue).

•  Monitor for rebound hyperkalemia.

•  Provide food rich in potassium (e.g., salt substitutes, dried fruits, bananas, green vegetables, tomatoes, yellow vegetables, chocolate, and dairy products), as appropriate.

NIC intervention activities selected from McCloskey, J.C., & Bulechek, G.M. (Eds.). (2000). Nursing intervention classification (NIC) (3rd ed.). St. Louis: Mosby. No part of this work is to be altered without prior written permission from the Publisher. Gl, Gastrointestinal; Pao₂, partial pressure of arterial oxygen; Paco₂, partial pressure of ar­terial carbon dioxide.

 Planning and Implementation

    RISK FOR INJURY

PLANNING: EXPECTED OUTCOMES. The client with hypokalemia is expected to avoid injury and have a re­turn to a normal seram potassium level.

INTERVENTIONS

 ELECTROLYTE MANAGEMENT: HYPOKALEMIA. In­terventions for hypokalemia aim to prevent potassium loss, increase seram potassium levels, and provide a safe environ­ment for the client (Chart 13-2). Drug and diet therapies help to restore normal seram potassium levels.DRUG THERAPY. Drag therapies for the treatment and prevention of hypokalemia include additional potassium and drugs to prevent potassium loss.

Potassium Supplements. Most potassium supplements are potassium chloride, potassium gluconate, potassium cit­rate, or a combination of these salts. The amount and the route of potassium replacement depend on the degree of potassium loss. A client with a seram potassium level of 3 mEq/L needs 100 to 200 mEq of potassium supplement; a client with a seram potassium level of 2.0 mEq/L needs 500 to 600 mEq (Tannen, 1996).

Potassium is given intravenously for severe hy­pokalemia. A dilution of no more than 1 mEq/10 mL of solution is recommended. The maximum recommended infu­sion rate is 5 to 10 mEq/hr; this rate is never to exceed 20 mEq/hr under any circumstances. Older clients may not be able to handle this rate. Because the rapid infusion of potas­sium can cause cardiac arrest, potassium is seldom given by intravenous (IV) push.

Potassium is a severe tissue irritant and is never admin­istered as an intramuscular or subcutaneous injection. Tissues damaged by potassium can become necrotic and slough, leading to a loss of function and requiring recon­structive surgery. IV potassium solutions irritate veins and can cause phlebitis. The nurse checks the orders carefully to ensure that the client receives the correct amount of potassium. The IV site is assessed every 2 hours, and the client is asked whether he or she feels burning or pain at the site. The IV solution is stopped immediately if infiltration occurs.

Oral potassium preparations may be administered as liq­uids or solids. Potassium chloride has a strong, unpleasant taste that is difficult to mask. Because potassium chloride can cause nausea and vomiting, it should not be taken on an empty stomach.

Potassium-Sparing Diuretics. Diuretics that increase the renal excretion of potassium commonly cause hypoka­lemia. These classes of diuretics include high-ceiling (loop) diuretics (e.g., furosemide [Lasix, Furoside^], bumetanide [Bumex], and ethacrynic acid [Edecrin]) and the thiazide di­uretics (chlorothiazide [Diuril], hydrochlorothiazide [Esidrix, HydroDIURIL, Urozide^], and quinethazone [Hydromox]). These drags are avoided in clients with actual hypokalemia and in those who are at risk for hypokalemia. A potassium-sparing diuretic may be appropriate for clients with hypo­kalemia who require diuretic therapy. Potassium-sparing di­uretics increase urine output without increasing potassium excretion. Potassium-sparing diuretics include spironolactone (Aldactone, Novospiroton^), triamterene (Dyrenium), and amiloride (Midamor).

DIET THERAPY. The nurse consults with the dietitian in teaching the client how to increase dietary potassium intake. Eating foods that are naturally rich in potassium helps to re­store normal potassium levels and prevent further loss. Table 11-7 lists the potassium content of common foods.

SAFETY MEASURES. For a client with muscle weakness from hypokalemia, the nurse uses safety measures, eliminates hazards, and assists with ambulation. Obstacles or slippery ar­eas are removed from the ambulation path, and the client wears nonslip footgear. When ambulating with assistance, the client wears a gait belt around the waist.

INEFFECTIVE BREATHING PATTERN

 PLANNING: EXPECTED OUTCOMES. The client with hypokalemia is expected to have a breathing pattern ad­equate to maintain gas exchange.

INTERVENTIONS. The nurse monitors the client’s respiratory rate and depth at least once per hour, noting in particular increased rate and decreased depth. The effective­ness of the respiratory muscles can also be determined by assessing the client’s ability to cough. The face, oral mu-cosa, and nail beds are examined for pallor or cyanosis. The nurse evaluates arterial blood gas values for hypoxemia (decreased blood oxygen concentration) and hypercapnia (increased arterial carbon dioxide concentration). Chapters 27 and 28 discuss respiratory assessment and interventions in more detail.

Hyperkalemia     

OVERVIEW

Hyperkalemia is a serum potassium level greater than 5.0 mEq/L (mmol/L). Because the range of normal serum potassium values is narrow, even slight increases above normal values can have serious adverse effects on the physiologic function of excitable tissues, especially the heart.

■       Pathophysiology

An elevated serum potassium level decreases the potassium concentration difference between the intracellular fluid (ICF) and the extracellular fluid (ECF). This decreased dif­ference increases cell excitability; as a result, excitable tis­sues respond to less intense stimuli and may even discharge spontaneously.

 COLLABORATIVE MANAGEMENT

Assessment

The client’s age is an important factor because renal function decreases with aging. The nurse asks about chronic illnesses (particularly renal disease and diabetes mellitus), recent medical or surgical interventions, and urine output, including fre­quency and amount of voidings. The nurse also inquires about medication use, particularly potassium-sparing diuretics. A diet history is obtained to determine the intake of potassium-rich foods or the use of salt substitutes, many of which con­tain potassium.

The nurse collects data regarding symptoms related to hy­perkalemia. The client is asked if he or she has experienced palpitations, skipped heartbeats, other cardiac irregularities, muscle twitching, weakness in the leg muscles, and unusual tingling or numbness in the hands, feet, or face.

PHYSICAL ASSESSMENT/CLINICAL MANIFESTATIONS

The clinical manifestations of hyperkalemia are summarized in Chart 13-4. Cardiovascular changes are the most severe re­sults of hyperkalemia and are the most common cause of death in clients with hyperkalemia (Chmielewski, 1998). Cardiac manifestations of hyperkalemia include bradycardia, hy­potension, and electrocardiographic (ECG) changes of tall, peaked T waves, prolonged PR intervals, flat or absent P waves, and wide QRS complexes (Figure 13-1). As serum potassium levels rise, ectopic beats (beats generated outside the normal conduction system in the ventricles) may appear. Complete heart block, ventricular standstill, and ventricular fibrillation are major life-threatening complications of severe hyperkalemia. The neuromuscular response to hyperkalemia has two phases. Skeletal muscles twitch in the early stages of hyper­kalemia, and the client may be aware of unusual nerve sensations (e.g., tingling and burning) that are followed by numbness in the hands and feet and around the mouth (paresthesia). As hyperkalemia progresses, muscle twitching changes to weakness followed by flaccid paralysis. The weakness ascends from the distal to the proximal areas and initially affects the muscles of the arms and legs. Trunk, head, and respiratory muscles are not affected until serum potassium levels reach lethal levels.

The smooth muscle of the gastrointestinal tract responds to hyperkalemia by increasing peristalsis. As a result, the client may experience diarrhea and spastic colonic activity.

The nurse listens to bowel sounds and observes stools. Bowel sounds are hyperactive, with frequent audible rushes and gurgles. Bowel movements may be frequent, watery, and explosive.

 LABORATORY ASSESSMENT

A serum potassium value greater than 5.0 mEq/L confirms hyperkalemia. If hyperkalemia results from dehydration, lev­els of other serum electrolytes, hematocrit, and hemoglobin may be elevated. Hyperkalemia associated with renal failure is usually accompanied by elevated levels of serum creatinine and blood urea nitrogen, decreased blood pH, and normal or low hematocrit and hemoglobin levels.

 Interventions

 ELECTROLYTE    MANAGEMENT:     HYPERKALEMIA.

Interventions for hyperkalemia are aimed at immediately reducing the serum potassium level. Drug therapy is useful for restoring normal potassium balance by eliminating potassium administration, enhancing potassium excretion, and promoting the movement of potassium from the extracellular fluid (ECF) into the cells. Monitoring the client’s re­sponse to intervention is another major nursing responsibility

Eliminating potassium administration by stopping infu­sions of potassium-containing IV solutions and by keeping the IV catheter open is useful in managing hyperkalemia. The nurse withholds oral potassium supplements, and a potas­sium-restricted diet is ordered.

Increasing potassium excretion can be effective in manag­ing hyperkalemia if renal function is not impaired. The physician orders the administration of potassium-excreting diuretics, such as furosemide (Miekley, 1998). For a client with renal problems, drug therapy to increase potassium ex­cretion includes cation exchange resins that promote gas­trointestinal sodium absorption and potassium excretion, such as sodium polystyrene sulfonate (Kayexalate). However, it may take sodium polystyrene sulfonate many hours to reduce potassium levels. If potassium levels are dangerously high, additional measures, such as dialysis and ultrafiltration, are necessary.

Promoting the movement of potassium from the extracellu­lar fluid (ECF) to the intracellular fluid (ICF) can help reduce serum potassium levels temporarily. Potassium movement from the ECF into the cells is enhanced by the presence of in­sulin. Insulin increases the activity of the membrane-bound sodium-potassium pump, resulting in the movement of potas­sium from the blood and other ECFs into the cell (Chmielewski, 1998). The physician may order IV flu­ids that contain substantial amounts of glucose and insulin to help decrease serum potassium levels (usually 100 mL of 10% to 20% glucose with 10 to 20 units of regular insulin). These IV solutions are hypertonic and are administered through a central venous catheter or in a vein with a high blood flow to avoid local vein inflammation. The nurse ob­serves the client for signs and symptoms of hypokalemia and hypoglycemia during this therapy.

INTERVENTION ACTIVITIES for The Client with Hyperkalemia

Electrolyte Management: Hyperkalemia: Promotion of potassium balance and prevention of complications resulting from serum potassium levels higher than desired

•  Administer electrolyte-binding and electrolyte-excreting resins (e.g., Kayexalate) as prescribed, if appropriate.

•  Monitor lab values for changes in oxygenation or acid- base balance, as appropriate.

•  Administer prescribed medications to shift potassium into the cell (e.g., 50% dextrose and insulin, sodium bicarbonate, calcium chloride, and calcium gluconate), as appropriate.

•  Avoid potassium-sparing medications (e.g., spironolactone [Aldactone] and triamterene [Dyrenium]), as appropriate.

•  Maintain potassium restrictions.

•  Administer prescribed diuretics, as appropriate.

•  Monitor fluid status, including intake and output, as appropriate.

•  Monitor potassium levels after diuresis.

•  Monitor cardiac manifestations of hyperkalemia (e.g., de­creased cardiac output, heart blocks, peaked T waves, fibrillation, or systole).

•  Respond to cardiac arrest.

Cardiac monitoring can help to prevent lethal dysrhyth-mias and allow for the early recognition of signs and symp­toms of the adverse response of cardiac muscle. The nurse compares recent ECG tracings with the client’s baseline trac­ings or with tracings obtained when the client’s serum potassium level was close to normal.

Health teaching is a key factor in the prevention of hyper­kalemia and in the early detection of its life-threatening com­plications. The teaching plan for the client at risk for hyper­kalemia includes diet, medications, and recognition of the signs and symptoms of hyperkalemia. Diet education in­cludes knowledge of foods to avoid (those high in potassium) and permissible foods containing little potassium

Hyponatremia

 OVERVIEW

Hyponatremia is a serum sodium (Na⁺) level below 135 mEq/L (mmol/L). Because sodium is the major cation of the blood and interstitial fluid and maintains the osmolarity of these fluids, sodium imbalances are often associated with fluid volume imbalances.

 Pathophysiology

The pathologic changes caused by hyponatremia involve two mechanisms. The first mechanism is a change in cell ex­citability or activity. As the concentration of sodium in the blood and other extracellular fluid decreases, the difference in sodium concentration between the extracellular fluid (ECF) and the intracellular fluid (ICF) also decreases. Less sodium is available to move across the excitable membrane, causing delayed and slower membrane depolarization. The second mechanism is the movement of water from the ECF space into the ICF space. Cells swell, and their functions are impaired.

■ Etiology

Many conditions can lead to hyponatremia by causing either an actual or a relative decrease in sodium content (Table 13-3). Hyponatremia can result from the loss of total body sodium, the movement of sodium from the blood to other fluid spaces (such as in burns, extensive inflammatory re­sponses, or severe crushing injuries), or the dilution of serum sodium as a result of excessive water in the plasma.

WOMEN’S HEALTH CONSIDERATIONS Hyponatremia as a complication during early postoperative recovery has a relatively high occurrence in the United States, ranging from 1 % to 5%. Although this complication occurs with equal frequency among men and women, more women develop brain damage and die from coma or seizure activity.

 COLLABORATIVE MANAGEMENT

 Assessment

The clinical manifestations of hyponatremia are caused by its effects on excitable cellular activity. The cells especially af­fected are those involved in cerebral, neuromuscular, and gas­tric smooth muscle functions (Chart 13-7).

   CEREBRAL MANIFESTATIONS

Changes in cerebral function are the most obvious signs and symptoms of hyponatremia. Because these changes may be seen as either depressed activity or excessive activity (and sometimes both), establishing the client’s usual cerebral func tion and behavioral patterns is essential to detecting the changes caused by hyponatremia. Behavioral changes result from cerebral edema and increased intracranial pressure. The nurse closely observes and documents the client’s behavior and level of consciousness.

NEUROMUSCULAR MANIFESTATIONS

The client’s neuromuscular status is assessed during each nursing shift for changes from baseline values. The neuro­muscular response to hyponatremia is generalized muscle weakness. Muscle tone and deep tendon reflexes diminish.

Muscle weakness occurs bilaterally and is worse in the ex­tremities. The nurse assesses deep tendon reflexes by lightly tapping the patellar (knee) tendons and Achilles (heel) ten­dons with a reflex hammer and documenting the degree of re­flex movement.

    GASTROINTESTINAL MANIFESTATIONS

The smooth muscle of the gastrointestinal system responds to decreased serum sodium levels with increased motility, causing nausea, diarrhea, and abdominal cramping. The gastrointestinal system is assessed by listening to bowel sounds and observing stools. Bowel sounds are hyperactive, with frequent rushes and gurgles, especially over the splenic flexure and in the lower left quadrant. Bowel movements are frequent, watery, and explosive. Peristaltic movements may be palpated through the abdominal wall and may even be visible on the abdominal surface.

  CARDIOVASCULAR MANIFESTATIONS

Hyponatremia has little direct effect on cardiac muscle contractility; however, alterations in cardiac output are associated with hyponatremia. When hyponatremia is accompanied by changes in blood volume, these fluid changes alter cardiac function. In general, the cardiac responses to hyponatremia with accompanying hypovolemia (decreased plasma volume, or fluid deficit) are a rapid, weak, thready pulse. Peripheral pulses are difficult to palpate and are easily blocked with light pressure. Neck veins may be flat when the client is in the supine position. Blood pressure, especially diastolic pressure, is decreased. The client may experience severe hypotension when moving from a lying or sitting position to a standing po­sition. The central venous pressure is low.

When hyponatremia is accompanied by hypervolemia (increased plasma volume or fluid excess), cardiac manifestations include a rapid, full pulse. Blood pressure is normal or elevated. Central venous pressure is normal or ele­vated depending on how well the left ventricle handles the extra fluid. Peripheral pulses are full and difficult to block; however, the peripheral pulses may not be palpable if edema is present.

 Interventions

 ELECTROLYTE     MANAGEMENT:     HYPONATREMIA.

Interventions with drug therapy and diet therapy aim to re­store serum sodium levels to normal values and prevent fur­ther decreases in serum sodium levels (Chart 13-8).

CHART 13-8

> INTERVENTION ACTIVITIES for The Client with Sodium Imbalances

Electrolyte Management: Hyponatremia:

Promotion of sodium balance and prevention of complications resulting from serum sodium levels lower than desired

•  Monitor for electrolyte imbalances associated with hyponatremia (e.g., hypokalemia, metabolic acidosis, and hypoglycemia), as appropriate.

•  Monitor for renal loss of sodium (oliguria).

•  Monitor intake and output.

•  Weigh daily and monitor trends.

•  Monitor for indications of fluid overload/retention (e.g., crackles, elevated CVP or pulmonary capillary wedge pressure, edema, neck vein distension, and ascites), as appropriate.

•  Administer hypertonic (3% to 5%) saline at 3 mL/kg/hr or per policy for rapid correction of hyponatremia, as appropriate.

•  Maintain fluid restriction, as appropriate.

•  Monitor for neurologic and/or neuromuscular manifestations of hyponatremia (e.g., lethargy, ICR confusion, headache, seizures, coma, fatigue, tremors, apprehend sion, muscle weakness, and hyperreflexia).

•  Monitor for cardiac manifestations of hyponatremia (e.g., elevated blood pressure, cold and clammy skin, and hypo- or hypervolemia).

Electrolyte Management: Hypernatremia: Promotion of sodium balance and prevention of complications resulting from serum sodium levels higher than desired

•  Monitor for indications of dehydration (e.g., decreased sweating, decreased urine, decreased skin turgor, and dry mucous membranes).

•  Monitor vital signs, as appropriate.

•  Weigh daily and monitor trends.

•  Provide comfort measures to decrease thirst.

•  Maintain patent IV access.

•  Monitor intake and output,

•  Provide frequent oral hygiene.

•  Administer isotonic (0.9%) saline, hypotonic (0.45%) saline, hypotonic (5%) dextrose, or diuretics, as appropriate, based on fluid status and urine osmolality.

•  Maintain sodium restrictions.

NIC intervention activities selected from McCloskey, J.C., & Bulechek, G.M. (Eds.). (2000). Nursing interventions classification (NIC) (3rd ed.). St. Louis: Mosby. No part of this work is to be altered without prior written permission from the Publisher. CVP, Central venous pressure; ICP, intracranial pressure.

DRUG THERAPY. Drug therapy can restore serum sodium levels to normal. Drug therapy regimens vary de­pending on whether or not fluid imbalance accompanies hy­ponatremia and how fast the imbalance has developed. In chronic or asymptomatic hyponatremia, sodium is replaced slowly and carefully.

When hyponatremia occurs with a fluid deficit (hypovolemia), the physician orders IV saline infusions to restore both sodium content and fluid volume. Severe hyponatremia may be treated with small-volume infusions of hypertonic (2% to 3%) saline. The infusions are delivered through a controller to prevent accidental increases in infusion rate. The nurse monitors the infusion rate and the client’s response. When hyponatremia is accompanied by fluid excess, drug therapy includes the administration of osmotic diuretics that primarily promote the excretion of water rather than sodium, such as mannitol (Osmitrol). The nurse assesses the client hourly for signs of an excessive loss of fluids or potassium and for dramatic increases in sodium levels. Drug therapy for hyponatremia caused by inappropriate secretion of antidiuretic hormone (ADH) includes agents that antagonize ADH, such as lithium and demeclocycline (Declomycin).

DIET THERAPY. Diet therapy can help to restore normal sodium balance in mild hyponatremia. The nurse collaborates with the dietitian in teaching the client about which foods to increase in the diet. Therapy consists of increasing oral sodium intake and restricting oral fluid intake. Fluid restric­tion may be a long-term regimen when overhydration with oral fluids is the cause of the hyponatremia or when renal fluid excretion is impaired. The nurse or assistive nursing per­sonnel measures fluid intake and output and reinforces the purpose of the fluid restriction.

Hypernatremia

   OVERVIEW

Hypernatremia is a serum sodium level greater than 145 mEq/L. Increased serum sodium levels can be caused by or can cause changes in fluid volumes.

As the extracellular sodium level rises, a larger difference in sodium concentration occurs between the extracellular fluid (ECF) and the intracellular fluid (ICF). More sodium is available to move rapidly across cell membranes. With mild hypernatremia, almost all excitable tissues are excited more easily. This condition is called irritability and causes ex­citable tissues to overrespond to stimuli. In addition, the os-molarity of the ECF also increases as the concentration of ex­tracellular sodium increases. This situation causes water to move from the cells into the ECF as a compensatory action to dilute the hyperosmolar ECF. Therefore when hypernatremia persists or worsens, the compensatory action causes severe cellular dehydration, and excitable tissues may no longer be able to respond to stimuli.

COLLABORATIVE MANAGEMENT

 Assessment

The clinical manifestations of hypernatremia vary with the severity of imbalance and whether a fluid imbalance is also present. Rapid increases in serum sodium level generally cause more obvious and severe symptoms. Gradual increases in serum sodium levels may produce no observable physical changes, even when sodium levels increase to ranges that are well above normal.

  CENTRAL NERVOUS SYSTEM MANIFESTATIONS

Altered cerebral function is the most common manifesta­tion of hypernatremia. The nurse assesses the client’s men­tal status in terms of attention span, recall of recent events, and ability to perform cognitive functions. In hyperna­tremia with normal or decreased fluid volumes, the client may have a short attention span and be agitated or confused about recent events. Manic episodes or seizures may occur if serum sodium concentration continues to increase. When hypernatremia is accompanied by a blood volume overload, the client may be lethargic, drowsy, stuporous, and even comatose.

 

   NEUROMUSCULAR MANIFESTATIONS

Skeletal muscles respond differently to various degrees of hy-pernatremia. Mild hypernatremia causes muscle twitching and irregular muscle contractions. As hypernatremia worsens, the muscles and nerves are less able to respond to a stimulus. The muscles become progressively weaker and show rigid paralysis. Deep tendon reflexes are reduced or absent. Muscle weakness associated with hypernatremia occurs bilaterally and has no specific pattern. Neuromuscular status is assessed by observing for twitching in muscle groups. The nurse also assesses muscle strength by having the client perform hand­grip and arm flexion against resistance. Peripheral nerve re­sponses are assessed by lightly tapping the patellar (knee) tendons and Achilles (heel) tendons with a reflex hammer and measuring the degree of movement.

 CARDIOVASCULAR MANIFESTATIONS

Increased serum sodium levels slow the movement of calcium into the heart cells, which decreases contractility. The nurse assesses cardiovascular status by measuring blood pressure and the rate and quality of the apical and peripheral pulses. Pulse rate and blood pressure may be normal, above normal, or below normal during hypernatremia, depending on the fluid volume and the speed with which the imbalance occurs. Pulse rate is increased in clients with hypernatremia and hypovolemia. Peripheral pulses may be difficult to palpate and are easily blocked with light pressure. Hypotension and severe orthostatic (postural) hypotension are present, and pulse pressure is greatly diminished. Clients with hypernatremia and hypervolemia have slow to normal bounding pulses. Peripheral pulses are full and diffi­cult to block. Neck veins are distended, even with the client in the upright position. Blood pressure, especially diastolic blood pressure, is increased.

 Interventions

ELECTROLYTE   MANAGEMENT:   

HYPERNATREMIA.

Drug therapy and diet therapy aim to prevent further increases in serum sodium levels and decrease elevated serum sodium levels (see Chart 13-8). Other interventions used when hyper­natremia becomes life threatening include hemodialysis, peri­toneal dialysis, and blood ultrafiltration.

DRUG THERAPY. When hypernatremia is caused by fluid loss, drug therapy is used to restore fluid balance. The physi­cian orders hypotonic IV infusions, usually 0.225% or 0.45% sodium chloride. Hypernatremia caused by fluid and sodium losses may necessitate fluid replacement with IV administra­tion of isotonic sodium chloride (NaCl) solutions. Hyperna­tremia caused by inadequate renal excretion of sodium re­quires drug therapy with diuretics that promote sodium loss, such as furosemide (Lasix, Furoside^”¹), bumetanide (Bumex), and ethacrynic acid (Edecrin). The nurse assesses the client hourly for symptoms that indicate an excessive loss of fluids, sodium, or potassium.

DIET THERAPY. Mild hypernatremia can be prevented or corrected by ensuring adequate water intake among older adults or those who may not have self-access to water. Dietary sodium restriction may be needed to prevent hypernatremiawhen renal problems are present. In addition, fluids must of­ten be restricted. The nurse collaborates with the dietitian in helping the client to understand how to determine the sodium content of foods, beverages, and medications, as well as the importance of complying with the diet.

CALCIUM IMBALANCES _

Hypocalcemia

 OVERVIEW

Hypocalcemia is a total serum calcium (Ca²⁺) level below 9.0 mg/dL or 2.25 mmol/L. Calcium is stored in bone, with only a small fraction of total body calcium present in extracellular fluid (ECF). Because the normal serum level of calcium is so low, small changes in serum calcium levels have major effects on body function.

 Pathophysiology

Calcium ions decrease the permeability of excitable mem­branes to sodium ions, thereby preventing spontaneous depo­larization. Calcium is a membrane stabilizer, regulating depolarization and the generation of action potentials. Low serum calcium levels increase the permeability of excitable mem­branes to sodium, and as a result depolarization occurs more easily and at inappropriate times.

Excitable tissues vary in their sensitivity to low serum cal­cium levels. Peripheral nerves, skeletal muscles, cardiac mus­cle, and gastrointestinal smooth muscle are most sensitive to decreased serum calcium levels. The severity of the manifestations associated with hypocalcemia depends on the degree of calcium imbalance.

Hypocalcemia also has pathologic effects on bone. Bone is the primary storage site for calcium and can release calcium into the blood wheeeded. Excessive calcium loss from bone can weaken bone. Chronic hypocalcemia leads to progressive osteoporosis, which decreases bone density and makes the bones more susceptible to fracture or deformity. (See Chapter 51 for a discussion of osteoporosis.)

CULTURAL CONSIDERATIONS

 Many African-American and Asian clients have a lac­tose intolerance caused by a deficiency of the enzyme lactase. These clients cannot use the nutrients present in milk and experience cramping, diarrhea, and abdominal pain after ingesting dairy products. Dairy products, especially milk, area common and rich source of calcium and vitamin D. Therefore clients with lactose intolerance may experience difficulty in obtaining enough calcium and vitamin D from other sources to maintaiormal calcium levels in the blood and bones.

 

CONSIDERATIONS FOR OLDER ADULTS

Older adults are at risk for most electrolyte imbalances. Major organs and body systems undergo changes with aging. For example, older adults have a smaller fluid volume per body weight than younger adults, and therefore any variation in fluid volumes or electrolyte levels leads to imbalances more quickly. They are also more likely to be taking prescription or over-the-counter medications that affect fluid or electrolyte balance. Some older adults have dietary calcium or vitamin D deficits because of economic conditions or general problems with obtaining, preparing, or eating food.

COLLABORATIVE MANAGEMENT •

Assessment

The diet history is a critical factor in assessing for the risk of hypocalcemia. The nurse asks the client about his or her in­take of calcium-containing foods and whether a calcium sup­plement is taken regularly.

One indicator of hypocalcemia is a report of frequent, painful muscle spasms (“charley horses”) in the calf or foot during periods of inactivity or sleep. Other information that can alert the nurse to a possible risk of hypocalcemia is a history of recent orthopedic surgery or bone healing. En­docrine disturbances and treatments are risk factors for hypocalcemia. A history of thyroid surgery, therapeutic irra­diation of the upper middle chest and neck area, or a recent anterior neck injury predisposes the client to hypocalcemia. The most common clinical manifestations of hypocalcemia are caused by overstimulation of the nerves and muscles.

 NEUROMUSCULAR MANIFESTATIONS

The client usually notices symptoms first in the limbs, with distal to proximal movement from the hands and feet. Pares-thesias may be noted initially, with sensations of tingling al­ternating with sensations of numbness. If hypocalcemia con­tinues or worsens, these sensations may progress to actual muscle twitching or painful cramps and spasms. Paresthesias may also affect the lips, nose, and ears.

 

 

 

 

 

INTERVENTION ACTIVITIES/or The Client with Calcium Imbalances

Electrolyte Management: Hypocalcemia:

Promotion of calcium balance and prevention of complications resulting from serum calcium levels lower than desired

•  Monitor trends in serum levels of calcium (e.g., ionized calcium), as available.

•  Monitor fluid status, including intake and output, as appropriate.

•  Administer appropriate prescribed calcium salt (e.g., cal cium carbonate, calcium chloride, and calcium gluconate), as indicated.

•  Monitor for side effects of IV administration of ionized calcium (e.g., calcium chloride), such as throm­ bophlebitis, soft tissue damage with extravasation, clotting, and thrombus formation, as appropriate.

•  Encourage intake of calcium (e.g., dairy products, seafood, nuts, broccoli, spinach, and supplements), as appropriate.

•  Provide adequate intake of vitamin D (e.g., vitamin sup­ plement and organ meats) to facilitate Gl absorption of calcium, as appropriate.

•  Monitor for neuromuscular manifestations of hypocalcemia (e.g., tetany, muscle twitching, cramping, grimac­ing, seizure, altered deep tendon reflexes, and spasm).

•  Monitor for cardiovascular manifestations of hypocalcemia (e.g., decreased contractility, decreased cardiac output, hypotension, lengthened ST segment, and prolonged QT interval).

•  Monitor for overcorrection and hypercalcemia.

Electrolyte Management: Hypercalcemia: Promotion of calcium balance and prevention of complications resulting from serum calcium levels higher than desired

•  Monitor intake and output.

•  Monitor trends in serum levels of calcium (e.g., ionized calcium), as available.

•  Monitor for fluid overload resulting from hydration therapy (e.g., daily weight, urine output, jugular vein distention, lung sounds, and right atrial pressure), as appropriate.

•  Monitor for neuromuscular manifestations of hypocalcemia (e.g., weakness, malaise, paresthesias, myalgia, hypotonia, decreased deep tendon reflexes, and poor coordination).

•  Administer indomethacin (Indocin), calcitonin, or pli-camycin (Mithracin), as appropriate.

•  Encourage mobilization to prevent bone resorption.

•  Monitor for recurring hypercalcemia 1 to 3 days after cessation of therapeutic measures

•  The nurse assesses for hypocalcemia by testing for Trousseau’s and Chvostek’s signs.

•  To test for Trousseau’s sign, the nurse places a blood pressure cuff around the upper arm, inflates the cuff to greater than the client’s systolic pressure, and keeps the cuff inflated for 1 to 4 minutes. Under these hypoxic conditions, a positive Trousseau’s sign occurs if the hand and fingers go into spasm in palmar flexion (Figure 13-2).

 

Figure   13-2 Palmar flexion—positive Trousseau‘s sign in hypocalcemia.

Figure 13-3 Facial muscle response—positive Chvostek‘s sign in hypocalcemia.

 To test for Chvostek’s sign, the nurse taps on the face just below and anterior to the ear (over the facial nerve) to trigger facial twitching of one side of the mouth, nose, and cheek).