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NUR308 Exam 1 Study Guide

Terms in this set (161)

Diffusion is the free movement of particles (solute) across a permeable membrane from an area of higher concentration to an area of lower concentration (down a concentration gradient). This action controls the movement of solute particles in solution across various body membranes. Diffusion is important in the transport of most electrolytes and other particles through cell membranes. Unlike capillary membranes, which permit the diffusion of most small-size particles down a gradient, cell membranes are selective in which particles can diffuse. They permit diffusion of some particles but not others. Some particles cannot move across a cell membrane, even when a steep "downhill" gradient exists, because the membrane is impermeable (not open) to that particle. For these particles, the concentration gradient is maintained across the membrane. In some instances, diffusion cannot occur without help, even down steep concentration gradients, because of selective membrane permeability. One example is glucose. Even though the amount of glucose may be 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, it binds to insulin receptors on cell membranes, which then makes the membranes much more permeable to glucose. As a result, glucose can cross the cell membrane down its concentration gradient until equilibrium of glucose concentration is achieved. Diffusion across a cell membrane that requires the assistance of a membrane-altering system (e.g., insulin) is called facilitated diffusion or facilitated transport. This type of movement is still a form of diffusion.
Water molecules in a confined space constantly press outward against the confining walls. This pressing of water molecules is hydrostatic pressure. It is a "water-pushing" pressure, because it is the force that pushes water outward from a confined space through a membrane. The amount of water in any body fluid space determines the hydrostatic pressure of that space. Blood, a fluid that is "thicker" than water (more viscous), is confined within the blood vessels. Blood has hydrostatic pressure because of its weight and volume. An additional factor that affects blood hydrostatic pressure in arteries is the pumping action of the heart. This action has little impact on the hydrostatic pressure in the capillaries and veins. The hydrostatic pressures of two fluid spaces can be compared whenever a porous (permeable) membrane separates the two spaces. If the hydrostatic pressure is the same in both fluid spaces, there is no pressure difference between the two spaces and the hydrostatic pressure is now at equilibrium. If the hydrostatic pressure is not the same in both spaces, disequilibrium exists. This means that the two spaces have a graded difference (gradient) for hydrostatic pressure: one space has a higher hydrostatic pressure than the other. The human body constantly seeks equilibrium. When a gradient exists, water movement (filtration) occurs until the hydrostatic pressure is the same in both spaces. When nothing stops it, water moves through the membrane (filters) from the space with higher hydrostatic pressure to the space with lower pressure. This filtration continues only as long as the hydrostatic pressure gradient exists. Equilibrium is reached when enough fluid leaves one space and enters the other space to make the hydrostatic pressure in both spaces equal. At this point, water molecules may be exchanged evenly between two spaces in equilibrium but no net further filtration of fluid occurs. Neither space gains or loses water molecules, and the hydrostatic pressure in both spaces remains the same.
Because the kidney is a major regulator of water and sodium balance to maintain blood pressure and perfusion to all tissues and organs, the kidneys monitor blood pressure, blood volume, blood oxygen levels, and blood osmolarity (related to sodium concentration). When the kidneys sense that any one of these parameters is getting low, they begin to secrete a substance called renin that sets into motion a group of hormonal and blood vessel responses to ensure that blood pressure is raised back up to normal. So, the triggering event is any change in the blood that indicates to the kidney that tissue and organ perfusion are at risk. Low blood pressure is a triggering event because when it gets too low, blood cannot flow through vessels into tissues and organs. Low blood volume is a triggering event because it is directly related to blood pressure. Anything that reduces blood volume (e.g., dehydration, hemorrhage) below a critical level always lowers blood pressure. Low blood oxygen levels also are triggering events because with too little oxygen in the blood, even if the blood reaches the tissues and organs, it cannot supply the needed oxygen and the tissues and organs could die. A low blood sodium level also is a triggering event because sodium and water are closely linked. Where sodium goes, water follows. So, anything that causes the blood to have too little sodium prevents water from staying in the blood. The result is low blood volume with low blood pressure and poor tissue perfusion. Once the kidneys sense that tissue and organ perfusion are at risk, special cells in the kidney tubule (in an area of the nephron known as the juxtaglomerular complex) begin to secrete renin into the bloodstream. Renin is an enzyme that activates some blood proteins, one of which is angiotensinogen. Activated angiotensinogen is angiotensin I, which is relatively weak and has little action. It is then acted on by another enzyme known as angiotensin-converting enzyme or ACE, which converts angiotensin I into its most active form, angiotensin II. Angiotensin II starts several different activities that all work to increase blood volume and blood pressure. First, because angiotensin II is a powerful vasoconstrictor, it causes constriction of small arteries and veins throughout the body. This action increases peripheral resistance and reduces the size of the vascular bed, which raises blood pressure without adding more blood volume. At the same time, a second action of angiotensin II is that it constricts the size of the arterioles that feed the kidney nephrons. This action results in a lower glomerular filtration rate and a huge reduction of urine output. Decreasing urine output prevents further loss of water so that more is retained in the blood to help raise blood pressure. The last and slightly slower action of angiotensinogen II is to cause the adrenal glands to secrete the hormone aldosterone. Aldosterone is nicknamed the "water- and sodium-saving hormone" because it causes the kidneys to reabsorb water and sodium, preventing them from being excreted into the urine. This response allows more water and sodium to be returned to the blood, increasing blood pressure and blood volume. All of these actions help maintain perfusion to vital organs.
Nearly all body systems are affected by dehydration to some degree. The most obvious changes occur in the cardiovascular and integumentary systems.

Cardiovascular changes are good indicators of hydration status because of the relationship between plasma fluid volume and blood pressure. Heart rate increases in an attempt to maintain blood pressure with less blood volume. Peripheral pulses are weak, difficult to find, and easily blocked with light pressure. The blood pressure also decreases, as does the pulse pressure, with a greater decrease in the systolic blood pressure. Hypotension is more severe with the patient in the standing position than in the sitting or lying position (orthostatic or postural hypotension). Because the blood pressure with the patient standing may be much lower than in other positions, first measure blood pressure with the patient lying down, then sitting, and finally standing. (These measures are also called "ortho checks" or "ortho changes.") As the blood pressure decreases when changing position, the person may not have sufficient blood flow to the brain, causing the sensations of light-headedness and dizziness. This problem increases the risk for falling, especially among older adults.

Neck veins are normally distended when a patient is in the supine position, and hand veins are distended when lower than the level of the heart. Neck veins normally flatten when the patient moves to a sitting position. With dehydration, neck and hand veins are flat, even when the neck and hands are not raised above the level of the heart.

Respiratory changes include an increased rate because the decreased blood volume reduces perfusion and oxygenation. The increased respiratory rate is an attempt to maintain oxygen delivery when perfusion is decreased.

Skin changes can indicate dehydration. Assess the skin and mucous membranes for color, moisture, and turgor. In older patients, this information is less reliable because of poor skin turgor resulting from the loss of elastic tissue and increased skin dryness from the loss of tissue fluids with aging. Assess skin turgor by checking:

• How easily the skin over the back of the hand and arm can be gently pinched between the thumb and the forefinger to form a "tent"

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

In generalized dehydration, skin turgor is poor, with the tent remaining for minutes after pinching the skin, and no skin depressions occur with gentle pressure. The skin is dry and scaly.

Considerations for Older Adults

Assess skin turgor in an older adult by pinching the skin over the sternum or on the forehead, rather than the back of the hand, because these areas more reliably indicate hydration (Fig. 13-9). As a person ages, the skin loses elasticity and tents on hands and arms 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. This manifestation may not be accurate for assessing dehydration in patients taking drugs that have the side effect of dry mouth.

Neurologic changes with dehydration include alterations of mental status and body temperature status because blood flow in the brain is reduced. Mental status changes, especially confusion, are more common among older adults and may be the first indication of a fluid balance problem. Check to determine whether the patient is alert and oriented. Chapter 43 provides more information about assessment of mental status.

The patient with dehydration often has a low-grade fever, and fever can also cause dehydration. A patient with a temperature higher than 102° F (39° C) for longer than 6 hours is especially at risk because the increased body temperature increases the rate at which fluids are lost. For every degree (Celsius) increase in body temperature above normal, a minimum of an additional 500 mL of body fluid is lost. The older adult begins to lose more body water at lower levels of fever.

Kidney changes in dehydration affect urine volume and composition. Monitor urine output, comparing total output with total fluid intake and daily weights. The urine may be concentrated, with a specific gravity greater than 1.030. The color is dark amber and has a strong odor. Urine output below 500 mL/day for any patient without kidney disease is cause for concern. Weigh the patient each day at the same time and on the same scale. When possible, have the patient wear the same amount and type of clothing for each weigh-in. Any weight loss over a half pound per day is fluid loss

No single laboratory test result confirms or rules out dehydration. Instead, dehydration is determined by laboratory findings along with clinical manifestations (see Table 13-1). Usually, laboratory findings with dehydration show elevated levels of hemoglobin, hematocrit, serum osmolarity, glucose, protein, blood urea nitrogen, and various electrolytes because more water is lost and other substances remain, increasing the osmolarity or concentration of the blood (hemoconcentration). Hemoconcentration is not present when dehydration is caused by hemorrhage, because loss of all blood and plasma products occurs together.
Patients with fluid overload often have pitting edema. Other manifestations are usually seen in the cardiovascular, respiratory, neuromuscular, integumentary, and GI systems.

Fluid overload is diagnosed based on assessment findings and the results of laboratory tests. Usually, serum electrolyte values are normal, but decreased hemoglobin, hematocrit, and serum protein levels may result from excessive water in the vascular space (hemodilution).

The focus of priority nursing interventions for patients with fluid overload is to ensure patient safety, restore normal fluid balance, provide supportive care until the imbalance is resolved, and prevent future fluid overload. Drug therapy, nutrition therapy, and monitoring are the basis of intervention.

Patient safety is the first priority. Interventions are implemented to prevent fluid overload from becoming worse, leading to pulmonary edema and heart failure. Any patient with fluid overload, regardless of age, is at risk for these complications. Older adults or those with cardiac problems, kidney problems, pulmonary problems, or liver problems are at greater risk.

Monitor for indicators of increased fluid overload (bounding pulse, increasing neck vein distention, presence of crackles in lungs, increasing peripheral edema, reduced urine output) at least every 2 hours.

Pulmonary edema can occur very quickly and can lead to death. Notify the health care provider of any change that indicates the fluid overload either is not responding to therapy or is becoming worse.

The patient with fluid overload and edema is at risk for skin breakdown. Use a pressure-reducing or pressure-relieving overlay on the mattress. Assess skin pressure areas daily for signs of redness or open area, especially the coccyx, elbows, hips, and heels. Because many patients with fluid overload may be receiving oxygen by mask or nasal cannula, check the skin integrity around the mask, nares, and ears and under the elastic band. Help the patient change positions every 2 hours, or ensure that unlicensed assistive personnel (UAP) perform this action.

Cardiovascular Changes
• Increased pulse rate
• Bounding pulse quality
• Full peripheral pulses
• Elevated blood pressure
• Decreased pulse pressure
• Elevated central venous pressure
• Distended neck and hand veins
• Engorged varicose veins
• Weight gain

Respiratory Changes
• Increased respiratory rate
• Shallow respirations
• Increased dyspnea with exertion or in the supine position
• Moist crackles present on auscultation

Skin and Mucous Membrane Changes
• Pitting edema in dependent areas
• Skin pale and cool to touch

Neuromuscular Changes
• Altered level of consciousness
• Headache
• Visual disturbances
• Skeletal muscle weakness
• Paresthesias

Gastrointestinal Changes
• Increased motility
• Enlarged liver

Drug therapy focuses on removing the excess fluid. Diuretics are prescribed for fluid overload if kidney failure is not the cause. These drugs increase kidney water or sodium excretion. High-ceiling (loop) diuretics, such as furosemide (Lasix, Furoside ), may be prescribed. (See Chapter 38 for discussion of diuretic therapy.) If there is concern that too much sodium and other electrolytes would be lost using loop diuretics or if the patient has syndrome of inappropriate antidiuretic hormone (SIADH), conivaptan (Vaprisol) or tolvaptan (Samsca) may be prescribed.

Monitor the patient for response to drug therapy, especially weight loss and increased urine output. Observe for manifestations of electrolyte imbalance, especially changes in electrocardiogram (ECG) patterns. Assess laboratory findings, especially sodium and potassium values, every 8 hours or whenever they are drawn.

Nutrition therapy for the patient with chronic fluid overload may involve restrictions of both fluid and sodium intake to control fluid volume. Review the patient's serum sodium levels whenever fluid overload is present. Often sodium restriction involves only "no added salt" to ordinary table foods when fluid overload is mild. For more severe fluid overload, the patient may be restricted to 2 g/day to 4 g/day of sodium. When sodium restriction is ongoing, teach the patient and family how to check food labels for sodium content and how to keep a daily record of sodium ingested. Explain to the patient and family the reason for any fluid restriction and the importance of adhering to the prescribed restriction.

Monitoring intake and output and weight provides information on therapy effectiveness. Teach UAP that these measurements need to be accurate, not just estimated, because treatment decisions are based on these findings. In addition to regulating the total amount of fluid ingested in a 24-hour period, schedule fluid offerings throughout the 24 hours. Teach UAP to check urine for color and character and to report these findings. Check the urine specific gravity (a specific gravity below 1.005 may indicate fluid overload). If the patient is receiving IV therapy, infuse the exact amount prescribed.

Fluid retention may not be visible. Remember that rapid weight gain is the best indicator of fluid retention and overload. Metabolism can account for no more than a half pound of weight gain in one day. Each pound of weight gained (after the first half pound) equates to 500 mL of retained water. Weigh the patient at the same time every day (before breakfast), using the same scale. Whenever possible, have the patient wear the same type of clothing for each weigh-in.

If the patient is discharged to home before the fluid overload has completely resolved or has continuing risk for fluid overload, teach him or her and the family to monitor weight at home. Suggest that a record of these daily weights be kept to show the health care provider at checkups. Also, instruct the patient to call his or her health care provider for more than a 3-pound gain in a week or more than a 1- to 2-pound gain in 24 hours.
Adequate catheter securement is vital to prevent many complications. Tape, sutures, and specially designed securement devices can be used for this purpose. For a short peripheral catheter, tape strips are most common; however, the tape should be clean. Tape strips from a peripheral IV start kit are preferred. Strips of tape should not be taken from rolls of tape moved between patient's rooms, from other procedures, or from uniform pockets. Precutting tape and placing it on the patient's bedrails, your uniform or scrubs, or other object should also be avoided to prevent infection.

Newer securement devices are designed for all catheter types and provide an evidence-based method to prevent VAD movement (INS, 2006). Recent studies have shown that these devices, such as the StatLock IV stabilization device, prevent peripheral and central catheters from becoming dislodged (Fig. 15-14). In addition, they prevent catheter complications, like phlebitis and infiltration. Use of securement devices, rather than tape, also provides significant cost savings by decreasing the number of IV restarts. To prevent skin tears, remove the adhesive on a StatLock with 70% alcohol.

Sterile dressings used over the insertion site protect the skin and puncture site. For a short peripheral catheter, the transparent membrane dressings do not require routine changes; site rotation is every 72 to 96 hours. Tape and sterile gauze or a transparent membrane dressing can be used for midline catheters and all types of central venous dressings. Tape and gauze dressings should be changed every 48 hours; transparent membrane dressings, such as Tegaderm, are changed at least every 7 days (Gorski, 2007). The initial dressing on a midline catheter or PICC is usually tape and gauze, changed within 24 hours after insertion because some bleeding is likely. Transparent membrane dressings can be used for subsequent dressing. Document all sterile dressing changes and IV site assessments in the appropriate patient record per agency policy.

Nursing Safety Priority Action Alert
Site protection may be needed for short peripheral catheters or for port access needles. Plastic shields can be placed over the site to prevent accidental bumping or pressure from clothing. Make sure you can easily assess the site frequently. Never place a restraint or opaque dressing over a peripheral IV site, especially when infusing an irritant or vesicant.

Describe the nursing care for a patient with the following vascular access devices:
Peripheral IV, Central line, PICC line. Describe peripheral IV site selection and
Assessment of peripheral IV site and nursing considerations, complications.
The current trend in health care demands that we partner with our patients to provide the best patient-centered care. In 2010, The Joint Commission added the requirement that all patients who have central lines placed in the hospital must have education on prevention of catheter-related bloodstream infection (CR-BSI). Before catheter insertion, educate the patient and family about:
• The type of catheter to be used
• Hand hygiene and aseptic technique for care of the catheter
• The therapy required
• Alternatives to the catheter and therapy
• Activity limitations
• Any signs or symptoms of complications that should be reported to a health care professional

Provide written information before placement of a long-term catheter, and continue to assess the patient's knowledge level and provide more information or answers as needed. Most manufacturers of PICCs, tunneled catheters, and implanted ports provide patient information booklets. However, specific information about the chosen procedures and supplies may be required. Conversation and pictures will be helpful for patients who are literacy challenged (have a low reading level).

Performing the Nursing Assessment
All central VADs require a postinsertion chest x-ray to document the tip location. The initial verbal and subsequent written report should contain specific information about the catheter tip location in relation to anatomic structures. The nurse's knowledge of accurate tip location is required before beginning infusion through the catheter. Repeating the x-ray during catheter use may be necessary if the patient reports unusual pain or sensation.

Nursing assessment for all infusion systems should be systematic. Begin with the insertion site and work upward, following the tubing. Know the type of catheter your patient has in place. Be sure to find out the length of catheter, the insertion site, and tip location to perform a complete assessment. Assess the insertion site by looking for redness, swelling, hardness, or drainage. Lightly palpate the area over the dressing. When a midline catheter or PICC is used, assess the entire extremity and upper chest for signs of phlebitis and thrombosis. When a tunneled catheter is used, assess the exit site, the entire length of the tunnel, and the point where the catheter enters the vein. For a well-healed catheter, it may not be possible to detect the vein entrance site. On newly inserted catheters, there could be a small puncture site with a suture or securement device. For implanted ports, assess the incision and surgically created subcutaneous pocket.

Assess the integrity of the dressing, making sure it is clean, dry, and adherent to the skin on all sides. Check all connections on the administration set, and ensure that they are secure. Be sure they are not taped. Check the rate of infusion for all fluids by either counting drops or checking the infusion pump. Assess the amount of fluid that has infused from the container. Is it accurate, or is it infusing too fast or too slow? Adjust the rate to the prescribed flow rate. Check all labels on fluid containers for the patient's name and fluid or medication. Be sure that the correct solution is being infused!

Describe the nursing care for a patient with the following vascular access devices:
Peripheral IV, Central line, PICC line. Describe peripheral IV site selection and
Assessment of peripheral IV site and nursing considerations, complications.
A peripherally inserted central catheter (PICC) is a long catheter inserted through a vein of the antecubital fossa (inner aspect of the bend of the arm) or the middle of the upper arm. Nurses who insert these CVADs require special training and certification.

In adults, the PICC length ranges from 18 to 29 inches (45-72 cm) with the tip residing in the superior vena cava (SVC) (Fig. 15-6). Placement of the catheter tip in veins distal to the SVC is avoided. This inappropriate tip location, often called a mid-clavicular catheter, is associated with much higher rates of thrombosis than when the tip is located in the SVC. Mid-clavicular tip locations are used only when anatomic or pathophysiologic changes prohibit placing the catheter into the SVC.

PICCs should be inserted early in the course of therapy before veins of the extremity have been damaged from multiple venipunctures and infusions. Insertion methods using guidewires and ultrasound systems greatly improve insertion success. The basilic vein is the preferred site for insertion; the cephalic vein can be used if necessary. Sterile technique is used for insertion to reduce the risk for catheter-related bloodstream infections (CR-BSIs). Before the catheter can be used for infusion, a chest x-ray indicating that the tip resides in the lower SVC is required when the catheter is not placed under fluoroscopy.

PICCs and nontunneled percutaneous central catheters may be sutured in place; however, this creates additional breaks in the skin that could become infected. If these sutures are loose or broken, notify the health care provider to replace them. IV catheter sutures are being replaced with securement devices in some facilities.

The initial dressing on a midline catheter or PICC is usually tape and gauze, changed within 24 hours after insertion because some bleeding is likely. Transparent membrane dressings can be used for subsequent dressing. Document all sterile dressing changes and IV site assessments in the appropriate patient record per agency policy.

Teach patients with a PICC to perform usual ADLs; however, they should avoid excessive physical activity. Muscle contractions in the arm from physical activity like heavy lifting can lead to catheter dislodgment and possible lumen occlusion. PICCs may be contraindicated in paraplegic patients who rely on their arms for mobility.

Describe the nursing care for a patient with the following vascular access devices:
Peripheral IV, Central line, PICC line. Describe peripheral IV site selection and
Assessment of peripheral IV site and nursing considerations, complications.
Hyponatremia is a serum sodium (Na+) level below 136 mEq/L (mmol/L). Sodium imbalances often occur with fluid volume imbalances because the same hormones regulate both sodium and water balance. The problems caused by hyponatremia involve two mechanisms—reduced excitable membrane depolarization and cellular swelling.

Excitable cell membrane depolarization depends on high extracellular fluid (ECF) levels of sodium being available to cross cell membranes and move into cells in response to a stimulus. Hyponatremia makes depolarization slower so that excitable membranes are less excitable.

With hyponatremia, the osmolarity of the ECF is lower than that of the intracellular fluid (ICF). As a result, water moves into the cell, causing swelling. Even a small amount of swelling can reduce cell function. Larger amounts of swelling can make the cell burst and die (lysis).

Many conditions and drugs can lead to hyponatremia (Table 13-5). One of the most common causes of low sodium levels is the prolonged use and overuse of diuretics, especially in older adults or in anyone who is also restricting sodium intake. When these drugs are used to manage fluid overload, sodium is lost along with the extra water. Hyponatremia can result from the loss of total body sodium, the movement of sodium from the blood to other fluid spaces, or the dilution of serum sodium from excessive water in the plasma.

TABLE 13-5 COMMON CAUSES OF HYPONATREMIA

Actual Sodium Deficits
• Excessive diaphoresis
• Diuretics (high-ceiling diuretics)
• Wound drainage (especially gastrointestinal)
• Decreased secretion of aldosterone
• Hyperlipidemia
• Kidney disease (scarred distal convoluted tubule)
• Nothing by mouth
• Low-salt diet
• Cerebral salt-wasting syndrome
• Hyperglycemia

Relative Sodium Deficits (Dilution)
• Excessive ingestion of hypotonic fluids
• Psychogenic polydipsia
• Freshwater submersion accident
• Kidney failure (nephrotic syndrome)
• Irrigation with hypotonic fluids
• Syndrome of inappropriate antidiuretic hormone secretion
• Heart failure

Patient-Centered Collaborative Care
Assessment

The manifestations of hyponatremia are caused by its effects on excitable cellular activity. The cells especially affected are those involved in cerebral, neuromuscular, intestinal smooth muscle, and cardiovascular functions.

Cerebral changes are the most obvious problems of hyponatremia. First establishing the patient's usual cognitive and behavioral patterns is essential because either depressed activity or excessive activity (and sometimes both) may occur. Behavioral changes result from cerebral edema and increased intracranial pressure. Closely observe and document the patient's behavior, level of consciousness, and mental status. A sudden onset of acute confusion or increased confusion is often seen in older adults who have low serum sodium levels.

Neuromuscular changes are seen as general muscle weakness. Assess the patient's neuromuscular status during each nursing shift for changes from baseline. Deep tendon reflexes diminish, and muscle weakness is worse in the legs and arms. Assess muscle strength in several ways, including arm muscle strength and leg muscle strength. Test arm muscle strength first by having the patient squeeze your hand. Another way to test arm muscle strength is to have the patient flex his or her arms against the chest and keep them flexed while you attempt to pull them away from the chest. Test leg muscle strength by having the patient push both feet against a flat surface (like a box or a board) while you apply resistance to the opposite side of the flat surface.

Nursing Safety Priority Action Alert
If muscle weakness is present, immediately check respiratory effectiveness because ventilation depends on adequate strength of respiratory muscles.

Intestinal changes include increased motility, causing nausea, diarrhea, and abdominal cramping. Assess the GI system by listening to bowel sounds and observing stools. Bowel sounds are hyperactive, with rushes and gurgles over the splenic flexure and in the lower left quadrant. Bowel movements are frequent and watery.

Cardiovascular changes are seen as changes in cardiac output. The cardiac responses to hyponatremia with hypovolemia (decreased plasma volume) include a rapid, weak, thready pulse. Peripheral pulses are difficult to palpate and are easily blocked with light pressure. Blood pressure is decreased, and the patient may have severe hypotension when moving from a lying or sitting position to a standing position (orthostatic hypotension), leading to light-headedness or dizziness. The central venous pressure is low.

When hyponatremia occurs with hypervolemia (fluid overload), cardiac changes include a full or bounding pulse with normal or high blood pressure. Peripheral pulses are full and difficult to block; however, they may not be palpable if edema is present.

Interventions
The health care provider determines the specific cause of the low sodium level to plan the most appropriate medical treatment. Interventions with drug therapy and nutrition therapy are used to restore serum sodium levels to normal and prevent complications from fluid overload or a too-rapid change in serum sodium level. The priorities for nursing care of the patient with hyponatremia are monitoring the patient's response to therapy and preventing hypernatremia and fluid overload.

Drug therapy first involves reducing the doses of any drugs that increase sodium loss, such as loop diuretics and thiazide diuretics. Other regimens vary depending on whether fluid imbalance occurs with hyponatremia. When hyponatremia occurs with a fluid deficit, IV saline infusions are prescribed to restore both sodium and fluid volume. Severe hyponatremia may be treated with small-volume infusions of hypertonic (2%-3%) saline. These infusions are delivered using a controller to prevent accidental increases in infusion rate. Monitor the infusion rate and the patient's response.

When hyponatremia occurs with fluid excess, drug therapy includes giving drugs that promote the excretion of water rather than sodium, such as conivaptan (Vaprisol) or tolvaptan (Samsca). Drug therapy for hyponatremia caused by inappropriate secretion of antidiuretic hormone (ADH) may also include agents that antagonize ADH, such as lithium and demeclocycline (Declomycin). Assess hourly for signs of excessive fluid loss, potassium loss, and increased sodium levels.

Nutrition therapy can help restore normal sodium balance in mild hyponatremia. Collaborate with the registered dietitian (RD) to teach the patient about which foods to increase in the diet. Therapy involves increasing oral sodium intake and restricting oral fluid intake. Fluid restriction may be needed long-term when fluid overload is the cause of the hyponatremia or when kidney fluid excretion is impaired. Nursing actions for patient safety, skin protection, measurement of fluid intake and output, and patient and family teaching are the same as those for fluid overload on pp. 179-180.
Hypernatremia is a serum sodium level over 145 mEq/L (mmol/L). High serum sodium levels can be caused by or can cause changes in fluid volumes. Table 13-6 lists common causes of hypernatremia.

As serum sodium level rises, a larger difference in sodium levels occurs between the extracellular fluid (ECF) and the intracellular fluid (ICF). More sodium is present to move rapidly across cell membranes during depolarization, making excitable tissues more easily excited. This condition is called irritability, and excitable tissues over-respond to stimuli. In addition, water moves from the cells into the ECF to dilute the hyperosmolar ECF. So, when serum sodium levels are high, severe cellular dehydration occurs. Eventually the dehydrated excitable tissues may no longer be able to respond to stimuli.

Patient-Centered Collaborative Care
Assessment
The manifestations of hypernatremia vary with the severity of sodium imbalance and whether a fluid imbalance is also present. Changes are first seen in excitable membrane activity, especially nerve, skeletal muscle, and cardiac function.

Nervous system changes start with altered cerebral function. Assess the patient's mental status for attention span, recall of recent events, and cognitive function. In hypernatremia with normal or decreased fluid volumes, the patient may have a short attention span and be agitated or confused about recent events. Manic episodes or seizures may occur if serum sodium continues to rise. When hypernatremia occurs with fluid overload, the patient may be lethargic, drowsy, stuporous, and even comatose.

Skeletal muscle changes vary with the degree of sodium increases. Mild rises cause muscle twitching and irregular muscle contractions. As hypernatremia worsens, the muscles and nerves are less able to respond to a stimulus and muscles become progressively weaker. Late, the deep tendon reflexes are reduced or absent. Muscle weakness occurs bilaterally and has no specific pattern. Observe for twitching in muscle groups. Assess muscle strength by having the patient perform handgrip and arm flexion against resistance as described on p. 181. The advanced practice nurse may check reflexes by lightly tapping the patellar (knee) tendons and Achilles (heel) tendons with a reflex hammer and measuring the movement.

Cardiovascular changes include decreased contractility because high sodium levels slow the movement of calcium into the heart cells. Measure 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, depending on the fluid volume and how rapidly the imbalance occurred.

Pulse rate is increased in patients with hypernatremia and hypovolemia. Peripheral pulses are difficult to palpate and are easily blocked. Hypotension and severe orthostatic (postural) hypotension are present, and pulse pressure is reduced.

Patients 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 patient in the upright position. Blood pressure, especially diastolic blood pressure, is increased.

Interventions
Drug and nutrition therapies are used to prevent further increases in serum sodium and decrease high serum sodium levels. Other medical interventions used when sodium levels become life threatening include hemodialysis and blood ultrafiltration. Priorities for nursing care of the patient with hypernatremia include monitoring his or her response to therapy and ensuring patient safety by preventing hyponatremia and dehydration.

Drug therapy is used to restore fluid balance when hypernatremia is caused by fluid loss. Hypotonic IV infusions, usually 0.225% sodium chloride, are prescribed. Hypernatremia caused by fluid and sodium losses (in which sodium losses are less than fluid losses) may require fluid replacement with IV infusions of solutions that are still hypotonic but contain slightly higher concentrations of sodium (e.g., 0.45% sodium chloride). Hypernatremia caused by poor kidney excretion of sodium requires drug therapy with diuretics that promote sodium loss, such as furosemide (Lasix, Furoside ) or bumetanide (Bumex). Assess the patient hourly for symptoms of excessive losses of fluid, sodium, or potassium.

Nutrition therapy can prevent or correct mild hypernatremia by ensuring adequate water intake, especially among older adults or those who may not have self-access to water. Dietary sodium restriction may be needed to prevent sodium excess when kidney problems are present. In addition, fluids must often be restricted. Collaborate with the dietitian to teach the patient how to determine the sodium content of foods, beverages, and drugs. Nursing actions for patient safety, skin protection, measurement of fluid intake and output, and patient and family teaching are similar to those for fluid overload on pp. 179-180.
Because 98% of total body potassium (K+) is inside cells, 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). It can be life threatening because every body system is affected.

Low serum potassium levels increase the difference in the amount of potassium between the fluid inside the cells (ICF) and the fluid outside the cells (ECF). This increased difference reduces the excitability of cells. As a result, the cell membranes of all excitable tissues, such as nerve and muscle, are less responsive to normal stimuli.

TABLE 13-7 COMMON CAUSES OF HYPOKALEMIA
Actual Potassium Deficits
• Inappropriate or excessive use of drugs:
• Diuretics
• Digitalis
• Corticosteroids
• Increased secretion of aldosterone
• Cushing's syndrome
• Diarrhea
• Vomiting
• Wound drainage (especially gastrointestinal)
• Prolonged nasogastric suction
• Heat-induced excessive diaphoresis
• Kidney disease impairing reabsorption of potassium
• Nothing by mouth

Relative Potassium Deficits
• Alkalosis
• Hyperinsulinism
• Hyperalimentation
• Total parenteral nutrition
• Water intoxication
• IV therapy with potassium-poor solutions

When the loss of ECF potassium is gradual, cells adjust and cellular potassium decreases in proportion to the ECF potassium level. The potassium difference between the two fluid spaces remains unchanged, and symptoms of hypokalemia may not appear until the potassium loss is extreme. Rapid reduction of serum potassium levels causes dramatic changes in function.

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 13-7 lists the common causes of hypokalemia.

Actual potassium depletion occurs when potassium loss is excessive or when potassium intake is not adequate to match normal potassium loss. Relative hypokalemia occurs when total body potassium levels are normal but the potassium distribution between fluid spaces is abnormal, or it is diluted by excess water.

Patient-Centered Collaborative Care
Assessment

Age is important because the kidneys' ability to concentrate urine decreases with aging, which increases potassium loss. Older adults are more likely to use drugs that lead to potassium loss.

Drugs, especially diuretics, corticosteroids, and beta-adrenergic agonists or antagonists, can increase potassium loss through the kidneys. Ask about prescription and over-the-counter drug use. A common cause of hypokalemia is the prolonged use and misuse of diuretics. In patients taking digoxin (Lanoxin, Novodigoxin ), hypokalemia increases the sensitivity of the cardiac muscle to the drug and may result in digoxin toxicity, even when the digoxin level is within the therapeutic range. Ask whether the patient takes a potassium supplement, such as potassium chloride (KCl), or eats foods that have high concentrations of potassium, such as bananas, citrus fruits or juices, raisins, and meat. The patient may not be taking the supplement as prescribed because of its unpleasant taste.

Disease can lead to potassium loss. Ask the patient about chronic disorders, as well as recent illnesses and medical or surgical interventions. A thorough nutrition history, including a typical day's food and beverage intake, helps identify patients at risk for hypokalemia.

Respiratory changes are likely because of weakness of the muscles needed for breathing. Skeletal muscle weakness results in shallow respirations. Thus respiratory status should be assessed first in any patient who might have hypokalemia. Assess the patient's breath sounds, ease of respiratory effort, color of nail beds and mucous membranes, and rate and depth of respiration. Assess respiratory status at least every 2 hours because respiratory insufficiency is a major cause of death.

Musculoskeletal changes include skeletal muscle weakness in response to hypokalemia. A stronger stimulus is needed to begin muscle contraction. A patient may be so weak that he or she cannot stand. Hand grasps are weak, and a decreased response to deep tendon reflex stimulation (hyporeflexia) may be seen. Severe hypokalemia causes flaccid paralysis. Assess for muscle weakness, and determine the patient's ability to perform ADLs.

Cardiovascular changes are assessed by first palpating the peripheral pulses. In the patient with hypokalemia, the pulse is usually thready and weak. Palpation is difficult, and the pulse is easily blocked with light pressure. The pulse rate can range from very slow to very rapid, and an irregular heartbeat (dysrhythmia) may be present. Measure blood pressure with the patient in the lying, sitting, and standing positions, because orthostatic (postural) hypotension occurs with hypokalemia.

Neurologic changes from hypokalemia include altered mental status. The patient may have short-term irritability and anxiety followed by lethargy that progresses to acute confusion and coma as hypokalemia worsens.

Behavioral changes caused by hypokalemia can occur quickly. If needed, obtain information about the patient's behavior from close family members or friends if the patient is confused. The patient may be lethargic and unable to perform simple problem-solving tasks such as counting by threes. As hypokalemia progresses, the patient may become more confused, especially to time and place. In severe hypokalemia, coma may develop.

Intestinal changes occur with hypokalemia because smooth muscle contractions in the intestinal tract are decreased, which leads to decreased peristalsis. The patient has hypoactive bowel sounds and may have nausea, vomiting, constipation, and abdominal distention. Assess distention by measuring abdominal girth. Auscultate for bowel sounds in all four abdominal quadrants to assess the extent of decreased peristalsis. Severe hypokalemia can cause the absence of peristalsis (paralytic ileus).

Laboratory data confirm hypokalemia (serum potassium value below 3.5 mEq/L [mmol/L]). Hypokalemia causes ECG changes in the heart, including ST-segment depression, flat or inverted T waves, and increased U waves. Dysrhythmias can lead to death, particularly in older adults who are taking digoxin.

Interventions

Interventions for hypokalemia aim to prevent potassium loss, increase serum potassium levels, and ensure patient safety. Drug and nutrition therapies help restore normal serum potassium levels. The priorities for nursing care of the patient with hypokalemia are (1) ensuring adequate oxygenation, patient safety for falls prevention, and prevention of injury from potassium administration and (2) monitoring the patient's response to therapy. Chart 13-7 highlights best practice activities when caring for a patient with hypokalemia.

Drug therapy for the treatment and prevention of hypokalemia includes additional potassium and drugs to prevent potassium loss. Most potassium supplements are potassium chloride, potassium gluconate, or potassium citrate. The amount and the route of potassium replacement depend on the degree of loss.

Potassium is given IV for severe hypokalemia. The drug is available in different concentrations, and this drug carries a high alert warning as a concentrated electrolyte solution. The Joint Commission has mandated that concentrated potassium be diluted and added to IV solutions only in the pharmacy by a registered pharmacist and that vials of concentrated potassium not be available in patient care areas. Before infusing any IV solution containing potassium chloride (KCl), check and re-check the dilution of the drug in the IV solution container.

Chart 13-7
Best Practice for Patient Safety & Quality Care
The Patient with Hypokalemia
• Question the continued use of drugs that increase excretion of potassium (e.g., thiazide and loop diuretics).
• Administer prescribed oral potassium supplement, well diluted and with a meal or just after a meal or snack to prevent nausea and vomiting.
• Prevent accidental overdose of IV potassium by checking and re-checking the concentration of potassium in the IV solution, ensuring that the maximum concentration is no greater than 1 mEq/10 mL of solution.
• Establish an IV access in a large vein with a high volume of flow, avoiding the hand.
• Assess the IV access for placement and an adequate blood return before administering potassium-containing solutions.
• Use a controller for solution delivery, maintaining an infusion rate not faster than 5 to 10 mEq of potassium per hour.
• Assess the IV site hourly.
• Stop the infusion immediately if the patient reports pain or burning or if any manifestation of infiltration occurs.
• If possible, monitor electrocardiography (ECG) continuously.
• Monitor patient responses every 1 to 2 hours to determine therapy effectiveness and the potential for hyperkalemia.
• Indications of therapy effectiveness:
• Respiratory rate is greater than 12 breaths per minute
• Oxygen saturation is at least 95% (or has returned to the patient's normal baseline)
• The patient can cough effectively
• Hand grasp strength increases
• Deep tendon reflexes are present
• Bowel sounds are present and active
• Pulse is easily palpated and regular
• Systolic blood pressure when standing remains within 20 mm Hg of the systolic pressure obtained when the patient is sitting or lying down
• ST segment returns to the isoelectric line
• T waves increase in size and are positive
• U waves decrease or disappear
• Patient's cognition resembles his or her prehypokalemic state
• Serum potassium level is between 3.5 and 5.0 mEq/L
• Indications of hyperkalemia:
• Heart rate is less than 60 beats per minute
• P waves are absent
• T waves are tall
• PR intervals are prolonged
• QRS complexes are wide
• Deep tendon reflexes are hyperactive
• Bowel sounds are hyperactive
• Numbness or tingling is present in the hands and feet and around the mouth
• The patient is anxious
• Serum potassium level is above 5.0 mEq/L
• Keep patient on bedrest until hypokalemia resolves, or provide assistance when out of bed to prevent falls.

Nursing Safety Priority Drug Alert
A dilution no greater than 1 mEq of potassium to 10 mL of solution is recommended for IV administration. The maximum recommended infusion rate is 5 to 10 mEq/hr; this rate is never to exceed 20 mEq/hr under any circumstances. Older patients may not be able to handle this rate. In accordance with the National Patient Safety Goals (NPSGs), potassium is not given by IV push to avoid causing cardiac arrest.

Potassium is a severe tissue irritant and is never given by IM or subcutaneous injection. Tissues damaged by potassium can become necrotic and slough, causing loss of function and requiring reconstructive surgery. IV potassium solutions irritate veins and can cause phlebitis. Check the prescription carefully to ensure that the patient receives the correct amount of potassium. Assess the IV site hourly, and ask the patient whether he or she feels burning or pain at the site.

Nursing Safety Priority Action Alert
If infiltration of an IV solution containing potassium occurs, stop the IV solution immediately, remove the venous access, and notify the health care provider or Rapid Response Team. Document these actions along with a complete description of the IV site.

Oral potassium preparations may be taken as liquids or solids. Potassium has a strong, unpleasant taste that is difficult to mask, although it can be mixed with many liquids. Some preparations are already flavored. Because potassium chloride can cause nausea and vomiting, give the drug during or after a meal and advise patients using the drug at home not to take it on an empty stomach.

Diuretics that increase the kidney excretion of potassium can cause hypokalemia. These classes of diuretics include high-ceiling (loop) diuretics (e.g., furosemide [Lasix, Furoside ] and bumetanide [Bumex]) and the thiazide diuretics. Avoid these drugs in patients with hypokalemia. A potassium-sparing diuretic may be prescribed for patients with hypokalemia who need diuretic therapy. Potassium-sparing diuretics increase urine output without increasing potassium loss. Potassium-sparing diuretics include spironolactone (Aldactone, Novospiroton ), triamterene (Dyrenium), and amiloride (Midamor).

Nutrition therapy involves coordination with a dietitian to teach the patient how to increase dietary potassium intake. Eating foods that are naturally rich in potassium helps prevent further loss, but supplementation is needed to restore normal potassium levels when hypokalemia is present.

Implement safety measures with a patient who has muscle weakness from hypokalemia, including the falls precautions listed in Chart 13-4. Measures include eliminating hazards and assisting with ambulation. Instruct UAP to remove obstacles or slippery areas from the ambulation path, and make certain the patient wears nonslip footgear. Be sure to have the patient wear a gait belt when ambulating with assistance.

Respiratory monitoring is performed at least hourly for severe hypokalemia and includes rate and depth, especially checking for increasing rate and decreasing depth. Also check oxygen saturation by pulse oximetry to determine breathing effectiveness. Assess respiratory muscle effectiveness by checking the patient's ability to cough. Examine the face, oral mucosa, and nail beds for pallor or cyanosis. Evaluate arterial blood gas values (when available) for decreased blood oxygen levels (hypoxemia) and increased arterial carbon dioxide levels (hypercapnia), which indicate inadequate breathing effectiveness.
Hyperkalemia is a serum potassium level higher than 5.0 mEq/L (mmol/L). The normal range for serum potassium values is narrow, so even slight increases above normal values can affect excitable tissues, especially the heart.

A high serum potassium level decreases the potassium difference between the intracellular fluid (ICF) and the extracellular fluid (ECF). This decreased difference increases cell excitability; as a result, most excitable tissues respond to less intense stimuli and may even discharge spontaneously. The heart is very sensitive to serum potassium increases, and the most serious complications of hyperkalemia are heart block and ventricular fibrillation.

The problems that occur with hyperkalemia are related to how rapidly ECF potassium levels increase. Sudden rises in serum potassium cause severe problems at potassium levels between 6 and 7 mEq/L. When serum potassium rises slowly, problems may not occur until potassium levels reach 8 mEq/L or higher.

Hyperkalemia may result from an actual increase in total body potassium or from the movement of potassium from the cells into the blood. Hyperkalemia is rare in people with normal kidney function. Most cases of hyperkalemia occur in hospitalized patients and in those undergoing medical treatment. Those at greatest risk for hyperkalemia are chronically ill patients, debilitated patients, and older adults. Table 13-8 lists common causes of hyperkalemia.

Patient-Centered Collaborative Care
Assessment
Age is important because kidney function decreases with aging. Ask about chronic illnesses (particularly kidney disease and diabetes mellitus), recent medical or surgical treatment, and urine output, including frequency and amount of voidings. Ask about drug use, particularly potassium-sparing diuretics and angiotensin-converting enzyme (ACE) inhibitors. Obtain a nutrition history to determine the intake of potassium-rich foods and the use of salt substitutes (which contain potassium).

Collect specific information about symptoms related to hyperkalemia. Ask whether the patient has had palpitations, skipped heartbeats, other cardiac irregularities, muscle twitching, weakness in the leg muscles, or unusual tingling or numbness in the hands, feet, or face. Ask about recent changes in bowel habits, especially diarrhea.

Cardiovascular changes are the most severe problems from hyperkalemia and are the most common cause of death in patients with hyperkalemia. Cardiac manifestations of hyperkalemia include bradycardia, hypotension, and ECG changes of tall, peaked T waves, prolonged PR intervals, flat or absent P waves, and wide QRS complexes. As serum potassium levels rise, heartbeats generated outside the normal conduction system in the ventricles (ectopic beats) may appear. Complete heart block, asystole, and ventricular fibrillation are life-threatening complications of severe hyperkalemia.

Neuromuscular changes with hyperkalemia have two phases. Skeletal muscles twitch in the early stages of hyperkalemia, and the patient may be aware of tingling and burning sensations followed by numbness in the hands and feet and around the mouth (paresthesia). As hyperkalemia worsens, muscle twitching changes to weakness followed by flaccid paralysis. The weakness moves up from the hands and feet and first affects the muscles of the arms and legs. Respiratory muscles are not affected until serum potassium levels reach lethal levels.

Intestinal changes include increased motility. The patient may have diarrhea and spastic colonic activity. Bowel sounds are hyperactive, with audible rushes and gurgles. Bowel movements are frequent and watery.

Laboratory data confirm hyperkalemia (potassium level over 5.0 mEq/L). If it is caused by dehydration, levels of other electrolytes, hematocrit, and hemoglobin also are elevated. Hyperkalemia caused by kidney failure occurs with elevated serum creatinine and blood urea nitrogen, decreased blood pH, and normal or low hematocrit and hemoglobin levels.

Interventions
Interventions for hyperkalemia focus on rapidly reducing the serum potassium level, preventing recurrences, and ensuring patient safety during the electrolyte imbalance. Drug therapy is the main medical intervention. The priorities for nursing care of the patient with hyperkalemia are monitoring to prevent cardiac complications, patient safety for falls prevention, monitoring the patient's response to therapy, and health teaching.

Drug therapy can restore normal potassium balance by enhancing potassium excretion and promoting the movement of potassium from the extracellular fluid (ECF) into the cells.

Eliminate extra potassium by stopping potassium-containing infusions. Keeping the IV access open is useful in managing hyperkalemia. Withhold oral potassium supplements, and provide a potassium-restricted diet.

Increasing potassium excretion helps reduce hyperkalemia if kidney function is normal. Potassium-excreting diuretics, such as furosemide, are prescribed. For a patient with kidney problems, drug therapy to increase potassium excretion includes cation exchange resins that promote intestinal sodium absorption and potassium excretion, such as sodium polystyrene sulfonate (Kayexalate). However, this therapy may take many hours to reduce potassium levels. If potassium levels are dangerously high, additional measures, such as dialysis, are needed.

Movement of potassium from the extracellular fluid (ECF) to the intracellular fluid (ICF) can help reduce serum potassium levels temporarily. Potassium movement into the cells is enhanced by insulin. Insulin increases the activity of the sodium-potassium pumps, which move potassium from the ECF into the cell. IV fluids containing glucose and insulin are prescribed 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 infused through a central line or in a vein with a high blood flow to avoid local vein inflammation. Observe the patient for manifestations of hypokalemia and hypoglycemia during this therapy.

Cardiac monitoring allows for the early recognition of dysrhythmias and other manifestations of hyperkalemia on cardiac muscle. Compare recent ECG tracings with the patient's baseline tracings or with tracings obtained when the patient's serum potassium level was close to normal.

Nursing Safety Priority Critical Rescue

Notify the health care provider or Rapid Response Team if the patient's heart rate falls below 60 beats per minute or if the T waves become spiked, both of which accompany hyperkalemia.

Health teaching is key to the prevention of hyperkalemia and the early detection of complications. The teaching plan for the patient at risk for hyperkalemia includes diet, drugs, and recognition of the manifestations of hyperkalemia. Collaborate with the dietitian to teach the patient and family about which foods to avoid (those high in potassium). Foods that contain little potassium and are allowed are listed in Chart 13-8. Instruct the patient and family to read the labels on drug and food packages to determine the potassium content. Warn them to avoid salt substitutes, which contain potassium.
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 amount of total body calcium present in extracellular fluid (ECF). Because the normal blood level of calcium is so low, any change in calcium levels has major effects on function.

Calcium is an excitable membrane stabilizer, regulating depolarization and the generation of action potentials. It decreases sodium movement across excitable membranes, slowing the rate of depolarization. Low serum calcium levels increase sodium movement across excitable membranes, allowing depolarization to occur more easily and at inappropriate times.

Hypocalcemia is caused by many chronic and acute conditions, as well as medical or surgical treatments. Table 13-9 lists the common causes of hypocalcemia. Acute hypocalcemia results in the rapid onset of life-threatening manifestations, even when the serum calcium level is not very low. Chronic hypocalcemia occurs slowly over time, and excitable membrane manifestations may not be severe because the body has adjusted to the gradual reduction of serum calcium levels.

TABLE 13-9 COMMON CAUSES OF HYPOCALCEMIA
Actual Calcium Deficits
• Inadequate oral intake of calcium
• Lactose intolerance
• Malabsorption syndromes:
• Celiac sprue
• Crohn's disease
• Inadequate intake of vitamin D
• End-stage kidney disease
• Kidney failure—polyuric phase
• Diarrhea
• Steatorrhea
• Wound drainage (especially gastrointestinal)

Relative Calcium Deficits
• Hyperproteinemia
• Alkalosis
• Calcium chelators or binders
• Citrate
• Mithramycin
• Penicillamine
• Sodium cellulose phosphate (Calcibind)
• Aredia
• Acute pancreatitis
• Hyperphosphatemia
• Immobility
• Removal or destruction of parathyroid glands

Actual calcium loss (a reduction in total body calcium) occurs when the absorption of calcium from the GI tract slows or when calcium is lost from the body. Relative calcium loss causes total body calcium amounts to remain normal while serum calcium levels are low. This problem occurs when the unbound calcium in the body is reduced or when parathyroid gland function is decreased.

Cultural Awareness
Lactose intolerance caused by a deficiency of the enzyme lactase occurs in 75% to 90% of all Asians, Blacks, and American Indians (McCance et al., 2010). Although this problem also does occur in Caucasians, the incidence is much higher in nonwhites. People with lactose intolerance cannot use the nutrients in milk and have cramping, diarrhea, and abdominal pain after ingesting dairy products. Dairy products, especially milk, are common and rich sources of both calcium and vitamin D. People with lactose intolerance may, therefore, have difficulty obtaining enough calcium and vitamin D from other sources to maintain normal calcium levels in the blood and bones.

Women's Health Considerations
Postmenopausal women are at risk for chronic calcium loss. This problem is related to reduced weight-bearing activities and a decrease in estrogen levels. In general, women have smaller frames than men and the female skeleton does not bear as much weight as the male skeleton. As they age, many women decrease weight-bearing activities such as running and walking, which allows osteoporosis to occur at a more rapid rate. Also, the estrogen secretion that protects against osteoporosis diminishes. (See Chapter 53 for a complete discussion of osteoporosis.)

Patient-Centered Collaborative Care
Assessment

The nutrition history is important to assess for the risk for hypocalcemia. Ask the patient about his or her intake of dairy products and whether he or she takes a calcium supplement regularly.

One indicator of hypocalcemia is a report of frequent, painful muscle spasms ("charley horses") in the calf or foot during rest or sleep. Other information that indicates possible 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 increases the risk for hypocalcemia. Most manifestations of acute hypocalcemia are caused by overstimulation of the nerves and muscles.

Neuromuscular changes often occur first in the hands and feet. Paresthesias occur at first, with sensations of tingling and numbness. If hypocalcemia continues or worsens, actual muscle twitching or painful cramps and spasms occur. Tingling may also affect the lips, nose, and ears. These problems may signal the onset of neuromuscular overstimulation and tetany.

Assess for hypocalcemia by testing for Trousseau's and Chvostek's signs. To test for Trousseau's sign, place a blood pressure cuff around the upper arm, inflate the cuff to greater than the patient's systolic pressure, and keep the cuff inflated for 1 to 4 minutes. Under these hypoxic conditions, a positive Trousseau's sign occurs when the hand and fingers go into spasm in palmar flexion (Fig. 13-14). To test for Chvostek's sign, tap the face just below and in front of the ear (over the facial nerve) to trigger facial twitching of one side of the mouth, nose, and cheek (Fig. 13-15).

Cardiovascular changes involve heart rate and ECG changes. The heart rate may be slower or slightly faster than normal, with a weak, thready pulse. Severe hypocalcemia causes severe hypotension and ECG changes of a prolonged ST interval and a prolonged QT interval.

Intestinal changes include increased peristaltic activity. Auscultate the abdomen for hyperactive bowel sounds. The patient may report painful abdominal cramping and diarrhea.

Skeletal changes are most common with chronic hypocalcemia. Calcium is moved from bone storage sites, causing a loss of bone density (osteoporosis). The bones are less dense, more brittle, and fragile. These bones break easily with even slight trauma. Vertebrae become more compact and may bend forward, leading to an overall loss of height. See Chapter 53 for more discussion about osteoporosis.

Ask about changes in height and any unexplained bone pain. Observe for spinal curvatures and any unusual bumps or protrusions in bones that may indicate old fractures.

Interventions
Interventions focus on restoring normal calcium levels and preventing complications. These include drug therapy, nutrition therapy, reducing environmental stimuli, and preventing injury. Patient safety during restoration of serum calcium levels is a priority of nursing care.

Drug therapy for hypocalcemia includes direct calcium replacement (oral and IV) and drugs that enhance the absorption of calcium, such as aluminum hydroxide and vitamin D. When neuromuscular manifestations are troublesome, drugs that decrease nerve and muscle responses also may be used. These drugs may include magnesium sulfate and various muscle relaxants.

Nutrition therapy involves a high-calcium diet for patients with mild hypocalcemia and for those with chronic conditions that cause them to be at continuous risk for hypocalcemia. Coordinate with the dietitian to assist the patient in selecting calcium-rich foods.

Environmental management for safety is needed because the excitable membranes of the nervous system and the skeletal system are overstimulated in hypocalcemia. Interventions to reduce stimulation include keeping the room quiet, limiting visitors, adjusting the lighting, and using a soft but reassuring voice.

Use seizure precautions for the patient with hypocalcemia. Such precautions include either keeping the bed in the lowest possible position and the siderails of the bed in the "up" position. Alternately, a mattress can be placed on the floor on the side of the bed with the siderail down. Keep emergency equipment (e.g., oxygen, suction) at the bedside. Keep an emergency cart equipped with emergency drugs and an endotracheal tray just outside the patient's room. If the patient does not have an IV access, one should be started.

Injury prevention strategies are needed because the patient with long-standing calcium loss may have brittle, fragile bones that fracture easily and cause little pain. When lifting or moving a patient with fragile bones, use a lift sheet rather than pulling the patient. Observe for normal range of joint motion and for any unusual surface bumps or depressions over bony areas.
Hypercalcemia is a total serum calcium level above 10.5 mg/dL, or 2.75 mmol/L. Because the normal range for serum calcium is so narrow, even small increases have severe effects. Although the effects of hypercalcemia occur first in excitable tissues, all systems are affected.

Hypercalcemia means either that the amount of serum calcium is so great that the normal calcium-controlling mechanisms cannot keep pace or that at least one control mechanism is not functioning properly (Table 13-10). Hypercalcemia causes excitable tissues to be less sensitive to normal stimuli, thus requiring a stronger stimulus to function. The excitable tissues affected most by hypercalcemia are the heart, skeletal muscles, nerves, and intestinal smooth muscles.

Calcium is needed by many of the enzymes involved in blood clotting. Hypercalcemia causes faster clotting times. Clots may form when they are not needed to control bleeding. Excessive clotting from hypercalcemia occurs more easily in vessels with slow blood flow.

Patient-Centered Collaborative Care
Assessment

The manifestations of hypercalcemia are related to its severity and how quickly the imbalance occurred. The patient with a mild but rapidly occurring calcium excess usually has more severe problems than the patient whose imbalance is severe but has developed slowly.

Cardiovascular changes are the most serious and life-threatening problems of hypercalcemia. Mild hypercalcemia at first causes increased heart rate and blood pressure. Severe or prolonged calcium imbalance depresses electrical conduction, slowing heart rate.

Measure pulse rate and blood pressure, and observe for indications of poor tissue blood flow, such as cyanosis and pallor. Examine ECG tracings for dysrhythmias, especially a shortened QT interval.

Hypercalcemia allows blood clots to form more easily whenever blood flow is poor. Blood clotting is more likely in the lower legs, the pelvic region, areas where blood flow is blocked by internal or external constrictions, and areas where venous obstruction occurs.

Assess for slowed or impaired blood flow. Measure and record calf circumferences with a soft tape measure. Assess the feet for temperature, color, and capillary refill to determine the blood flow to and from the area.

Neuromuscular changes include severe muscle weakness and decreased deep tendon reflexes without paresthesia. The patient may have an altered level of consciousness that can range from confusion and lethargy to coma. Psychiatric problems also can occur.

Intestinal changes are first reflected as decreased peristalsis. Constipation, anorexia, nausea, vomiting, and abdominal pain are common. Bowel sounds are hypoactive or absent. The abdomen increases in size because the intestinal contents remain in the tract instead of being moved forward. Assess abdominal size by measuring abdominal girth with a soft tape measure in a line circling the abdomen at the umbilicus.

Interventions
Interventions for hypercalcemia aim to reduce serum calcium levels through drug therapy and dialysis. Rehydration and cardiac monitoring are also important.

Drug therapy involves preventing increases in calcium, as well as drugs to lower calcium levels. IV solutions containing calcium (e.g., Ringer's lactate) are stopped. Oral drugs containing calcium or vitamin D (e.g., calcium-based antacids) are discontinued.

Fluid volume replacement can help restore normal serum calcium levels. IV normal saline (0.9% sodium chloride) is usually given because sodium increases kidney excretion of calcium.

Thiazide diuretics are discontinued and are replaced with diuretics that enhance the excretion of calcium, such as furosemide (Lasix, Furoside ). Calcium chelators (calcium binders) help lower serum calcium levels. Such drugs include plicamycin (Mithracin) and penicillamine (Cuprimine, Pendramine ).

Drugs to prevent hypercalcemia include agents that inhibit calcium resorption from bone, such as phosphorus, calcitonin (Calcimar), bisphosphonates (etidronate), and prostaglandin synthesis inhibitors (aspirin, NSAIDs).

Dialysis is used when severe hypercalcemia causes life-threatening cardiac problems and drug therapy may not reduce serum calcium levels fast enough to prevent death. Methods of dialysis for rapid calcium reduction are usually hemodialysis or blood ultrafiltration.

Cardiac monitoring of patients with hypercalcemia is needed to identify dysrhythmias and decreased cardiac output. Compare recent ECG tracings with the patient's baseline tracings. Especially look for changes in the T waves and the QT interval and changes in rate and rhythm.

TABLE 13-10 COMMON CAUSES OF HYPERCALCEMIA

Actual Calcium Excesses
• Excessive oral intake of calcium
• Excessive oral intake of vitamin D
• Kidney failure
• Use of thiazide diuretics

Relative Calcium Excesses
• Hyperparathyroidism
• Malignancy:
• Direct invasion (cancers of breast, lung, prostate, and osteoclastic bone and multiple myeloma)
• Indirect resorption (liver cancer, small cell lung cancer, and cancer of the adrenal gland)
• Hyperthyroidism
• Immobility
• Use of glucocorticoids
• Dehydration
Hypomagnesemia is a serum magnesium (Mg2+) level below 1.3 mEq/L. Most problems leading to hypomagnesemia are caused by decreased magnesium intake or increased magnesium loss. As a result, hypomagnesemia reflects a decrease in the total body magnesium content.

The effects of hypomagnesemia are caused by increased membrane excitability and the accompanying serum calcium and potassium imbalances. Excitable membranes, especially nerve cell membranes, may depolarize spontaneously.

Hypomagnesemia is caused by decreased absorption of dietary magnesium or increased kidney magnesium excretion. Table 13-12 lists the specific causes of hypomagnesemia.

Patient-Centered Collaborative Care
Common clinical manifestations of hypomagnesemia are seen in the neuromuscular, central nervous, and intestinal systems.

Neuromuscular changes are caused by increased nerve impulse transmission. Normally, magnesium inhibits nerve impulse transmission at synapse areas. Decreased levels increase impulse transmission from nerve to nerve or from nerve to skeletal muscle. The patient has hyperactive deep tendon reflexes, numbness and tingling, and painful muscle contractions. Positive Chvostek's and Trousseau's signs may be present because hypomagnesemia may occur with hypocalcemia (see the earlier discussion of these assessment signs of neuromuscular changes on pp. 189-190 in the Hypocalcemia section). Skeletal muscle weakness occurs when intracellular magnesium levels are also decreased. The patient may have tetany and seizures as hypomagnesemia worsens.

Central nervous system (CNS) changes are caused by increased nerve impulse transmission. These changes may present as psychological depression, psychosis, and confusion.

Intestinal changes are from decreased intestinal smooth muscle contraction. Reduced motility, anorexia, nausea, constipation, and abdominal distention are common. A paralytic ileus may occur when hypomagnesemia is severe.

Interventions for hypomagnesemia aim to correct the imbalance and manage the specific problem that caused it. In addition, because hypocalcemia often occurs with hypomagnesemia, interventions also aim to restore normal serum calcium levels.

Drugs that promote magnesium loss, such as high-ceiling (loop) diuretics, osmotic diuretics, aminoglycoside antibiotics, and drugs containing phosphorus, are discontinued. Magnesium is replaced intravenously with magnesium sulfate (MgSO4) when hypomagnesemia is severe. The IV route is used because MgSO4 causes pain and tissue damage when injected IM. Assess deep tendon reflexes at least hourly in the patient receiving IV magnesium to monitor effectiveness and prevent hypermagnesemia. Oral magnesium often causes diarrhea and can increase magnesium loss. If hypocalcemia is also present, drug therapy to increase serum calcium levels is prescribed.

TABLE 13-12 COMMON CAUSES OF MAGNESIUM IMBALANCE
Hypomagnesemia
• Malnutrition
• Starvation
• Diarrhea
• Steatorrhea
• Celiac disease
• Crohn's disease
• Drugs (diuretics, aminoglycoside antibiotics, cisplatin, amphotericin B, cyclosporine)
• Citrate (blood products)
• Ethanol ingestion
Hypermagnesemia is a serum magnesium level above 2.1 mEq/L. Magnesium is a membrane stabilizer. When magnesium excess occurs, excitable membranes are less excitable and need a stronger-than-normal stimulus to respond. With severe hypermagnesemia, excitable membranes may not respond to any stimulus.

The imbalance results from increased intake of magnesium coupled with decreased kidney excretion of magnesium. Table 13-12 lists the specific causes of hypermagnesemia.

Patient-Centered Collaborative Care
Most manifestations of hypermagnesemia occur as a result of reduced membrane excitability. They usually are not apparent until serum magnesium levels exceed 4 mEq/L. The most common problems are seen in the cardiac, central nervous, and neuromuscular systems.

Cardiac changes include bradycardia, peripheral vasodilation, and hypotension. These problems become more severe as serum magnesium levels increase. ECG changes show a prolonged PR interval with a widened QRS complex. Bradycardia can be severe, and cardiac arrest is possible. Hypotension is also severe, with a diastolic pressure lower than normal. Patients with severe hypermagnesemia are in grave danger of cardiac arrest.

Central nervous system changes result from depressed nerve impulse transmission. Patients may be drowsy or lethargic. Coma may occur if the imbalance is prolonged or severe.

Neuromuscular changes result from decreased nerve impulse transmission to the skeletal muscles. Deep tendon reflexes are reduced or even absent. Voluntary skeletal muscle contractions become progressively weaker and finally stop.

Hypermagnesemia has no direct effect on the lungs; however, when the respiratory muscles are weak, respiratory insufficiency can lead to respiratory failure and death.

Interventions for hypermagnesemia aim to reduce the serum level and correct the underlying problem that caused the imbalance.

All oral and parenteral magnesium is discontinued. When kidney failure is not present, giving magnesium-free IV fluids can reduce serum magnesium levels. High-ceiling (loop) diuretics such as furosemide (Lasix, Furoside ) can further reduce serum magnesium levels. When cardiac problems are severe, giving calcium may reverse the cardiac effects of hypermagnesemia.

TABLE 13-12 COMMON CAUSES OF MAGNESIUM IMBALANCE
Label: Important
Hypermagnesemia
• Increased magnesium intake:
• Magnesium-containing antacids and laxatives
• IV magnesium replacement
• Decreased kidney excretion of magnesium resulting from kidney disease
Pre-op assessment establishes a baseline (for comparison after surgery) and ids any risks.
Ask about allergies. If they say they are allergic to PCN for example, then ask the pt "what happens when you take PCN."
Ask about meds, herbs, supplements, drugs, alcohol: the key supplements to look out for are gingko, ginger, garlic & vit E (all cause bleeding); St Johns Wort prolongs the effects of anesthesia. Ideally pt should stop taking these several weeks before.
Cultural/religious considerations: e.g. Jehovah's witnesses won't use blood products
Assess support: who will care for them after sx, how will drive them home after sx
Functional assessment
Do an assmnt for alcohol: Screening tests for alcoholism are the CAGE (cutdown, annoyed, guilty, eye-opener) assessment, or AUDIT (Alcohol Use Disorders Identification Test). If the pt drinks a lot then the pt could go into withdrawl aka delirium tremors if they have to abruptly stop their alcoholic intake. To help with this the pt is prescribed Librium and in some cases Alcohol.

Meds that affect anesthesia & sx response:
Anticoagulants: risk for bleeding
Nonsteroidal anti-inflammatory drugs (NSAIDS): risk for bleeding, pt is asked to stop taking a week before the procedure
Steroids: delays wound healing r/t suppressed immune response
Antihypertensives: you don't automatically want to hold these drugs b/c they are important!!! So you need to question this, sometimes contact the Dr.
Diuretics
Insulin, oral diabetics
Analgesics
Antihistamines/decongestants: blood pressure, can lead to HTN
Monoamine oxidase (MAO) inhibitors: interact w/ everything, but ask the provider b4 surgery whether or not to stop giving them
***TQ: If the pt is NPO before an operation but they need to take their meds then the nurse needs to consider how important these meds are. BP meds are pretty important, you should call the Dr and question the order. Colace stool softener is not important, so don't call the Dr. Often times the hosp allows an NPO status pt to receive a little bit of water in order to take meds.

Pre-Operative Assessment
Level of anxiety, knowledge
Past medical and surgical history
Pain level
Degree of surgical risk- Elderly
Ask the pt if they have ever had or a family member has ever had Malignant hyperthermia!
Ask pain level b4 surgery to get a baseline, remember elderly tend to under-report pain.
Increased degree of surgical risk: Elderly, long procedures, head/neck surgery, extensive medical history
***Smoking: If pt smokes try to have pt stop 6-8wks b4 surgery or at least have them cut down. Offer smoking cessation programs.
***Infection: Assess for fever, ask about recent colds or infections. Generally, pt SHOULD NOT have sx if they are fighting an infection (check WBC)!!!

Renal Status
Gastrointestinal status
Neurological Status
Hematologic Status
Endocrine Status
Immunologic
Nutrition
Do a baseline neuro assmt:
2 most common problems, esp in the elderly: Delirium & stroke
Bleeding disorder
Endocrine: hypothyroidism be cautious when using sedation b/c it takes them longer to clear the drugs
Nutrition is important for proper wound healing

Pre-Operative Diagnostics
CBC: WBC with a differential, H & H, RBC
Basic Met Panel: electrolytes, glucose, BUN/Cre
Coagulation: Pt, Ptt, INR
HCG: human chorionic gonadotropin; pregnancy test
EKG & Chest x ray: depends on the age and the pt condition, may not be done
PFTs:
U/A: urine analysis,
"Type and screen": blood is drawn and it is screened, done if there is any chance that you might need blood. But if there is a significant chance that you may need blood, then a "Coomb's test" is done that checks for more than just the basic A/B/O, it also tests Rh and other things. It actually mixes the pts blood w/ the donor blood.

Dietary Restrictions
NPO: Patient advised not to ingest anything by mouth for 6 to 8 hours before surgery:
Decreases the risk for aspiration.
Patients should be given written and oral directions to stress adherence.
Surgery can be cancelled if not followed.

Pre-Operative Assessment Risk for Pulmonary Aspiration
Why the incr risk for aspiration w/ Diabetics: they are prone to get gastroparesis (stomach slows down, it's an autonomic response)
*Def'n of Gastroparesis: a condition that reduces the ability of the stomach to empty its contents, but there is no blockage (obstruction), cause is unknown, may be from disruption of nerve signals to the stomach. The condition is a common complication of diabetes and can be a complication of some surgeries.


Describe the pre-operative management of a patient including: informed consents, NPO status, psychosocial needs, premedication(safety), need for assistance post operatively and patient teaching.

Explain the significance of preoperative assessment in order to identify patient's at
risk for complications. Use of herbal products(refer to notes), smoking etc
Nursing management related to NPO status and patient's prescribed scheduled
medications such as HTN meds, insulin
Scrubbed persons function within a sterile field; gowns and gloves provide a barrier to transfer of microorganisms from person to surgical wound.
Sterile drapes create a sterile field and impede movement of microorganisms from a nonsterile to sterile area.
All items used in sterile field are sterile.
Sterile field is monitored and maintained during movement of persons and instruments.
Surgical scrub reduces the number of resident bacteria.
Preoperative skin preparation reduces risk of postoperative wound infection.

Surgical scrub is typically a 3-5 min process before going into the surgical room.
Usually in the "anteroom." The scrub starts with nails (no Acrylic nails!!!), brush under the nails. Wash arms.
They dry with sterile towel, start with fingers and work their way up being cautious not to let the towel hit the sink or any unsterile surface.
The surgeon's hands will not be sterile but this cleaning process drastically reduces the amount of residual bacteria.
Pt may be asked to shower the night before in Chlorhexidine (CHD) or Betadine. The CDC recommends CHD.
If pt must be shaved an electrical razor is used (not wax, just kidding )
Surgical room: kept cold (reduce bacteria growth), there is some humidity to reduce fire b/c the pt is an oxygen (fire accelerant). The pt is grounded to prevent electric shock b/c the surgeons use electrical instruments and there is blood and liquids around and traffic in & out of the OR is minimized.

Surgical Attire
Hat: Put on first; prevents contamination of scrubs
Scrubs: Closely woven, shirt tied or tucked
Shoe covers: Worn if splashes or spills anticipated
Masks: Prevent contamination by droplets
Face shields and eyewear: Protect from splashing and spraying
Lead aprons and thyroid shields: Protect from exposure to radiation
Ideally you come to work in your street clothes and you change in the OR locker room into your scrubs. Don't wear your scrubs into the OR, it brings outside contaminates into the OR.
If there is any chance you may be splashed with body fluids you MUST wear eye protection!!!
If they are using any Xrays protect yourself against radiation. Xray can be used to check the procedure or to find missing sponges.

Describe surgical considerations including surgical scrub, basic principles of asepsis.
Circulating nurses or "circulators" are registered nurses who coordinate, oversee, and are involved in the patient's nursing care in the OR. The circulating nurse's actions are vital to the smooth flow of events before, during, and after surgery. He or she is responsible for coordinating all activities within that particular OR. The circulator sets up the OR and ensures that supplies, including blood products and diagnostic support, are available as needed. All anticipated equipment is gathered and inspected by the circulator to make certain that it is safe and functional before the surgery. Depending on the procedure and position required, the circulator makes up the operating bed (OR table) with gel pads (to prevent pressure ulcers), safety straps and armboards (for patient positioning), and either heating pads under the sheets or disposable warming blankets placed over the patient as indicated (to prevent hypothermia)

If there is no holding area nurse, the circulator assumes the responsibilities of that nursing role as well. Even when there is a holding area nurse, The Joint Commission's National Patient Safety Goals (NPSGs) require that the circulator also greets the patient and reviews findings with the holding area nurse.

Once the patient is ready to be moved into the OR, the circulating nurse, along with the OR team, assists the patient in transferring to the operating bed. The nurse positions the patient, protecting bony areas with extra padding while providing comfort and reassurance. While observing the patient, the circulating nurse also assists the anesthesia provider with the induction of anesthesia by positioning the patient and applying cricoid pressure, when requested. The circulator then may assist with additional positioning, insert a Foley catheter if needed, apply the grounding pad, test equipment, and "prep" (scrub) the surgical site before the patient is draped with sterile drapes.

Throughout the surgery, the circulating nurse:
•Protects the patient's privacy
•Ensures the patient's safety
•Monitors traffic in the room
•Assesses the amount of urine and blood loss
•Reports findings to the surgeon and anesthesia provider
•Ensures that the surgical team maintain sterile technique and a sterile field
•Anticipates the patient's and surgical team's needs, providing supplies and equipment
•Communicates information about the patient's status to family members during long or unique procedures
•Documents care, events, interventions, and findings

Depending on facility policy, the circulating nurse may record drugs, blood, and blood components given. (This also may be a function of the anesthesia provider.)

Before the procedure is over, the circulating nurse completes documentation in the OR and nursing records, including the presence of drains or catheters, the length of the surgery, and a count of all sponges, "sharps" (needles, blades), and instruments. He or she notifies the postanesthesia care unit (PACU) of the patient's estimated time of arrival and any special needs.
Physiologic responses to surgery & anesthesia include:
Neuroendocrine: stress response
Metabolic: incr MBR r/t the stress
Thermoregulatory:
Unplanned hypothermia
Malignant Hyperthermia
Muscle rigidity, resp and metabolic acidosis
Treatment: remove cause, hyperventilate, cool (cool the fluids down)
Dantrolene
***TQ: Unplanned hypothermia: The OR is cold, body exposed , warm pt using blankets and machines, you can warm the fluids and blood instead of giving cold. 1 hr after the start of surgery is when the pt can become hypothermic. If pt is cold, they may shiver, which increases metabolic rate like 300%, then they need more O2, also HR may go down and clotting decreases when you're cold
***TQ: Malignant Hyperthermia: genetic defect, hyperthermia, high risk group is adolescent males, obtain personal hx & family hx b/c it is genetic disorder. If it's happened to pt before there is a high chance it will happen again. The underlying prob is that the pt becomes very hypermetabolic, in particular the skeletal muscles are effected (uncontrolled metabolism in the muscles). It can happen initially following induction and in rare cases can occur up to 48-72hrs after the surgery. But most likely it will occur during the actual surgery. Usually classified into early signs and later signs. The early signs are incr CO2 and tachy, decr 02 sat, ACIDOSIS, prob metabolic. Later sign is the actual hyperthermia and it can go pretty high (112°), elevates the BMR, electrolyte disturbances, elevated K & Ca. Mu
What to do for malignant hyperthermia: remove the agent causing it (give DANTROLENE, a muscle skeletal relaxer), hyperventilate manually or bag the pt (not just hyperoxygenating b/c that doesn't treat the acidosis), cool the pt (cool the IV fluids), give bicarb for acidosis, insulin for hyperkalemia & d50

Identification Safety: make sure it's the right pt, ask their name (not "are you Mr Smith" instead ask "what is your name"), check their id bracelet
Assessment: upon arrival to OR & intraoperative
***TQ: Positioning: set the pt up appropriately for the type of surgery, minimize pressure ulcers and nerve damage
Risk for pressure ulcer in surgery: long procedure, elderly skin, poor nutritional background

When repositioning pt after surgery, put legs down slowly, put on pillows first, then slowly lower them to flat.
All the blood is in the trunk you don't want to cause hypotension
This position could also cause abdominal compartment syndrome

Nursing interventions for the patient undergoing surgery might include:
Preventing and reducing complications related to prolonged immobility
Promoting electrical, chemical, physical, and environmental safety in OR
Monitoring and maintaining patient core temperature
Monitoring fluid volume balance
Monitoring and maintaining aseptic technique
Teaching patient/family perioperative routines

Postanesthesia Care
Phase I encompasses care of the patient from emergence from anesthesia until physiologically stable, including return of protective reflexes and motor function.
Phase II begins with the return to baseline level of consciousness, patent airway with upper airway reflexes, manageable pain, and stable pulmonary, cardiac, and renal functioning.
Phase III practice settings include 23-hour observation suites, in-hospital units, and recovery care centers within the hospital or community. Nursing care continues until the patient completely recovers from anesthesia and surgery and is ready to resume activities of daily living.

Focus of Nursing Care in the Immediate Postoperative Period
Maintaining ventilation and circulation
Monitoring oxygenation and level of consciousness
Preventing shock
Managing pain/anxiety
Preventing complications
Maintaining safety
1st concern immediately post op is Airway.
Assess the pt, look at vital signs, ABCs, pain (make sure pt has good ABCs b4 giving pain meds!!!)
Optimal way to manage pain post-op for someone who is alert: PCA, usually of morphine (lowers RR, and causes constipation)
PCA pump can be set in diff ways.
Basal means that the pt gets a certain rate at specific intervals
Bolus means that the pt is allowed to get a certain range within a certain range of time e.g. 5-10mg each hr, but no more than 20mg every 2 hrs

Scenario: pt is sleeping w/ low resp rate. What do you do?
Assess first then act. In this case you wake the person up. Pt is responsive and breathes more and you don't have to do anything further

Scenario: pt is sleeping, unresponsive w/ RR of 2
Assess and act, don't leave pt. Stay w/ pt and have someone get the NARCAN then administer

Immediate Respiratory Complications
Respiratory complications are the leading cause of morbidity and mortality in the immediate postoperative period.
Immediate respiratory complications that might occur include:
Airway obstruction
Hypoxemia
Aspiration
Laryngospasm: If someone is having a laryngospasm you will hear STRIDOR!!! This is an emergency.
Risk factors for respiratory complications include chronic obstructive pulmonary disease (COPD), smoking, advanced age, and obesity.
Atelectasis : incentive spirometer, coughing, deep breathing, get pts out of bed right after surgery, that night, or next morning. Administer pain med'n before doing these things!!!
Pneumonia
Pulmonary embolus

Immediate Cardiovascular Complications
Hypotension
Hypertension
Cardiac dysrhythmias
The incidence of perioperative myocardial infarction is expected to increase as the population ages and more surgical procedures are performed on older adults.
***TQ: If you notice HTN in the pt upon admission to PACU: 1st ask does pt have a hx of HTN, also consider that they are in pain
***TQ: What if pt has a change in level of consciousness: this often is an 1st indicator of resp problems. But if their O2 sat is fine then consider pain

Thermoregulation
Both hypothermia and hyperthermia are associated with physiologic alterations that may interfere with immediate postoperative recovery.
Hypothermia: Shivering increases oxygen demand up to 400%, impairs coagulation, and causes decreased cerebral blood flow.
Hyperthermia: This can be caused by an infectious process, sepsis, or malignant hyperthermia (might occur or recur as late as 24-72 hours after surgery).

Neurologic System
Cerebral functioning
Motor and sensory assessment important after epidural or spinal anesthesia:
Motor function—simple commands; patient to move extremities
Return of sympathetic nervous system tone: gradually elevate head (esp for spinal and epidural anesthesia, if raised too quickly can cause hypotension) and monitor for hypotension

Acute Pain
Negative Effects of Pain
Assessment
Interventions include:
Drug therapy
Complementary and alternative therapies such as:
Positioning
Massage
Relaxation and diversion techniques

GI Complications
Nausea and vomiting: Occur in 25%-30% of surgical patients
Abdominal distention
Paralytic ileus
Stress ulcer
Abdominal compartment syndrome
N&V is major concern b/c pt can aspirate.
Lateral position is probably the best position.
Give them Zofran or anti-emetic. Have suction at the beside. They may need a nasogastric tube or they may already have one.
***TQ: If a pt has an NG tube and they are nauseous...Make sure the suction is working.
Paralytic ileus: sympathetic nervous system takes over when the pt has surgery b/c of the stressful procedure, also any GI surgery may have manipulated the GI tract. Sign of decr peristalsis is absent bowel signs.
What are we concerned about w/ paralytic ileus: increases the risk of ASPIRATION
Stress ulcer: pt given PPI prophylactically

Urinary Retention
Characterized by inability to void over a 6- to 8-hour period
Can occur after spinal anesthesia; surgery of the rectum, colon, gynecologic structures
Usually resolves within 48 hours
Urinary tract infection
***TQ: Pt should void w/in 6-8hrs after procedure. What to do if not? Assess-look & palpate for distention, if no distention and pt still cannot void, what do you do.
Think non-invasive: run water, help them stand and get out of bed, put their hand under the warm water, lightly push on the bladder.
If these methods don't work then you catheterize the pt

Potential Complications Related to Wounds
Wound healing: Factors include advanced age, nutritional status, vascular disease, diabetes
Hemorrhage: Most likely to occur within 48 hours postoperatively; might be related to sutures or small vessel leakage
Infection: Factors include hematoma, foreign body, dead space, hypothermia
Dehiscence and evisceration: Usually occur 3-10 days postoperatively; separation associated with technical factors, obesity, coughing, infection

Priorities of Care
Pre Operative: assess the pt to id risk factors
Intra Operative: safety, positioning, sterility
Post Operative: #1 concern is AIRWAY!!!, resp, HR, BP, pain


What are the most common postoperative complications and the interventions for
each? Ie-Aspiration, Respiratory Complications, Nausea/vomiting, pain(PCA), urinary retention, wound dehiscence etc
Malignant hyperthermia (MH) is an acute, life-threatening complication of certain drugs used for general anesthesia. The reaction begins in skeletal muscle exposed to specific agents, causing increased calcium levels in muscle cells and increased muscle metabolism. Serum calcium and potassium levels are increased, as is the metabolic rate, leading to acidosis, cardiac dysrhythmias, and a high body temperature. Onset of MH may occur immediately after induction of anesthesia, several hours into the procedure, or, rarely, even after the anesthetic has been terminated. Clinical features reflect the increased muscle calcium level and the greatly increased body metabolism. Manifestations include tachycardia, dysrhythmias, muscle rigidity (especially of the jaw and upper chest), hypotension, tachypnea, skin mottling, cyanosis, and myoglobinuria (presence of muscle proteins in the urine). The most sensitive indication is an unexpected rise in the end-tidal carbon dioxide level with a decrease in oxygen saturation. Another early indication is sinus tachycardia. Extremely elevated temperature, as high as 111.2° F (44° C), is a late sign of MH. Survival depends on early diagnosis and the actions of the entire surgical team. Time is crucial when MH is diagnosed. Dantrolene sodium, a skeletal muscle relaxant, is the drug of choice along with other interventions (Kaplow, 2010). For a known history or risk, the patient can be treated before, during, and after surgery with dantrolene to prevent this problem. Chart 17-1 lists best practices for care of the patient with MH. The AORN recommends that all operating rooms have a dedicated MH cart containing drugs for management (normal saline, dantrolene, sodium bicarbonate, insulin, 50% dextrose, lidocaine, and calcium chloride), a protocol card listing interventions, and the MH hotline number. Additional nursing support is needed during this true perioperative emergency.

Emergency Care of the Patient with Malignant Hyperthermia
•Stop all inhalation anesthetic agents and succinylcholine.
•Ventilate the patient with 100% oxygen, using the highest possible flow rate.
•Administer dantrolene sodium (Dantrium) IV at a dose of 2 to 3 mg/kg.
•Administer 100% oxygen.
•If possible, terminate surgery. If termination is not possible, continue surgery using anesthetic agents that do not trigger malignant hyperthermia (MH).
•Assess arterial blood gases (ABGs) and serum chemistries for metabolic acidosis and hyperkalemia.
•If metabolic acidosis is evident by ABG analysis, administer sodium bicarbonate IV.
•If hyperkalemia is present, administer 10 units of regular insulin in 50 mL of 50% dextrose IV.
•Use active cooling techniques:
•Administer iced saline (0.9% NaCl) IV at a rate of 15 mL/kg every 15 minutes as needed.
•Apply a cooling blanket over the torso.
•Pack bags of ice around the patient's axillae, groin, neck, and head.
•Lavage the stomach, bladder, rectum, and open body cavities with sterile iced normal saline.
•Insert a nasogastric tube and a rectal tube.
•Monitor core body temperature to assess effectiveness of interventions and to avoid hypothermia.
•Monitor cardiac rhythm by electrocardiography (ECG) to assess for dysrhythmias.
•Insert a Foley catheter to monitor urine output.
•Treat any dysrhythmias that do not resolve on correction of hyperthermia and hyperkalemia with antidysrhythmic agents other than calcium channel blockers.
•Administer IV fluids at a rate and volume sufficient to maintain urine output above 2 mL/kg/hr.
•Monitor urine for presence of blood or myoglobin.
•If urine output falls below 2 mL/kg/hr, consider using osmotic or loop diuretics, depending on the patient's cardiac and kidney status.
•Contact the Malignant Hyperthermia Association of the United States (MHAUS) hotline for more information regarding treatment: (800) 644-9737.
•Transfer the patient to the intensive care unit (ICU) when stable.
•Continue to monitor the patient's temperature, ECG, ABGs, electrolytes, creatine kinase, coagulation studies, and serum and urine myoglobin levels until they have remained normal for 24 hours.
•Instruct the patient and family about testing for MH risk.
•Refer the patient and family to the Malignant Hyperthermia Association of the United States at (800) 986-4287 or www.mhaus.org.
•Report the incident to the North American Malignant Hyperthermia Registry at the University of Pittsburgh: (412) 692-5464.

MH is a genetic disorder with an autosomal dominant pattern of inheritance. The patient with a genetic predisposition for MH is at risk for this complication from halothane, enflurane, isoflurane, desflurane, sevoflurane, and succinylcholine. This rare syndrome is most common in young adults. Males are affected more often than females (despite the autosomal dominant pattern of inheritance) because of gender differences in muscle mass. Once a patient or family history of MH is known, family members can have a muscle biopsy to determine whether they are at risk. The muscle biopsy tested with the caffeine halothane contracture test (CHCT) is still considered the "gold standard" for MH testing even though this disorder is inherited. Currently, no definitive genetic test identifies all people at risk for MH. When a patient is determined to be at risk for MH, he or she can still have anesthesia and surgery; however, more precautions are needed and different anesthetic agents are used.
Peripheral arterial disease (PAD) is a chronic, long-term problem with frequent complications. Patients may benefit from a case manager who can follow them across the continuum of care. The desired outcome is that the patient can be maintained in the home.

Management at home often requires an interdisciplinary team approach, including several home care visits. Chart 38-5 outlines the assessment highlights for home care patients with peripheral vascular disease (PVD).

Instruct patients on methods to promote vasodilation. Teach them to avoid raising their legs above the level of the heart unless venous stasis is also present. Provide written and oral instructions on foot care and methods to prevent injury and ulcer development (Chart 38-6).

Patients who have had surgery require additional instruction on incision care (see Chapter 18). Encourage all patients to avoid smoking and to limit dietary fat intake to less than 30% of the total daily calories. Remind them to drink adequate fluids to prevent dehydration.

Patients with chronic arterial obstruction may fear recurrent occlusion or further narrowing of the artery. They often fear that they might lose a limb or become debilitated in other ways. Indeed, chronic PAD may worsen, especially in those with diabetes mellitus. Reassure them that participation in prescribed exercise, nutrition therapy, and drug therapy, along with cessation of smoking, can limit further formation of atherosclerotic plaques.

Home Care Assessment: The Patient with Peripheral Vascular Disease
Assess tissue perfusion to affected extremity(ies), including:
• Distal circulation, sensation, and motion
• Presence of pain, pallor, paresthesias, pulselessness, paralysis, poikilothermy (coolness)
• Ankle-brachial index

Assess adherence to therapeutic regimen, including:
• Following foot care instructions
• Quitting smoking
• Maintaining dietary restrictions
• Participating in exercise regimen
• Avoiding exposure to cold and constrictive clothing

Assess ability to manage wound care and prevent further injury, including:
• Use of compression stockings or compression pumps as directed
• Use of various dressing materials
• Signs and symptoms to report to nurse

Assess coping ability of patient and family members.

Assess home environment, including:
• Safety hazards, especially related to falls

Patient and Family Education: Preparing for Self-Management
Foot Care for the Patient with Peripheral Vascular Disease
• Keep your feet clean by washing them with a mild soap in room-temperature water.
• Keep your feet dry, especially the ankles and between the toes.
• Avoid injury to your feet and ankles. Wear comfortable, well-fitting shoes. Never go without shoes.
• Keep your toenails clean and filed. Have someone cut them if you cannot see them clearly. Cut your toenails straight across.
• To prevent dry, cracked skin, apply a lubricating lotion to your feet.
• Prevent exposure to extreme heat or cold. Never use a heating pad on your feet.
• Avoid constricting garments.
• If a problem develops, see a podiatrist or physician.
• Avoid extended pressure on your feet or ankles, such as occurs when you lean against something.



Describe teaching regarding lifestyle modification for HTN and PVD
Identify the signs and symptoms for PVD. What is the significance of
intermittent claudication and rest pain?
Raynaud's phenomenon is caused by vasospasm of the arterioles and arteries of the upper and lower extremities, usually unilaterally. Raynaud's disease occurs bilaterally. The two terms are sometimes used interchangeably. Although they are related, there are some differences. Raynaud's phenomenon usually occurs in people older than 30 years. Raynaud's disease can occur between the ages of 17 and 50 years. Raynaud's phenomenon can occur in either gender, Raynaud's disease is more common in women.

The pathophysiology is the same for both entities. The etiology is unknown. Patients often have an associated systemic connective tissue disease such as systemic lupus erythematosus or progressive systemic sclerosis (see Chapter 20).

As a result of vasospasm, the superficial skin vessels are constricted and blanching of the extremity occurs, followed by cyanosis. When the vasospasm is relieved, the tissue becomes reddened or hyperemic (Fig. 38-8). The patient's extremities are numb and cold, and he or she may report pain and swelling. Ulcers may also be present. These attacks are intermittent and can be aggravated by cold or stress. In severe cases, the attack lasts longer and gangrene of the digits can occur.

Management involves relieving or preventing the vasoconstriction by drug therapy. Commonly prescribed drugs are nifedipine (Procardia), cyclandelate (Cyclospasmol), and phenoxybenzamine (Dibenzyline). These vasodilating agents may help relieve the symptoms, but they can cause uncomfortable side effects such as facial flushing, headaches, hypotension, and dizziness.

For severe symptoms that are not reduced by drugs, a lumbar sympathectomy may be performed. The surgeon cuts the sympathetic nerve fibers that cause vasoconstriction of blood vessels in the legs. This method is effective for foot symptoms. For the upper extremities, a similar procedure—sympathetic ganglionectomy—may provide symptom relief. The long-term effectiveness of these treatments is questionable.

Patient education is important in prevention of complications. Explain methods to prevent vasoconstriction, such as minimizing exposure to cold, reducing caffeine intake, smoking cessation (if the patient smokes), and decreasing stress. Teach the patient to wear warm clothes, socks, and gloves when exposed to cool or cold temperatures. He or she should keep the home at a comfortably warm temperature and wear gloves to the grocery store. Help the patient identify stressors, and provide suggestions for reducing them. (See Chapter 20 for further discussion of Raynaud's phenomenon as it relates to connective tissue disease.)
Buerger's disease (thromboangiitis obliterans) is an uncommon occlusive disease of the arteries and veins in the distal portion of the upper and lower extremities. The disease often extends into the tissues around the vessels, resulting in fibrosis and scarring that bind the artery, vein, and nerve firmly together. Larger arteries such as the femoral and brachial become involved in the late stages of the disease. The veins are less commonly involved.

The cause of Buerger's disease is unknown although there is a strong association with tobacco smoking and is typically identified in young adult men who smoke. Cessation of cigarette smoking usually arrests the disease process. Continued smoking causes occlusion in the more proximal vessels. A familial or genetic predisposition and autoimmune etiologic factors are also possible

Assessment
The first clinical manifestation of Buerger's disease is usually claudication (muscle pain caused by an inadequate blood supply) of the arch of the foot. Intermittent claudication may occur in the lower extremities. The pain may be ischemic, occurring in the digits while the patient is at rest. Often there is an aching pain that is more severe at night. Intermittent shocklike pain can be the result of ischemic neuropathy. Patients often have increased sensitivity to cold and report coldness and numbness. On physical examination, pulses are often diminished in the distal extremities and the extremities are cool and red or cyanotic in the dependent position.

A diagnosis of Buerger's disease is based on a physical finding of peripheral ischemia. Ulcerations and gangrene may be seen in the digits. The ulcerations are usually sharply demarcated. The gangrenous lesion can be small or can affect the entire digit.

Arteriograms can be useful in delineating the degree of disease in the arteries. Commonly, arteriography reveals multiple segmental occlusions in the smaller arteries of the forearm, hand, leg, and foot. Plethysmographic studies of the fingers or toes may be diagnostic of the disease in the early stages. These studies can also be useful in following the progression of the disease in more proximal arteries (see Chapter 35 for discussion of these tests).

Interventions
Nursing interventions are directed toward:
• Preventing the progression of the disease
• Avoiding vasoconstriction
• Promoting vasodilation
• Relieving pain
• Managing ulceration and gangrene

To prevent the progression of Buerger's disease, complete abstinence from tobacco in all forms is essential. Teach the patient to avoid extreme cold or prolonged exposure to cold to prevent vasoconstriction. Instruct him or her about drugs that may be used for vasodilation (e.g., nifedipine [Procardia]). The collaborative care for Buerger's disease is similar to that for peripheral arterial disease (PAD) (see the discussion of Interventions on p. 787 in the Peripheral Arterial Disease section).
Abdominal aortic aneurysms (AAAs) account for most aneurysms, are commonly asymptomatic, and frequently rupture. Most of these are located between the renal arteries and the aortic bifurcation (dividing area).

Aneurysms can cause symptoms by exerting pressure on surrounding structures or by rupturing. Rupture is the most frequent complication and is life threatening because abrupt and massive hemorrhagic shock results. Thrombi within the wall of an aneurysm can also be the source of emboli in distal arteries below the aneurysm.

Atherosclerosis is the most common cause of aneurysms, with hypertension, hyperlipidemia, and cigarette smoking being contributing factors. Age, gender, and family history also play a role (Forsdahl et al., 2009). Syphilis (a sexually transmitted disease), Marfan syndrome (a connective tissue disease), and Ehlers-Danlos syndrome (a rare genetic disorder) are other causes of AAAs. Chronic inflammation (aortitis) and blunt trauma, usually from motor vehicle crashes, can cause aneurysms in the descending thoracic aorta (Hiratzka et al., 2010).

Abdominal aortic aneurysm rupture remains a significant cause of death in the United States. Death occurs more often in male patients and those older than 65 years (Forsdahl et al., 2009). Thoracic aortic aneurysms also occur most often in older adults and have a high mortality rate even with surgical intervention.

Most patients with abdominal or thoracic aneurysms are asymptomatic when their aneurysms are first discovered by routine examination or during an imaging study performed for another reason. However, a few patients do have symptoms that bring them to their health care provider or the emergency department.

Assess patients with a known or suspected abdominal aortic aneurysm (AAA) for abdominal, flank, or back pain. Pain is usually described as steady with a gnawing quality, unaffected by movement, and lasting for hours or days.

A pulsation in the upper abdomen slightly to the left of the midline between the xyphoid process and the umbilicus may be present. A detectable aneurysm is at least 5 cm in diameter. Auscultate for a bruit over the mass, but avoid palpating the mass because it may be tender and there is risk for rupture! If expansion and impending rupture of an AAA are suspected, assess for severe pain of sudden onset in the back or lower abdomen, which may radiate to the groin, buttocks, or legs.

Patients with a rupturing AAA are critically ill and in hemorrhagic (hypovolemic) shock. Signs include hypotension, diaphoresis, decreased level of consciousness, oliguria (scant urine output), loss of pulses distal to the rupture, and dysrhythmias. Retroperitoneal hemorrhage is manifested by hematomas in the flanks (lower back). Rupture into the abdominal cavity causes abdominal distention.

Immediately after surgery, the patient is typically admitted to a critical care unit for 24 hours, depending on his or her age and condition. Limit elevation of the head of the bed to 45 degrees or less to avoid flexion of the graft. In addition to providing the usual care discussed in Chapter 18, assess for and assist in prevention of the postoperative complications that can occur after an AAA repair.

Complications include:
• Myocardial infarction
• Graft occlusion or rupture causing hemorrhage
• Hypovolemia and/or renal failure
• Respiratory distress
• Paralytic ileus

During the immediate postoperative period, the patient's blood pressure is monitored with an arterial catheter. Continuous cardiac monitoring is used to detect any dysrhythmias. Hemodynamic monitoring is used to detect low cardiac output and other findings consistent with an acute myocardial infarction. Other signs of myocardial infarction include chest pain, shortness of breath, diaphoresis (excessive sweating), anxiety, and restlessness.

Nursing Safety Priority Action Alert
A major priority for nursing care after an AAA surgical repair is to assess for signs of graft occlusion or rupture. Assess vital signs and circulation every 15 minutes for the first hour and then hourly, with assessment of pulses distal to the graft site (including the posterior tibial and dorsalis pedis pulses). Report signs of graft occlusion or rupture, including:
• Changes in pulses
• Cool to cold extremities below the graft
• White or blue extremities or flanks
• Severe pain
• Abdominal distention
• Decreased urine output

Hypovolemia and acute renal failure may occur because of blood loss during surgery or before if rupture occurred. Assess urine output hourly. If urine output is less than 50 mL/hr, notify the surgeon immediately. Although advances in surgical technique have decreased the risk for renal failure after clamping during surgery, renal failure may occur. Renal failure caused by acute tubular necrosis (ATN) is more common after emergency surgery. In addition to monitoring urine output, in collaboration with the physician, monitor serum creatinine and blood urea nitrogen (BUN) levels daily.

Assess respiratory rate and depth every hour and auscultate breath sounds every 4 hours to monitor for respiratory complications. The patient may be mechanically ventilated and should be extubated as soon as he or she is stable. While the patient is intubated, turn and suction him or her as needed. Administer opioids for pain as prescribed. After extubation, assist the patient to a bedside chair within 24 hours. Early mobility decreases the risk for atelectasis and deep vein thrombosis. Teach him or her to use firm abdominal support of the incision with a pillow or bath blanket during coughing exercises.

Paralytic ileus after AAA repair is expected for 2 to 3 days. Patients usually have a nasogastric tube set to low suction until they begin to pass flatus. Listen for bowel sounds and assess for flatus every 8 hours. Report when bowel sounds return and any flatus to the physician. Some surgeons begin to introduce fluids or soft food to stimulate peristalsis. Prolonged absence of flatus and presence of abdominal distention may indicate a paralytic ileus or a bowel infarction.
• Pericarditis-inflammatory process of the visceral or parietal pericardium (lining that surrounds the heart)
Causes:
• Secondary to a myocardial infarction
• Infection:may be viral, fungal, or bacterial
• Seen in cancer patients
• Autoimmune disorders like lupus
• Renal Failure
Pericarditis may be seen as (2) types:
a) Effusive-meaning fluid + inflammation
b) Non-effusive - just inflammation, no fluid
Clinical Manifestations:
• Pericardial friction "rub"-effusion-fluid involved, when you auscultate, sounds like sandpaper rubbing against each other
• Chest pain
• Fever and increase in WBC-due to inflammation/infection
• ESR- Erythrocyte Sedimentation Rate, measures time erythrocytes take to settle, the higher the number, the more inflammation there is; an elevated ESR is significant for infection, yet it is a non-specific marker, it is not specific to pericarditis, but helpful in indicating that there is an inflammation or infection somewhere in the body
Pericardial effusion may cause cardiac tamponade (potential complication of pericarditis)- pumping action of the heart is affected, so much fluid builds up leading to cardiogenic shock related to cardiac tamponade
S/S:
• Beck's triad:
1-hypotension
2-muffled/distant heart sounds
3-JVD-jugular venous distension, indicating right-sided heart failure
• Pulsus paradoxus- systolic BP drops greater than 10 mmHg during inspiration
Management:
• Treatment specific to the cause- i.e. if its infectious in nature, treat the infection
• Pericardiocentesis- a needle is inserted into the pericardial sac, fluid is removed and sent to lab for analysis
• Monitoring vital signs and heart sounds- monitor for bleeding, infection, pneumothorax, also irritation to the heart from pericardiocentesis may trigger dysrhythmias
• Anti inflammatory medication-NSAID's are used but contraindicated in patients with hx of renal failure and/or GI bleed
• Promoting comfort, providing rest
• Managing pain- meds stronger than NSAID's may be needed
• Patient and family teaching
• An alternative measure to pericardiocentesis may be used: pericardiotomy- "pericardial window," a small opening or window is made into the pericardial sac allowing the fluid to drain into the chest where it is then reabsorbed
Infective Endocarditis(IE)- involves the endocardium; damage to the endothelium, pathogen introduction forms mass on valve called vegetation, can be an infectious process and growth can embolize and travel to other parts of the body causing PE/CVA
• May develop rapidly or gradually
• Turbulent blood flow promote vegetative growth
• Related to the valves
• May be acute or chronic
• Growth occurs on valves leading to IE, may dislodge and become embolus
Risk Factors:
• Rheumatic Heart disease- common complication of RHD is valvular incompetency
• Valve Replacement- prosthetic heart increases risk of IE
• A patient has been diagnosed with infective endocarditis. While obtaining a nursing history the nurse specifically asks the patient about:
1. IV drug abuse- may be source of bacteria, risk factor for IE
Clinical Manifestations:
• Fever- b/c it is an infectious process
• H/A- not sure if this means headache? It is what I found when I looked up abbrv.
• Arthralgia- joint pain
• Arthritis
• Chest pain- due to valvular problems or emboli
• Lab values such as WBC (high)
• Spleenomegaly
• Osler's nodes- tender, raised areas that occur on the fingers and toes
• Janeway nodes- non-tender nodes that occur in the palms of the hands and the soles of the feet
• Murmurs- nurse will assess for murmurs
Diagnositics:
• Blood cultures- used to identify the source
• C&S-culture and sensitivity testing is done to see which antibiotic the infectious source is sensitive or resistant to. When the culture returns, patient is put on empiric therapy, based on s/s, this is what we think is going on and we treat with broad spectrum antibiotics. When sensitivity test returns, therapeutic therapy is initiated-specific to infectious source.
• Echocardiography- to see heart structures/valves
1. non-invasive, external Doppler- observe valvular function
2. TEE- trans-esophageal echocardiogram, tube is inserted down into pt's esophagus which produces a better image; note that with this test a numbing agent is given since we are inserting a tube down into the esophagus; the nurse must anticipate that upon the patient's return they will have a decreased gag reflex, putting them at risk for aspiration; do not feed until reflex returns.
Management:
• Antibiotics- given appropriate to microbe based on sensitivity testing; long term therapy is expected, 4-6 weeks; at times patient will go home with port or catheter to continue antibiotic therapy at home; we must be cautious when sending home an IV drug abuser with a central line
• Rest- to decrease metabolic demands
• Valvular repair
• Monitoring for new murmurs
• Embolic events- PE or CVA(assess neuro status)
• Prophylactic antibiotics- esp on pt's with hx of IE and/or valve repairs, prophylactic antibiotics are given before routine dental procedures
• Patient and family teaching- has been shown that poor dental hygiene increases the risk of IE; provide teaching on good dental hygiene.
• The SBAR procedure or similar established protocol is used for successful communication between caregivers and between health care agencies.
• SBAR is a formal method of communication between two or more members of the health care team which includes these four steps:
o Situation: Describe what is happening to require this communication.
o Background: Explain any relevant background information.
o Assessment: Provide an analysis of the problem based on assessment data.
o Recommendation: State what is needed or what the desired outcome is.
• Nurses delegate certain nursing tasks and activities to unlicensed assistive personnel (UAP), such as patient care technicians (PCTs) or patient care assistants (PCAs).
• Delegation is the process of transferring to a competent person the authority to perform a selected nursing task or activity in a selected patient care situation.
• Five rights are followed when delegating and supervising a nursing task or activity to a UAP:
o Right task
o Right circumstances
o Right person
o Right communication
o Right supervision
• Evidence-based practice (EBP) is the integration of best current evidence to make decisions about patient care. It considers the patient's preferences and values, as well as one's own clinical expertise.
• Nurses are active participants in the systematic quality improvement process in their health care agency.
• Informatics involves using information and technology to communicate, manage knowledge, mitigate error, and support decision-making.
• Informatics and technology are used for patient documentation, electronic data access, and health care resource tracking.
• Nurses play a key role in promoting safety and preventing errors, including "missed nursing care."
• Learning about the special needs of older adults is important for health care professionals in a variety of settings.
• The percentage of people older than age 65 years in the United States is about 13%.
• The four subgroups of the older adult population are the young old, middle old, old old, and elite old.
• The fastest growing subgroup is the old old, sometimes referred to as the advanced older adult population. Members of this subgroup are sometimes referred to as the "frail elderly," although a number of 85 to 95 year olds are very healthy.
• Frailty is a clinical syndrome in which the older adult has unintentional weight loss, weakness and exhaustion, and slowed physical activity, including walking. Frail elders are also at high risk for adverse outcomes.
• Health status can affect the ability to perform daily activities and participate in social activities.
• Increased dependence on others may have a negative effect on morale and life satisfaction.
• Loss of autonomy is a painful event with far reaching effects.
• The older adult often experiences personal losses that can affect their sense of control over their lives.
• Many older adults are not prepared for retirement in view of increased expenses and income that is not adequate to meet basic needs, health care treatments, and medications.
• Many are discharged from health care facilities and require home health services or live in long-term care settings.
• Coordinate care by collaborating with members of the health care team when providing care to older adults in the community or inpatient setting.
• Stress can speed up the aging process over time, or it can lead to diseases that increase the rate of degeneration. It can also impair the reserve capacity of older adults and lessen their ability to respond and adapt to changes in their environment.
o Relocation stress syndrome is the physical and emotional distress that occurs after the person moves from one setting to another and may cause sleep disturbance and physical symptoms, such as GI distress.
• Decreased reaction time to stimuli and an impairment of memory for recent events are changes in cognition that are age related.
o Two forms of competence exist: legal competence and clinical competence.
o If determined in court that a person is not legally competent, a guardian is appointed to make financial and health care decisions.
o A clinically competent person is legally competent and capable of making clinical decisions.
o Depression is the most common yet most underdiagnosed and undertreated mental health/behavioral health disorder among older adults. The Geriatric Depression Scale was developed as a basic screening measure for depression in older adults.
o Depression is broadly defined as a mood disorder that can have cognitive, affective, and physical manifestations.
o Depression increases with admission to the hospital or nursing home.
o Dementia is a broad term used for a syndrome that involves a slowly progressive cognitive decline, sometimes called chronic confusion.
o Delirium is an acute state of confusion. Delirium differs from dementia in that it is usually short-term and reversible, often occurring in unfamiliar settings.
o Confusion is not part of the normal aging process.
o Promote sleep and rest for older adults to decrease the incidence of delirium and prevent falls.
• Screen older adults for alcohol abuse or alcoholism and refer those with identified problems to appropriate resources. The CAGE questionnaire has four items and is used frequently in primary care for screening for alcohol misuse in older adults.
• Neglect or abuse may occur in older adults, especially those who are dependent.
o The abuser is often a family member who becomes frustrated or distraught over the burden of caring for the older adult.
o Abuse may be comprised of neglect or failure to provide basic needs, physical abuse, financial abuse, or emotional abuse.
• Medication use in older adults is often a problem when they commit errors when self-medicating, avoid needed medications, or have problems understanding their medication regimen.
o Physiologic changes of aging predispose older adults to toxic effects of medication; drugs are absorbed, metabolized, and distributed more slowly. They are also excreted more slowly by the kidneys.
o Older adults may not tolerate standard dosing traditionally prescribed for younger adults.
o Chronic disease added to physiologic changes of aging results in drug reactions with a more dramatic effect and a longer time to correct.
o Older adults may commit errors when self-medicating, avoid needed medications, or have problems understanding their medication regimen.
o Polypharmacy is the use of multiple drugs, duplicative drug therapy, high-dosage medications, and drugs prescribed for too long a period of time.
o The Beers Criteria for Potentially Inappropriate Medication Use in Older Adults assessment tool is very useful in screening for medication-related risks in older adults who have chronic health problems.
• Patients with chronic and disabling health problems often participate in rehabilitation programs to prevent further disability, maintain functional ability, and restore as much function as possible.
• Rehabilitation is the process of learning to live with chronic and disabling conditions.
• The most common settings for care are freestanding rehabilitation hospitals, rehabilitation units within hospitals, and skilled nursing facilities.
• Rehab patients typically receive care for 1 to 3 weeks.
• A chronic health problem is one that has existed for at least 3 months.
• A disabling health problem is any physical or mental health problem that can cause disability.
• Chronic and disabling illnesses affect almost half of the population in the United States.
• Complications of chronic disease accounts for the majority of all deaths and associated medical costs account for over two thirds of the nation's health care cost.
• The rate of chronic and disabling conditions is expected to increase as more "baby boomers" approach late adulthood.
• Younger adults are also living longer with potentially disabling congenital or genetic disorders which in the past would have shortened life expectancy.
• Accidents are a leading cause of death among young and middle-aged adults.
• Increasing accident survival rates means that individuals are often faced with chronic or disabling conditions, such as traumatic brain injuries and spinal cord injuries.
• The main outcome of rehabilitation is that the patient will return to the best possible physical, mental, social, vocational, and economic capacity.
• Patients in a rehabilitation setting are managed by an interdisciplinary team of health care professionals; the patient and family are also members of the team.
• Collaborate with the rehabilitation health care team when planning and providing patient
• A physician who specializes in rehabilitative medicine is called a physiatrist.
• As the coordinator of the patient's care, the nurse collaborates with the rehabilitation health team when planning and providing patient care to restore and maintain the patient's function.
• Patients may not require the services of all health care team members.
• Patient assessment is a key collaborative function.
o Collect the history of the patient's present condition, any current drug therapy, and any treatment programs in progress.
o Assess the patient's usual daily schedule and habits of everyday living, including hygiene practices, eating, elimination, sexual activity, and sleep.
o Collect the physical assessment data systematically according to major body systems, on admission for baseline and every day.
o Assess associated signs and symptoms of decreased cardiac output or respiratory distress such as chest pain, shortness of breath, and fatigue.
o Fear associated with any inability to breathe normally can make a person dependent in many aspects of life.
o Some disorders of the respiratory system can be resolved or diminished, but some chronic diseases, such as emphysema, often continue to worsen.
o Determine when the patient experiences these symptoms and what relieves them.
o Determine the level of activity that can be accomplished without experiencing shortness of breath.
o Monitor the patient's oral intake and pattern of eating, checking for the presence of anorexia or dysphagia.
o Ask about the patient's baseline urinary patterns, including the number of times the patient usually voids.
o Determine whether he or she routinely awakens during the night to empty the bladder or has uninterrupted sleep.
o Neurologic assessment includes motor function, sensation, and cognition.
o Assess the patient's pre-existing problems, general physical condition, and communication abilities.
o Assess patients in rehabilitation for risk factors that make them likely to develop skin breakdown. Identify actual or potential interruptions in skin integrity.
• Assess the patient's psychosocial needs adequately through verbal indicators and descriptions of self-care.
o Chronic or disabling health problems may cause changes in the patient's self-esteem and body image.
o Assess the patient's self-esteem and changes in body image caused by chronic or disabling health problems.
o Assess the patient's and family's response to chronic and disabling conditions, including feelings of loss and grief, coping, and the availability of support systems.
• Functional ability refers to the ability to perform activities of daily living, such as bathing, dressing, feeding, and ambulating.
o Independent living skills include activities such as using the telephone, shopping, preparing food, and housekeeping.
o These skills are sometimes referred to as instrumental activities of daily living.
• In coordination with the physical and occupational therapists, the nurses assess the patient's ability to perform activities using a functional assessment process.
o Functional assessment tools are used to assess a patient's abilities.
o The Functional Independence Measure (FIM) system is one assessment tool used to assess functional ability of the patient in rehabilitation.
o As a basic indicator of the severity of a disability, the FIM attempts to quantify what the person actually does, whatever the diagnosis or impairment.
o Similar to the FIM form, the Interdisciplinary Minimum Data Set is used to assess patients in long-term care settings.
o The resident's motor ability, sensation, and cognition are evaluated, as well as overall health status.
• Following assessment, the rehabilitation team devises a plan of care and education.
o Use evidence-based Safe Patient Handling practices when assessing and moving patients.
o The members of the interdisciplinary team teach patients transfer, bed mobility, and gait training techniques.
o The patient is taught how to perform ADLs with or without using adaptive devices; encourage the patient to be as independent as possible.
o Assess patients in rehabilitation for risk factors that make them likely to develop skin breakdown; interventions to prevent skin problems include repositioning and adequate nutrition.
o Prevent complications of immobility for the patient and teach patients and families how to prevent complications.
o Patients with bladder and bowel problems are managed by training programs. Patients with neurogenic bladder and bowel problems are managed by training programs; overactive (spastic or reflex) and underactive (hypotonic or flaccid) elimination problems are managed differently.
• Encourage the family to allow the patient to perform as many functions as possible independently to promote feelings of self-worth.
• Evaluate the ability of patients to use assistive or adaptive devices to promote independence.
• After assessing the home environment, the case manager, occupational therapist, and rehabilitation nurse make recommendations to the patient and family about home modifications.
• Vocational counselors can help the patient find meaningful training, education, or employment after discharge from the rehabilitation setting.
• Normal body fluid pH remains at a near-neutral value when the acids and bases are nearly balanced, limiting the total number of free or unbalanced hydrogen ions.
• Balance occurs through control of hydrogen ion (H+) production and elimination.
• The more hydrogen ions present, the more acidic the fluid.
• The fewer hydrogen ions present, the more alkaline the fluid.
• Abnormal pH interferes with many normal physiologic functions, including:
o the function of hormones and enzymes,
o the distribution of other electrolytes,
o activity of the heart, nerves, muscles, and GI tract,
o the effectiveness of many drugs.
• Acids are substances that release hydrogen ions when dissolved in water (H2O).
• A base is a substance that binds free hydrogen ions in solution.
• Liquids with a pH of 7.0 are neutral—they have a free hydrogen ion level in which the number and strength of acids and bases are equal.
• Acid-base balance is regulated by chemical, respiratory, and kidney actions.
• The lungs control the amount of CO2 that is retained or exhaled.
• The kidneys regulate the amount of hydrogen and bicarbonate ions that are retained or excreted by the body.
• Compensation is the process in which the body uses its three regulatory mechanisms (chemical, respiratory, and renal) to correct for changes in the pH of body fluids.
• If a lung problem causes retention of carbon dioxide, the healthy kidney compensates by increasing the amount of bicarbonate that is produced and retained.
• The best way to determine acid-base balance is to analyze arterial blood gases (ABGs).
• Check the serum potassium level for any patient who has acidosis.
• Assess heart rate and rhythm at least every 2 hours for any patient with an acid-base imbalance.
• Compensation is the process in which the body uses its chemical, respiratory, and renal regulatory mechanisms to keep the free hydrogen ion level within the narrow range of normal.
• Chemical buffers are the immediate way that acid-base imbalances are corrected.
• Chemical buffers are paired mixtures, usually a weak base and an acid salt.
• Buffers can either release a hydrogen ion into a fluid or bind a hydrogen ion from a fluid to try to bring the fluid as close as possible to normal.
• The common buffers are bicarbonate, phosphate, and proteins.
• The respiratory system is the second line of defense against changes.
• The respiratory system's response in acid-base balance is rapid—efforts occur within seconds to minutes.
• Respiratory compensation occurs through the lungs, usually to correct for acid-base imbalances from metabolic problems.
• Breathing controls the amount of free hydrogen ions by controlling the amount of carbon dioxide in arterial blood.
• As the amount of CO2 begins to rise above normal in brain blood and tissues, these central receptors trigger the neurons to increase the rate and depth of breathing; this is called hyperventilation.
• When the amount of arterial CO2 returns to normal, the rate and depth of breathing return to levels that are normal for the person.
• Central receptors also sense low CO2 levels and stop or slow the neuron activity in the respiratory centers, decreasing the rate and depth of breathing; this is called hypoventilation.
• Acidosis reduces the excitability of cardiovascular muscle, neurons, skeletal muscle, and GI smooth muscle.
• Acidosis can result from an actual or relative increase in the amount or strength of acids.
• Acidosis can be caused by metabolic problems, respiratory problems, or combined metabolic and respiratory problems.
• Four processes can result in metabolic acidosis: overproduction of hydrogen ions, underelimination of hydrogen ions, underproduction of bicarbonate ions, and overelimination of bicarbonate ions.
• Respiratory acidosis results when any area of respiratory function is impaired, reducing the exchange of oxygen and carbon dioxide, causing CO2 retention.
• Respiratory acidosis results from only one process: retention of CO2, causing increased production of free hydrogen ions.
• Respiratory acidosis is caused by four types of problems: respiratory depression, inadequate chest expansion, airway obstruction, and reduced alveolar-capillary diffusion.
• The hallmark of a base excess acidosis is an ABG result with an elevated pH and an elevated bicarbonate level along with normal oxygen and carbon dioxide levels.
• Remember that metabolic and respiratory acidosis can occur at the same time.
• To manage acidosis, collect data about risk factors related to the development of acidosis, specifically age, nutrition, and presenting symptoms.
• Remember that older adults are more at risk for problems leading to acid-base imbalance, including cardiac, renal, or pulmonary impairment.
• Some manifestations of acidosis include central nervous system, neuromuscular, cardiovascular, respiratory, skin, and behavioral changes.
• The best way to determine acid-base balance and evaluate the effectiveness of therapy is by analyzing arterial blood gases. Arterial blood pH is the laboratory value used to confirm acidosis.
• Be alert for fluid volume changes, decreased cardiac output, falls related to skeletal muscle weakness, impaired memory, ineffective breathing, and fatigue.
• Interventions for metabolic acidosis include hydration and drugs or treatments to control the problem causing the acidosis.
• Interventions for respiratory acidosis aim to maintain a patent airway and enhance gas exchange.
• Assess the airway and oxygenation status of any patient who has acute respiratory acidosis or acute confusion.
• Instruct all patients at continuing risk for respiratory acidosis to stop smoking.
• Advances in surgical techniques, anesthesia, pharmacology, medical devices, and supportive interventions have provided many benefits to perioperative patients.
• Surgical procedures are categorized by the purpose, body location, extent, and degree of urgency.
• The terms outpatient and ambulatory refer to a patient who goes to the surgical area the day of the surgery and returns home on the same day.
• Hospital-based ambulatory surgical centers, freestanding surgical centers, physicians' offices, and ambulatory care centers are common settings.
• More than half of all surgical procedures in North America are performed in ambulatory centers.
• More patients are admitted as inpatients after a procedure than preoperatively.
• Together, patient care provided during the preoperative, intraoperative, and postoperative periods is known as the perioperative experience.
• Perioperative nurses function as an educator, an advocate, and a promoter of health.
• The preoperative period begins when the patient is scheduled for surgery and ends at the time of transfer to the surgical suite.
• Preoperative care focuses on preparing the patient for the surgery, including education and interventions required to reduce anxiety and complications and to promote patient cooperation for postoperative procedures.
• Use at least two appropriate identifiers (e.g., hospital number, the identification band, asking the patient to state his or her name) to identify the patient. Room number or bed numbers are not used to identify patients.
o Ensure that the patient is wearing proper identification, including allergy bracelets, if applicable.
• Patients are screened preoperatively for problems that increase the risk for complications during and after surgery.
o Identify current health problems, potential complications from anesthesia, and complications that may occur after surgery.
o Age, drugs, herbs, and substance use may affect patient responses to anesthesia and pain medication.
o Many chronic illnesses increase surgical risks and need to be considered when planning care.
o Complications from anesthesia occur more often in patients with cardiac problems.
o Pulmonary complications are more likely to occur in older patients, those with chronic respiratory problems, and smokers.
o Sensitivities or allergies to certain substances, especially latex, may cause reactions to anesthetic agents or to perioperative substances.
o Laboratory tests before surgery provide baseline data about the patient's health and help predict potential complications.
o Preoperative imaging studies are based on patient need, medical history, and the nature of the surgical procedure.
o An electrocardiogram may be required for all patients older than a specific age that is to have general anesthesia or for those with a history of or risk for cardiac disease.
o Any abnormal assessment findings are reported to the surgeon and anesthesiology personnel.
o Psychosocial assessment determines the patient's level of anxiety, coping ability, and support systems.
o Most patients have some degree of anxiety before surgery while others may be fearful after surgery.
o Reactions vary according to the type of surgery, perceived effects of the surgery, and potential outcomes.
• Pace the interview to match the learning needs and style of the individual patient.
• Encourage the patient to express his or her feelings regarding the surgical procedure or its possible outcome.
• Explain and provide written information for all diagnostic procedures, restrictions, and follow-up care to the patient and his or her family.
• Communicate any concerns or fears the patient has to the surgeon and anesthesia personnel.
• Communicate to the surgeon and anesthesia personnel any physical or laboratory change that may alter the patient's response to drugs, anesthesia, or surgery.
• Autologous blood donation for surgery can be made by the patient up to 5 weeks before the scheduled surgery date.
• Increased use of bloodless surgery and minimally invasive surgery provide alternatives for patients with religious or medical restrictions to blood transfusions.
• Discharge planning should be started for all patients before surgery by assessing the patient's home environment, self-care capabilities, and support systems.
• Morbidity and mortality during or after surgery are higher in older and chronically ill patients.
• Preoperative education may begin in the surgeon's office for planned or elective surgery using pamphlets, written instructions, and videotapes.
• Information about informed consent, dietary restrictions, bowel and skin preps, exercises after surgery, and plans for pain management promote patients' participation and help achieve the desired outcome.
• Education should be documented in the patient record, including who was involved in teaching, what was taught, and the educational materials given to the patient.
• Ask the patient to explain in his or her own words what surgical procedure is being done and why.
• If the patient's explanation of the scheduled surgery is not consistent with the documentation, notify the surgeon and request that he or she speak to the patient.
• Surgery of any type requires informed consent from the patient or legal guardian.
• Surgical procedures that are site specific, such as left, right, or bilateral, require patient identification before surgery.
o Patient or staff marks the site to ensure the correct site is used.
o Check that documentation for any procedure to be performed on one of a paired organ or extremity clearly indicates which organ or extremity is involved.
• Patients have the right to have or to initiate advance directives, such as a living will or durable power of attorney. Ask the patient if an advance directive has been completed.
• Preoperative drugs may be prescribed to reduce anxiety, promote relaxation, reduce nasal and oral secretions, prevent laryngospasm, reduce vagal-induced bradycardia, inhibit gastric secretions, and decrease the amount of anesthetic needed for the induction and maintenance of anesthesia.
• In the immediate preoperative period, the medical record is reviewed, teaching is reinforced, patient is dressed for surgery, and preoperative drugs are administered.
• On the day of surgery, the patient's usual drug schedule may need to be altered in consultation with the medical physician and anesthesia provider.
• Ensure that dentures and any other personal items are removed from the patient before the patient is transferred to the surgical suite.
• Bowel or intestinal preparations are performed to prevent injury to the colon and to reduce the number of intestinal bacteria when a patient is having major abdominal, pelvic, perineal, or perianal surgery.
• In some cases, a urinary catheter is inserted to prevent injury to bladder and to measure accurate output.
• Prepare the patient for possible postoperative placement of tubes, drains, and vascular access devices.
o Follow Physician's orders for proper care of these devices.
o Monitor proper positioning of patient to maintain patency of tubes, drains, and vascular access devices.
• Teach the patient and family members about exercises and procedures that will be performed after surgery.
o Family members can be helpful in reminding patients to perform these exercises.
o Teaching before surgery reduces apprehension and fear for patients and families.
o Teach patients about dietary restrictions and preoperative preparations.
o Teach the patient specific interventions to perform after surgery to prevent complications, such as incision splinting, deep-breathing exercises, and range-of-motion exercises.
o Discussion, demonstration with return demonstration, and practice by the patient aid in the ability to perform various breathing and leg exercises, including incentive spirometry, coughing, and splinting.
• A certified registered nurse anesthetist (CRNA) is a registered nurse with additional education and credentials who delivers anesthetic agents under supervision.
• The anesthesia provider induces and maintains anesthesia, delivers other drugs as needed, and monitors cardiopulmonary function, capnography, vital signs, and intake and output.
• Perioperative, or operating room, nurses include the holding area nurse, circulating nurse, scrub nurse, and specialty nurse.
• OR nurses use clinical decision-making skills, develop a plan of care, and coordinate care delivery to patients and their family members.
• Holding area nurses work in presurgical holding areas coordinating care, reviewing the medical record and preoperative checklist, verifying that the operative consent forms are signed, and documenting the risk assessment.
• Circulating nurses or "circulators" are registered nurses who coordinate patient's nursing care in the OR, setting up the OR, and ensuring that supplies are available as needed. The circulator may assume the responsibilities of the holding area role.
• The circulator also assists the OR team in the patient transfer to the bed, positioning the patient and protecting bony areas, providing comfort and reassurance, inserting a Foley catheter if needed, and scrubbing the surgical site.
• Scrub nurses set up the sterile field, drape the patient, and hand sterile supplies, sterile equipment, and instruments to the surgeon and the assistant.
• A specially trained person who is not a nurse may perform the scrub role; these include operating room technicians or surgical technologists.
• Correct identification of the patient is the responsibility of every member of the health care team. The patient's identity is verified with two types of identifiers according to hospital policy.
• When the procedure involves a specific site, validating the side on which a procedure is to be performed is the responsibility of each health care professional before and at the time of surgery.
• The Joint Commission now recommends that the patient and the professional who knows the most about the patient (usually the surgeon performing the surgery) mark the surgical site.
• The circulating nurse and anesthesia provider review the patient's medical record in the holding area or the operating room.
• Review preoperative checklist and informed consent forms.
• Review allergies and previous reactions to anesthesia or blood transfusions.
• Highlight any known allergies.
• Apply grounding pads as needed.
• Complete any needed skin preparation.
• Ask the patient when was the last time he or she had anything to eat or drink.
• Assess the patient for tachycardia, increased end-tidal carbon dioxide level, and increased body temperature as indicators of malignant hyperthermia.
• Perform a final assessment for threats to patient safety.
• Report to the surgeon any discrepancy between what type of surgery the patient says is going to be performed and what the informed consent form indicates.
• Check the patient's attire to ensure adherence with facility policy.
• Perform an accurate "sharps" and sponge count with the scrub nurse or surgical technologist.
• Maintain the malignant hyperthermia cart.
• Encourage the patient to express his or her feelings about the surgical procedure or its possible outcome.
• Communicate patient preferences or fears about anesthesia to the anesthesia provider.
• Assess the incision site in the PACU and each shift on the medical-surgical nursing unit.
• Clean surgical wound heals at skin level in about 2 weeks in the absence of trauma, connective tissue disease, malnutrition, infection, or the use of some drugs, such as steroids.
o Smokers, older patients, obese patients, diabetic patients, and those with reduced immunity have delayed wound healing.
o Complete healing of all tissue layers within the wound may take 6 months to 2 years.
• The surgeon usually performs the first dressing change to assess the wound, remove any packing, and advance or remove drains.
• Use aseptic technique during all dressing changes.
• Patients frequently have pain or discomfort after surgery.
• Pain is a subjective experience and may be more intense than the health care professional can appreciate.
• Pain after surgery is related to the surgical wound, tissue manipulation, drains, positioning during surgery, presence of an endotracheal tube, and the patient's experience with pain.
• Priority nursing diagnoses after surgery include impaired gas exchange, impaired skin integrity, acute pain, and potential for hypoxemia.
• Wound infection is a major complication after surgery resulting from contamination during surgery, preoperative infection, debilitation, or immunosuppression.
• If dehiscence or evisceration occurs, apply a sterile nonadherent or saline dressing to the wound, have the patient lie flat with knees bent to reduce intra-abdominal pressure, and notify the surgeon.
• Assess the patient's report of pain to differentiate the pain of angina and myocardial infarction (MI) from other noncardiac causes; discomfort, indigestion, squeezing, heaviness, and viselike are common terms used to describe chest pain of cardiac origin.
• Expand on the description of symptoms by obtaining information about their onset, duration, sequence, frequency, location, quality, intensity, associated symptoms, and precipitating, aggravating, and relieving factors.
• Major symptoms usually identified by patients with CVD include chest pain or discomfort, dyspnea, fatigue, palpitations, weight gain, syncope, and extremity pain.
• Women often present with a "triad" of symptoms, including indigestion or abdominal fullness, chronic fatigue despite adequate rest, and inability to catch one's breath.
• Dyspnea that is associated with activity is referred to as dyspnea on exertion. It is usually an early symptom of heart failure and may be the only symptom in women.
• Extremity pain may be caused by ischemia from atherosclerosis and/or venous insufficiency of the peripheral blood vessels.
• Patients may be classified according to the New York Heart Association's Functional Classification or other system to indicate the degree to which ordinary physical activities are affected by heart disease.
• Physical assessment begins with an assessment of appearance, including general build, skin color, distress level, level of consciousness, shortness of breath, position, and verbal responses.
• Recognize that denial is a common and normal response to help patients cope with threatening circumstances.
• Be aware that coping behaviors of those who have cardiovascular problems vary from patient to patient.
• Allow the patient to express feelings about an actual or perceived loss of health or social status related to cardiovascular disease.
• Assess vital signs carefully in patients having invasive cardiovascular testing; report new dysrhythmias after testing.
• After invasive cardiovascular diagnostic testing, such as angiography and cardiac catheterization, monitor the insertion site for bleeding and hematoma formation.
• Identify patients at risk for cardiovascular disease, especially those with hyperlipidemia, hypertension, excess weight, physical inactivity, smoking, psychological stress, a positive family history, and diabetes.
• Teach patients how to reduce the risk of heart disease through exercise, diet modification, smoking cessation, and medications, as needed.
• The American Heart Association provides guidelines to combat obesity and improve cardiac health include ingesting more nutrient-rich foods which have vitamins, minerals, fiber, and other nutrients, but are low in calories. To get the necessary nutrients, teach patients to choose foods like vegetables, fruits, whole-grain products, and fat-free dairy products most often.
• Inform patients that genetics and other nonmodifiable risk factors, such as family history and gender, contribute to the development of CVD.
• The electrophysiologic properties of cardiac cells regulate heart rate and rhythm.
• Specialized cardiac muscle cells possess unique properties: automaticity, excitability, conductivity, and contractility.
• The cardiac conduction system specialized cells are responsible for the generation and conduction of electrical impulses that cause atrial and ventricular depolarization.
• The conduction system consists of the sinoatrial node, atrioventricular junctional area, and bundle branch system.
• The electrocardiogram (ECG) provides a graphic representation, or picture, of cardiac electrical activity.
• A lead provides one view of the heart's electrical activity, but multiple leads, or views, can be obtained.
• Some units have full-disclosure monitors, which continuously store ECG rhythms in memory up to a certain amount of time, allowing nurses and health care providers to access and print them for more thorough patient assessment and management.
• Routine strips and changes in rhythm are documented in the patient's record.
• Analysis of an ECG rhythm strip requires a systematic approach using a five-step method facilitated by use of a measurement tool called an ECG caliper.
• The five steps consist of determining the heart rate and the rhythm, analyzing P waves, measuring the PR interval, and measuring the QRS duration.
• An 80-lead ECG looks at the heart from 80 views instead of only 12 and gives a 360-degree view of the heart.
o Evaluation of this 80-lead ECG revealed a 15% increase in diagnosing MIs, particularly in the posterior wall which was missed in the 12-lead ECG.
• The Vaughn-Williams classification is commonly used to categorize anti-dysrhythmic drugs according to their effects on the action potential of cardiac cells.
o Class I antidysrhythmics are membrane-stabilizing agents used to decrease automaticity.
o Class II antidysrhythmics control dysrhythmias associated with excessive beta-adrenergic stimulation by competing for receptor sites, and thereby decreasing heart rate and conduction velocity.
o Class III antidysrhythmics lengthen the absolute refractory period and prolong repolarization and the action potential duration of ischemic cells.
o Class IV antidysrhythmics impede the flow of calcium into the cell during depolarization, thereby depressing the automaticity of the SA and AV nodes, decreasing heart rate, and prolonging AV nodal refractory period and conduction.
• Temporary pacing is a nonsurgical intervention that provides a timed electrical stimulus to the heart when either the impulse initiation or the conduction system of the heart is defective.
• Electrical stimuli may be delivered to the right atrium or right ventricle (with single-chamber pacemakers) or to both (with dual-chamber pacemakers).
• Patients with AF who have valvular disease are particularly at risk for venous thromboembolism.
o Monitor patients carefully for these complications.
• Dronedarone (Multaq) is a new drug similar to amiodarone, yet better tolerated by patients, for maintenance of sinus rhythm after cardioversion.
o Dronedarone should not be used in patients with a history or current congestive heart failure because it can cause an exacerbation of cardiac symptoms.
• Noninvasive pacing is an emergency measure to provide demand ventricular pacing in patients with profound bradycardia or asystole. Teach patients to expect possible discomfort.
• Automated external defibrillators are used by medical and lay personnel as an essential intervention for VF.
• Do not perform CPR while the patient is being defibrillated.
• Radiofrequency catheter ablation is an invasive procedure that may be used to abolish an irritable focus causing a supraventricular or ventricular tachydysrhythmia.
• The evidence indicates an increase in the number and complexity of catheter ablation procedures for AF.
• The implantable cardioverter/defibrillator is indicated for patients who have experienced one or more episodes of spontaneous sustained ventricular tachycardia.
• Some patients use a lightweight, automatic wearable cardioverter defibrillator.
• Be very careful to protect patients and staff to prevent electrical injury when assisting with invasive pacemakers, cardioversion, and defibrillation.
• Teach patients with dysrhythmias the correct drug, dose, route, time, and side effects of prescribed medications, and to notify their physicians if adverse effects occur.
• Teach family members where to learn cardiopulmonary resuscitation to decrease their anxiety while living with a patient with dysrhythmias.
• Teach patients the importance of adhering to their prescribed cardiac regimen, such as checking their pulse to ascertain pacemaker function.
• The NRCPR established "Gold Standards" for resuscitation efforts. Data from the NRCPR are used to make CPR process improvements in individual facilities.
• Recent evidence suggests that percutaneous coronary intervention combined with mild therapeutic hypothermia is not associated with increased cardiac or neurological risk.
• Venous disease causes blood to back up into the distal areas and can lead to edema and thromboses that can become emboli, a life-threatening complication.
• Venous thromboembolism refers to deep vein thrombosis and pulmonary embolism, with symptoms of tenderness and pain or asymptomatic.
• Deep vein thrombosis is the most common type of peripheral vascular problem. When symptoms are present, they include swelling, redness, localized pain, and warmth.
• The preferred diagnostic test is venous duplex ultrasonography, a noninvasive test.
• It is most often treated medically using a combination of rest, drug therapy such as anticoagulants, and preventive measures.
• Closely observe the patient receiving anticoagulants or thrombolytics for signs of bleeding and monitor appropriate laboratory values for desired outcome values.
• Inferior vena caval interruption may be indicated for recurrent thrombosis or emboli not responding to treatment and for patients who cannot tolerate anticoagulation.
• Venous insufficiency occurs as a result of prolonged venous hypertension which results in edema, venous stasis ulcers, swelling, and cellulitis.
• Treatment of chronic venous insufficiency is primarily nonsurgical, unless it is complicated by a venous stasis ulcer that requires surgical débridement.
• Varicose veins are distended, protruding veins that appear darkened and tortuous.
• Postoperatively, assess the groin and leg for bleeding through the elastic bandage, keep legs elevated, and perform range-of-motion exercises of the legs at least hourly.
• Radio frequency energy use and laser treatment are alternatives to surgery.
• Teach patients ways to prevent deep vein thrombosis and subsequent embolism. In the hospital setting, provide measures, such as wearing graduated compression stockings, to prevent or manage DVT.
• Teach patients about self-care when they have venous insufficiency.
• An amputation is the removal of a part of the body.
• A traumatic amputation requires rapid emergency care to possibly save the severed body part for reattachment and prevent hemorrhage.
• Advances in microvascular surgical procedures, antibiotic therapy, and improved surgical techniques for trauma and bone neoplasm help to reduce the incidence of amputation.
• The psychosocial aspects of the procedure are often more devastating than the physical impairments that result since the loss is complete and permanent.
• Collaborate with members of the health care team, including prosthetists, rehabilitation therapists, psychologists, case managers, and physiatrists when providing care to the patient who has an amputation. Collaborate with the rehabilitation therapists to improve ambulation and/or enable the patient to be independent in ADLs.
• The most common complications of elective or traumatic amputations are hemorrhage, infection, phantom limb pain, neuroma, and flexion contractures.
• Phantom limb pain is a frequent complication of amputation where sensation is felt in the amputated part after surgery, but is more common in patients who had chronic limb pain before surgery and rare in those who have traumatic amputations.
• Observe for hemorrhage and infection in the patient having an amputation.
• Postoperatively, assess for and promptly manage phantom limb pain in the patient who has an amputation; collaborate with specialists to incorporate complementary and alternative therapies into the patient's plan of care.
• Several community organizations, such as the Amputee Coalition of America, are available to help patients and their families cope with the loss of a body part.
• Recognize that the patient having an amputation may need to adjust to an altered lifestyle; however, new custom prosthetics improve mobility.
• Help the patient with an amputation or other musculoskeletal trauma and the family to set realistic outcomes and take one day at a time.
• For patients with severe trauma or amputation, assess coping skills and encourage verbalization.